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Prologue 
PARTI From the Beginning... 


WO ON DU BRWNY 


A 
© 


. Captured in a Bottle 

. The Deaf to Hear, and the Lame to Walk 

. Electrical Sensitivity 

. The Road Not Taken 

. Chronic Electrical Illness 

. The Behavior of Plants 

. Acute Electrical Illness 

. Mystery on the Isle of Wight 

. Earth's Electric Envelope 

. Porphyrins and the Basis of Life 

PART II .. 
11. 
12, 
13. 
14. 
15. 
16. 


. To the Present 

Irritable Heart 

The Transformation of Diabetes 
Cancer and the Starvation of Life 
Suspended Animation 

You mean you can hear electricity? 
Bees, Birds, Trees, and Humans 


Photographs 


[7 


Notes 


In the Land of the Blind 


Bibliography 


About the Author 


Prologue 





So weak were the cosmic 
radio waves that they would have been invisible, and so life never 
developed organs that could see them. 

The even longer waves, the low-frequency pulsations given off by 
lightning, are also invisible. When lightning flashes, it momentarily fills the 
air with them, but they are almost gone in an instant; their echo, 
reverberating around the world, is roughly ten billion times weaker than the 
light from the sun. We never evolved organs to see this either. 

But our bodies know that those colors are there. The energy of our cells 
whispering in the radio frequency range is infinitesimal but necessary for 
life. Every thought, every movement that we make surrounds us with low 
frequency pulsations, whispers that were first detected in 1875 and are also 
necessary for life. The electricity that we use today, the substance that we 
send through wires and broadcast through the air without a thought, was 
identified around 1700 as a property of life. Only later did scientists learn to 
extract it and make it move inanimate objects, ignoring—because they 
could not see—its effects on the living world. It surrounds us today, in all of 
its colors, at intensities that rival the light from the sun, but we still cannot 
see it because it was not present at life’s birth. 


We live today with a number of devastating diseases that do not belong 
here, whose origin we do not know, whose presence we take for granted and 
no longer question. What it feels like to be without them is a state of vitality 
that we have completely forgotten. 

" Anxiety disorder," afflicting one-sixth of humanity, did not exist before 
the 1860s, when telegraph wires first encircled the earth. No hint of it 
appears in the medical literature before 1866. 

Influenza, in its present form, was invented in 1889, along with 
alternating current. It is with us always, like a familiar guest—so familiar 
that we have forgotten that it wasn't always so. Many of the doctors who 
were flooded with the disease in 1889 had never seen a case before. 

Prior to the 1860s, diabetes was so rare that few doctors saw more than 
one or two cases during their lifetime. It, too, has changed its character: 
diabetics were once skeletally thin. Obese people never developed the 
disease. 

Heart disease at that time was the twenty-fifth most common illness, 
behind accidental drowning. It was an illness of infants and old people. It 
was extraordinary for anyone else to have a diseased heart. 

Cancer was also exceedingly rare. Even tobacco smoking, in non- 
electrified times, did not cause lung cancer. 





PARI ONE 





1. Captured in a Bottle 





His midwives—Kleist, Cunaeus, Allamand, and Musschenbroek— 
warned that they had helped give birth to an enfant terrible, whose shocks 
could take away your breath, boil your blood, paralyze you. The public 
should have listened, been more cautious. But of course the colorful reports 
of those scientists only encouraged the crowds. 

Pieter van Musschenbroek, professor of physics at the University of 
Leyden, had been using his usual friction machine. It was a glass globe that 
he spun rapidly on its axis while he rubbed it with his hands to produce the 
“electric fluid”—what we know today as static electricity. Hanging from the 
ceiling by silk cords was an iron gun barrel, almost touching the globe. It 
was called the “prime conductor,” and was normally used to draw sparks of 
static electricity from the rubbed, rotating glass sphere. 


Mani. do Lido. R. doa Se t748. pag Y3 plL. 








Llassrare rwie. 


Line engraving from Mémoires de l’Académie Royale des Sciences Plate 1, p. 23, 1746 


But electricity, in those early days, was of limited use, because it always 
had to be produced on the spot and there was no way to store it. So 
Musschenbroek and his associates designed an ingenious experiment—an 
experiment that changed the world forever: they attached a wire to the other 
end of the prime conductor and inserted it in a small glass bottle partly 
filled with water. They wanted to see if the electric fluid could be stored in 
a jar. And the attempt succeeded beyond their wildest expectations. 

“I am going to tell you about a new but terrible experiment,” 
Musschenbroek wrote to a friend in Paris, “which I advise you never to try 
yourself, nor would I, who have experienced it and survived by the grace of 


God, do it again for all the Kingdom of France." He held the bottle in his 
right hand, and with the other hand he tried to draw sparks from the gun 
barrel. *Suddenly my right hand was hit with such force, that my whole 
body shook as though struck by lightning. The glass, although thin, did not 
break, and my hand was not knocked away, but my arm and whole body 
were affected more terribly than I can express. In a word, I thought I was 
done for.”! His companion in invention, biologist Jean Nicolas Sébastien 
Allamand, when he tried the experiment, felt a “prodigious blow.” “I was so 
stunned,” he said, “that I could not breathe for some moments.” The pain 
along his right arm was so intense that he feared permanent injury.” 

But only half the message registered with the public. The fact that 
people could be temporarily or, as we will see, permanently injured or even 
killed by these experiments became lost in the general excitement that 
followed. Not only lost, but soon ridiculed, disbelieved, and forgotten. Then 
as now, it was not socially acceptable to say that electricity was dangerous. 
Just two decades later, Joseph Priestley, the English scientist who is famous 
for his discovery of oxygen, wrote his History and Present State of 
Electricity, in which he mocked the “cowardly professor” Musschenbroek, 
and the “exaggerated accounts" of the first experimenters.? 

Its inventors were not the only ones who tried to warn the public. 
Johann Heinrich Winkler, professor of Greek and Latin at Leipzig, 
Germany, tried the experiment as soon as he heard about it. *I found great 
convulsions in my body," he wrote to a friend in London. *It put my blood 
into great agitation; so that I was afraid of an ardent fever; and was obliged 
to use refrigerating medicines. I felt a heaviness in my head, as if I had a 
stone lying upon it. It gave me twice a bleeding at my nose, to which I am 
not inclined. My wife, who had only received the electrical flash twice, 
found herself so weak after it, that she could hardly walk. A week after, she 
received only once the electrical flash; a few minutes after it she bled at the 
nose." 

From their experiences Winkler took away the lesson that electricity was 
not to be inflicted upon the living. And so he converted his machine into a 
great beacon of warning. “I read in the newspapers from Berlin," he wrote, 
“that they had tried these electrical flashes upon a bird, and had made it 


suffer great pain thereby. I did not repeat this experiment; for I think it 
wrong to give such pain to living creatures." He therefore wrapped an iron 
chain around the bottle, leading to a piece of metal underneath the gun 
barrel. *When then the electrification is made," he continued, *the sparks 
that fly from the pipe upon the metal are so large and so strong, that they 
can be seen (even in the day time) and heard at the distance of fifty yards. 
They represent a beam of lightning, of a clear and compact line of fire; and 
they give a sound that frightens the people that hear it." 

The general public did not react as he planned, however. After reading 
reports like Musschenbroek's in the proceedings of France's Royal 
Academy of Sciences, and his own in the Philosophical Transactions of the 
Royal Society of London, eager men and women by the thousands, all over 
Europe, lined up to give themselves the pleasure of electricity. 

Abbé Jean Antoine Nollet, a theologian turned physicist, introduced the 
magic of the Leyden jar into France. He tried to satisfy the insatiable 
demands of the public by electrifying tens, hundreds of people at once, 
having them take each other by the hand so as to form a human chain, 
arranged in a large circle with the two ends close together. He would place 
himself at one of the ends, while the person who represented the last link 
took hold of the bottle. Suddenly the learned abbot, touching with his hand 
the metal wire inserted in the flask, would complete the circuit and 
immediately the shock would be felt simultaneously by the whole line. 
Electricity had become a social affair; the world was possessed, as some 
Observers called it, by *electromania." 

The fact that Nollet had electrocuted several fish and a sparrow with the 
same equipment did not deter the crowds in the least. At Versailles, in the 
presence of the king, he electrified a company of 240 soldiers of the French 
Guard holding each other by the hands. He electrified a community of 
monks at the Carthusian monastery in Paris, stretched out in a circle more 
than a mile around, each connected to his neighbors by iron wires. 

The experience became so popular that the public began to complain of 
not being able to give themselves the pleasure of an electric shock without 
having to wait in line or consult a physician. A demand was created for a 
portable apparatus that everyone could purchase for a reasonable price and 


enjoy at their leisure. And so the “Ingenhousz bottle?” was invented. 
Enclosed in an elegant-looking case, it was a small Leyden jar joined to a 
varnished silk ribbon and a rabbit skin with which to rub the varnish and 
charge the jar.^ 

Electric canes were sold, “priced for all pocketbooks.”> These were 
Leyden jars cleverly disguised as walking canes, which you could charge 
surreptitiously and trick unsuspecting friends and acquaintances into 
touching. 

Then there was the “electric kiss,’ a form of recreation that even 
preceded the invention of the Leyden jar but became much more exciting 
afterwards. Physiologist Albrecht von Haller, at the University of 
Göttingen, declared incredulously that such parlor games had “taken the 
place of quadrille.” “Could one believe,” he wrote, “that a lady’s finger, that 
her whale-bone petticoat, should send forth flashes of true lightning, and 
that such charming lips could set on fire a house?” 








| 


Line engraving c. 1750, reproduced in Jürgen Teichmann, Vom Bernstein zum Elektron, Deutsches 
Museum 1982 


She was an "angel," wrote German physicist Georg Matthias Bose, with 
“white-swan neck” and “blood-crowned breasts,” who “steals your heart 
with a single glance” but whom you approach at your peril. He called her 
“Venus Electrificata” in a poem, published in Latin, French, and German, 
that became famous throughout Europe: 


If a mortal only touches her hand 

Of such a god-child even only her dress, 

The sparks burn the same, through all of one’s limbs, 
As painful as it is, he seeks it again. 


Even Benjamin Franklin felt compelled to give instructions: *Let A and 
B stand on wax; or A on wax and B on the floor; give one of them the 
electrised phial in hand; let the other take hold of the wire; there will be a 
small spark; but when their lips approach, they will be struck and shock’d.”® 

Wealthy ladies hosted such entertainment in their homes. They hired 
instrument makers to craft large, ornate electrical machines that they 
displayed like pianos. People of more moderate means bought off-the-shelf 
models that were available in an assortment of sizes, styles, and prices. 

Aside from entertainment, electricity, assumed to be related to or 
identical with the life force, was used primarily for its medical effects. Both 
electrical machines and Leyden jars found their way into hospitals, and into 
the offices of doctors wanting to keep up with the times. An even greater 
number of “electricians” who were not medically trained set up office and 
began treating patients. One reads of medical electricity being used during 
the 1740s and 1750s by practitioners in Paris, Montpellier, Geneva, Venice, 
Turin, Bologna, Leipzig, London, Dorchester, Edinburgh, Shrewsbury, 
Worcester, Newcastle-Upon-Tyne, Uppsala, Stockholm, Riga, Vienna, 
Bohemia, and The Hague. 

The famous French revolutionary and doctor Jean-Paul Marat, also a 
practitioner of electricity, wrote a book about it titled Mémoire sur 
l'électricité médicale (“Memoir on Medical Electricity”). 

Franklin treated patients with electricity in Philadelphia—so many of 
them that static electric treatments later became known, in the nineteenth 
century, as “franklinization.” 

John Wesley, the founder of the Methodist Church, published a 72-page 
tract in 1759 titled Desideratum; or, Electricity Made Plain and Useful. He 
called electricity “the noblest Medicine yet known in the World,” to be used 
in diseases of the nervous system, skin, blood, respiratory system, and 
kidneys. “A person standing on the ground,” he felt obliged to add, “cannot 
easily kiss an electrified person standing on the rosin.”” Wesley himself 
electrified thousands of people at the headquarters of the Methodist 
movement and at other locations around London. 

And it wasn’t just prominent individuals who were setting up shop. So 
many non-medical people were buying and renting machines for medical 


use that London physician James Graham wrote, in 1779: “I tremble with 
apprehension for my fellow creatures, when I see in almost every street in 
this great metropolis a barber — a surgeon — a tooth-drawer — an apothecary, 
or a common mechanic turned electrical operator." 

Since electricity could initiate contractions of the uterus, it became a 
tacitly understood method of obtaining abortions. Francis Lowndes, for 
example, was a London electrician with an extensive practice who 
advertised that he treated poor women gratis *for amenorrhea."? 

Even farmers began testing electricity on their crops and proposing it as 
a means of improving agricultural production, as we will see in chapter 6. 

The use of electricity on living beings in the eighteenth century was so 
widespread in Europe and America that a wealth of valuable knowledge 
was collected about its effects on people, plants, and animals, knowledge 
that has been entirely forgotten, that is far more extensive and detailed than 
what today’s doctors are aware of, who see daily, but without recognition, 
its effects on their patients, and who do not even know such knowledge ever 
existed. This information is both formal and informal—letters from 
individuals describing their experiences; accounts written up in newspapers 
and magazines; medical books and treatises; papers read at meetings of 
scientific societies; and articles published in newly founded scientific 
journals. 

As early as the 1740s, ten percent of all articles published in the 
Philosophical Transactions were related to electricity. And during the last 
decade of that century, fully seventy percent of all articles on electricity in 
the prestigious Latin journal, Commentarii de rebus in scientis naturali et 
medicina gestis, had to do with its medical uses and its effects on animals 
and people.!? 

But the floodgates were wide open, and the torrent of enthusiasm about 
electricity rushed on unhindered, and would continue to do so during the 
coming centuries, sweeping caution against the rocks, crushing hints of 
danger like so many bits of driftwood, obliterating whole tracts of 
knowledge and reducing them to mere footnotes in the history of invention. 


2. The Deaf to Hear, and the Lame to 
Walk 


A BURMESE ELEPHANT has the same set of genes whether it toils in a 
logging camp or runs free in the forest. But its DNA will not tell you the 
details of its life. In the same way, electrons cannot tell us what is most 
interesting about electricity. Like elephants, electricity has been forced to 
bear our burdens and move great loads, and we have worked out more or 
less precisely its behavior while in captivity. But we must not be fooled into 
believing we know everything important about the lives of its wild cousins. 

What is the source of thunder and lightning, that causes clouds to 
become electrified and discharge their fury upon the earth? Science still 
does not know. Why does the earth have a magnetic field? What makes 
combed hair frizzy, nylon cling, and party balloons stick to walls? This 
most common of all electrical phenomena is still not well understood. How 
does our brain work, our nerves function, our cells communicate? How is 
our body's growth choreographed? We are still fundamentally ignorant. 
And the question raised in this book— "What is the effect of electricity on 
life?"—,is one that modern science doesn't even ask. Science’s only concern 
today is to keep human exposure be-low a level that will cook your cells. 
The effect of nonlethal electricity is something mainstream science no 
longer wants to know. But in the eighteenth century, scientists not only 
asked the question, but began to supply answers. 

Early friction machines were capable of being charged to about ten 
thousand volts—enough to deliver a stinging shock, but not enough, then or 
now, to be thought dangerous. By way of comparison, a person can 
accumulate thirty thousand volts on their body in walking across a synthetic 
carpet. Discharging it stings, but won't kill you. 


A one-pint Leyden jar could deliver a more powerful shock, containing 
about 0.1 joules of energy, but still about a hundred times less than what is 
thought to be hazardous, and thousands of times less than shocks that are 
routinely delivered by defibrillators to revive people who are in cardiac 
arrest. According to mainstream science today, the sparks, shocks, and tiny 
currents used in the eighteenth century should have had no effects on 
health. But they did. 

Imagine you were a patient in 1750 suffering from arthritis. Your 
electrician would seat you in a chair that had glass legs so that it was well 
insulated from the ground. This was done so that when you were connected 
to the friction machine, you would accumulate the "electric fluid" in your 
body instead of draining it into the earth. Depending on the philosophy of 
your electrician, the severity of your disease, and your own tolerance for 
electricity, there were a number of ways to “electrize” you. In the “electric 
bath," which was the most gentle, you would simply hold in your hand a 
rod connected to the prime conductor, and the machine would be cranked 
continuously for minutes or hours, communicating its charge throughout 
your body and creating an electrical *aura" around you. If this was done 
gently enough, you would feel nothing— just as a person who shuffles their 
feet on a carpet can accumulate a charge on their body without being aware 
of it. 

After you were thus “bathed,” the machine would be stopped and you 
might be treated with the “electric wind.” Electricity discharges most easily 
from pointed conductors. Therefore a grounded, pointed metal or wooden 
wand would be brought toward your painful knee and you would again feel 
very little—perhaps the sensation of a small breeze as the charge that had 
built up in your body slowly dissipated through your knee into the grounded 
wand. 

For a stronger effect, your electrician might use a wand with a rounded 
end, and instead of a continuous current draw actual sparks from your ailing 
knee. And if your condition were severe—say your leg was paralyzed—he 
could charge up a small Leyden jar and give your leg a series of strong 
shocks. 


Electricity was available in two flavors: positive, or “vitreous” 
electricity, obtained by rubbing glass, and negative, or “resinous” 
electricity, originally obtained by rubbing sulfur or various resins. Your 
electrician would most likely treat you with positive electricity, as it was the 
variety normally found on the surface of the body in a state of health. 

The goal of electrotherapy was to stimulate health by restoring the 
electrical equilibrium of the body where it was out of balance. The idea was 
certainly not new. In another part of the world, the use of natural electricity 
had been developed to a fine art over thousands of years. Acupuncture 
needles, as we will see in chapter 9, conduct atmospheric electricity into the 
body, where it travels along precisely mapped pathways, returning to the 
atmosphere through other needles that complete the circuit. By comparison 
electrotherapy in Europe and America, although similar in concept, was an 
infant science, using instruments that were like sledgehammers. 

European medicine in the eighteenth century was full of 
sledgehammers. If you went to a conventional doctor for your rheumatism, 
you might expect to be bled, purged, vomited, blistered, and even dosed 
with mercury. It’s easy to understand that going to an electrician instead 
might seem a very attractive alternative. And it remained attractive until the 
beginning of the twentieth century. 

After more than half a century of unceasing popularity, electrotherapy 
fell temporarily out of favor during the early 1800s in reaction to certain 
cults, one of which had grown up in Europe around Anton Mesmer and his 
so-called “magnetic” healing, and another in America around Elisha 
Perkins and his “electric” tractors—three-inch-long metallic pencils with 
which one made passes over a diseased part of the body. Neither man used 
actual magnets or electricity at all, but they gave both those methods, for a 
while, a bad name. By mid-century electricity was again mainstream, and in 
the 1880s ten thousand American physicians were administering it to their 
patients. 

Electrotherapy finally fell permanently out of favor in the early 
twentieth century, perhaps, one suspects, because it was incompatible with 
what was then going on in the world. Electricity was no longer a subtle 
force that had anything to do with living things. It was a dynamo, capable 


of propelling locomotives and executing prisoners, not curing patients. But 
sparks delivered by a friction machine, a century and a half before the 
world was wired, carried quite different associations. 

There is no doubt that electricity sometimes cured diseases, both major 
and minor. The reports of success, over almost two centuries, were 
sometimes exaggerated, but they are too numerous and often too detailed 
and well-attested to dismiss them all. Even in the early 1800s, when 
electricity was not in good repute, reports continued to emerge that cannot 
be ignored. For example, the London Electrical Dispensary, between 
September 29, 1793, and June 4, 1819, admitted 8,686 patients for electrical 
treatment. Of these, 3,962 were listed as “cured,” and another 3,308 as 
"relieved" when they were discharged—an 84 percent success rate.! 

Although the main focus of this chapter will be on effects that are not 
necessarily beneficial, it is important to remember why eighteenth century 
society was enthralled with electricity, just as we are today. For almost three 
hundred years the tendency has been to chase its benefits and dismiss its 
harms. But in the 1700s and 1800s, the daily use of electricity in medicine 
was a constant reminder, at least, that electricity was intimately connected 
with biology. Here in the West, electricity as a biological science remains in 
its infancy today, and even its cures have been long forgotten. I will recall 
just one of them. 


Making the Deaf Hear 

In 1851, the great neurologist Guillaume Benjamin Duchenne de Boulogne 
achieved renown for something for which he is least remembered today. A 
well-known figure in the history of medicine, he was certainly no quack. He 
introduced modern methods of physical examination that are still in use. He 
was the first physician ever to take a biopsy from a living person for the 
purpose of diagnosis. He published the first accurate clinical description of 
polio. A number of diseases that he identified are named for him, most 
notably Duchenne muscular dystrophy. He is remembered for all those 
things. But in his own time he was the somewhat unwilling center of 
attention for his work with the deaf. 


Duchenne knew the anatomy of the ear in great detail, in fact it was for 
the purpose of elucidating the function of the nerve called the chorda 
tympani, which passes through the middle ear, that he asked a few deaf 
people to volunteer to be the subjects of electrical experiments. The 
incidental and unexpected improvement in their hearing caused Duchenne 
to be inundated with requests from within the deaf community to come to 
Paris for treatments. And so he began to minister to large numbers of people 
with nerve deafness, using the same apparatus that he had designed for his 
research, which fit snugly into the ear canal and contained a stimulating 
electrode. 

His procedure, to a modern reader, might seem unlikely to have had any 
effect at all: he exposed his patients to pulses of the feeblest possible 
current, spaced half a second apart, for five seconds at a time. Then he 
gradually increased the current strength, but never to a painful level, and 
never for more than five seconds at a time. And yet by this means he 
restored good hearing, in a matter of days or weeks, to a 26-year-old man 
who had been deaf since age ten, a 21-year-old man who had been deaf 
since he had measles at age nine, a young woman recently made deaf by an 
overdose of quinine, given for malaria, and numerous others with partial or 
complete hearing loss.? 

Fifty years earlier, in Jever, Germany, an apothecary named Johann 
Sprenger became famous throughout Europe for a similar reason. Though 
he was denounced by the director of the Institute for the Deaf and Dumb in 
Berlin, he was besieged by the deaf themselves with requests for treatment. 
His results were attested in court documents, and his methods were adopted 
by contemporary physicians. He himself was reported to have fully or 
partially restored hearing to no less than forty deaf and hard of hearing 
individuals, including some deaf from birth. His methods, like Duchenne's, 
were disarmingly simple and gentle. He made the current weaker or 
stronger according to the sensitivity of his patient, and each treatment 
consisted of brief pulses of electricity spaced one second apart for a total of 
four minutes per ear. The electrode was placed on the tragus (the flap of 
cartilage in front of the ear) for one minute, inside the ear canal for two 
minutes, and on the mastoid process behind the ear for one minute. 


And fifty years before Sprenger, Swedish physician Johann Lindhult, 
writing from Stockholm, reported the full or partial restoration of hearing, 
during a two-month period, to a 57-year-old man who had been deaf for 
thirty-two years; a youth of twenty-two, whose hearing loss was recent; a 
seven-year-old girl, born deaf; a youth of twenty-nine, hard of hearing since 
age eleven; and a man with hearing loss and tinnitus of the left ear. “All 
patients," wrote Lindhult, *were treated with gentle electricity, either the 
simple current or the electric wind." 

Lindhult, in 1752, was using a friction machine. Half a century later, 
Sprenger used galvanic currents from an electric pile, forerunner of today's 
batteries. Half a century after that, Duchenne used alternating current from 
an induction coil. British surgeon Michael La Beaume, similarly successful, 
used a friction machine in the 1810s and galvanic currents later on. What 
they all had in common was their insistence on keeping their treatments 
brief, simple, and painless. 


Seeing and Tasting Electricity 

Aside from attempting to cure deafness, blindness, and other diseases, early 
electricians were intensely interested in whether electricity could be directly 
perceived by the five senses—another question about which modern 
engineers have no interest, and modern doctors have no knowledge, but 
whose answer is relevant to every modern person who suffers from 
electrical sensitivity. 

When he was still in his early twenties, the future explorer Alexander 
von Humboldt lent his own body to the elucidation of this mystery. It would 
be several years before he left Europe on the long voyage that was to propel 
him far up the Orinoco River and to the top of Mount Chimborazo, 
collecting plants as he went, making systematic observations of the stars 
and the earth and the cultures of Amazonian peoples. Half a century would 
pass before he would begin work on his five-volume Kosmos, an attempt to 
unify all existing scientific knowledge. But as a young man supervising 
mining operations in the Bayreuth district of Bavaria, the central question 
of his day occupied his spare time. 


Is electricity really the life force, people were asking? This question, 
gnawing gently at the soul of Europe since the days of Isaac Newton, had 
suddenly become insistent, forcing itself out of the lofty realms of 
philosophy and into dinnertime discussions around the tables of ordinary 
people whose children would have to live with the chosen answer. The 
electric battery, which produced a current from the contact of dissimilar 
metals, had just been invented in Italy. Its implications were huge: friction 
machines—bulky, expensive, unreliable, subject to atmospheric conditions 
—might no longer be necessary. Telegraph systems, already designed by a 
few visionaries, might now be practical. And questions about the nature of 
the electric fluid might come closer to being answered. 

In the early 1790s, Humboldt threw himself into this research with 
enthusiasm. He wished, among other things, to determine whether he could 
perceive this new form of electricity with his own eyes, ears, nose, and taste 
buds. Others were doing similar experiments—Alessandro Volta in Italy, 
George Hunter and Richard Fowler in England, Christoph Pfaff in 
Germany, Peter Abilgaard in Denmark—but none more thoroughly or 
diligently than Humboldt. 

Consider that today we are accustomed to handling nine-volt batteries 
with our hands without a thought. Consider that millions of us are walking 
around with silver and zinc, as well as gold, copper, and other metals in the 
fillings in our mouths. Then consider the following experiment of 
Humboldt’s, using a single piece of zinc, and one of silver, that produced an 
electric tension of about a volt: 

“A large hunting dog, naturally lazy, very patiently let a piece of zinc be 
applied against his palate, and remained perfectly tranquil while another 
piece of zinc was placed in contact with the first piece and with his tongue. 
But scarcely one touched his tongue with the silver, than he showed his 
aversion in a humorous manner: he contracted his upper lip convulsively, 
and licked himself for a very long time; it sufficed afterwards to show him 
the piece of zinc to remind him of the impression he had experienced and to 
make him angry.” 

The ease with which electricity can be perceived, and the variety of the 
sensations, would be a revelation to most doctors today. When Humboldt 


touched the top of his own tongue with the piece of zinc, and its point with 
the piece of silver, the taste was strong and bitter. When he moved the piece 
of silver underneath, his tongue burned. Moving the zinc further back and 
the silver forward made his tongue feel cold. And when the zinc was moved 
even further back he became nauseated and sometimes vomited—which 
never happened if the two metals were the same. The sensations always 
occurred as soon as the zinc and silver pieces were placed in metallic 
contact with each other.’ 

A sensation of sight was just as easily elicited, by four different 
methods, using the same one-volt battery: by applying the silver “armature” 
on one moistened eyelid and the zinc on the other; or one in a nostril and 
the other on an eye; or one on the tongue and one on an eye; or even one on 
the tongue and one against the upper gums. In each case, at the moment the 
two metals touched each other, Humboldt saw a flash of light. If he repeated 
the experiment too many times, his eyes became inflamed. 

In Italy, Volta, the inventor of the electric battery, succeeded in eliciting 
a sensation of sound, not with one pair of metals, but with thirty, attached to 
electrodes in each ear. With the metals he originally used in his “pile,” using 
water as an electrolyte, this may have been about a twenty-volt battery. 
Volta heard only a crackling sound which could have been a mechanical 
effect on the bones of his middle ears, and he did not repeat the experiment, 
fearing that the shock to his brain might be dangerous.‘ It remained for 
German physician Rudolf Brenner, seventy years later, using more refined 
equipment and smaller currents, to demonstrate actual effects on the 
auditory nerve, as we will see in chapter 15. 


Speeding up the Heart and Slowing it Down 

Back in Germany, Humboldt, armed with the same single pieces of zinc and 
silver, turned his attention next to the heart. Together with his older brother 
Wilhelm, and supervised by well-known physiologists, Humboldt removed 
the heart of a fox and prepared one of its nerve fibers so that the armatures 
could be applied to it without touching the heart itself. “At each contact 
with the metals the pulsations of the heart were clearly changed; their 


speed, but especially their force and their elevation were augmented," he 
recorded. 

The brothers next experimented on frogs, lizards, and toads. If the 
dissected heart beat 21 times in a minute, after being galvanized it beat 38 
to 42 times in a minute. If the heart had stopped beating for five minutes, it 
restarted immediately upon contact with the two metals. 

Together with a friend in Leipzig, Humboldt stimulated the heart of a 
carp that had almost stopped beating, pulsing only once every four minutes. 
After massaging the heart proved to have no effect, galvanization restored 
the rate to 35 beats per minute. The two friends kept the heart beating for 
almost a quarter of an hour by repeated stimulation with a single pair of 
dissimilar metals. 

On another occasion, Humboldt even managed to revive a dying linnet 
that was lying feet up, eyes closed on its back, unresponsive to the prick of 
a pin. *I hastened to place a small plate of zinc in its beak and a small piece 
of silver in its rectum," he wrote, “and I immediately established a 
communication between the two metals with an iron rod. What was my 
astonishment, when at the moment of contact the bird opened its eyes, 
raised itself on its feet and beat its wings. It breathed again for six or eight 
minutes and then calmly died."^ 

Nobody proved that a one-volt battery could restart a human heart, but 
scores of observers before Humboldt had reported that electricity increased 
the human pulse rate—knowledge that is not possessed by doctors today. 
German physicians Christian Gottlieb Kratzenstein®é and Carl Abraham 
Gerhard,’ German physicist Celestin Steiglehner,®? Swiss physicist Jean 
Jallabert,? French physicians François Boissier de Sauvages de la Croix," 
Pierre Mauduyt de la Varenne," and Jean-Baptiste Bonnefoy,? French 
physicist Joseph Sigaud de la Fond, and Italian physicians Eusebio 
Sguario'^ and Giovan Giuseppi Veratti!^ were just a few of the observers 
who reported that the electric bath increased the pulse rate by anywhere 
from five to thirty beats per minute, when positive electricity was used. 
Negative electricity had the opposite effect. In 1785, Dutch pharmacist 
Willem van Barneveld conducted 169 trials on 43 of his patients—men, 
women, and children aged nine to sixty—finding an average five percent 


increase in the pulse rate when the person was bathed with positive 
electricity, and a three percent decrease in the pulse rate when the person 
was bathed with negative electricity.'? When positive sparks were drawn the 
pulse increased by twenty percent. 

But these were only averages: no two individuals reacted the same to 
electricity. One person's pulse always increased from sixty to ninety beats 
per minute; another's always doubled; another's pulse became much 
slower; another reacted not at all. Some of van Barneveld's subjects reacted 
in a manner opposite to the majority: a negative charge always accelerated 
their pulse, while a positive charge slowed it down. 


“Tstupidimento” 

Observations of these kinds came quickly and abundantly, so that by the 
end of the eighteenth century a basic body of knowledge had been built up 
about the effects of the electric fluid—usually the positive variety—on the 
human body. It increased both the pulse rate, as we have seen, and the 
strength of the pulse. It augmented all of the secretions of the body. 
Electricity caused salivation, and made tears to flow, and sweat to run. It 
caused the secretion of ear wax, and nasal mucus. It made gastric juice flow, 
stimulating the appetite. It made milk to be let down, and menstrual blood 
to issue. It made people urinate copiously and move their bowels. 

Most of these actions were useful in electrotherapy, and would continue 
to be so until the early twentieth century. Other effects were purely 
unwanted. Electrification almost always caused dizziness, and sometimes a 
sort of mental confusion, or “istupidimento,” as the Italians called it." It 
commonly produced headaches, nausea, weakness, fatigue, and heart 
palpitations. Sometimes it caused shortness of breath, coughing, or asthma- 
like wheezing. It often caused muscle and joint pains, and sometimes 
mental depression. Although electricity usually caused the bowels to move, 
often with diarrhea, repeated electrification could result in constipation. 

Electricity caused both drowsiness and insomnia. 

Humboldt, in experiments on himself, found that electricity increased 
blood flow from wounds, and caused serum to flow copiously out of 
blisters.!® Gerhard divided one pound of freshly drawn blood into two equal 


parts, placed them next to each other, and electrified one of them. The 
electrified blood took longer to clot.'? Antoine Thillaye-Platel, pharmacist 
at the Hótel-Dieu, the famous hospital in Paris, agreeing, said that 
electricity is contraindicated in cases of hemorrhage.” Consistent with this 
are numerous reports of nosebleeds from electrification. Winkler and his 
wife, as already mentioned, got nosebleeds from the shock of a Leyden jar. 
In the 1790s, Scottish physician and anatomist Alexander Monro, who is 
remembered for discovering the function of the lymphatic system, got 
nosebleeds from just a one-volt battery, whenever he tried to elicit the 
sensation of light in his eyes. “Dr. Monro was so excitable by galvanism 
that he bled from the nose when, having the zinc very gently inserted in his 
nasal fossae, he put it in contact with an armature applied to his tongue. The 
hemorrhage always took place at the moment when the lights appeared.” 
This was reported by Humboldt.? In the early 1800s, Conrad Quensel, in 
Stockholm, reported that galvanism "frequently" caused nosebleeds.?? 


Recherches fur lElectricité 5$Disc Plo." Pag. 4o22 





Line engraving from Abbé Nollet, Recherches sur les Causes Particulières des Phénomènes 
Électriques, Paris: Frères Guérin, 1753 


Abbé Nollet proved that at least one of these effects—perspiration— 
occurred merely from being in an electric field. Actual contact with the 
friction machine wasn’t even necessary. He had electrified cats, pigeons, 
several kinds of songbirds, and finally human beings. In carefully 
controlled repeatable experiments, accompanied by modern-looking data 
tables, he had demonstrated measurable weight loss in all of his electrified 
subjects, due to an increase in evaporation from their skin. He had even 
electrified five hundred houseflies in a gauze-covered jar for four hours and 


found that they too had lost extra weight—4 grains more than their non- 
electrified counterparts in the same amount of time. 

Then Nollet had the idea to place his subjects on the floor underneath 
the electrified metal cage instead of in it, and they still lost as much, and 
even a bit more weight than when they were electrified themselves. Nollet 
had also observed an acceleration in the growth of seedlings sprouted in 
electrified pots; this too occurred when the pots were only placed on the 
floor beneath. “Finally,” wrote Nollet, “I made a person sit for five hours on 
a table near the electrified metal cage.” The young woman lost 4% drams 
more weight than when she had actually been electrified herself.” 

Nollet was thus the first person, back in 1753, to report significant 
biological effects from exposure to a DC electric field—the kind of field 
that according to mainstream science today has no effect whatsoever. His 
experiment was later replicated, using a bird, by Steiglehner, professor of 
physics at the University of Ingolstadt, Bavaria, with similar results.?^ 

Table 1 lists the effects on humans, reported by most early electricians, 
of an electric charge or small currents of DC electricity. Electrically 
sensitive people today will recognize most if not all of them. 


Table 1 - Effects of Electricity as Reported in the Eighteenth Century 


Therapeutic and neutral effects Non-therapeutic effects 
Change in pulse rate Dizziness 

Sensations of taste, light, Nausea 

and sound Headaches 

Increase of body temperature Nervousness 

Pain relief Irritability 

Restoration of muscle tone Mental confusion 
Stimulation of appetite Depression 

Mental exhilaration Insomnia 

Sedation Drowsiness 
Perspiration Fatigue 

Salivation Weakness 

Secretion of ear wax Numbness and tingling 
Secretion of mucus Muscle and joint pains 


Menstruation, uterine Muscle spasms and cramps 


contraction 
Lactation 
Lacrimation 
Urination 
Defecation 


Backache 

Heart palpitations 

Chest pain 

Colic 

Diarrhea 

Constipation 

Nosebleeds, hemorrhage 
Itching 

‘Tremors 

Seizures 

Paralysis 

Fever 

Respiratory infections 
Shortness of breath 
Coughing 

Wheezing and asthma attacks 
Eye pain, weakness, and fatigue 
Ringing in the ears 

Metallic taste 


3. Electrical Sensitivity 


“I HAVE ALMOST ENTIRELY given up the electrical experiments.” The 
author of these words, in referring to his own inability to tolerate electricity, 
wrote them not in the modern era of alternating currents and radio waves, 
but in the mid-eighteenth century when all there was was static electricity. 
French botanist Thomas-Frangois Dalibard confided his reasons to 
Benjamin Franklin in a letter dated February 1762. “First, the different 
electrical shocks have so strongly attacked my nervous system that I am left 
with a convulsive tremor in my arm so that I can scarcely bring a glass to 
my mouth; and if I now were to touch one electrical spark I would be 
unable to sign my name for 24 hours. Another thing that I notice is that it is 
almost impossible for me to seal a letter because the electricity of the 
Spanish wax, communicating itself to my arm, increases my tremor.” 

Dalibard was not the only one. Benjamin Wilson’s 1752 book, A 
Treatise on Electricity, helped promote the popularity of electricity in 
England, but he himself did not fare so well by it. “Upon repeating those 
shocks often for several weeks together,” he wrote, “I at last was weakened 
so much that a very small quantity of electric matter in the vial would shock 
me to a great degree, and cause an uncommon pain. So that I was obliged to 
desist from trying any more.” Even rubbing a glass globe with his hand— 
the basic electrical machine of his day—gave him “a very violent 
headache.”! 

The man who authored the first book in German devoted solely to 
electricity, _ Neu-Entdeckte Phenomena von  Bewunderns-wurdigen 
Wiirckungen der Natur (“Newly Discovered Phenomena of the Wonderful 
Workings of Nature,” 1744), became gradually paralyzed on one side of his 
body. Called the first electrical martyr, Johann Doppelmayer, professor of 


mathematics at Nuremberg, stubbornly persisted in his researches and died 
of a stroke in 1750 after one of his electrical experiments.” 

These were just three of the earliest casualties—three scientists who 
helped birth an electrical revolution in which they themselves could not 
participate. 

Even Franklin developed a chronic neurological illness that began 
during the period of his electrical researches and that recurred periodically 
for the rest of his life. Although he also suffered from gout, this other 
problem worried him more. Writing on March 15, 1753, of a pain in his 
head, he said, “I wish it were in my foot, I think I could bear it better." One 
recurrence lasted for the better part of five months while he was in London 
in 1757. He wrote to his doctor about *a giddiness and a swimming in my 
head," *a humming noise," and "little faint twinkling lights" that disturbed 
his vision. The phrase “violent cold,’ appearing often in his 
correspondence, was usually accompanied by mention of that same pain, 
dizziness, and problems with his eyesight? Franklin, unlike his friend 
Dalibard, never recognized a connection to electricity. 

Jean Morin, professor of physics at the Collége Royale de Chartres, and 
author, in 1748, of Nouvelle Dissertation sur l'Électricité (“New 
Dissertation on Electricity”), thought that it was never healthy to expose 
oneself to electricity in any form, and to illustrate his point he described an 
experiment conducted not with a friction machine but with his pet cat. “I 
stretched out a large cat on the cover of my bed,” he recounted. “I rubbed it, 
and in the darkness I saw sparks fly.” He continued this for more than half 
an hour. “A thousand tiny fires flew here and there, and continuing the 
friction, the sparks grew until they seemed like spheres or balls of fire the 
size of a hazelnut... I brought my eyes near one ball, and I immediately felt 
a lively and painful stinging in my eyes; there was no shock in the rest of 
my body; but the pain was followed by a faintness that made me fall to the 
side, my strength failed me, and I battled, so to speak, against passing out, I 
fought against my own weakness from which I did not recover for several 
minutes.” 

Such reactions were by no means confined to scientists. What is known 
to few doctors today was known universally to all eighteenth-century 


electricians, and to the nineteenth-century electrotherapists who followed 
them: electricity had side effects and some individuals were enormously 
and unaccountably more sensitive to it than others. “There are persons,” 
wrote Pierre Bertholon, a physicist from Languedoc, in 1780, “on whom 
artificial electricity made the greatest impression; a small shock, a simple 
spark, even the electric bath, feeble as it is, produced profound and lasting 
effects. I found others in whom strong electrical operations seemed not to 
cause any sensation at all... Between these two extremes are many nuances 
that correspond to the diverse individuals of the human species."^ 

Sigaud de la Fond’s numerous experiments with the human chain never 
produced the same results twice. “There are people for whom electricity can 
be unfortunate and very harmful,” he declared. “This impression being 
relative to the disposition of the organs of those who experience it and of 
the sensitivity or irritability of their nerves, there are probably not two 
persons in a chain composed of many, who experience strictly the same 
degree of shock.” 

Mauduyt, a physician, proposed in 1776 that “the face of the 
constitution depends in great part on the communication between the brain, 
the spinal cord and the different parts by means of the nerves. Those in 
whom this communication is less free, or who experience the nervous 
illness, are then more affected than others.” 

Few other scientists made any attempt to explain the differences. They 
simply reported them as fact—a fact as ordinary as that some people are fat 
and some thin, some tall and some short—but a fact that one had to take 
into account if one were going to offer electricity as a treatment, or 
otherwise expose people to it. 

Even Abbé Nollet, popularizer of the human chain and electricity’s 
leading missionary, reported this variability in the human condition from 
the very beginning of his campaign. “Pregnant women especially, and 
delicate persons,” he wrote in 1746, “should not be exposed to it.” And 
later: “Not all persons are equally appropriate to the experiments of 
electricity, be it for exciting that virtue, be it for receiving it, be it finally for 
feeling its effects.”® 


British physician William Stukeley, in 1749, was already so familiar 
with the side effects of electricity that he observed, after an earthquake at 
London on March 8 of that year, that some felt “pains in their joints, 
rheumatism, sickness, headach, pain in their back, hysteric and nervous 
disorders... exactly as upon electrification; and to some it has proved 
fatal."? He concluded that electrical phenomena must play an important role 
in earthquakes. 

And Humboldt was so amazed by the extraordinary human variability 
that he wrote, in 1797: “It is observed that susceptibility to electrical 
irritation, and electrical conductivity, differ as much from one individual to 
another, as the phenomena of living matter differ from those of dead 
material." 

The term "electrical sensitivity," in use again today, reveals a truth but 
conceals a reality. The truth is that not everyone feels or conducts electricity 
to the same degree. In fact if most people were aware of how vast the 
spectrum of sensitivity really is, they would have reason to be as astonished 
as Humboldt was, and as I still am. But the hidden reality is that however 
great the apparent differences between us, electricity is still part and parcel 
of our selves, as necessary to life as air and water. It is as absurd to imagine 
that electricity doesn't affect someone because he or she is not aware of it, 
as to pretend that blood doesn't circulate in our veins when we are not 
thirsty. 

Today, people who are electrically sensitive complain about power lines, 
computers, and cell phones. The amount of electrical energy being 
deposited into our bodies incidentally from all this technology is far greater 
than the amount that was deposited deliberately by the machines available 
to electricians during the eighteenth and early nineteenth centuries. The 
average cell phone, for example, deposits about 0.1 joule of energy into 
your brain every second. For a one-hour phone call, that's 360 joules. 
Compare that to a maximum of only 0.1 joule from the complete discharge 
of a one-pint Leyden jar. Even the 30-element electric pile which Volta 
attached to his ear canals could not have delivered more than 150 joules in 
an hour, even if all the energy were absorbed by his body. 


Consider also that a static charge of thousands of volts accumulates on 
the surface of computers screens—both old desktop computers and new 
wireless laptops—whenever they are in use, and that part of this charge is 
deposited on the surface of your body when you sit in front of one. This is 
probably less charge than was provided by the electric bath, but no one was 
subjected to the electric bath for forty hours a week. 

Electrotherapy is indeed an anachronism. In the twenty-first century we 
are all engaged in it whether we like it or not. Even if occasional use was 
once beneficial to some, perpetual bombardment is not likely to be so. And 
modern researchers trying to determine the biological effects of electricity 
are a bit like fish trying to determine the impact of water. Their eighteenth 
century predecessors, before the world was inundated, were in a much 
better position to record its effects. 

The second phenomenon pointed out by Humboldt has equally profound 
implications for both modern technology and modern medicine: not only 
were some people more sensitive to its effects than others, but individuals 
differed extremely in their ability to conduct electricity and in their 
tendency to accumulate a charge on the surface of their body. Some people 
could not help gathering a charge wherever they went, simply by moving 
and breathing. They were walking spark generators, like the Swiss woman 
whom the Scottish writer Patrick Brydone heard about in his travels. Her 
sparks and shocks, he wrote, were “strongest in a clear day, or during the 
passage of thunder-clouds, when the air is known to be replete with that 
fluid." Something was physiologically different about such individuals. 

And, conversely, human non-conductors were found, people who 
conducted electricity so poorly, even when their hands were well 
moistened, that their presence in a human chain interrupted the flow of 
current. Humboldt performed many experiments of this type with so-called 
“prepared frogs.” When the person at one end of a chain of eight people 
grasped a wire connected to the sciatic nerve of a frog while the person at 
the other end grasped a wire connected to its thigh muscle, the completing 
of the circuit made the muscle convulse. But not if there was a human non- 
conductor anywhere in the chain. Humboldt himself interrupted the chain 
one day when he was running a fever and was temporarily a non-conductor. 


He also could not elicit the flash of light in his eyes with the current on that 
day." 

In the Transactions of the American Philosophical Society for 1786 is a 
report along the same lines by Henry Flagg about experiments that took 
place at Rio Essequibo (now Guyana), in which a many-personed chain 
grasped the two ends of an electric eel. “If someone was present who 
constitutionally was not apt to receive the impression of the electric fluid,” 
wrote Flagg, “that person did not receive the shock at the moment of 
contact with the fish.” Flagg mentioned one such woman who, like 
Humboldt, had a mild fever at the time of the experiment. 

This led some eighteenth century scientists to postulate that both 
electrical sensitivity and electrical conductivity were indicators of one’s 
overall state of health. Bertholon observed that a Leyden bottle drew feebler 
sparks more slowly from a patient who was running a fever than an 
identical bottle did from a healthy person. During episodes of the chills, the 
opposite was true: the patient then seemed to be a super-conductor and the 
sparks drawn from him or her were stronger than normal. 

According to Benjamin Martin, “a person who has the small-pox cannot 
be electrified by any means whatever.” 13 

But despite the above observations, neither electrical sensitivity nor 
electrical conductivity were reliable indicators of either good health or bad. 
Most often they seemed to be random attributes. Musschenbroek, for 
example, in his Cours de Physique, mentioned three individuals whom he 
was never, at any time, able to electrify at all. One was a vigorous, healthy 
50-year-old man; the second a healthy, pretty 40-year-old mother of two; 
and the third a 23-year-old paralyzed man.'^ 

Age and sex seemed to be factors. Bertholon thought that electricity had 
a greater effect on mature young men than on infants or the elderly. 
French surgeon Antoine Louis agreed. *A man of twenty-five years," he 
wrote, “is electrified more easily than a child or an old person."!6 According 
to Sguario, “women generally are electrized more easily, and in a better 
manner, than men, but in one or the other sex a fiery and sulfurous 
temperament better than others, and youths better than old people." 
According to Morin, “adults and persons with a more robust temperament, 


more hot-blooded, more fiery, are also more susceptible to the movement of 
this substance.”!® These early observations that vigorous young adults are in 
some way more susceptible to electricity than others may seem surprising. 
But we will see later the importance of this observation to the public health 
problems of the modern era, including especially the problem of influenza. 

To illustrate in some detail the typical reactions of electrically sensitive 
people, I have chosen Benjamin Wilson's report on the experiences of his 
servant, who volunteered to be electrified in 1748 when he was twenty-five 
years of age. Wilson, being electrically sensitive himself, was naturally 
more attentive to these effects than some of his colleagues. Present-day 
electrically sensitive people will recognize most of the effects, including the 
after-effects that lasted for days. 

“After the first and second experiments,” wrote Wilson, “he complained 
of his spirits being depressed, and of being a little sick. Upon making the 
fourth experiment, he became very warm, and the veins of his hands and 
face swelled to a great degree. The pulse beat more than ordinary quick, and 
he complained of a violent oppression at his heart (as he called it) which 
continued along with the other symptoms near four hours. Upon uncovering 
his breast, it appeared to be much inflamed. He said that his head ached 
violently, and that he felt a pricking pain in his eyes and at his heart; and a 
pain in all his joints. When the veins began to swell, he complained of a 
sensation which he compared to that arising from strangling, or a stock 
tying too tight about the neck. Six hours after the making of the 
experiments most of these complaints left him. The pain in his joints 
continued till the next day, at which time he complained of weakness, and 
was very apprehensive of catching cold. On the third day he was quite 
recovered. 

“The shocks he received were trifling,’ Wilson added, “compared with 
those which are commonly received by most persons when they join hands 
to compleat the circuit for amusement."!? 

Morin, who stopped subjecting himself to electricity before 1748, also 
highlighted its ill effects in some detail. *Persons who are electrified on 
resin cakes, or on a wool cushion, often become like asthmatics," he 
observed. He reported the case of a young man of thirty who, after being 


electrified, suffered from a fever for thirty-six hours and a headache for 
eight days. He denounced medical electricity, concluding from his own 
experiments on people with rheumatism and gout that “all left suffering 
much more than before.” “Electricity brings with it symptoms to which it is 
not prudent to expose oneself,” he said, “because it is not always easy to 
repair the damage.” He especially disapproved of the medical use of the 
Leyden jar, telling the story of a man with eczema on his hand who, 
receiving a shock from a small jar containing only two ounces of water, was 
rewarded with a pain in his hand that endured more than a month. “He was 
not so eager after that,” said Morin, “to be the whipping boy for the 
electrical phenomena.” 

Whether electricity did more good than harm was not a trivial issue for 
people who lived at that time. 

Morin, who was electrically sensitive, and Nollet, who was not, came to 
loggerheads over the future of our world, there at the dawn of the electrical 
era. Their debate played out very publicly in the books and magazines of 
their time. Electricity was, first and foremost, known to be a property of 
living things and to be necessary for life. Morin thought of electricity as a 
kind of atmosphere, an exhalation that surrounded material bodies, 
including living bodies, and communicated itself to others by proximity. He 
was frightened by Nollet's notion that electricity might instead be a 
substance that flowed in a direction from one place to another, that could 
not flow out unless more of it flowed in from somewhere else, a substance 
that humanity had now captured and could send anywhere in the world at 
will. The debate began in 1748, just two years after the invention of the 
Leyden jar. 

“Tt would be easy,” prophesied Nollet with amazing accuracy, “to make 
a great number of bodies feel the effects of electricity at the same time, 
without moving them, without inconveniencing them, even if they are at 
very considerable distances; because we know that this virtue is transmitted 
with enormous ease to a distance by chains or by other contiguous bodies; 
some metal pipes, some iron wires stretched far away... a thousand other 
means even easier, that ordinary industry could invent, would not fail to put 


these effects within reach of the whole world, and to extend the use of it as 
far as one would wish."?! 

Morin was shocked. What would become of the bystanders, he 
immediately thought? “The living bodies, the spectators, would quickly lose 
that spirit of life, that principle of light and of fire that animates them... To 
put the whole universe, or at least a sphere of immense size in play, in 
action, in movement for a simple crackling of a little electrical spark, or for 
the formation of a luminous halo five to six inches long at the end of an iron 
bar, that would be truly to create a great commotion for no good reason. To 
make the electrical material penetrate in the interior of the densest metals, 
and then to make it radiate out with no obvious cause; that is perhaps to 
speak of good things; but the whole world will not agree.”22 

Nollet responded with sarcasm: “Truly, I don’t know if the whole 
universe must feel thus the experiments that I make in a small corner of the 
world; how will this flowing material that I cause to come toward my globe 
from nearby, how will its flow be felt in China, for example? But that 
would be of great consequence! Hey! What would become, as Mr. Morin 
remarks so well, of the living bodies, of the spectators!” 

Like other prophets who have shouted warnings instead of praise for 
new technologies, Morin was not the most popular scientist of his time. I 
have even seen him condemned by one modern historian as a “pompous 
critic,” a “gladiator” who “rose against” the electrical visionary Nollet.4 
But the differences between the two men were in their theories and 
conclusions, not their facts. The side effects of electricity were known to 
everyone, and continued to be so until the dawn of the twentieth century. 

George Beard and Alphonso Rockwell’s authoritative 1881 textbook on 
Medical and Surgical Electricity devoted ten pages to these phenomena. 
The terms they used were “electro-susceptibility,” referring to those who 
were easily injured by electricity, and “electro-sensibility,” referring to 
those who sensed electricity to an extraordinary degree. One hundred and 
thirty years after Morin’s first warnings, these physicians said: “There are 
individuals whom electricity always injures, the only difference in the effect 
on them between a mild and a severe application being, that the former 
injures less than the latter. There are patients upon whom all 


electrotherapeutic skill and experience are wasted; their temperaments are 
not en rapport with electricity. It matters not what may be the special 
disease or symptoms of disease from which they suffer— paralysis, or 
neuralgia, or neurasthenia, or hysteria, or affections of special organs—the 
immediate and the permanent effects of galvanization or faradization, 
general or localized, are evil and only evil." The symptoms to watch out for 
were the same as in the previous century: headache and backache; 
irritability and insomnia; general malaise; excitation or increase of pain; 
over-excitation of the pulse; chills, as though the patient were catching a 
cold; soreness, stiffness, and dull aching; profuse perspiration; numbness; 
muscle spasms; light or sound sensitivity; metallic taste; and ringing in the 
ears. 

Electro-susceptibility runs in families, said Beard and Rockwell, and 
they made the same observations about gender and age that early 
electricians had made: women, on average, were a little more susceptible to 
electricity than men, and active adults between twenty and fifty bore 
electricity more poorly than at other ages. 

Like Humboldt, they were also astonished by the people who were 
insensitive to the electrical energy. “It should be added,” they said, “that 
some persons are indifferent to electricity—they can bear almost any 
strength of either current very frequently and for long applications, without 
experiencing any effect either good or evil. Electricity may be poured over 
them in limitless measures; they may be saturated with it, and they may 
come out from the applications not a whit better or worse.” They were 
frustrated that there was no way to predict whether a person was en rapport 
with electricity or not. “Some women,” they observed, “even those who are 
exquisitely delicate, can bear enormous doses of electricity, while some 
men who are very hardy can bear none at all.” 

Obviously electricity is not, as so many modern doctors would have it— 
those who recognize that it affects our health at all—an ordinary kind of 
stressor, and it is a mistake to assume that one’s vulnerability to it is an 
indicator of one’s state of health. 

Beard and Rockwell did not give any estimates of the numbers of people 
not en rapport with electricity, but in 1892, otologist Auguste Morel 


reported that twelve percent of healthy subjects had a low threshold for at 
least the auditory effects of electricity. In other words, twelve percent of the 
population was, and presumably still is, able in some way to hear unusually 
low levels of electric current. 


Weather Sensitivity 

Unlike electrical sensitivity per se, the study of human sensitivity to the 
weather has a venerable history going back five thousand years in 
Mesopotamia, and possibly as long in China and Egypt. In his treatise on 
Airs, Waters and Places, written about 400 B.C., Hippocrates said that the 
human condition is largely determined by the climate of the place where 
one lives, and its variations. This is a discipline that, however much ignored 
and underfunded, is mainstream. And yet the name of this science, 
“biometeorology,” hides an open secret: some thirty percent of any 
population, no matter their ethnic origin, are weather sensitive and 
therefore, according to some textbooks in that field, electrically sensitive.?9 

The International Society for Biometeorology was founded in 1956 by 
Dutch geophysicist Solco Tromp with headquarters in, appropriately, 
Leyden, the city that launched the electrical age over two centuries before. 
And for the next forty years—until cell phone companies began to put 
pressure on researchers to repudiate an entire, long- established scientific 
discipline?—bioelectricity and biomagnetism were the subjects of intensive 
research and were the focus of one of the Society's ten permanent Study 
Groups. In 1972, an International Symposium was held in the Netherlands 
on the “Biological Effects of Natural Electric, Magnetic and 
Electromagnetic Fields.” In 1985, the Fall issue of the International Journal 
of Biometeorology was devoted entirely to papers on the effects of air ions 
and atmospheric electricity. 

“We do great injustice to the electrosensitive patients,” wrote Felix Gad 
Sulman, “when we treat them as psychiatric patients.” Sulman was a 
medical doctor at Hadassah University Medical Center in Jerusalem, and 
chair of the Medical School’s Bioclimatology Unit. In 1980, he published a 
400-page monograph titled The Effects of Air Ionization, Electric Fields, 
Atmospherics and Other Electric Phenomena on Man and Animal. Sulman, 


together with fifteen colleagues in other medical and technical fields, had 
studied 935 weather-sensitive patients over a period of fifteen years. One of 
their most riveting findings was that eighty percent of these patients could 
predict weather changes twelve to forty-eight hours before they happened. 
“The ‘prophetic’ patients were all sensitive to the electrical changes 
preceding the arrival of a weather change,” Sulman wrote. “They reacted by 
serotonin release to ions and atmospherics which naturally arrive with the 
speed of electricity—before the slow pace of the weather winds.” 

Weather sensitivity had emerged from within the walls of centuries of 
imprecise medical hearsay and was being exposed to the light of rigorous 
laboratory analysis. But this put the field of biometeorology on a collision 
course with an emerging technological dynamo. For if a third of the earth’s 
population are that sensitive to the gentle flow of ions and the subtle 
electromagnetic whims of the atmosphere, what must the incessant rivers of 
ions from our computer screens, and the turbulent storms of emissions from 
our cell phones, radio towers, and power lines be doing to us all? Our 
society is refusing to make the connection. In fact, at the 19th International 
Congress of Biometeorology held September 2008 in Tokyo, Hans Richner, 
professor of physics at the Swiss Federal Institute of Technology, stood up 
and actually told his colleagues that because cell phones are not dangerous, 
and their electromagnetic fields are so much stronger than those from the 
atmosphere, therefore decades of research were wrong and 
biometeorologists should not study human interactions with electric fields 
any more.? In other words, since we are all using cell phones, therefore we 
have to presume that they're safe, and so all the effects on people, plants 
and animals from mere atmospheric fields that have been reported in 
hundreds of laboratories could not have happened! It is no wonder that 
long-time biometeorological researcher Michael Persinger, professor at 
Laurentian University in Ontario, says that the scientific method has been 
abandoned.? 

But in the eighteenth century, electricians did make the connection. The 
reactions of their patients to the friction machine shed new light on an 
ancient mystery. The problem was framed by Mauduyt. *Men and animals," 
he explained, “experience a sort of weakness and languor on stormy days. 


This depression reaches its highest degree at the moment preceding the 
storm, it diminishes shortly after the storm has burst, and especially when a 
certain quantity of rain has fallen; it dissipates and terminates with it. This 
fact is well known, important, and has occupied physicians for a long time 
without their being able to find a sufficient explanation.”*! 

The answer, said Bertholon, was now at hand: “Atmospheric electricity 
and artificial electricity depend on one and the same fluid that produces 
various effects relative to the animal economy. A person who is insulated 
and electrized by the bath represents one who stands on the earth when it is 
electrified to excess; both are filled to overabundance with the electric fluid. 
It is accumulated around them in the same fashion."?? The electric circuit 
created by a machine was a microcosm of the grand circuit created by the 
heavens and the earth. 

Italian physicist Giambatista Beccaria described the global electrical 
circuit in surprisingly modern terms (see chapter 9). *Previous to rain," he 
wrote, *a quantity of electrical matter escapes out of the earth, in some 
place where there was a redundancy of it; and ascends to the higher regions 
of the air... The clouds that bring rain diffuse themselves from over those 
parts of the earth which abound with the electric fire, to those parts which 
are exhausted of it; and, by letting fall their rain, restore the equilibrium 
between them. ”33 

Eighteenth century scientists were not the first to discover this. The 
Chinese model, formulated in the Yellow Emperor's Classic of Internal 
Medicine, written in the fourth century B.C., is similar. In fact, if one 
understands that “Qi” is electricity, and that “Yin” and “Yang” are negative 
and positive, the language is almost identical: “The pure Yang forms the 
heaven, and the turbid Yin forms the earth. The Qi of the earth ascends and 
turns into clouds, while the Qi of the heaven descends and turns into rain."*^ 

Famous weather sensitive—and therefore electrically sensitive— 
individuals have included Lord Byron, Christopher Columbus, Dante, 
Charles Darwin, Benjamin Franklin, Goethe, Victor Hugo, Leonardo da 
Vinci, Martin Luther, Michelangelo, Mozart, Napoleon, Rousseau, and 
Voltaire. 


4. The Road Not Taken 


DURING THE 1790s, European science faced an identity crisis. For 
centuries, philosophers had been speculating about the nature of four 
mysterious substances that animated the world. They were light, electricity, 
magnetism, and caloric (heat). Most thought the four fluids were somehow 
related to one another, but it was electricity that was most obviously 
connected with life. Electricity alone breathed motion into nerves and 
muscles, and pulsations into the heart. Electricity boomed from the heavens, 
stirred winds, tossed clouds, pelted the earth with rain. Life was movement, 
and electricity made things move. 

Electricity was "an electric and elastic spirit" by which "all sensation is 
excited, and the members of animal bodies move at the command of the 
will, namely, by the vibrations of this spirit, mutually propagated along the 
solid filaments of the nerves, from the outward organs of sense to the brain, 
and from the brain into the muscles."! So spoke Isaac Newton in 1713, and 
for the next century few disagreed. 

Electricity was: 


"an element that is to us more intimate than the very air 
that we breathe." 
Abbé Nollet, 1746? 


"the principle of animal functions, the instrument of will 
and the vehicle of sensations." 
French physicist Marcelin Ducarla-Bonifas, 1779? 


"that fire necessary to all bodies and which gives them 
life... that is both attached to known matter and yet apart 
from it." 

Voltaire, 17724 


*one of the principles of vegetation; it's what fertilizes 
our fields, our vines, our orchards, and what brings 
fecundity to the depths of the waters." 

Jean-Paul Marat, M.D., 17825 


“the Soul of the Universe” that “produces and sustains 
Life thro-out all Nature, as well in Animals as in 
Vegetables” 

John Wesley, founder of the Methodist Church, 1760.5 


Then came Luigi Galvani's stunning announcement that simply 
touching a brass hook to an iron wire would cause a frog's leg to contract. 
A modest professor of obstetrics at the Institute of Sciences of Bologna, 
Galvani thought this proved something about physiology: each muscle fiber 
must be something like an organic Leyden jar. The metallic circuit, he 
reasoned, released the “animal electricity” that was manufactured by the 
brain and stored in the muscles. The function of the nerves was to discharge 
that stored electricity, and the dissimilar metals, in direct contact with the 
muscle, somehow mimicked the natural function of the animal’s own 
nerves. 

But Galvani’s countryman, Alessandro Volta, held an opposing, and at 
that time heretical opinion. The electric current, he claimed, came not from 
the animal, but from the dissimilar metals themselves. The convulsions, 
according to Volta, were due entirely to the external stimulus. Furthermore, 
he proclaimed, “animal electricity” did not even exist, and to try to prove it 
he made his momentous demonstration that the electric current could be 
produced by the contact of different metals alone, without the intervention 
of the animal. 

The combatants represented two different ways of looking at the world. 
Galvani, trained as a physician, sought his explanations in biology; the 
metals, to him, were an adjunct to a living organism. Volta, the self-taught 
physicist, saw precisely the opposite: the frog was only an extension of the 
non-living metallic circuit. For Volta, the contact of one conductor with 
another was a sufficient cause, even for the electricity within the animal: 


muscles and nerves were nothing more than moist conductors, just another 
kind of an electric battery. 

Their dispute was a clash not just between scientists, not just between 
theories, but between centuries, between mechanism and spirit, an 
existential struggle that was ripping the fabric of western civilization in the 
late 1790s. Hand weavers were shortly to rise in revolt against mechanical 
looms, and they were destined to lose. The material, in science as in life, 
was displacing and obscuring the vital. 

Volta, of course, won the day. His invention of the electric battery gave 
an enormous boost to the industrial revolution, and his insistence that 
electricity had nothing to do with life also helped steer its direction. This 
mistake made it possible for society to harness electricity on an industrial 
scale—to wire the world, even as Nollet had envisioned—without worrying 
about the effects such an enterprise might have on biology. It permitted 
people to begin to disregard the accumulated knowledge gained by 
eighteenth century electricians. 

Eventually, one learns if one reads the textbooks, Italian physicists 
Leopoldo Nobili and Carlo Matteucci, and then a German physiologist 
named Emil du Bois-Reymond, came along and proved that electricity did 
after all have something to do with life, and that nerves and muscles were 
not just moist conductors. But the mechanistic dogma was already 
entrenched, resisting all attempts to properly restore the marriage between 
life and electricity. Vitalism was permanently relegated to religion, to the 
realm of the insubstantial, divorced forever from the domain of serious 
investigative science. The life force, if it existed, could not be subjected to 
experiment, and it certainly could not be the same stuff that turned electric 
motors, lit light bulbs, and traveled thousands of miles on copper wires. 
Yes, electricity had finally been discovered in nerves and muscles, but its 
action was only a by-product of the journeys of sodium and potassium ions 
across membranes and the flight of neurotransmitters across synapses. 
Chemistry, that was the thing, the fertile, seemingly endless scientific soil 
that nurtured all biology, all physiology. Long-range forces were banished 
from life. 


The other, even more significant change that occurred after 1800 is that 
gradually people even forgot to wonder what the nature of electricity was. 
They began to build a permanent electrical edifice, whose tentacles snaked 
everywhere, without noticing, or thinking about, its consequences. Or, 
rather, they recorded its consequences in minute detail without ever making 
the connection to what they were building. 


5. Chronic Electrical IlIness 


IN 1859, THE CITY of London underwent an astonishing metamorphosis. 
A tangle of electric wires, suddenly and inescapably, was brought to the 
streets, shops, and residential rooftops of its two and a half million 
inhabitants. I will let one of the most famous English novelists, who was an 
eyewitness, begin the story. 

"About twelve years ago," wrote Charles Dickens, *when the tavern 
fashion of supplying beer and sandwiches at a fixed price became very 
general, the proprietor of a small suburban pothouse reduced the system to 
an absurdity by announcing that he sold a glass of ale and an electric shock 
for fourpence. That he really traded in this combination of science and drink 
is more than doubtful, and his chief object must have been to procure an 
increase of business by an unusual display of shopkeeping wit. Whatever 
motive he had to stimulate his humor, the fact should certainly be put upon 
record that he was a man considerably in advance of his age. He was 
probably not aware that his philosophy in sport would be made a science in 
earnest in the space of a few years, any more than many other bold 
humorists who have been amusing on what they know nothing about. The 
period has not yet arrived when the readers of Bishop Wilkin's famous 
discourse upon aerial navigation will be able to fly to the moon, but the 
hour is almost at hand when the fanciful announcement of the beer-shop 
keeper will represent an every-day familiar fact. A glass of ale and an 
electric shock will shortly be sold for fourpence, and the scientific part of 
the bargain will be something more useful than a mere fillip to the human 
nerves. It will be an electric shock that sends a message across the house- 
tops through the web of wires to any one of a hundred and twenty district 
telegraph stations, that are to be scattered amongst the shopkeepers all over 
the town. 


"The industrious spiders have long since formed themselves into a 
commercial company, called the London District Telegraph Company 
(limited), and they have silently, but effectively, spun their trading web. 
One hundred and sixty miles of wire are now fixed along parapets, through 
trees, over garrets, round chimney-pots, and across roads on the southern 
side of the river, and the other one hundred and twenty required miles will 
soon be fixed in the same manner on the northern side. The difficulty 
decreases as the work goes on, and the sturdiest Englishman is ready to give 
up the roof of his castle in the interests of science and the public good, 
when he finds that many hundreds of his neighbors have already led the 
way." 

English citizens did not necessarily welcome the prospect of electric 
wires being attached to their homes. “The British householder has never 
seen a voltaic battery kill a cow,” wrote Dickens, “but he has heard that it is 
quite capable of such a feat. The telegraph is worked, in most cases, by a 
powerful voltaic battery, and therefore the British householder, having a 
general dread of lightning, logically keeps clear of all such machines.” 
Nonetheless, Dickens tells us, the agents of the London District Telegraph 
Company persuaded nearly three thousand five hundred property owners to 
lend their rooftops as resting places for the two hundred and eighty miles of 
wires that were crisscrossing all of London, and that were shortly to drop 
into the shops of grocers, chemists, and tavern-keepers all over the city.! 

A year later, the electrical web above London homes became even more 
densely woven when the Universal Private Telegraph Company opened its 
doors. In contrast to the first company, whose stations accepted only public 
business, Universal rented telegraph facilities to individuals and businesses 
for private use. Cables containing up to a hundred wires each formed the 
backbone of the system, each wire departing from its companions at the 
nearest approach to its destination. By 1869, this second company had 
strung more than two thousand five hundred miles of cable, and many times 
as much wire over the heads and under the feet of Londoners, to serve about 
fifteen hundred subscribers scattered throughout the city. 

A similar transformation was occurring more or less everywhere in the 
world. The rapidity and intensity with which this happened is not 


appreciated today. 

The systematic electrification of Europe had begun in 1839 with the 
opening of the magnetic telegraph on the Great Western Railway between 
West Drayton and London. The electrification of America began a few 
years later, when Samuel Morse's first telegraph line marched from 
Baltimore to Washingon in 1844 along the Baltimore and Ohio Railroad. 
Even earlier, electric doorbells and annunciators began decorating homes, 
offices, and hotels, the first complete system having been installed in 1829 
in Boston's Tremont House, where all hundred and seventy guest rooms 
were connected by electric wires to a system of bells in the main office. 

Electric burglar alarms were available in England by 1847, and soon 
afterwards in the United States. 

By 1850, telegraph lines were under construction on every continent 
except Antarctica. Twenty-two thousand miles of wire had been energized 
in the United States; four thousand miles were advancing through India, 
where “monkeys and swarms of large birds" were alighting on them"?; one 
thousand miles of wire were spreading in three directions from Mexico 
City. By 1860, Australia, Java, Singapore, and India were being joined 
undersea. By 1875, thirty thousand miles of submarine cable had 
demolished oceanic barriers to communication, and the tireless weavers had 
electrified seven hundred thousand miles of copper web over the surface of 
the earth—enough wire to encircle the globe almost thirty times. 

And the traffic of electricity accelerated even more than the number of 
wires, as first duplexing, then quadriplexing, then automatic keying meant 
that current flowed at all times—not just when messages were being sent— 
and that multiple messages could be sent over the same wire at the same 
time, at a faster and faster rate. 

Almost from the beginning, electricity became a presence in the average 
urban dweller's life. The telegraph was never just an adjunct to railroads 
and newspapers. In the days before telephones, telegraph machines were 
installed first in fire and police stations, then in stock exchanges, then in the 
offices of messenger services, and soon in hotels, private businesses, and 
homes. The first municipal telegraph system in New York City was built by 
Henry Bentley in 1855, connecting fifteen offices in Manhattan and 


Brooklyn. The Gold and Stock Telegraph Company, incorporated in 1867, 
supplied instantaneous price quotations from the Stock, Gold, and other 
Exchanges telegraphically to hundreds of subscribers. In 1869, the 
American Printing Telegraph Company was created to provide private 
telegraph lines to businesses and individuals. The Manhattan Telegraph 
Company was organized in competition two years later. By 1877, the Gold 
and Stock Telegraph Company had acquired both those companies and was 
operating 1,200 miles of wire. By 1885, the industrious spiders linking 
almost thirty thousand homes and businesses had to spin webs over New 
York even more intricate than the ones over Dickens' London. 


In the midst of this transformation, a slender, slightly deaf clergyman's son 
wrote the first clinical histories of a previously unknown disease that he 
was observing 

as only three years out of medical school. Yet his paper was 
accepted and published, in 1869, in the prestigious Boston Medical and 
Surgical Journal, later renamed the New England Journal of Medicine. 

A self-assured young man, possessed of a serenity and hidden sense of 
humor that attracted people to him, Beard was a sharp observer who, even 
so early in his career, was not afraid to break new medical ground. 
Although he was sometimes ridiculed by his elders for his novel ideas, one 
of his colleagues was to say many years after his death that Beard "never 
said an unkind word against anyone."? Besides this new disease, he also 
specialized in electrotherapy and hypnotherapy, both of which he was 
instrumental in restoring to good repute, half a century after the death of 
Mesmer. In addition, Beard contributed to the knowledge of the causes and 
treatment of hay fever and seasickness. And in 1875 he collaborated with 
Thomas Edison in investigating an “etheric force” that Edison had 
discovered, which was able to travel through the air, causing sparks in 
nearby objects without a wired circuit. Beard correctly surmised, a decade 
before Hertz and two decades before Marconi, that this was high frequency 
electricity, and that it might one day revolutionize telegraphy.^ 





George Miller Beard, M.D. (1839-1883) 





Although some of its symptoms 
resembled other diseases, neurasthenia seemed to attack at random and for 
no reason and no one was expected to die from it. Beard certainly didn't 
connect the disease with electricity, which was actually his preferred 
treatment for neurasthenia—when the patient could tolerate it. When he 
died in 1883, the cause of neurasthenia, to everyone's frustration, had still 
not been identified. But in a large portion of the world where the term 
“neurasthenia” is still in everyday use among doctors—and the term is used 
in most of the world outside of the United States—electricity is recognized 
today as one of its causes. And the electrification of the world was 
undoubtedly responsible for its appearance out of nowhere during the 
1860s, to become a pandemic during the following decades. 

Today, when million-volt power lines course through the countryside, 
twelve-thousand-volt lines divide every neighborhood, and sets of thirty- 
ampere circuit breakers watch over every home, we tend to forget what the 
natural situation really is. None of us can begin to imagine what it would 
feel like to live on an unwired earth. Not since the presidency of James Polk 
have our cells, like puppets on invisible strings, been given a second’s rest 
from the electric vibrations. The gradual increase in voltage during the past 


century and a half has been only a matter of degree. But the sudden 
overwhelming of the earth's own nurturing fields, during the first few 
decades of technological free-for-all, had a drastic impact on the very 
character of life. 

In the earliest days telegraph companies, in countryside and in cities, 
built their lines with only one wire, the earth itself completing the electric 
circuit. None of the return current flowed along a wire, as it does in 
electrical systems today; all of it traveled through the ground along 
unpredictable paths. 

Twenty-five-foot-high wooden poles supported the wires on their 
journeys between towns. In cities, where multiple telegraph companies 
competed for customers and space was at a premium, forests of overhead 
wires tangled their way between housetops, church steeples, and chimneys, 
to which they attached themselves like vines. And from those vines hung 
electric fields that blanketed the streets and byways and the spaces within 
the homes to which they clung. 

The historical numbers provide a clue to what happened. According to 
George Prescott's 1860 book on the Electric Telegraph, a typical battery 
used for a 100-mile length of wire in the United States was "fifty cups of 
Grove," or fifty pairs of zinc and platinum plates, which provided an 
electric potential of about 80 volts.5 In the earliest systems, the current only 
flowed when the telegraph operator pressed the sending key. There were 
five letters per word and, in the Morse alphabet, an average of three dots or 
dashes per letter. Therefore, if the operator was proficient and averaged 
thirty words per minute, she pressed the key at a rhythm of 7.5 strokes per 
second. This is the very near the fundamental resonant frequency (7.8 Hz) 
of the biosphere, to which all living things, as we will see in chapter 9, are 
tuned, and whose average strength—about a third of a millivolt per meter— 
is given in textbooks. It is easy to calculate, using these simple assumptions, 
that the electric fields beneath the earliest telegraph wires were up to 30,000 
times stronger than the natural electric field of the earth at that frequency. In 
reality the rapid interruptions in telegraph keying also produced a wide 
range of radio frequency harmonics, which also traveled along the wires 
and radiated through the air. 


The magnetic fields can also be estimated. Based on the values for 
electrical resistance for wires and insulators as given by Samuel Morse 
himself, the amount of current on a typical long-distance wire varied from 
about 0.015 ampere to 0.1 ampere, depending on the length of the line and 
the weather. Since the insulation was imperfect, some current escaped down 
each telegraph pole into the earth, a flow which increased when it rained. 
Then, using the published value of 10? gauss for the magnetic field of the 
earth at 8 Hz, one may calculate that the magnetic field from a single early 
telegraph wire would have exceeded the earth's natural magnetic field at 
that frequency for a distance of two to twelve miles on either side of the 
line. And since the earth is not uniform, but contains underground streams, 
iron deposits, and other conductive paths over which the return current 
would travel, exposure of the population to these new fields varied widely. 

In cities, each wire carried about 0.02 ampere and exposure was 
universal. The London District Telegraph Company, for example, 
commonly had ten wires together, and the Universal Private Telegraph 
Company had up to one hundred wires together, strung above the streets 
and rooftops over a large part of town. Although the apparatus and alphabet 
of London District differed from those used in America, the current through 
its wires fluctuated at a similar rate—about 7.2 vibrations per second if the 
operator transmitted 30 words per minute." And Universal's dial telegraph 
was a hand-cranked magneto-electric machine that actually sent alternating 
current through the wires. 

One enterprising scientist, professor of physics John Trowbridge at 
Harvard University, decided to put to the test his own conviction that 
signals riding on telegraph wires that were grounded at both ends were 
escaping from their appointed paths and could easily be detected at remote 
locations. His test signal was the clock at the Harvard Observatory, which 
transmitted time signals four miles by wire from Cambridge to Boston. His 
receiver was a newly-invented device—a telephone—connected to a length 
of wire five hundred feet long and grounded to the earth at both ends. 
Trowbridge found that by tapping the earth in this way he could clearly hear 
the ticking of the observatory clock up to a mile from the observatory at 
various points not in the direction of Boston. The earth was being massively 


polluted with stray electricity, Trowbridge concluded. Electricity originating 
in the telegraph systems of North America should even be detectable on the 
other side of the Atlantic Ocean, he said after doing some calculations. If a 
powerful enough Morse signal, he wrote, were sent from Nova Scotia to 
Florida over a wire that was grounded at both ends, someone on the coast of 
France should be able to hear the signal by tapping the earth using his 
method. 

A number of historians of medicine who have not dug very deep have 
asserted that neurasthenia was not a new disease, that nothing had changed, 
and that late nineteenth and early twentieth century high society was really 
suffering from some sort of mass hysteria.? 

A list of famous American neurasthenes reads like a Who's Who of 
literature, the arts, and politics of that era. They included Frank Lloyd 
Wright, William, Alice and Henry James, Charlotte Perkins Gilman, Henry 
Brooks Adams, Kate Chopin, Frank Norris, Edith Wharton, Jack London, 
Theodore Dreiser, Emma Goldman, George Santayana, Samuel Clemens, 
Theodore Roosevelt, Woodrow Wilson, and a host of other well-known 
figures. 

Historians who think they have found neurasthenia in older textbooks 
have been confused by changes in medical terminology, changes that have 
prevented an understanding of what happened to our world a hundred and 
fifty years ago. For example, the term "nervous" was used for centuries 
without the connotations given to it by Freud. It simply meant, in today's 
language, “neurological.” George Cheyne, in his 1733 book, The English 
Malady, applied the term "nervous disorder" to epilepsy, paralysis, tremors, 
cramps, contractions, loss of sensation, weakened intellect, complications 
of malaria, and alcoholism. Robert Whytt's 1764 treatise on "nervous 
disorders" is a classic work on neurology. It can be confusing to see gout, 
tetanus, hydrophobia, and forms of blindness and deafness called “nervous 
disorders” until one realizes that the term “neurological” did not replace 
“nervous” in clinical medicine until the latter half of the nineteenth century. 
“Neurology,” at that time, meant what “neuroanatomy” means today. 

Another source of confusion for a modern reader is the old use of the 
terms “hysterical” and “hypochondriac” to describe neurological conditions 


of the body, not the mind. The “hypochondria” were the abdominal regions 
and “hystera,” in Greek, was the uterus; as Whytt explained in his treatise, 
hysterical and hypochondriac disorders were those neurological diseases 
that were believed to have their origins in the internal organs, “hysterical” 
traditionally being applied to women’s diseases and “hypochondriac” to 
men’s. When the stomach, bowels and digestion were involved, the illness 
was called hypochondriac or hysterical depending on the patient’s sex. 
When the patient had seizures, blackouts, tremors, or palpitations, but the 
internal organs were not affected, the illness was called simply “nervous.” 

Confounding this confusion still further were the Draconian treatments 
that were standard medical practice until well into the nineteenth century, 
which themselves often caused serious neurological problems. These were 
based on the humoral theory of medicine as set forth by Hippocrates in the 
fifth century B.C. For thousands of years all sickness was believed to be 
caused by an imbalance of “humors”—the four humors being phlegm, 
yellow bile, black bile, and blood—so that the goal of medical treatment 
was to strengthen the deficient humors and drain off those that were in 
excess. Therefore all medical complaints, major and minor, were subject to 
treatment by some combination of purging, vomiting, sweating, bleeding, 
medicines, and dietary prescriptions. And the drugs were liable to be 
neurotoxic, preparations containing heavy metals such as antimony, lead, 
and mercury being frequently prescribed. 

By the early nineteenth century, some doctors had begun to question the 
humoral theory of disease, but the term “neurology” had not yet acquired its 
modern meaning. During this time the realization that many illnesses were 
still being called “hysterical” and “hypochondriac” when there was nothing 
wrong with the uterus or internal organs led a number of physicians to try 
out new names for diseases of the nervous system. In the eighteenth century 
Pierre Pomme’s “vaporous conditions” included cramps, convulsions, 
vomiting, and vertigo. Some of these patients had total suppression of urine, 
spitting of blood, fevers, smallpox, strokes, and other illnesses that 
sometimes took their lives. When the disease didn’t kill them the frequent 
bleedings often did. Thomas Trotter’s book, A View of the Nervous 
Temperament, written in 1807, included cases of worms, chorea, tremors, 


gout, anemia, menstrual disorders, heavy metal poisonings, fevers, and 
convulsions leading to death. A series of later French doctors tried out 
names like “proteiform neuropathy,” “nervous hyperexcitability,” and “the 
nervous state.” Claude Sandras’ 1851 Traité Pratique des Maladies 
Nerveuses (“Practical Treatise on Nervous Diseases”) is a conventional 
textbook on neurology. Eugéne Bouchut’s 1860 book on “l'état nerveux” 
(“the nervous state”) contained many case histories of patients suffering 
from the effects of blood-letting, tertiary syphilis, typhoid fever, 
miscarriage, anemia, paraplegia, and other acute and chronic illnesses of 
known causes, some lethal. Beard’s neurasthenia is not to be found. 

In fact, the first description anywhere of the disease to which Beard 
called the world’s attention is in Austin Flint’s textbook of medicine 
published in New York in 1866. A professor at the Bellevue Hospital 
Medical College, Flint devoted two brief pages to it and gave it almost the 
Same name Beard was to popularize three years later. Patients with 
“nervous asthenia,” as he called it, “complain of languor, lassitude, want of 
buoyancy, aching of the limbs, and mental depression. They are wakeful 
during the night, and enter upon their daily pursuits with a sense of 
fatigue."? These patients did not have anemia or any other evidence of 
organic disease. They also did not die of their disease; on the contrary, as 
Beard and others were later to also observe, they seemed to be protected 
from ordinary acute illnesses and lived, on average, longer than others. 

These first publications were the beginning of an avalanche. *More has 
been written about neurasthenia in the course of the last decade," wrote 
Georges Gilles de la Tourette in 1889, “than on epilepsy or hysteria, for 
example, during the last century.” !° 

The best way to familiarize the reader with both the disease and its 
cause is to introduce another prominent New York City physician who 
herself suffered from it—though by the time she told her story the 
American medical profession had been trying to find the cause of 
neurasthenia for nearly half a century and, not finding one, had concluded 
that the illness was psychosomatic. 

Dr. Margaret Abigail Cleaves, born in the territory of Wisconsin, had 
graduated from medical school in 1879. She had first worked at the State 


Hospital for the Insane at Mt. Pleasant, Iowa, and from 1880 to 1883 had 
served as chief physician to the female patients of the Pennsylvania State 
Lunatic Hospital. In 1890 she had moved to the big city, where she had 
opened a private practice in gynecology and psychiatry. It was not until 
1894, at the age of 46, that she was diagnosed with neurasthenia. What was 


new was her heavy exposure to electricity: she had begun to specialize in 
electrotherapy. 













‘There remained all the usual pain of nerve trunks or peripheral 
nerve endings, the exquisite sensitiveness of the body, the inability to bear a 
touch heavier than the brush of a butterfly’s wing, the insomnia, lack of 
strength, the recurrence of depression of spirits, the inability to use my 
brain at my study and writing as I wished.” 

“Tt was with the greatest difficulty,” she wrote on another occasion, “to 
even use knife and fork at the table, while the routine carving was an 
impossibility.” 


Cleaves had chronic fatigue, poor digestion, headaches, heart 
palpitations and tinnitus. She found the sounds of the city unbearable. She 
smelled and tasted “phosphorus.” She became so sensitive to the sun that 
she lived in darkened rooms, able to go outdoors only at night. She 
gradually lost her hearing in one ear. She became so affected by 
atmospheric electricity that, by her sciatica, her facial pain, her intense 
restlessness, her feeling of dread, and her sensation “of a crushing weight 
bowing me to the earth,” she could predict with certainty 24 to 72 hours in 
advance that the weather was going to change. “Under the influence of 
oncoming electrical storms," she wrote, “my brain does not function."!! 

And yet through it all, suffering until the end of her life, she was 
dedicated to her profession, exposing herself day in and day out to 
electricity and radiation in their various forms. She was a founding and very 
active officer of the American Electro-Therapeutic Association. Her 
textbook on Light Energy taught the therapeutic uses of sunlight, arc light, 
incandescent light, fluorescent light, X-rays, and radioactive elements. She 
was the first physician to use radium to treat cancer. 

How could she not have known? And yet it was easy. In her day as in 
ours, electricity did not cause disease, and neurasthenia—it had finally been 
decided—resided in the mind and emotions. 

Other related illnesses were described in the late nineteenth and early 
twentieth centuries, occupational diseases suffered by those who worked in 
proximity to electricity. “Telegrapher’s cramp,” for example, called by the 
French, more accurately, “mal télégraphique” (“telegraphic sickness”) 
because its effects were not confined to the muscles of the operator’s hand. 
Ernest Onimus described the affliction in Paris in the 1870s. These patients 
suffered from heart palpitations, dizziness, insomnia, weakened eyesight, 
and a feeling “as though a vice were gripping the back of their head.” They 
suffered from exhaustion, depression, and memory loss, and after some 
years of work a few descended into insanity. In 1903, Dr. E. Cronbach in 
Berlin gave case histories for seventeen of his telegraphist patients. Six had 
either excessive perspiration or extreme dryness of hands, feet, or body. 
Five had insomnia. Five had deteriorating eyesight. Five had tremors of the 
tongue. Four had lost a degree of their hearing. Three had irregular 


heartbeats. Ten were nervous and irritable both at work and at home. *Our 
nerves are shattered,” wrote an anonymous telegraph worker in 1905, “and 
the feeling of vigorous health has given way to a morbid weakness, a 
mental depression, a leaden exhaustion... Hanging always between sickness 
and health, we are no longer whole, but only half men; as youths we are 
already worn out old men, for whom life has become a burden... our 
strength prematurely sapped, our senses, our memory dulled, our 
impressionability curtailed.” These people knew the cause of their illness. 
“Has the release of electrical power from its slumber,” asked the 
anonymous worker, “created a danger for the health of the human race?”!? 
In 1882, Edmund Robinson encountered similar awareness among his 
telegraphist patients from the General Post Office at Leeds. For when he 
suggested treating them with electricity, they “declined trying anything of 
the kind.” 

Long before that, an anecdote from Dickens could have served as a 
warning. He had toured St. Luke’s Hospital for Lunatics. “We passed a deaf 
and dumb man,” he wrote, “now afflicted with incurable madness.” Dickens 
asked what employment the man had been in. “‘Aye,’ says Dr. Sutherland, 
‘that is the most remarkable thing of all, Mr. Dickens. He was employed in 
the transmission of electric-telegraph messages.’” The date was January 15, 
1858.13 

Telephone operators, too, often suffered permanent injury to their health. 
Ernst Beyer wrote that out of 35 telephone operators that he had treated 
during a five-year period, not a single one had been able to return to work. 
Hermann Engel had 119 such patients. P. Bernhardt had over 200. German 
physicians routinely attibuted this illness to electricity. And after reviewing 
dozens of such publications, Karl Schilling, in 1915, published a clinical 
description of the diagnosis, prognosis, and treatment of illness caused by 
chronic exposure to electricity. These patients typically had headaches and 
dizziness, tinnitus and floaters in the eyes, racing pulse, pains in the region 
of the heart, and palpitations. They felt weak and exhausted and were 
unable to concentrate. They could not sleep. They were depressed and had 
anxiety attacks. They had tremors. Their reflexes were elevated, and their 
senses were hyperacute. Sometimes their thyroid was hyperactive. 


Occasionally, after long illness, their heart was enlarged. Similar 
descriptions would come throughout the twentieth century from doctors in 
the Netherlands, Belgium, Denmark, Austria, Italy, Switzerland, the United 
States, and Canada." In 1956, Louis Le Guillant and his colleagues reported 
that in Paris “there is not a single telephone operator who doesn’t 
experience this nervous fatigue to one degree or another.” They described 
patients with holes in their memory, who couldn’t carry on a conversation 
or read a book, who fought with their husbands for no reason and screamed 
at their children, who had abdominal pains, headaches, vertigo, pressure in 
their chest, ringing in their ears, visual disturbances, and weight loss. A 
third of their patients were depressed or suicidal, almost all had anxiety 
attacks, and over half had disturbed sleep. 

As late as 1989, Annalee Yassi reported widespread “psychogenic 
illness” among telephone operators in Winnipeg, Manitoba and St. 
Catharines, Ontario, and in Montreal, Bell Canada reported that 47 percent 
of its operators complained of headaches, fatigue, and muscular aches 
related to their work. 

Then there was “railway spine,” a misnamed illness that was 
investigated as early as 1862 by a commission appointed by the British 
medical journal Lancet. The commissioners blamed it on vibrations, noise, 
speed of travel, bad air, and sheer anxiety. All those factors were present, 
and no doubt contributed their share. But there was also one more that they 
did not consider. Because by 1862, every rail line was sandwiched between 
one or more telegraph wires running overhead and the return currents from 
those lines coursing beneath, a portion of which flowed along the metal 
rails themselves, upon which the passenger cars rode. Passengers and train 
personnel commonly suffered from the same complaints later reported by 
telegraph and telephone operators: fatigue, irritability, headaches, chronic 
dizziness and nausea, insomnia, tinnitus, weakness, and numbness. They 
had rapid heart beat, bounding pulse, facial flushing, chest pains, 
depression, and sexual dysfunction. Some became grossly overweight. 
Some bled from the nose, or spat blood. Their eyes hurt, with a *dragging" 
sensation, as if they were being pulled into their sockets. Their vision and 
their hearing deteriorated, and a few became gradually paralyzed. A decade 


later they would have been diagnosed with neurasthenia—as many railroad 
employees later were. 

The most salient observations made by Beard and the late nineteenth 
century medical community about neurasthenia are these: 

It spread along the routes of the railroads and telegraph lines. 

It affected both men and women, rich and poor, intellectuals and 
farmers. 

Its sufferers were often weather sensitive. 

It sometimes resembled the common cold or influenza. 

It ran in families. 

It seized most commonly people in the prime of their life, ages 15 to 45 
according to Beard, 15 to 50 according to Cleaves, 20 to 40 according to H. 
E. Desrosiers, 20 to 50 according to Charles Dana. 

It lowered one’s tolerance for alcohol and drugs. 

It made people more prone to allergies and diabetes. 

Neurasthenes tended to live longer than average. 

And sometimes—a sign whose significance will be discussed in chapter 
10—neurasthenes passed reddish or dark brown urine. 

It was the German physician Rudolf Arndt who finally made the 
connection between neurasthenia and electricity. His patients who could not 
tolerate electricity intrigued him. “Even the weakest galvanic current,” he 
wrote, “so weak that it scarcely deflected the needle of a galvanometer, and 
was not perceived in the slightest by other people, bothered them in the 
extreme.” He proposed in 1885 that “electrosensitivity is characteristic of 
high-grade neurasthenia.” And he prophesied that electrosensitivity “may 
contribute not insubstantially to the elucidation of phenomena that now 
seem puzzling and inexplicable.” 

He wrote this in the middle of an intense, unrelenting haste to wire the 
whole world, driven by an unquestioning embrace of electricity, even an 
adoration, and he wrote it as though he knew he was risking his reputation. 
A large obstacle to the proper study of neurasthenia, he suggested, was that 
people who were less sensitive to electricity did not take its effects at all 
seriously: instead, they placed them in the realm of superstition, “lumped 
together with clairvoyance, mind-reading and mediumship.”!® 


That obstacle to progress confronts us still today. 


The Renaming 
In December 1894, an up-and-coming Viennese psychiatrist wrote a paper 
whose influence was enormous and whose consequences for those who 
came after have been profound and unfortunate. Because of him, 
neurasthenia, which is still the most common illness of our day, is accepted 
as a normal element of the human condition, for which no external cause 
need be sought. Because of him, environmental illness, that is, illness 
caused by a toxic environment, is widely thought not to exist, its symptoms 
automatically blamed on disordered thoughts and out-of-control emotions. 
Because of him, we are today putting millions of people on Xanax, Prozac, 
and Zoloft instead of cleaning up their environment. For over a century ago, 
at the dawn of an era that blessed the use of electricity full throttle not just 
for communication but for light, power, and traction, Sigmund Freud 
renamed neurasthenia “anxiety neurosis” and its crises “anxiety attacks.” 
Today we call them also “panic attacks.” 

The symptoms listed by Freud, in addition to anxiety, will be familiar to 
every doctor, every “anxiety” patient, and every person with electrical 
sensitivity: 


Irritability 

Heart palpitations, arrhythmias, and chest pain 
Shortness of breath and asthma attacks 
Perspiration 

Tremor and shivering 

Ravenous hunger 

Diarrhea 

Vertigo 

Vasomotor disturbances (flushing, cold extremities, etc.) 
Numbness and tingling 

Insomnia 

Nausea and vomiting 

Frequent urination 

Rheumatic pains 


Weakness 
Exhaustion 





In the International Classification of Diseases (ICD-10), there is a 
unique code for neurasthenia, F48.0, but in the version used in the United 
States (ICD-10-CM), F48.0 has been removed. In the American version, 
neurasthenia is only one among a list of “other nonpsychotic mental 
disorders” and is almost never diagnosed. Even in the Diagnostic and 
Statistical Manual (DSM-V), the official system for assigning codes to 
mental diseases in American hospitals, there is no code for neurasthenia. 

It was a death warrant only in North America and Western Europe, 
however. Half the world still uses neurasthenia as a diagnosis in the sense 
intended by Beard. In all of Asia, Eastern Europe, Russia and the former 
Soviet Republics, neurasthenia is today the most common of all psychiatric 
diagnoses as well as one of the most frequently diagnosed diseases in 
general medical practice.'” It is often considered a sign of chronic toxicity.!? 

In the 1920s, just as the term was being abandoned in the West, it was 
first coming into use in China.!° The reason: China was just beginning to 
industrialize. The epidemic that had begun in Europe and America in the 
late nineteenth century had not yet reached China at that time. 

In Russia, which began to industrialize along with the rest of Europe, 
neurasthenia became epidemic in the 1880s.? But nineteenth century 
Russian medicine and psychology were heavily influenced by 
neurophysiologist Ivan Sechenov, who emphasized external stimuli and 
environmental factors in the workings of the mind and body. Because of 


Sechenov's influence, and that of his pupil Ivan Pavlov after him, the 
Russians rejected Freud's redefinition of neurasthenia as anxiety neurosis, 
and in the twentieth century Russian doctors found a number of 
environmental causes for neurasthenia, prominent among which are 
electricity and electromagnetic radiation in their various forms. And as 
early as the 1930s, because they were looking for it and we weren't, a new 
clinical entity was discovered in Russia called *radio wave sickness," which 
is included today, in updated terms, in medical textbooks throughout the 
former Soviet Union and ignored to this day in Western countries, and to 
which I will return in later chapters. In its early stages the symptoms of 
radio wave sickness are those of neurasthenia. 

As living beings, not only do we possess a mind and a body, but we also 
have nerves that join the two. Our nerves are not just conduits for the ebb 
and flow of electric fluid from the universe, as was once believed, nor are 
they just an elaborate messenger service to deliver chemicals to muscles, as 
is currently thought. Rather, as we will see, they are both. As a messenger 
service, the nervous system can be poisoned by toxic chemicals. As a 
network of fine transmission wires, it can easily be damaged or unbalanced 
by a great or unfamiliar electric load. This has effects on both mind and 
body that we know today as anxiety disorder. 


6. The Behavior of Plants 


WHEN I FIRST ENCOUNTERED the works of (Sir Jagadis Chunder Bose, 


I was stunned. The son of a public official in East Bengal, Bose was 
educated in Cambridge, where he received a degree in natural science that 
he took back to his home country. 





He performed 
conduction experiments on the nerves of ferns in the same way 
physiologists do with the sciatic nerves of frogs. 





Sir Jagadis Chunder Bose (1858-1937) 


Bose also located pulsating cells in a plant's stem which he showed are 
responsible for pumping the sap, which have special electrical properties, 
and he built what he called a magnetic sphygmograph that magnified the 
pulsations ten million times and measured changes in sap pressure. 

I was astonished, because you can search botanical textbooks today 
without finding so much as a hint that plants have anything like a heart and 
a nervous system. Bose's books, including Plant Response (1902), The 
Nervous Mechanism of Plants (1926), Physiology of the Ascent of Sap 
(1923), and Plant Autographs and Their Revelations (1927), languish in the 
archives of research libraries. 

But Bose did more than just find the nerves of plants. He demonstrated 
the effects of electricity and radio waves on them, and he obtained similar 
results with sciatic nerves of frogs, proving the exquisite sensitivity of all 
living things to electromagnetic stimuli. His expertise in these areas was 
beyond question. He had been appointed Officiating Professor of Physics at 
the Presidency College in Calcutta in 1885. He made contributions in the 
field of solid-state physics, and is credited with the invention of the device 
—called a coherer—that was used to decode the first wireless message sent 
across the Atlantic Ocean by Marconi. In fact, Bose had given a public 
demonstration of wireless transmission in a lecture hall in Calcutta in 1895, 
more than a year before Marconi's first demonstration on Salisbury Plain in 
England. But Bose took out no patents, and sought no publicity for his 
invention of the radio. Instead he gave up those technical pursuits to devote 
the rest of his life to the more humble study of plant behavior. 

In applying electricity to plants, Bose built on a tradition that was 
already a century and a half old. 

The first to electrify a plant with a friction machine was a Dr. Mainbray 
of Edinburgh, who connected two myrtle trees to a machine throughout 
October 1746; the two trees sent out new branches and buds that autumn as 
though it were springtime. The following October, Abbé Nollet, having 
received this news, conducted the first of a series of more rigorous 
experiments in Paris. In addition to Carthusian monks and soldiers of the 


French guard, Nollet was electrifying mustard seeds as they sprouted in tin 
bowls back in his laboratory. The electrified sprouts grew four times as tall 
as normal, but with stems that were weaker and more slender.! 

That December, around Christmas time, Jean Jallabert electrified 
jonquil, hyacinth, and narcissus bulbs in carafes of water.? The following 
year Georg Bose electrified plants at Wittenberg,? and Abbé Menon at 
Angers, and for the rest of the eighteenth century plant growth 
demonstrations were de rigeur among scientists studying frictional 
electricity. The energized plants sprouted earlier, grew faster and longer, 
opened their flowers sooner, sent out more leaves, and were generally—but 
not always—sturdier. 

Jean-Paul Marat even watched electrified lettuce seeds germinate in the 
month of December when the ambient temperature was two degrees above 
freezing.® 

Giambattista Beccaria in Turin was the first, in 1775, to suggest the use 
of these effects for the benefit of agriculture. Soon afterwards Francesco 
Gardini, also in Turin, stumbled upon the opposite effect: plants deprived of 
the natural atmospheric field did not grow as well. A network of iron wires 
had been stretched over the ground for the purpose of detecting atmospheric 
electricity. But the wires happened to run above part of a monastery’s 
garden, shielding it from the atmospheric fields that the wires were 
measuring. For the three years that the wire net had been in place, the 
gardeners tending that section had complained that their harvests of fruits 
and seeds were fifty to seventy percent less than in the rest of their gardens. 
So the wires were removed, and production returned to normal. Gardini 
drew a remarkable inference. “Tall plants,’ he said, “have a harmful 
influence on the development of plants that grow at their base, not only by 
depriving them of light and heat, but also because they absorb atmospheric 
electricity at their expense.”® 

In 1844, W. Ross was the first of many to apply electricity to a field of 
crops, using a one-volt battery much like the one from which Humboldt had 
so successfully elicited sensations of light and taste, only larger. He buried a 
copper plate five feet by fourteen inches at one end of a row of potatoes, a 
zinc plate two hundred feet away at the other end, and connected the two 


plates with a wire. And in July he harvested potatoes averaging two and a 
half inches in diameter from the electrified row, versus only one-half inch 
from the untreated row.’ 

In the 1880s, Professor Selim Lemström of the University of 
Helsingfors in Finland conducted large-scale experiments on crops with a 
friction machine, suspending over his crops a network of pointed wires 
connected to the positive pole of the machine. Over a period of years he 
found that electricity stimulated the growth of some crops—wheat, rye, 
barley, oats, beets, parsnips, potatoes, celeriac, beans, leeks, raspberries, and 
strawberries—while it stunted the growth of peas, carrots, kohlrabi, 
rutabagas, turnips, cabbages, and tobacco. 

And in 1890, Brother Paulin, Director of the Agricultural Institute at 
Beauvais, France, invented what he called a “géomagnétifére” to draw 
down atmospheric electricity like Benjamin Franklin had once done with 
his kite. Perched atop a tall pole 40 to 65 feet high was an iron collecting 
rod, terminating in five pointed branches. Four such poles were planted on 
every hectare of land, and the electricity collected by them was carried to 
the soil and distributed to the crops by means of underground wires. 

According to contemporary newspaper accounts the effect was visually 
startling. Like supercrops, all of the potato plants within a sharply 
delineated ring were greener, taller, and “twice as vigorous” as the 
surrounding plants. The yield of potatoes within the electrified areas was 
fifty to seventy percent greater than outside them. Repeated in a vineyard, 
the experiment produced grape juice with seventeen percent more sugar, 
and wine with an exceptional alcohol content. Further trials in fields of 
spinach, celery, radishes, and turnips were just as impressive. Other 
farmers, using similar apparatus, improved their yields of wheat, rye, 
barley, oats, and straw.® 

All these experiments with frictional electricity, feeble electric batteries, 
and atmospheric fields might make one suspect that it doesn’t take very 
much current to affect a plant. But until the end of the nineteenth century 
the experiments lacked precision, and accurate Measurements were not 
available. 

Which brings me back to Jagadis Chunder Bose. 


In 1859, Eduard Pflüger had formulated a simple model of how electric 
currents affect animal nerves. If two electrodes are attached to a nerve and 
the current is suddenly turned on, the negative electrode, or cathode, 
momentarily stimulates the section of nerve near it, while the positive 
electrode, or anode, has a deadening effect. The reverse occurs at the 
moment the current is broken. The cathode, said Pflüger, increases 
excitability at “make,” and decreases excitability at “break,” while the 
anode does just the opposite. While the current is flowing and not changing, 
supposedly nervous activity is not affected whatsoever by the current. 
Pfliiger’s Law, formulated a century and a half ago, is widely believed until 
the present day, and is the basis for modern electrical safety codes that are 
designed to prevent shocks at “make” or “break” of circuits but that do not 
prevent low-level continuous currents from being induced in the body 
because they are presumed to be of no consequence. 

Unfortunately Pfliiger’s Law is not true and Bose was the first to prove 
it. One problem with Pfliiger’s Law is that it was based on experiments 
using relatively strong electric currents, on the order of one milliampere (a 
thousandth of an ampere). But, as Bose showed, it is not even correct at 
those levels.? Experimenting on himself in much the same way Humboldt 
had done a century before, Bose applied an electromotive force of 2 volts to 
a skin wound, and to his surprise the cathode, both at make, and as long as 
the current flowed, made the wound much more painful. The anode, both at 
make and while the current flowed, soothed the wound. But exactly the 
opposite occurred when he applied a much lower voltage. At a third of a 
volt, the cathode soothed and anode irritated. 

After experimenting on his own body, Bose, being a botanist, tried a 
similar experiment on a plant. He took a twenty-centimer length of the 
nerve of a fern, and applied an electromotive force of only a tenth of a volt 
across the ends. This sent a current of about three ten-millionths of an 
ampere through the nerve, or about one thousand times less than the range 
of currents most modern physiologists and makers of safety regulations are 
used to thinking about. Again, at this low level of current, Bose found 
precisely the reverse of Pfliiger’s Law: the anode stimulated the nerve and 
the cathode made it less responsive. Evidently, in plants as well as in 


animals, electricity could have exactly opposite effects depending on the 
strength of the current. 

Still Bose was not satisfied, because under certain circumstances the 
effects did not consistently follow either pattern. Maybe, suspected Bose, 
Pflüger's model was not only wrong but simplistic. He speculated that the 
applied currents were actually altering the conductivity of the nerves and 
not just the threshold of their response. Bose questioned the received 
wisdom that nervous functioning was a neat all-or-nothing response based 
only on chemicals in a watery solution. 

His ensuing experiments confirmed his suspicions spectacularly. 
Contrary to existing theories—existing still today in the twenty-first century 
—of how nerves function, a constantly applied electric current, even though 
tiny, profoundly altered the conductivity of the animal and plant nerves 
Bose tested. If the applied current was in the same direction as nervous 
impulses, the speed of the impulses became slower and, in the animal, the 
muscular response to stimulation became weaker. If the applied current was 
in the opposite direction, nervous impulses traveled faster and muscles 
responded more vigorously. By manipulating the magnitude and direction 
of the applied current, Bose found that he could control nerve conduction at 
will, in animals and in plants, making nerves more or less sensitive to 
stimulation, or even blocking conduction altogether. And after the current 
was turned off, a rebound effect was observed. If a given amount of current 
depressed conduction, the nerve became hypersensitive after it was turned 
off, and remained so for a period of time. In one experiment a brief current 
of 3 microamperes—3 millionths of an ampere—produced nervous 
hypersensitivity for 40 seconds. 





In 1923, Vernon Blackman, an agricultural researcher at Imperial 
College in England, found in field experiments that electric currents 
averaging less than one milliampere (one thousandth of an ampere) per acre 
increased the yields of several types of crops by twenty percent. The current 
passing through each plant, he calculated, was only about 100 picoamperes 
—that's 100 trillionths of an ampere, about a thousand times less than the 
currents Bose had found were necessary to stimulate or deaden nerves. 

But the field results were inconsistent. So Blackman took his 
experiments into the laboratory where both exposure and growth conditions 
could be precisely controlled. Barley seeds were sprouted in glass tubes, 
and at varying heights above each plant was a metal point charged to about 
10,000 volts by a DC power supply. The current flowing through each plant 
was measured precisely with a galvanometer, and Blackman found that a 
maximal increase in growth was obtained with a current of only 50 
picoamperes, applied for just one hour per day. Increasing the time of 
application diminished the effect. Increasing the current to a tenth of a 
microampere was always harmful. 

In 1966, Lawrence Murr and colleagues at Pennsylvania State 
University, experimenting on sweet corn and bush beans, verified 
Blackman's finding that currents around one microampere inhibited growth 
and damaged leaves. They then took these experiments one step farther: 
they undertook to discover the smallest current that would affect growth. 
And they found that any current greater than one quadrillionth of an ampere 
would stimulate plant growth. 

In his radio experiments, Bose used a device he called a magnetic 
crescograph, which recorded the growth rate of plants, magnified ten 
million times." Remember that Bose was also an expert in wireless 
technology. When he set up a radio transmitter at one end of his property, 
and a plant attached to a receiving aerial at the other end, two hundred 
meters away, he found that even a brief radio transmission changed a plant's 
growth rate within a few seconds. The broadcast frequency, implied from 
his description, was about 30 MHz. We are not told what the power was. 
However, Bose recorded that a “feeble stimulus” produced an immediate 
acceleration of growth, and that “moderate” radio energy retarded growth. 


7. Acute Electrical Illness 


ON MARCH 103, 1876, seven famous words sent an even greater 
avalanche of wires cascading down over an already tangled world: “Mr. 
Watson, come here, I want you.” 

As though living in a desert that was waiting to be planted and watered, 
millions of people heard and heeded the call. For although in 1879 only 250 
people owned telephones in all of New York City, just ten years later, from 
that same soil, fertilized by an idea, dense forests of telephone poles were 
sprouting eighty and ninety feet tall, bearing up to thirty cross-branches 
each. Each tree in these electric groves supported up to three hundred wires, 
obscuring the sun and darkening the avenues below. 





2^ 


The Blizzard of 1888, New York City Courtesy of the Museum of the City of New York 


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Calvert and German Streets, Baltimore, Maryland, circa 1889. From E. B. Meyer, Underground 
Transmission and Distribution, McGraw-Hill, N.Y., 1916 





The electric light industry was conceived at roughly the same time. One 
hundred and twenty-six years after a few Dutch pioneers taught their eager 
pupils how to store a small quantity of electric fluid in a glass jar, the 
Belgian Zénobe Gramme gave to the descendants of those pioneers the 
knowledge, so to speak, of how to remove that jar's lid. His invention of the 
modern dynamo made possible the generation of virtually unlimited 
quantities of electricity. By 1875, dazzling carbon arc lamps were lighting 
outdoor public spaces in Paris and Berlin. By 1883, wires carrying two 
thousand volts were trailing across residential rooftops in the West End of 
London. Meanwhile, Thomas Edison had invented a smaller and gentler 
lamp, the modern incandescent, that was more suitable for bedrooms and 
kitchens, and in 1881 on Pearl Street in New York City he built the first of 
hundreds of central stations supplying direct current (DC) electric power to 





And then another species of invention was planted alongside: alternating 
current (AC). Although many, including Edison, wanted to eradicate the 
invader, to pull it out by the roots as being too dangerous, their warnings 
were to no avail. By 1885, the Hungarian trio of Károly Zipernowsky, Otis 
Bláthy, and Max Déri had designed a complete AC generation and 
distribution system and began installing these in Europe. 

In the United States, George Westinghouse adopted the AC system in 
the spring of 1887 and the “battle of the currents” escalated, Westinghouse 
vying with Edison for the future of our world. In one of the last salvos of 
that brief war, on page 16 of its January 12, 1889 issue, Scientific American 
published the following challenge: 


The direct and alternating current advocates are engaged in 
active attack upon each other on the basis of the relative 
harmfulness of the two systems. One engineer has suggested a 
species of electric duel to settle the matter. He proposes that he 
shall receive the direct current while his opponent shall receive 
the alternating current. Both are to receive it at the same 
voltage, and it is to be gradually increased until one succumbs, 
and voluntarily relinquishes the contest. 


The State of New York settled the matter by adopting the electric chair 
as its new means of executing murderers. Yet, although alternating current 
was the more dangerous, it won the duel which was even then playing out 
not between individual combatants, but between commercial interests. 
Long-distance suppliers of electricity had to find economical ways to 
deliver ten thousand times more power through the average wire than had 
previously been necessary. Using the technology available at that time, 
direct current systems could not compete. 

From these beginnings electrical technology, having been carefully 
sowed, fertilized, watered, and nurtured, shot skyward and outward toward 
and beyond every horizon. It was Nikola Tesla's invention of the polyphase 


AC motor, patented in 1888, enabling industries to use alternating current 
not just for lighting but for power, that provided the last necessary 
ingredient. In 1889, quite suddenly, the world was being electrified on a 
scale that could scarcely have been conceived when Dr. George Beard first 
described a disease called neurasthenia. The telegraph had “annihilated 
space and time," many had said at the time. But twenty years later the 
electric motor made the telegraph look like a child's toy, and the electric 
locomotive was poised to explode onto the countryside. 

In early 1888, just thirteen electric railways had operated in the United 
States on a total of forty-eight miles of track, and a similar number in all of 
Europe. So spectacular was the growth of this industry that by the end of 
1889, roughly a thousand miles of track had been electrified in the United 
States alone. In another year that number again tripled. 

Eighteen eighty-nine is the year manmade electrical disturbances of the 
earth's atmosphere took on a global, rather than local, character. In that year 
the Edison General Electric Company was incorporated, and the 
Westinghouse Electric Company was reorganized as the Westinghouse 
Electric and Manufacturing Company. In that year Westinghouse acquired 
Tesla's alternating current patents and put them to use in its generating 
stations, which grew to 150 in number in 1889, and to 301 in 1890. In the 
United Kingdom, amendment of the Electric Lighting Act in 1888 eased 
regulations on the electric power industry and made central power station 
development commercially feasible for the first time. And in 1889, the 
Society of Telegraph Engineers and Electricians changed its name to the 
now more appropriate Institution of Electrical Engineers. In 1889, sixty-one 
producers in ten countries were manufacturing incandescent lamps, and 
American and European companies were installing plants in Central and 
South America. In that year Scientific American reported that “so far as we 
know, every city in the United States is provided with arc and incandescent 
illumination, and the introduction of electric lighting is rapidly extending to 
the smaller towns.”! Also in that year, Charles Dana, writing in the Medical 
Record, reported on a new class of injuries, previously produced only by 
lightning. They were due, he said, to “the extraordinary increase now going 
on in the practical application of electricity, nearly $100,000,000 being 


already invested in lights and power alone.” In 1889, most historians agree, 
the modern electrical era opened. 

And in 1889, as if the heavens had suddenly opened as well, doctors in 
the Americas, Europe, Asia, Africa, and Australia were overwhelmed by a 
flood of critically ill patients suffering from a strange disease that seemed to 
have come like a thunderbolt from nowhere, a disease that many of these 
doctors had never seen before. That disease was influenza, and that 
pandemic lasted four continuous years and killed at least one million 
people. 


Influenza Is an Electrical Disease 

Suddenly and inexplicably, influenza, whose descriptions had remained 
consistent for thousands of years, changed its character in 1889. Flu had last 
seized most of England in November 1847, over half a century earlier. The 
last flu epidemic in the United States had raged in the winter of 1874-1875. 
Since ancient times, influenza had been known as a capricious, 
unpredictable disease, a wild animal that came from nowhere, terrorized 
whole populations at once without warning and without a schedule, and 
disappeared as suddenly and mysteriously as it had arrived, not to be seen 
again for years or decades. It behaved unlike any other illness, was thought 
not to be contagious, and received its name because its comings and goings 
were said to be governed by the “influence” of the stars. 


Deaths (per million] 





1850 1860 1870 1880 1890 1900 1910 1920 1930 1940 


Influenzal deaths per million in England and Wales, 1850-1940? 





Like “anxiety disorder,” influenza is so common and so seemingly 
familiar that a thorough review of its history is necessary to unmask this 
stranger and convey the enormity of the public health disaster that occurred 
one hundred and thirty years ago. It's not that we don't know enough about 
the influenza virus. We know more than enough. The microscopic virus 
associated with this disease has been so exhaustively studied that scientists 
know more about its tiny life cycle than about any other single 
microorganism. But this has been a reason to ignore many unusual facts 
about this disease, including the fact that it is not contagious. 





Such a trend is not the only aspect of this disease that has long puzzled 
virologists. In 1992, one of the world's authorities on the epidemiology of 


influenza, R. Edgar Hope-Simpson, published a book in which he reviewed 
the essential known facts and pointed out that they did not support a mode 
of transmission by direct human-to-human contact. Hope-Simpson had been 
perplexed by influenza for a long time, in fact ever since he had treated its 
victims as a young general practitioner in Dorset, England, during the 
1932-1933 epidemic—the very epidemic during which the virus that is 
associated with the disease in humans was first isolated. But during his 71- 
year career Hope-Simpson’s questions were never answered. “The sudden 
explosion of information about the nature of the virus and its antigenic 
reactions in the human host,” he wrote in 1992, had only “added to the 
features calling for explanation.” 

Why is influenza seasonal? he still wondered. Why is influenza almost 
completely absent except during the few weeks or months of an epidemic? 
Why do flu epidemics end? Why don’t out-of-season epidemics spread? 
How do epidemics explode over whole countries at once, and disappear just 
as miraculously, as if suddenly prohibited? He could not figure out how a 
virus could possibly behave like this. Why does flu so often target young 
adults and spare infants and the elderly? How is it possible that flu 
epidemics traveled at the same blinding speed in past centuries as they do 
today? How does the virus accomplish its so-called “vanishing trick”? This 
refers to the fact that when a new strain of the virus appears, the old strain, 
between one season and the next, has vanished completely, all over the 
world at once. Hope-Simpson listed twenty-one separate facts about 
influenza that puzzled him and that seemed to defy explanation if one 
assumed that it was spread by direct contact. 

He finally revived a theory that was first put forward by Richard Shope, 
the researcher who isolated the first flu virus in pigs in 1931, and who also 
did not believe that the explosive nature of many outbreaks could be 
explained by direct contagion. Shope, and later Hope-Simpson, proposed 
that the flu is not in fact spread from person to person, or pig to pig, in the 
normal way, but that it instead remains latent in human or swine carriers, 
who are scattered in large numbers throughout their communities until the 
virus is reactivated by an environmental trigger of some sort. 





variations in solar radiation, and that it may be electromagnetic in nature, as 
a good many of his predecessors during the previous two centuries had 
suggested. 

When Hope-Simpson was young and beginning his practice in Dorset, a 
Danish physician named Johannes Mygge, at the end of a long and 
distinguished career, had just published a monograph in which he too 
showed that influenza pandemics tended to occur during years of maximum 
solar activity, and further that the yearly number of cases of flu in Denmark 
rose and fell with the number of sunspots. In an era in which epidemiology 
was becoming nothing more than a search for microbes, Mygge admitted, 
and knew already from hard experience, that “he who dances out of line 
risks having his feet stomped on."^ But he was certain that influenza had 
something to do with electricity, and he had come to this conviction in the 
same way I did: from personal experience. 

In 1904 and 1905, Mygge had kept a careful diary of his health for nine 
months, and he later compared it to records of the electrical potential of the 
atmosphere, which he had recorded three times a day for ten years as part of 
another project. It turned out that his incapacitating migraine-like 
headaches, which he had always known were connected to changes in the 
weather, almost always fell on the day of, or one day before, a sudden 
severe rise or drop in the value of the atmospheric voltage. 

But headaches were not the only effects. On the days of such electrical 
turmoil, almost without exception, his sleep was broken and unrestful and 
he was bothered with dizziness, irritable mood, a feeling of confusion, 
buzzing sensations in his head, pressure in his chest, and an irregular 
heartbeat, and sometimes, he wrote, *my condition had the character of a 
threatening influenza attack, which in every case was not essentially 
different from the onset of an actual attack of that illness."^ 

Others who have connected influenza with sunspots or atmospheric 
electricity include John Yeung (2006), Fred Hoyle (1990), J. H. Douglas 
Webster (1940), Aleksandr Chizhevskiy (1936), C. Conyers Morrell (1936), 
W. M. Hewetson (1936), Sir William Hamer (1936), Gunnar Edstróm 
(1935), Clifford Gill (1928), C. M. Richter (1921), Willy Hellpach (1911), 
Weir Mitchell (1893), Charles Dana (1890), Louise Fiske Bryson (1890), 


Ludwig Buzorini (1841), Johann Schónlein (1841), and Noah Webster 
(1799). In 1836, Heinrich Schweich observed that all physiological 
processes produce electricity, and proposed that an electrical disturbance of 
the atmosphere may prevent the body from discharging it. He repeated the 
then-common belief that the accumulation of electricity within the body 
causes the symptoms of influenza. No one has yet disproven this. 

It is of interest that between 1645 and 1715, a period astronomers call 
the Maunder Minimum, when the sun was so quiet that virtually no 
sunspots were to be seen and no auroras graced polar nights—during which, 
according to native Canadian tradition, "the people were deserted by the 
lights from the sky,”® —there were also no worldwide pandemics of flu. In 
1715, sunspots reappeared suddenly after a lifetime’s absence. In 1716, the 
famous English astronomer Sir Edmund Halley, at sixty years of age, 
published a dramatic description of the northern lights. It was the first time 
he had ever seen them. But the sun was still not fully active. As though it 
had woken up after a long sleep, it stretched its legs, yawned, and lay down 
again after displaying only half the number of sunspots that it shows us 
today at the peak of each eleven-year solar cycle. It wasn’t until 1727 that 
the sunspot number surpassed 100 for the first time in over a century. And 
in 1728 influenza arrived in waves over the surface of the earth, the first flu 
pandemic in almost a hundred and fifty years. More universal and enduring 
than any in previously recorded history, that epidemic appeared on every 
continent, became more violent in 1732, and by some reports lasted until 
1738, the peak of the next solar cycle.? John Huxham, who practiced 
medicine in Plymouth, England, wrote in 1733 that “scarce any one had 
escaped it.” He added that there was “a madness among dogs; the horses 
were seized with the catarrh before mankind; and a gentleman averred to 
me, that some birds, particularly the sparrows, left the place where he was 
during the sickness."? An observer in Edinburgh reported that some people 
had fevers for sixty continuous days, and that others, not sick, “died 
suddenly."? By one estimate, some two million people worldwide perished 
in that pandemic.!? 

If influenza is primarily an electrical disease, a response to an electrical 
disturbance of the atmosphere, then it is not contagious in the ordinary 





evere outbreaks were reported in May of that year 
simultaneously in Bukhara, Uzbekistan; Greenland; and northern Alberta." 
Flu was reported in July in Philadelphia! and in Hillston, a remote town in 
Australia, and in August in the Balkans.'* This pattern being at odds with 
prevailing theories, many historians have pretended that the 1889 pandemic 
didn’t “really” start until it had seized the western steppes of Siberia at the 
end of September and that it then spread in an orderly fashion from there 
outward throughout the rest of the world, person to person by contagion. 
But the trouble is that the disease still would have had to travel faster than 
the trains and ships of the time. It reached Moscow and St. Petersburg 
during the third or fourth week of October, but by then, influenza had 
already been reported in Durban, South Africa!’ and Edinburgh, Scotland.'® 
New Brunswick, Canada,!” Cairo,'® Paris,? Berlin? and Jamaica? were 
reporting epidemics in November; London, Ontario on December 4;? 
Stockholm on December 9;? New York on December 11;^ Rome on 
December 12;?» Madrid on December 13;?6 and Belgrade on December 15.7? 





It was as if something fundamental had changed in the 
atmosphere, as if brush fires were being ignited by some unknown vandal 
randomly, everywhere in the world. 

One observer in East Central Africa, which was struck in September 
1890, asserted that influenza had never before appeared in that part of 
Africa at all, not within the memory of the oldest living inhabitants.?9 

"Influenza," said Dr. Benjamin Lee of the Pennsylvania State Board of 
Health, *spreads like a flood, inundating whole sections in an hour... It is 
scarcely conceivable that a disease which spreads with such astonishing 
rapidity, goes through the process of re-development in each person 
infected, and is only communicated from person to person or by infected 
articles.”29 





port of call, it was something to remember. In 1894, Charles Creighton 
described fifteen separate historical instances where entire ships or even 
many ships in a naval fleet were seized by the illness far from landfall, as if 
they had sailed into an influenzal fog, only to discover, in some cases, upon 
arriving at their next port, that influenza had broken out on land at the same 
time. Creighton added one report from the contemporary pandemic: the 
merchantship “Wellington” had sailed with its small crew from London on 
December 19, 1891, bound for Lyttelton, New Zealand. On the 26th of 
March, after over three months at sea, the captain was suddenly shaken by 
intense febrile illness. Upon arriving at Lyttelton on April 2, “the pilot, 
coming on board found the captain ill in his berth, and on being told the 
symptoms at once said, ‘It is the influenza: I have just had it myself.’”2° 

An 1857 report was so compelling that William Beveridge included it in 
his 1975 textbook on influenza: “The English warship Arachne was 
cruising off the coast of Cuba ‘without any contact with land.’ No less than 
114 men out of a crew of 149 fell ill with influenza and only later was it 
learnt that there had been outbreaks in Cuba at the same time.”*! 

The speed at which influenza travels, and its random and simultaneous 
pattern of spread, has perplexed scientists for centuries, and has been the 
most compelling reason for some to continue to suspect atmospheric 
electricity as the cause, despite the known presence of an extensively 
studied virus. Here is a sampling of opinion, old and modern: 


Perhaps no disease has ever been observed to affect so many 
people in so short a time, as the Influenza, almost a whole city, 
town, or neighborhood becoming affected in a few days, indeed 
much sooner than could be supposed to spread from contagion. 

Mercatus relates, that when it prevailed in Spain, in 1557, the 
greatest part of the people were seized in one day. 

Dr. Glass says, when it was rife in Exeter, in 1729, two 
thousand were attacked in one night. 

Shadrach Ricketson, M.D. (1808), A Brief History of 
the Influenza? 


The simple fact is to be recollected that this epidemic affects 
a whole region in the space of a week; nay, a whole continent as 
large as North America, together with all the West Indies, in the 
course of a few weeks, where the inhabitants over such vast 
extent of country, could not, within so short a lapse of a time, 
have had the least communication or intercourse whatever. This 
fact alone is sufficient to put all idea of its being propagated by 
contagion from one individual to another out of the question. 
Alexander Jones, M.D. (1827), Philadelphia Journal 
of the Medical and Physical Sciences? 


Unlike cholera, it outstrips in its course the speed of human 
intercourse. 
Theophilus Thompson, M.D. (1852), Annals of 
Influenza or Epidemic Catarrhal Fever in Great 
Britain from 1510 to 18375 





Sir Morell Mackenzie, M.D. (1893), Fortnightly 
Review? 


Usually influenza travels at the same speed as man but at 
times it apparently breaks out simultaneously in widely separated 
parts of the globe. 

Jorgen Birkeland (1949), Microbiology and Man*° 


[Before 1918] there are records of two other major epidemics 
of influenza in North America during the past two centuries. The 
first of these occurred in 1789, the year in which George 
Washington was inaugurated President. The first steamboat did 
not cross the Atlantic until 1819, and the first steam train did not 
run until 1830. Thus, this outbreak occurred when man's fastest 


conveyance was the galloping horse. Despite this fact, the 

influenza outbreak of 1789 spread with great rapidity; many 

times faster and many times farther than a horse could gallop. 
James Bordley III, M.D. and A. McGehee Harvey, 
M.D. (1976), Two Centuries of American Medicine, 
1776-1976? 





Why have epidemic patterns in Great Britain not altered in 
four centuries, centuries that have seen great increases in the 
speed of human transport? 

John J. Cannell, M.D. (2008), *On the Epidemiology 
of Influenza," in Virology Journal 





In the first wave of the pandemic of 1889 in England, neurological 
symptoms were most often prominent and respiratory symptoms absent.^ 
Most of Medical Officer Róhring's 239 flu patients at Erlangen, Bavaria, 
had neurological and cardiovascular symptoms and no respiratory disease. 
Nearly one-quarter of the 41,500 cases of flu reported in Pennsylvania as of 
May 1, 1890 were classified as primarily neurological and not respiratory.*! 
Few of David Brakenridge's patients in Edinburgh, or Julius Althaus' 
patients in London, had respiratory symptoms. Instead they had dizziness, 
insomnia, indigestion, constipation, vomiting, diarrhea, *utter prostration of 
mental and bodily strength," neuralgia, delirium, coma, and convulsions. 


Upon recovery many were left with neurasthenia, or even paralysis or 
epilepsy. Anton Schmitz published an article titled "Insanity After 
Influenza" and concluded that influenza was primarily an epidemic nervous 
disease. 


2EBEE some cases it seizes on that part of (the 


nervous system) which governs the machinery of respiration, 
in others on that which presides over the digestive functions; in 
others again it seems, as it were, to run up and down the 
nervous keyboard, jarring the delicate mechanism and stirring 
up disorder and pain in different parts of the body with what 
almost seems malicious caprice... As the nourishment of every 
tissue and organ in the body is under the direct control of the 
nervous system, it follows that anything which affects the 
latter has a prejudicial effect on the former; hence it is not 
surprising that influenza in many cases leaves its mark in 
damaged structure. Not only the lungs, but the kidneys, the 
heart, and other internal organs and the nervous matter itself 
may suffer in this way.“ 


Insane asylums filled up with patients who had had influenza, people 
suffering variously from profound depression, mania, paranoia, or 
hallucinations. “The number of admissions reached unprecedented 
proportions,” reported Albert Leledy at the Beauregard Lunatic Asylum, at 
Bourges, in 1891. “Admissions for the year exceed those of any previous 
year,” reported Thomas Clouston, superintending physician of the Royal 
Edinburgh Asylum for the Insane, in 1892. “No epidemic of any disease on 
record has had such mental effects,” he wrote. In 1893, Althaus reviewed 
scores of articles about psychoses after influenza, and the histories of 
hundreds of his own and others’ patients who had gone insane after the flu 
during the previous three years. He was perplexed by the fact that the 
majority of psychoses after influenza were developing in men and women 
in the prime of their life, between the ages of 21 and 50, that they were 


most likely to occur after only mild or slight cases of the disease, and that 
more than one-third of these people had not yet regained their sanity. 

The frequent lack of respiratory illness was also noted in the even 
deadlier 1918 pandemic. In his 1978 textbook Beveridge, who had lived 
through it, wrote that half of all influenza patients in that pandemic did not 
have initial symptoms of nasal discharge, sneezing, or sore throat.“ 

The age distribution is also wrong for contagion. In other kinds of 
infectious diseases, like measles and mumps, the more aggressive a strain of 
virus is and the faster it spreads, the more rapidly adults build up immunity 
and the younger the population that gets it every year. According to Hope- 
Simpson, this means that between pandem- ics influenza should be 
attacking mainly very young children. But influenza keeps on stubbornly 
targeting adults; the average age is almost always between twenty and forty, 
whether during a pandemic or not. The year 1889 was no exception: 
influenza felled preferentially vigorous young adults in the prime of their 
life, as if it were maliciously choosing the strongest instead of the weakest 
of our species. 

Then there is the confusion about animal infections, which are so much 
in the news year after year, scaring us all about catching influenza from 
swine or birds. 








hen the army of King Karlmann of Bavaria was seized by 
influenza in 876 A.D., the same disease also decimated the dogs and the 
birds.^ In later epidemics, up to and including the twentieth century, illness 
was commonly reported to break out among dogs, cats, horses, mules, 
sheep, cows, birds, deer, rabbits, and even fish at the same time as 
humans.*° Beveridge listed twelve epidemics during the eighteenth and 
nineteenth centuries in which horses caught the flu, usually one or two 
months before the humans. 





During the 1918-1919 pandemic, monkeys and baboons perished in great 
numbers in South Africa and Madagascar, sheep in northwest England, 


horses in France, moose in northern Canada, and buffalo in Yellowstone.^ 
There is no mystery here. We are not catching the flu from animals, nor 
they from us. If influenza is caused by abnormal electromagnetic conditions 
in the atmosphere, then it affects all living things at the same time, 
including living things that don't share the same viruses or live closely with 
one another. 

The obstacle to unmasking the stranger that is influenza is the fact that it 
is two different things. Influenza is a virus and it is also a clinical illness. 
The confusion comes about because since 1933, human influenza has been 
defined by the organism that was discovered in that year, and not by clinical 
symptoms. If an epidemic strikes, and you come down with the same 
disease as everyone else, but an influenza virus can't be isolated from your 
throat and you don't develop antibodies to one, then you are said not to 
have influenza. But the fact is that although influenza viruses are associated 
in some way with disease epidemics, they have never been shown to cause 
them. 

Seventeen years of surveillance by Hope-Simpson in and around the 
community of Cirencester, England, revealed that despite popular belief, 
influenza is not readily communicated from one person to another within a 
household. Seventy percent of the time, even during the *Hong Kong flu" 
pandemic of 1968, only one person in a household would get the flu. If a 
second person had the flu, both often caught it on the same day, which 
meant that they did not catch it from each other. Sometimes different minor 
variants of the virus were circulating in the same village, even in the same 
household, and on one occasion two young brothers who shared a bed had 
different variants of the virus, proving that they could not have caught it 
from each other, or even from the same third person.^ William S. Jordan, in 
1958, and P. G. Mann, in 1981, came to similar conclusions about the lack 
of spread within families. 

Another indication that something is wrong with prevailing theories is 
the failure of vaccination programs. Although vaccines have been proven to 
confer some immunity to particular strains of flu virus, several prominent 
virologists have admitted over the years that vaccination has done nothing 
to stop epidemics and that the disease still behaves just as it did a thousand 


years ago.^? In fact, after reviewing 259 vaccination studies from the British 
Medical Journal spanning 45 years, Tom Jefferson recently concluded that 
influenza vaccines have had essentially no impact on any real outcomes, 
such as school absences, working days lost, and flu-related illnesses and 
deaths.°° 





8. Mystery on the Isle of Wight 


IN 1904 THE BEES began to die. 

From this quiet island, 23 miles long and 13 miles wide, lying off 
England's southern coast, one looks across the English Channel toward the 
distant shores of France. In the preceding decade two men, one on each side 
of the Channel, one a physician and physicist, the other an inventor and 
entrepreneur, had occupied their minds with a newly discovered form of 
electricity. The work of each man had very different implications for the 
future of our world. 

At the westernmost end of the Isle of Wight, near offshore chalk 
formations called The Needles, in 1897, a handsome young man named 
Giuglielmo Marconi erected his own “needle,” a tower as tall as a twelve- 
story building. It supported the antenna for what became the world's first 
permanent radio station. Marconi was liberating electricity, vibrating at 
close to a million cycles per second, from its confining wires, and was 
broadcasting it freely through the air itself. He did not stop to ask if this was 
safe. 

A few years earlier, in 1890, a well-known physician, director of the 
Laboratory of Biological Physics at the Collége de France in Paris, had 
already begun investigations bearing on the important question Marconi 
was not asking: how does electricity of high frequencies affect living 
organisms? A distinguished presence in physics as well as medicine, 
Jacques-Arséne d' Arsonval is remembered today for his many contributions 
in both fields. He devised ultra-sensitive meters to measure magnetic fields, 
and equipment to measure heat production and respiration in animals; made 
improvements to the microphone and the telephone; and created a new 
medical specialty called darsonvalization, which is still practiced today in 
the nations of the former Soviet Bloc. In the West it has evolved into 


diathermy, which is the therapeutic use of radio waves to produce heat 
within the body. But darsonvalization is the use of radio waves medicinally 
at low power, without generating heat, to produce the kinds of effects 
d’Arsonval discovered in the early 1890s. 

He had first observed that electrotherapy, as then practiced, was not 
producing uniform results, and he wondered if this was because of lack of 
precision in the form of the electricity being applied. He therefore designed 
an induction machine capable of putting out perfectly smooth sine waves, 
“without jerks or teeth,”! that would not be injurious to the patient. When he 
tested this current on human subjects he found, as he had predicted, that at 
therapeutic doses it caused no pain, yet had potent physiological effects. 





Jacques-Arséne d’ Arsonval (1851-1940) 


“We have seen that with very steady sine waves, nerve and muscle are 
not stimulated,’ he wrote. “The passage of the current nevertheless is 
responsible for profound modification of metabolism as shown by the 
consumption of a greater amount of oxygen and the production of 
considerably more carbon dioxide. If the shape of the wave is changed, 
each electrical wave will produce a muscular contraction."? D' Arsonval had 
already discovered the reason, 125 years ago, why today's digital 
technologies, whose waves have nothing but “jerks and teeth,” are causing 
so much illness. 


D’Arsonval next experimented with alternating currents of high 
frequency. Using a modification of the wireless apparatus devised a few 
years earlier by Heinrich Hertz, he exposed humans and animals to currents 
of 500,000 to 1,000,000 cycles per second, applied either by direct contact 
or indirectly by induction from a distance. They were close to the 
frequencies Marconi was soon going to broadcast from the Isle of Wight. In 
no case did the subject’s body temperature increase. But in every case his 
subject’s blood pressure fell significantly, without—in the case of human 
subjects at least—any conscious sensation. 





These early results should have made anyone experimenting with radio 
waves think twice before exposing the whole world to them 
indiscriminately—should have at least made them cautious. Marconi, 
however, was unfamiliar with d' Arsonval's work. Largely self-educated, the 
inventor had no inkling of radio's potential dangers and no fear of it. 
Therefore when he powered up his new transmitter on the island he had no 
suspicion that he might be doing himself or anyone else any harm. 

If radio waves are dangerous, Marconi, of all people in the world, 
should have suffered from them. Let us see if he did. 

As early as 1896, after a year and a half of experimenting with radio 
equipment in his father's attic, the previously healthy 22-year-old youth 
began running high temperatures which he attributed to stress. These fevers 
were to recur for the rest of his life. By 1900 his doctors were speculating 
that perhaps he had unknowingly had rheumatic fever as a child. By 1904 
his bouts of chills and fevers had become so severe that it was thought they 
were recurrences of malaria. At that time he was occupied with building a 
permanent super-high-power radio link across the Atlantic Ocean between 
Cornwall, England and Cape Breton Island, Nova Scotia. Because he 
thought that longer distances required longer waves, he suspended 
tremendous wire net aerials, occupying acres of land, from multiple towers 
hundreds of feet tall on both sides of the ocean. 


On March 16, 1905, Marconi married Beatrice O'Brien. In May, after 
their honeymoon, he took her to live in the station house at Port Morien on 
Cape Breton, surrounded by twenty-eight huge radio towers in three 
concentric circles. Looming over the house, two hundred antenna wires 
stretched out from a center pole like the spokes of a great umbrella more 
than one mile in circumference. As soon as Beatrice settled in, her ears 
began to ring. 

















From: W. J. Baker, A History of the Marconi Company, St. Martin's Press, N.Y., 1971 


After three months there she was ill with severe jaundice. When 
Marconi took her back to England it was to live underneath the other 
monster aerial, at Poldhu Bay in Cornwall. She was pregnant all this time, 
and although she moved to London before giving birth, her child had spent 
most of its nine months of fetal life bombarded with powerful radio waves 
and lived only a few weeks, dying of *unknown causes." At about the same 
time Marconi himself collapsed completely, spending much of February 
through May of 1906 feverish and delirious. 

Between 1918 and 1921, while engaged in designing short wave 
equipment, Marconi suffered from bouts of suicidal depression. 

In 1927, during the honeymoon he took with his second wife Maria 
Cristina, he collapsed with chest pains and was diagnosed with a severe 


heart condition. Between 1934 and 1937, while helping to develop 
microwave technology, he suffered as many as nine heart attacks, the final 
one fatal at age 63. 

Bystanders sometimes tried to warn him. Even at his first public 
demonstration on Salisbury Plain in 1896, there were spectators who later 
sent him letters describing various nerve sensations they had experienced. 
His daughter Degna, reading them much later while doing research for the 
biography of her father, was particular taken by one letter, from a woman 
“who wrote that his waves made her feet tickle.” Degna wrote that her 
father received letters of this sort frequently. When, in 1899, he built the 
first French station in the coastal town of Wimereux, one man who lived 
close by “burst in with a revolver,” claiming that the waves were causing 
him sharp internal pains. Marconi dismissed all such reports as fantasy. 

In what may have been an even more ominous warning, Queen Victoria 
of England, in residence at Osborne House, her estate at the north end of the 
Isle of Wight, suffered a cerebral hemorrhage and died on the evening of 
January 22, 1901, just as Marconi was firing up a new, more powerful 
transmitter twelve miles away. He was hoping to communicate with Poldhu 
the next day, 300 kilometers distant, twice as far as any previously recorded 
radio broadcast, and he did. On January 23 he sent a telegram to his cousin 
Henry Jameson Davis, saying “Completely successful. Keep information 
private. Signed William.” 

And then there were the bees. 

In 1901, there were already two Marconi stations on the Isle of Wight— 
Marconi’s original station, which had been moved to Niton at the south end 
of the island next to St. Catherine’s Lighthouse, and the Culver Signal 
Station run by the Coast Guard at the east end on Culver Down. By 1904, 
two more had been added. According to an article published in that year by 
Eugene P. Lyle in World’s Work magazine, four Marconi stations were now 
operating on the small island, communicating with a steadily growing 
number of naval and commercial ships of many nations, steaming through 
the Channel, that were equipped with similar apparatus. It was the greatest 
concentration of radio signals in the world at that time. 


In 1906, the Lloyd's Signal Station, half a mile east of St. Catherine's 
Lighthouse, also acquired wireless equipment. At this point the bee 
situation became so severe that the Board of Agriculture and Fisheries 
called in biologist Augustus Imms of Christ's College, Cambridge, to 
investigate. Ninety percent of the honey bees had disappeared from the 
entire island for no apparent reason. The hives all had plenty of honey. But 
the bees could not even fly. *They are often to be seen crawling up grass 
stems, or up the supports of the hive, where they remain until they fall back 
to the earth from sheer weakness, and soon afterwards die," he wrote. 
Swarms of healthy bees were imported from the mainland, but it was of no 
use: within a week the fresh bees were dying off by the thousands. 





severe losses of bees being 
reported in parts of Australia, Canada, the United States, and South Africa.^ 
The disease was also reported in Italy, Brazil, France, Switzerland, and 
Germany. Although for years one or another parasitic mite was blamed, 
British bee pathologist Leslie Bailey disproved those theories in the 1950s 
and came to regard the disease itself as a sort of myth. Obviously bees had 
died, he said, but not from anything contagious. 

Over time, Isle of Wight disease took fewer and fewer bee lives as the 
insects seemed to adapt to whatever had changed in their environment. 
Places that had been attacked first recovered first. 

Then, in 1917, just as the bees on the Isle of Wight itself appeared to be 
regaining their former vitality, an event occurred that changed the electrical 
environment of the rest of the world. Millions of dollars of United States 
government money were suddenly mobilized in a crash program to equip 
the Army, Navy, and Air Force with the most modern communication 
capability possible. 





“Mr. Charles Schilke of Morganville, Monmouth County, a beekeeper 
with considerable experience operating about 300 colonies reported a great 
loss of bees from the hives in one of his yards located near Bradevelt,” read 


one report, published in August 1918.° “Thousands of dead were lying and 
thousands of dying bees were crawling about in the vicinity of the hive, 
collecting in groups on bits of wood, on stones and in depressions in the 
earth. The affected bees appeared to be practically all young adult workers 
about the age when they would normally do the first field work, but all ages 
of older bees were found. No abnormal condition within the hive was 
noticed at this time.” 

This outbreak was confined to Morganville, Freehold, Milhurst, and 
nearby areas of New Jersey, just a few miles seaward from one of the most 
powerful radio stations on the planet, the one in New Brunswick that had 
just been taken over by the government for service in the war. A 50,000- 
watt Alexanderson alternator had been installed in February of that year to 
supplement a less efficient 350,000-watt spark apparatus. Both provided 
power to a mile-long aerial consisting of 32 parallel wires supported by 12 
steel towers 400 feet tall, broadcasting military communications across the 
ocean to the command in Europe. 

For long distance 
communications there were no satellites, and no shortwave equipment. 
Vacuum tubes had not yet been perfected. Transistors were decades into the 
future. It was the era of immense radio waves, inefficient aerials the size of 
small mountains, and spark gap transmitters that scattered radiation like 
buckshot all over the radio spectrum to interfere with everyone else’s 
signals. Oceans were crossed by brute force, three hundred thousand watts 
of electricity being supplied to those mountains to achieve a radiated power 
of perhaps thirty thousand. The rest was wasted as heat. Morse code could 
be sent but not voice. Reception was sporadic, unreliable. 

Few of the great powers had had a chance to establish overseas 
communication with their colonies before war intervened in 1914. The 
United Kingdom had two ultra-powerful stations at home, but no radio links 
with a colony. The first such link was still under construction near Cairo. 
France had one powerful station at the Eiffel Tower, and another at Lyon, 
but no links with any of its overseas colonies. Belgium had a powerful 
station in the Congo State, but blew up its home station at Brussels after 
war broke out. Italy had one powerful station in Eritrea, and Portugal had 


one in Mozambique and one in Angola. Norway had one ultrapotent 
transmitter, Japan one, and Russia one. Only Germany had made much 
progress in building an Imperial Chain, but within months after the 
declaration of war, all of its overseas stations—at Togo, Dar-es-Salaam, 
Yap, Samoa, Nauru, New Pomerania, Cameroon, Kiautschou, and German 
East Africa—were destroyed.® 

Radio, in short, was in its faltering infancy, still crawling, its attempts to 
walk hindered by the onset of the European War. During 1915 and 1916, the 
United Kingdom made progress in installing thirteen long-range stations in 
various parts of the world in order to keep in contact with its navy. 

When the United States entered the war in 1917, it changed the terrain 
in a hurry. The United States Navy already had one giant transmitter at 
Arlington, Virginia and a second at Darien, in the Canal Zone. A third, in 
San Diego, began broadcasting in May 1917, a fourth, at Pearl Harbor, on 
October 1 of that year, and a fifth, at Cavite, the Philippines, on December 
19. The Navy also took over and upgraded private and foreign-owned 
stations at Lents, Oregon; South San Francisco, California; Bolinas, 
California; Kahuku, Hawaii; Heeia Point, Hawaii; Sayville, Long Island; 
Tuckerton, New Jersey; and New Brunswick, New Jersey. By late 1917, 
thirteen American stations were sending messages across two oceans. 

Fifty more medium and high powered radio stations ringed the United 
States and its possessions for communication with ships. To equip its ships 
the Navy manufactured and deployed over ten thousand low, medium, and 
high powered transmitters. By early 1918, the Navy was graduating over 
four hundred students per week from its radio operating courses. In the 
short course of a year, between April 6, 1917 and early 1918, the Navy built 
and was operating the world’s largest radio network. 

America’s transmitters were far more efficient than most of those built 
previously. When a 30-kilowatt Poulson arc was installed at Arlington in 
1913, it was found to be so much superior to the 100-kilowatt spark 
apparatus there that the Navy adopted the arc as its preferred equipment and 
ordered sets with higher and higher ratings. A 100-kilowatt arc was 
installed at Darien, a 200-kilowatt arc in San Diego, 350-kilowatt arcs at 


Pearl Harbor and Cavite. In 1917, 30-kilowatt arcs were being installed on 
Navy ships, outclassing the transmitters on most ships of other nations. 

Still, the arc was basically only a spark gap with electricity flowing 
across it continuously instead of in bursts. It still sprayed the airway with 
unwanted harmonics, transmitted voices poorly, and was not reliable 
enough for continuous day and night communication. So the Navy tried out 
its first high-speed alternator, the one it inherited at New Brunswick. 
Alternators did not have spark gaps at all. Like fine musical instruments, 
they produced pure continuous waves that could be sharply tuned, and 
modulated for crystal clear voice or telegraphic communication. Ernst 
Alexanderson, who designed them, also designed an antenna to go with 
them that increased radiation efficiency sevenfold. When tested against the 
350-kilowatt timed spark at the same station, the 50-kilowatt alternator 
proved to have a bigger range.’ So in February 1918, the Navy began to rely 
on the alternator to handle continuous communications with Italy and 
France. 

In July 1918, another 200-kilowatt arc was added to the system the 
Navy had taken over at Sayville. In September 1918, a 500-kilowatt arc 
went on the air at a new naval station at Annapolis, Maryland. Meanwhile 
the Navy had ordered a second, more powerful alternator for New 
Brunswick, of 200-kilowatt capacity. Installed in June, it too went on the air 
full time in September. New Brunswick immediately became the most 
powerful station in the world, outclassing Germany's flagship station at 
Nauen, and was the first that transmitted both voice and telegraphic 
messages across the Atlantic Ocean clearly, continuously, and reliably. Its 
signal was heard over a large part of the earth. 

The disease that was called Spanish influenza was born during these 
months. It did not originate in Spain. It did, however, kill tens of millions 
all over the world, and it became suddenly more fatal in September of 1918. 
By some estimates the pandemic struck more than half a billion people, or a 
third of the world's population. Even the Black Death of the fourteenth 
century did not kill so many in so short a period of time. No wonder 
everyone is terrified of its return. 


A few years ago researchers dug up four bodies in Alaska that had lain 
frozen in the permafrost since 1918 and were able to identify RNA from an 
influenza virus in the lung tissue of one of them. This was the monster germ 
that was supposed to have felled so many in the prime of their lives, the 
microbe that so resembles a virus of pigs, against whose return we are to 
exercise eternal vigilance, lest it decimate the world again. 





outbreak, laying low about 400 people, occurred in February in the Naval 
Radio School at Cambridge, Massachusetts.? In March, influenza spread to 
Army camps where the Signal Corps was being trained in the use of the 
wireless: 1,127 men contracted influenza in Camp Funston, in Kansas, and 
2,900 men in the Oglethorpe camps in Georgia. In late March and April, the 
disease spread to the civilian population, and around the world. 

Mild at first, the epidemic exploded with death in September, 
everywhere in the world at once. Waves of mortality traveled with 
astonishing speed over the global ocean of humanity, again and again until 
their force was finally spent three years later. 





Others bled from their 
gums, ears, skin, stomach, intestines, uterus, or kidneys, the most common 
and rapid route to death being hemorrhage in the lungs: flu victims drowned 
in their own blood. Autopsies revealed that as many as one-third of fatal 
cases had also hemorrhaged into their brain,? and occasionally a patient 
appeared to be recovering from respiratory symptoms only to die of a brain 
hemorrhage. 

“The regularity with which these various hemorrhages appeared 
suggested the possibility of there being a change in the blood itself,” wrote 
Drs. Arthur Erskine and B. L. Knight of Cedar Rapids, Iowa in late 1918. 


So they tested the blood from a large number of patients with influenza and 
pneumonia. “In every case tested without a single exception," they wrote, 
“the coagulability of the blood was lessened, the increase in time required 
for coagulation varying from two and one-half to eight minutes more than 
normal. Blood was tested as early as the second day of infection, and as late 
as the twentieth day of convalescence from pneumonia, with the same 
results... Several local physicians also tested blood from their patients, and, 
while our records are at this time necessarily incomplete, we have yet to 
receive a report of a case in which the time of coagulation was not 
prolonged.” 





Erskine and Knight saved their 
patients not by fighting infection, but by giving them large doses of calcium 
lactate to facilitate blood clotting. 

Another astonishing fact that makes no sense if this pandemic was 
infectious, but that makes good sense if it was caused by radio waves, is 
that instead of striking down the old and the infirm like most diseases, this 
one killed mostly healthy, vigorous young people between the ages of 
eighteen and forty—just as the previous pandemic had done, with a little 
less vehemence, in 1889. This, as we saw in chapter 5, is the same as the 
predominant age range for neurasthenia, the chronic form of electrical 
illness. Two-thirds of all influenza deaths were in this age range.'^ Elderly 
patients were rare.!° One doctor in Switzerland wrote that he “knew of no 
case in an infant and no severe case in persons over 50,” but that “one 
robust person showed the first symptoms at 4 p.m. and died before 10 the 
next morning."!6 A reporter in Paris went so far as to say that “only persons 
between 15 and 40 years of age are affected.” !” 

The prognosis was better if you were in poor physical condition. If you 
were undernourished, physically handicapped, anemic, or tuberculous, you 
were much less likely to get the flu and much less likely to die from it if 
you did.'? This was such a common observation that Dr. D. B. Armstrong 
wrote a provocative article, published in the Boston Medical and Surgical 


Journal, titled “Influenza: Is it a Hazard to Be Healthy?” Doctors were 
seriously discussing whether they were actually giving their patients a death 
sentence by advising them to keep fit! 

The flu was reported to be even more fatal for pregnant women. 

A further peculiarity that had doctors scratching their heads was that in 
most cases, after the patients’ temperature had returned to normal, their 
pulse rate fell below 60 and remained there for a number of days. In more 
serious cases the pulse rate fell to between 36 and 48, an indication of heart 
block.'® This too is puzzling for a respiratory virus, but will make sense 
when we learn about radio wave sickness. 

Patients also regularly lost some of their hair two to three months after 
recovering from the flu. According to Samuel Ayres, a dermatologist at 
Massachusetts General Hospital in Boston, this was an almost daily 
occurrence, most of these patients being young women. This is not an 
expected after-effect of respiratory viruses either, but hair loss has been 
widely reported from exposure to radio waves.”° 

Yet another puzzling observation was that so few patients in 1918 had 
sore throats, runny noses, or other initial respiratory symptoms.” But 
neurological symptoms, just as in the pandemic of 1889, were rampant, 
even in mild cases. They ranged from insomnia, stupor, dulled perceptions, 
unusually heightened perceptions, tingling, itching, and impairment of 
hearing to weakness or partial paralysis of the palate, eyelids, eyes, and 
various other muscles.? The famous Karl Menninger reported on 100 cases 
of psychosis triggered by influenza, including 35 of schizophrenia, that he 
saw during a three-month period.?? 

Although the infectious nature of this illness was widely assumed, 
masks, quarantines, and isolation were all without effect. Even in an 
isolated country like Iceland the flu spread universally, in spite of the 
quarantining of its victims. 

The disease seemed to spread impossibly fast. “There is no reason to 
suppose that it traveled more rapidly than persons could travel [but] it has 
appeared to do so,” wrote Dr. George A. Soper, Major in the United States 
Army.”° 


But most revealing of all were the various heroic attempts to prove the 
infectious nature of this disease, using volunteers. All these attempts, made 
in November and December 1918 and in February and March 1919, failed. 
One medical team in Boston, working for the United States Public Health 
Service, tried to infect one hundred healthy volunteers between the ages of 
eighteen and twenty-five. Their efforts were impressive and make 
entertaining reading: 

“We collected the material and mucous secretions of the mouth and nose 
and throat and bronchi from cases of the disease and transferred this to our 
volunteers. We always obtained this material in the same way. The patient 
with fever, in bed, had a large, shallow, traylike arrangement before him or 
her, and we washed out one nostril with some sterile salt solutions, using 
perhaps 5 c.c., which is allowed to run into the tray; and that nostril is 
blown vigorously into the tray. This is repeated with the other nostril. The 
patient then gargles with some of the solution. Next we obtain some 
bronchial mucus through coughing, and then we swab the mucous surface 
of each nares and also the mucous surface of the throat... Each one of the 
volunteers... received 6 c.c. of the mixed stuff that I have described. They 
received it into each nostril; received it in the throat, and on the eye; and 
when you think that 6 c.c. in all was used, you will understand that some of 
it was swallowed. None of them took sick.” 

In a further experiment with new volunteers and donors, the salt solution 
was eliminated, and with cotton swabs, the material was transferred directly 
from nose to nose and from throat to throat, using donors in the first, 
second, or third day of the disease. “None of these volunteers who received 
the material thus directly transferred from cases took sick in any way... All 
of the volunteers received at least two, and some of them three ‘shots’ as 
they expressed it.” 

In a further experiment 20 c.c. of blood from each of five sick donors 
were mixed and injected into each volunteer. “None of them took sick in 
any way.” 

“Then we collected a lot of mucous material from the upper respiratory 
tract, and filtered it through Mandler filters. This filtrate was injected into 


ten volunteers, each one receiving 3.5 c.c. subcutaneously, and none of 
these took sick in any way." 

Then a further attempt was made to transfer the disease “in the natural 
way,” using fresh volunteers and donors: “The volunteer was led up to the 
bedside of the patient; he was introduced. He sat down alongside the bed of 
the patients. They shook hands, and by instructions, he got as close as he 
conveniently could, and they talked for five minutes. At the end of the five 
minutes, the patient breathed out as hard as he could, while the volunteer, 
muzzle to muzzle (in accordance with his instructions, about 2 inches 
between the two), received this expired breath, and at the same time was 
breathing in as the patient breathed out... After they had done this for five 
times, the patient coughed directly into the face of the volunteer, face to 
face, five different times... [Then] he moved to the next patient whom we 
had selected, and repeated this, and so on, until this volunteer had had that 
sort of contact with ten different cases of influenza, in different stages of the 
disease, mostly fresh cases, none of them more than three days old... None 
of them took sick in any way.” 

“We entered the outbreak with a notion that we knew the cause of the 
disease, and were quite sure we knew how it was transmitted from person to 
person. Perhaps,” concluded Dr. Milton Rosenau, “if we have learned 
anything, it is that we are not quite sure what we know about the disease.”2’ 

Earlier attempts to demonstrate contagion in horses had met with the 
same resounding failure. Healthy horses were kept in close contact with 
sick ones during all stages of the disease. Nose bags were kept on horses 
that had nasal discharges and high temperatures. Those nose bags were used 
to contain food for other horses which, however, stubbornly remained 
healthy. As a result of these and other attempts, Lieutenant Colonel Herbert 
Watkins-Pitchford of the British Army Veterinary Corps wrote in July 1917 
that he could find no evidence that influenza was ever spread directly from 
one horse to another. 

The other two influenza pandemics of the twentieth century, in 1957 and 
1968, were also associated with milestones of electrical technology, 
pioneered once again by the United States. 


Radar, first used extensively during World War II, was deployed on a 
spectacular scale by the United States during the mid-1950s, as it sought to 
surround itself with a triple layer of protection that would detect any 
nuclear attack. The first and smallest barrier was the 39 stations of the 
Pinetree Line, which kept vigil from coast to coast across southern Canada 
and from Nova Scotia northward to Baffin Island. This line, completed in 
1954, was the roots, as it were, for a huge tree of surveillance that grew 
between 1956 and 1958, whose branches spread across mid- and high- 
latitude Canada, sent shoots into Alaska, and drooped down over the 
Atlantic and Pacific Oceans to guard the United States on east, west, and 
north. When it was complete hundreds of radar domes, resembling golf 
balls the size of buildings, littered the Canadian landscape from ocean to 
ocean, and from the American border to the Arctic. 

The Mid-Canada Line, extending 2,700 miles from Hopedale, Labrador 
to Dawson Creek, British Columbia, consisted of 98 powerful Doppler 
radars 30 miles apart and roughly 300 miles north of the Pinetree Line. 
Construction of the first station began on October 1, 1956, and the 
completed system was dedicated on January 1, 1958. 

The 58 stations of the Distant Early Warning or DEW Line kept their 
frozen watch roughly along the 69th parallel, 200 miles north of the Arctic 
Circle, in a chain extending from Baffin Island to the Northwest Territories 
and across Alaska. Each main site, of which there were 33, had two pulsed 
transmitters, one controlling a pencil beam for long-range precision 
tracking, the other a wider beam for general surveillance. Each beam had a 
peak power of 500 kilowatts, so that each site had a maximum peak 
capacity of one million watts. The frequency was between 1220 and 1350 
MHz. The other twenty-five "gap-filler" stations had continuous wave 
Dopplers rated at 1 kilowatt and operated at 500 MHz. Construction began 
in 1955 and the completed system was dedicated on July 31, 1957. 

The DEW Line extended down into the Atlantic and Pacific Oceans in 
lines of Navy ships—four in the Atlantic and five in the Pacific— 
supplemented by fleets of Lockheed aircraft that cruised in twelve- to 
fourteen-hour shifts at 3,000 to 6,000 feet in altitude. The radar-bearing 
ships and planes of the Atlantic Barrier were based in Maryland and 


Newfoundland and patrolled the waters out to the Azores. Atlantic 
operations began testing on July 1, 1956, and were fully deployed one year 
later. The Pacific Barrier, based in Hawaii and Midway, scanned the ocean 
off western North America and patrolled roughly from Midway to Kodiak 
Island. Its first two ships were assigned to Pearl Harbor in 1956, and the 
Barrier became fully operational on July 1, 1958. 

In addition, three “Texas Towers," equipped with long-range radars, 
were placed about 100 miles off the Atlantic coast and affixed to the ocean 
floor. The first, 110 miles east of Cape Cod, began operation in December 
1955, while the third, 84 miles southeast of New York Harbor, was 
activated in early summer 1957. 

Finally, every one of the 195 initial radar sites blanketing Canadian 
skies had to be able to send surveillance data from mostly very remote 
locations, and so high power radio transmitters were added to each site, 
typically operating in the microwave spectrum between 600 and 1000 MHz, 
with broadcast powers of up to 40 kilowatts. These used a technology called 
"tropospheric scatter." Huge antennas the shape of curved billboards aimed 
their signals above the distant horizon so as to bounce them off particles in 
the lower atmosphere six miles above the earth, and thereby reach a 
receiver hundreds of miles away. 

Another complete network of such antennas, called the White Alice 
Communications System, was installed throughout Alaska at the same time. 
The first ones were put into service on November 12, 1956, and the 
complete system was dedicated on March 26, 1958. 

The *Asian" influenza pandemic began about the end of February 1957 
and lasted for more than a year. The bulk of the mortality occurred in the 
fall and winter of 1957-1958. 

A decade later the United States launched the world's first constellation 
of military satellites into orbit at an altitude of about 18,000 nautical miles, 
right in the heart of the outer Van Allen radiation belt. Called the Initial 
Defense Communication Satellite Program (IDCSP), its 28 satellites 
became operational after the last eight were launched on June 13, 1968. The 
“Hong Kong” flu pandemic began in July 1968 and lasted until March 
1970. 


Although there had already been a few satellites in space, they had all 
been launched one at a time during the 1960s, and at the beginning of 1968 
there had been a total of only 13 operating satellites orbiting above the 
earth. In one fell swoop the IDCSP not only more than tripled the number, 
but placed them in the middle of the most vulnerable layer of the earth's 
magnetosphere. 





Those for whom this attachment was strongest, whose roots were most 
vital, whose life's rhythms were tuned most closely to the accustomed 
pulsations of our planet—in other words, vigorous, healthy young adults, 
and pregnant women—those were the individuals who most suffered and 
died. Like an orchestra whose conductor has suddenly gone mad, their 
organs, their living instruments, no longer knew how to play. 


9. Earth's Electric Envelope 


A 
All things by immortal power, 
Near or far, 
Hiddenly 


To each other linked are, 
That thou canst not stir a flower 
Without troubling of a star. 


FRANCIS THOMPSON, in The Mistress of Vision 


WHEN I LOOK at a flower, what I see is not the same as what a honey bee 
sees, who comes to drink its nectar. She sees beautiful patterns of ultraviolet 
that are invisible to me, and she is blind to the color red. A red poppy is 
ultraviolet to her. A cinquefoil flower, which looks pure yellow to me, is to 
her purple, with a yellow center luring her to its nectar. Most white flowers 
are blue-green to her eye. 

When I look upon the night sky, the stars appear as points of color 
twinkling through earth's atmosphere. Everywhere else, except for the 
moon and a few planets, is blackness. But it is the blackness of illusion. 

If you could see all the colors in the world, 





the radio waves, the X- 
rays, the gamma rays, the slow galactic pulsations, if you could see 
everything that is really there in its myriad shapes and hues, in all of its 
blinding glory, instead of blackness you'd see form and motion everywhere, 
day and night. 


Almost all of the matter in the universe is electrically charged, an 
endless sea of ionized particles called plasma, named after the contents of 
living cells because of the unpredictable, life-like behavior of electrified 
matter. The stars we see are made of electrons, protons, bare atomic nuclei, 
and other charged particles in constant motion. The space between the stars 
and galaxies, far from being empty, teems with electrically charged 
subatomic particles, swimming in vast swirling electromagnetic fields, 
accelerated by those fields to near-light speeds. Plasma is such a good 
conductor of electricity, far better than any metals, that filaments of plasma 
—invisible wires billions of light-years long—transport electromagnetic 
energy in gigantic circuits from one part of the universe to another, shaping 
the heavens. Under the influence of electromagnetic forces, over billions of 
years, cosmic whirlpools of matter collect along these filaments, like beads 
on a string, evolving into the galaxies that decorate our night sky. In 
addition, thin sheaths of electric current called double layers, like the 
membranes of biological cells, divide intergalactic space into immense 
compartments, each of which can have different physical, chemical, 
electrical, and magnetic properties. There may even, some speculate, be 
matter on one side of a double layer and antimatter on the other. Enormous 
electric fields prevent the different regions of space from mixing, just as the 
integrity of our own cells is preserved by the electric fields of the 
membranes surrounding them. 

Our own Milky Way, in which we live, a medium-sized spiral galaxy 
one hundred thousand light-years across, rotates around its center once 
every two hundred and fifty million earth years, generating around itself a 
galactic-size magnetic field. Filaments of plasma five hundred light-years 
long, generating additional magnetic fields, have been photographed 
looping out of our galactic center. 

Our sun, also made of plasma, sends out an ocean of electrons, protons, 
and helium ions in a steady current called the solar wind. Blowing at three 
hundred miles per second, it bathes the earth and all of the planets before 
diffusing out into the plasma between the stars. 

The earth, with its core of iron, rotates on its axis in the electric fields of 
the solar system and the galaxy, and as it rotates it generates its own 


magnetic field that traps and deflects the charged particles of the solar wind. 
They wrap the earth in an envelope of plasma called the magnetosphere, 
which stretches out on the night side of the planet into a comet-like tail 
hundreds of millions of miles long. Some of the particles from the solar 
wind collect in layers we call the Van Allen belts, where they circulate six 
hundred to thirty-five thousand miles above our heads. Driven along 
magnetic lines of force toward the poles, the electrons collide with oxygen 
and nitrogen atoms in the upper atmosphere. These fluoresce to produce the 
northern and southern lights, the aurorae borealis and australis, that dance in 
the long winter nights of the high latitudes. 

The sun also bombards our planet with ultraviolet light and X-rays. 
These strike the air fifty to two hundred and fifty miles above us, ionizing 
it, freeing the electrons that carry electric currents in the upper atmosphere. 
This, the earth's own layer of plasma, is called the ionosphere. 

The earth is also showered with charged particles from all directions 
called cosmic rays. These are atomic nuclei and subatomic particles that 
travel at velocities approaching the speed of light. From within the earth 
comes radiation emitted by uranium and other radioactive elements. Cosmic 
rays from space and radiation from the rocks and soil provide the small ions 
that carry the electric currents that surround us in the lower atmosphere. 

In this electromagnetic environment we evolved. 

We all live in a fairly constant vertical electric field averaging 130 volts 
per meter. In fair weather, the ground beneath us has a negative charge, the 
ionosphere above us has a positive charge, and the potential difference 
between ground and sky is about 300,000 volts. The most spectacular 
reminder that electricity is always playing around and through us, bringing 
messages from the sun and stars, is, of course, lightning. Electricity courses 
through the sky far above us, explodes downward in thunderstorms, rushes 
through the ground beneath us, and flows gently back up through the air in 
fair weather, carried by small ions. All of this happens continuously, as 
electricity animates the entire earth; about one hundred bolts of lightning, 
each delivering a trillion watts of energy, strike the earth every second. 
During thunderstorms the electric tension in the air around us can reach 
4,000 volts per meter and more. 


When I first learned about the global electrical circuit, twenty-five years 
ago, I drew the following sketch to help me think about it. 





Living organisms, as the drawing indicates, are part of the global circuit. 
Each of us generates our own electric fields, which keep us vertically 
polarized like the atmosphere, with our feet and hands negative with respect 
to our spine and head. Our negative feet walk on the negative ground, as 
our positive heads point to the positive sky. The complex electric circuits 
that course gently through our bodies are completed by ground and sky, and 
in this very real way the earth and sun, the Great Yin and the Great Yang of 
the Yellow Emperor s Classic, are energy sources for life. 

It is not widely appreciated that the reverse is also true: not only does 
life need the earth, but the earth needs life. The atmosphere, for example, 
exists only because green things have been growing for billions of years. 
Plants created the oxygen, all of it, and very likely the nitrogen too. Yet we 
fail to treat our fragile cushion of air as the irreplaceable treasure that it is, 
more precious than the rarest diamond. Because for every atom of coal or 
oil that we burn, for every molecule of carbon dioxide that we produce from 
them, we destroy forever one molecule of oxygen. The burning of fossil 
fuels, of ancient plants that once breathed life into the future, is really the 
undoing of creation. 

Electrically, too, life is essential. Living trees rise hundreds of feet into 
the air from the negatively charged ground. And because most raindrops, 
except in thunderstorms, carry positive charge down to earth, trees attract 


“As for men,” said Loren Eiseley, “those myriad little detached ponds 
with their own swarming corpuscular life, what were they but a way that 
water has of going about beyond the reach of rivers?”! Not only we, but 
especially trees, are the earth’s way of watering the desert. Trees increase 
evaporation and lower temperatures, and the currents of life speeding 
through their sap are continuous with the sky and the rain. 

We are all part of a living earth, as the earth is a member of a living 
solar system and a living universe. The play of electricity across the galaxy, 
the magnetic rhythms of the planets, the eleven-year cycle of sunspots, the 
fluctuations in the solar wind, thunder and lightning upon this earth, 
biological currents within our bodies—the one depends upon all the others. 
We are like tiny cells in the body of the universe. Events on the other side 
of the galaxy affect all life here on earth. And it is perhaps not too far- 
fetched to say that any dramatic change in life on earth will have a small but 
noticeable effect on the sun and stars. 


B 


When the City and South London Electric Railway began operating in 
1890, it interfered with delicate instruments at the Royal Observatory at 
Greenwich four and a half miles away.’ Little did the physicists there know 
that electromagnetic waves from that and every other electric railway were 
also radiating into space and altering the earth’s magnetosphere, a fact that 
would not be discovered until decades later. To understand its significance 
for life, let us return first to the story of lightning. 





German physicist who predicted their existence, and who, with his student 
Herbert Kónig, proved their constant presence in the atmosphere in 1953. 

It so happens that in a state of awake relaxation, our brains tune in to 
these precise frequencies. The dominant pattern of a human 
electroencephalogram, from before birth through adulthood—the well- 
known alpha rhythm, ranging from 8 to 13 Hz, or 7 to 13 Hz in a newborn 
—is bounded by the first two Schumann resonances. An old part of the 
brain called the limbic system, which is involved in emotions, and in long- 
term memory, produces theta waves, of 4 to 7 Hz, which are bounded above 
by the first Schumann resonance. The theta rhythm is more prominent in 
young children, and in adults in meditation. These same frequencies, alpha 
and theta, with surprisingly little variation, pulsate, so far as is known, in all 
animals. In a state of relaxation, dogs show an alpha rhythm, identical to 
ours, of 8 to 12 Hz. In cats the range is slightly wider, from 8 to 15 Hz. 
Rabbits, guinea pigs, goats and cows, frogs, birds, and reptiles all show 
nearly the same frequencies.? 

Schumann's student Kónig was so impressed by the resemblances these 
atmospheric waves bear to the electrical oscillations of the brain that he 
conducted a series of experiments with far-reaching implications. The first 
Schumann resonance, he wrote, is so completely identical to the alpha 
rhythm that even an expert is hard pressed to tell the difference between the 
tracings from the brain and the atmosphere. Kónig did not think this was a 
coincidence. The first Schumann resonance appears during fair weather, he 
noted, in calm, balanced conditions, just as the alpha rhythm appears in the 
brain in a calm, relaxed state. The delta rhythm, on the other hand, which 
consists of irregular, higher amplitude waves around 3 Hz, appears in the 
atmosphere under disturbed, unbalanced weather conditions, and in the 
brain in disturbed or disease states—headaches, spastic conditions, tumors, 
and so forth. 

In an experiment involving nearly fifty thousand people attending a 
Traffic Exhibition in Munich in 1953, Kónig was able to prove that these 
latter types of disturbed waves, when present in the atmosphere, 
significantly slow human reactions times, while the 8 Hz Schumann waves 
do just the opposite. The larger the Schumann signal in the atmosphere, the 


quicker people's reactions were on that day. Kónig then duplicated these 
effects in the laboratory: an artificial field of 3 Hz (delta range) slowed 
human reactions, while an artificial field of 10 Hz (alpha range) accelerated 
them. Kónig also noted that during the 3 Hz exposure some of his subjects 
complained of headaches, fatigue, tightness in their chest, or sweating from 
their palms.^ 

In 1965, James R. Hamer published the results of experiments along 
these same lines that he had conducted for Northrop Space Laboratories, in 
an article which he titled *Biological Entrainment of the Human Brain by 
Low Frequency Radiation." Like Kónig, he showed that frequencies above 
8 Hz quickened reaction times, while lower frequencies had the opposite 
effect. But he went further. He proved that the human brain could 
distinguish between frequencies that differed only slightly from each other 
—but only if the signal was weak enough. When he reduced the signal 
strength to 0.0038 volts per meter, which is close to the value of the earth's 
own fields, 742 Hz had a significantly different effect than 812 Hz, and 9% 
Hz than 10% Hz. 

Lightning is not yet done with its repertoire. In addition to the static 
field that we walk in and the low frequencies that speak to our brains, 
lightning also provides us with a steady symphony of higher frequencies 
called atmospherics, or just “sferics,” which reach thousands of cycles per 
second. They sound like twigs snapping if you listen to them on a very low 
frequency (VLF) radio, and usually originate in thunderstorms that may, 
however, be thousands of miles away. Other sounds, called whistlers, 
resembling the descending tones of a slide whistle, often originate in 
thunderstorms on the opposite end of the earth. Their falling tones are 
produced during the long journey these waves have taken as they are guided 
along magnetic field lines into outer space and back to earth in the opposite 
hemisphere. These waves may even bounce back and forth many times 
from one end of the earth to another, resulting in trains of whistles that 
seemed so unworldly when they were first discovered in the 1920s that they 
generated newspaper articles with not-so-inappropriate titles like “Voices 
From Outer Space.”® 


Among the other sounds one may hear, especially at higher latitudes, 
originating somewhere in the electrical environment of our planet, are a 
steady hiss, and a “dawn chorus,” so named because of its resemblance to 
chirping birds. Both of these sounds rise and fall gently every 10 seconds or 
so with the slow pulsations of the earth’s magnetic field. 






eaction times, amputees’ pains, and complaints of people with brain 
injuries all rose significantly on days with strong VLF sferics.9 

Our VLF environment regulates biological rhythms in both humans and 
animals. Golden hamsters, which have been popular pets since the 1930s, 
live in the wild near Aleppo, Syria where, every winter for about three 
months, they go in and out of hibernation. But scientists who have tried to 
use hamsters as a subject for hibernation studies in the laboratory have been 
puzzled by their inability to trigger hibernation in these animals by 
exposing them to prolonged cold, reducing hours of daylight, or controlling 
any other known environmental factor.’ 

In the mid-1960s, climatologists Wolfgang Ludwig and Reinhard Mecke 
took a different approach. They kept a hamster during the winter in a 
Faraday cage, shielded from all natural electromagnetic waves, and without 
any alteration of temperature or hours of daylight. At the beginning of the 
fourth week they introduced the natural outdoor atmospheric frequencies by 
means of an antenna, whereupon the hamster promptly fell asleep. During 
the following two months, the researchers were able to put the animal into 
and out of hibernation by introducing, or removing, either the natural 
outdoor frequencies, or artificial VLF fields that imitated the natural winter 
pattern. Then, at the beginning of the thirteenth week of the experiment, the 
frequencies in the enclosure were changed so as to imitate the natural 


summer pattern, and within half an hour, as if panicked by the sudden 
change in season, the animal woke up and began a “movement storm,” 
running day and night for an entire week until the experiment was 
terminated. In repetitions of this experiment on other hamsters, the 
researchers found that this high level of activity could not be induced unless 
the state of hibernation had been triggered first. The artificial fields they 
used were extremely weak—as small as 10 millivolts per meter for the 
electric field and 26.5 microamperes per meter for the magnetic field. 

One way to find out if the earth’s natural fields are as important to 
people as to hamsters would be to 










Which is exactly 
what behavioral physiologist Riitger Wever did at the Max Planck Institute 
in Germany. In 1967 he had an underground building constructed 
containing two isolation chambers. Both were carefully shielded against 
outside light and sound, and one was shielded also against electromagnetic 
fields. During the next two decades hundreds of people had their sleep 
cycles, body temperature, and other internal rhythms monitored while they 
lived in one or the other of these rooms, usually for a month at a time. 
Wever found that even without any variation in light and darkness, and 
without any clocks or time cues, the body’s sleep cycle and internal rhythms 
remained close to 24 hours, 

However, when those fields were excluded, the body’s 
rhythms usually became longer, erratic, and desynchronized with each 
other. The average “free-running” sleep cycle was 25 hours, but in 
individual cases was as short as 12 hours and as long as 65 hours. Variations 
in body temperature, potassium excretion, speed of mental processes, and 
other rhythms drifted at their own separate rates, completely different from 
one another, and no longer coinciding with the sleep-wake cycle at all. 








Life, residing between heaven and earth, partakes of both polarities. As we 
will see in the next chapter, the distribution of electric charge in living 
beings has been measured and mapped externally. In plants this was done 
by professor of anatomy Harold Saxton Burr, at Yale University, and in 
animals by orthopedic surgeon Robert O. Becker, at the State University of 
New York, Upstate Medical Center, Syracuse. The areas of greatest positive 
voltage in animals are the center of the head, the heart, and the lower 
abdomen, and in trees the crown. The places of greatest negative voltage, in 
trees, are the roots, and in animals, the four feet and the end of the tail. 
These are the places where the global electrical circuit enters and leaves the 
body on its way between heaven and earth. And the channels through which 
the electricity travels inside living beings, distributing the electricity of 
heaven and earth to every organ, were precisely mapped several thousand 
years ago, and are part of a body of knowledge that we know today as 
Chinese acupuncture. It was written down in the Huangdi Neijing, the 
Yellow Emperor 5 Classic of Internal Medicine, between 500 and 300 B.C. 

The very names of key acupuncture points reveal an understanding that 
the circuitry of the body is continuous with that of earth and sky. Kidney 1, 
for example, the point underneath the foot, in the center of the sole, is 
known in Chinese as yong quan, meaning “bubbling spring,” because earth 
energy bubbles up into the feet through these points and climbs up the legs 
into the rest of the body toward the heavens. Governing Vessel 20, the point 
on top of the head, in the center, is called bai hui, the “hundred 
convergences.” This is also the “thousand petal lotus” of Indian traditions, 
the place where the energy of heaven descends into our body toward the 
earth, and the flows of our body converge and reach toward the sky. 

But not until the 1950s did scientists, beginning with Yoshio Nakatani in 
Japan and Reinhold Voll in Germany, begin to actually measure the 
electrical conductivity of acupuncture points and meridians, and to finally 
translate the word “qi” (formerly spelled “chi”) into modern language: it 
means “electricity.” 

Hsiao-Tsung Lin is a professor of chemical and material science at 
National Central University in Taiwan. The qi that flows through our 
meridians, he tells us, is an electrical current that brings both power and 


information to our cells, current whose source is both internal and external. 
Every acupuncture point has a double function: as an amplifier for the 
internal electrical signals, boosting their strength as they travel along the 
meridians; and as an antenna that receives electromagnetic signals from the 
environment. The dantians, or energy centers of Chinese medicine, located 
in the head, heart, and abdomen—equivalent to the chakras of Indian 
tradition—are electromagnetic oscillators that resonate at particular 
frequencies, and that communicate with the meridians and regulate their 
flow. They have capacitance and inductance like oscillators in any 
electronic circuitry. 









As a result of the work of Nakatani, Voll, Becker, and others, 
electroacupuncture, using microampere currents, has taken its place 
alongside traditional acupuncture, and commercial point locators, which 
find acupuncture points by measuring the electrical conductivity of the skin, 
have come into use among nontraditional practitioners here in the West.? In 
China, electroacupuncture devices have been in use since 1934. They are a 
tacit acknowledgement that the body is an electrical instrument, and that its 
health or sickness depends on the proper distribution and balance of the 
electrical energies that constantly flow around and through us. But 
ironically they also prevent that scientific knowledge from becoming true 
knowledge, for to substitute artificial electricity for atmospheric electricity 
in replenishing the body is to forget that the electricity of the air is there, 
nourishing us and giving us life. 





and that electricity is not only a force that moves locomotives, 


but is the incredibly complex and delicate stuff of life. Typically, the 
electrical resistance of an acupuncture point is two to six times lower than 
the resistance of the surrounding skin, and its capacitance—its ability to 
store electrical energy—is five times as great. Commercial point locators 
do not always work, because sometimes—depending on the internal state of 
the individual—an acupuncture point can have a higher resistance than its 
surroundings. But the meridians always respond in an active and nonlinear 
way to electrical stimulation, and they react, say modern researchers, 
exactly like an electrical circuit.!? 

The physical structures of the conductive points and meridians have 
been tentatively identified. In the 1960s, a North Korean physician, Bong 
Han Kim, published detailed photographs of an entire network of tiny 
corpuscles, and threadlike structures that connect them, that exist 
throughout the body in our skin, in our internal organs and nervous system, 
and in and around our blood vessels. These ducts, he found, were 
electrically conductive and the fluid within them, surprisingly, contained 
large amounts of DNA. Their electrical pulsations were considerably slower 
than the heartbeat: in the skin of a rabbit, the pulsation rate was between 10 
and 20 per minute. 





The reason his work has been so completely ignored 
has partly to do with his relations with the North Korean government—Kim 
was expunged from official records in 1966, and rumor has it that he 


committed suicide—and partly with the fact that 
But in the mid-1980s, 


Jean-Claude Darras, a French physician working in the nuclear medicine 
department at Necker Hospital in Paris, replicated some of Kim's 
experiments. He injected a radioactive dye containing technetium-99 into 
various acupuncture points on the feet of volunteers, and found that the dye 


migrated precisely along the meridian pathways of classical acupuncture, 
just as Kim had found." 

In 2002, Kwang-Sup Soh, who had already been investigating the 
electromagnetic properties of acupuncture meridians, headed up a team at 
Seoul National University in South Korea, which looked for and found 
most of the threadlike duct system described by Kim. A breakthrough came 
in November 2008 with the discovery that trypan blue, a dye that was 
previously known to stain only dead cells, if injected into living tissue, will 
stain only the nearly invisible threads and corpuscles they had painstakingly 
begun to identify. The “primo vascular system,” as it was now called, 
suddenly became a subject of research in other centers in South and North 
Korea, as well as in China, Europe, Japan, and the United States. The ducts 
and corpuscles of this system were found, just as Kim had described, 
resting on the surface of and penetrating inside the internal organs, floating 
inside the large blood and lymphatic vessels, winding along the outside of 
major blood vessels and nerves, traveling inside the brain and spinal cord, 
and following the paths of the known meridians within the deep layers of 
the skin.? When the surface of the skin was stained with the dye, only 
points along the meridians absorbed it.'? 






held in Jecheon, 
Korea, Satoru Fujiwara, retired professor of anatomy at Osaka City 
University, Japan, reported tentative success at surgically identifying a 
superficial primo node—an acupuncture point—in the skin of a rabbit's 
abdomen.'* And in 2015, researchers at Seoul National University used a 
commercially available staining kit to reveal a threadlike vessel running just 
beneath the abdominal skin of anesthetized living rats.!° The vessel, colored 
dark blue from the stain, followed the pathway of the acupuncture meridian 
called the conception vessel, and connected discrete corpuscles 
corresponding in location to the known acupuncture points on that 
meridian. The fine structure of this system of nodes and ducts was revealed 
by electron microscopy. The staining process, they noted, takes less than ten 
minutes. 


D 


In the early 1970s, atmospheric physicists finally woke up to the fact that 
the earth's magnetic field was highly disturbed. Not all of those whistlers, 
hiss, chorus, lion roars, and other colorful sounds they had been listening to 
for half a century were caused by nature! This discovery came about as a 
result of efforts to deliberately alter the earth’s electromagnetic 
environment—efforts that have culminated, today, in the operation of 
Project HAARP, located in Gakona, Alaska (see chapter 16). 

Under contract with the Office of Naval Research, scientists at Stanford 
University’s Radioscience Laboratory had built a 100-kilowatt VLF 
transmitter at Siple Station, Antarctica, broadcasting in the 1.5 to 16 kHz 
range. The purposes of the 13-mile-long antenna that stretched over the 
frozen ice, according to Robert Helliwell, one of the members of the 
Stanford team, included “control of the ionosphere, control of the radiation 
belts and new methods of v.l.f. and u.l.f. communication."!5 It had been 
discovered accidentally in 1958 that VLF transmissions originating on the 
earth interact with particles in the magnetosphere, stimulating them to emit 
new VLF waves, which can then be received at the opposite end of the 
earth. The purpose of the Stanford project was to do this deliberately—to 
inject sufficient quantities of very low frequency energy into the 
magnetosphere so that it would not only trigger new waves, but that these 
triggered waves might in turn cause electrons to rain out of the earth's 
radiation belts into the atmosphere, altering the properties of the ionosphere 
for military purposes. A primary goal of the Department of Defense was to 
devise a method of stimulating the ionosphere to emit VLF (very low 
frequency), ELF (extra low frequency), or even ULF (ultra low frequency) 
waves in order to communicate with submarines submerged beneath the 
oceans." The VLF transmitter at Siple, and a VLF receiver in northern 
Quebec, at Roberval, were part of this early research. 

The data they collected were surprising. First, the signal received in 
Quebec, immediately after transmission from Antarctica, was larger than 
expected. The waves broadcast from Antarctica were not only triggering 
new emissions from particles in the magnetosphere, but were being 
amplified more than a thousandfold in the magnetosphere before returning 
to earth and being received in Quebec. Only half a watt of broadcast power 


o 


was required in order to be detected near the opposite pole of the earth after 
being relayed from the magnetosphere.'® The second surprise was that 
Roberval was receiving frequencies that were unrelated to the frequencies 
that originated at Siple, but that were instead multiples of 60 Hz. The Siple 
signal had been altered, on its journey through outer space, to bear the 
imprint of the electric power grid. 

Since those first discoveries, scientists have learned a great deal about 
this form of pollution, now known as “power line harmonic radiation.” It 
appears that harmonics from all of the world’s power grids leak 
continuously into the magnetosphere, where they are greatly amplified as 
they bounce back and forth between the northern and southern hemisphere, 
generating their own rising and falling whistlers just like radiation from 
lightning. 

But there is a fundamental difference. Before 1889, whistlers and other 
lightning-triggered sounds played continuously over the entire range of the 
terrestrial instrument. Today the music is stilted, dulled, often confined to 
multiples of 50 or 60 Hz. Every component of the natural symphony has 
been radically altered. The “dawn chorus” is quieter on Sundays than on 
other days of the week, and the starting frequencies of most chorus 
emissions are power line harmonics.!9 “It seems likely that the entire hiss 
band is caused by power line radiation,” wrote Helliwell in 1975. And the 
natural, slow pulsations of the earth’s magnetic field, below 1 Hz, which are 
also important to all life, are strongest on weekends, evidently because they 
are being suppressed by radiation from the power grid, and this radiation is 
stronger on weekdays.? Antony Fraser-Smith, also at Stanford, by 
analyzing geomagnetic activity data collected since 1868, showed that this 
is not a new phenomenon but has been happening since the first use of 
alternating current, and has been increasing over time.” Data collected 
between 1958 and 1992 showed that Pc 1 activity, representing 
geomagnetic pulsations between 0.2 and 5 Hz, has been fifteen to twenty 
percent greater on weekends than in the middle of the week.?? 

The structure of the Van Allen radiation belts seems also to have been 
altered. What the Department of Defense had wanted to do intentionally 
was apparently already being done massively by the world's electric power 


ie) 


grids. Why, physicists had long wondered, are there two electron-filled 
radiation belts around the earth, an inner and an outer, separated by a layer 
that is virtually empty of electrons? This "electron slot," some think, is 
continually drained of its electrons by their interaction with radiation from 
power lines.? These electrons, in turn, rain down over the earth, modifying 
the electrical properties of the atmosphere.?^ Not only may this increase the 
frequency of thunderstorms,” but it may shift the values of the Schumann 
resonances to which all living things are attuned.” 

In short, the electromagnetic environment of the entire earth is radically 
different today from what it was before 1889. 





E 


Influenza 


If the atmosphere is, at times, electrified beyond the 
degree which is usual, and necessary to preserve the body 
in a due state of excitement, the nerves must be too highly 
excited, and under a continued operation of undue 
stimulus, become extremely irritable, and subject to 
debility. 


NOAH WEBSTER, A Brief History of Epidemic and 
Pestilential Diseases, 1799, p. 38 


A large, rapid, qualitative change in the earth’s electromagnetic 
environment has occurred six times in history. 


In 1889, power line harmonic radiation began. From that year forward 
the earth's magnetic field bore the imprint of power line frequencies and 
their harmonics. In that year, exactly, the natural magnetic activity of the 
earth began to be suppressed. This has affected all life on earth. The power 
line age was ushered in by the 1889 pandemic of influenza. 

In 1918, the radio era began. It began with the building of hundreds of 
powerful radio stations at LF and VLF frequencies, the frequencies 
guaranteed to most alter the magnetosphere. The radio era was ushered in 
by the Spanish influenza pandemic of 1918. 

In 1957, the radar era began. It began with the building of hundreds of 
powerful early warning radar stations that littered the high latitudes of the 
northern hemisphere, hurling millions of watts of microwave energy 
skyward. Low-frequency components of these waves rode on magnetic 
field lines to the southern hemisphere, polluting it as well. The radar era 
was ushered in by the Asian flu pandemic of 1957. 

In 1968, the satellite era began. It began with the launch of dozens of 
satellites whose broadcast power was relatively weak. But since they were 
already in the magnetosphere, they had as big an effect on it as the small 
amount of radiation that managed to enter it from sources on the ground. 
The satellite era was ushered in by the Hong Kong flu pandemic of 1968. 

The other two mileposts of technology—the beginning of the wireless 
era and the activation of the High Frequency Active Auroral Research 
Program (HAARP)—belong to very recent times and will be discussed later 
in this book. 


10. Porphyrins and the Basis of Life 


I see little hope to be able to explain the subtle difference 
between a normal and a sick cell as long as we do not 
understand the basic difference between a cat and a stone. 


ALBERT SZENT-GYÖRGYI 


STRANGELY ENOUGH, “porphyrin” is not a household word. It is not a 
sugar, fat, or protein, nor is it a vitamin, mineral, or hormone. But it is more 
basic to life than any other of life’s components, because without it we 
would not be able to breathe. Plants could not grow. There would not be 
any oxygen in the atmosphere. Wherever energy is transformed, wherever 
electrons flow, there look for porphyrins. 





As I write this chapter, a dear friend has just died. For the last seven 
years she had had to live without electricity, hardly ever seeing the sun. She 
seldom ventured out in the daytime; when she did, she covered herself from 
head to foot in thick leather clothing, a broad-brimmed leather hat hiding 
her face, and glasses bearing two layers of dark lenses concealing her eyes. 
A former dancer who loved music, nature, and the outdoors, Bethany was 
virtually abandoned by a world in which she no longer belonged. 

Her condition, probably caused by her years of work for a computer 
company, was a classic example of an illness that has been known to 
medicine only since 1891, its emergence at that time being one of the side 
effects of the sudden worldwide expansion of electrical technology. Its 
connection with electricity was discovered a century later. Although it is 
now considered an extremely rare genetic disease, affecting as few as one 
person in fifty thousand, porphyria was originally thought to affect as many 


as ten percent of the population. Its supposed rarity is due in large part to 
the ostrich-like behavior of the medical profession after World War II. 

In the late 1940s, medical practitioners were staring at an impossible 
contradiction. Most synthetic chemicals were known poisons. But one of 
the legacies of the war was the ability to manufacture products from 
petroleum, easily and cheaply, to substitute for almost every consumer 
product imaginable. Now, thanks to the fledgling petrochemical industry, 
bringing us “Better Living Through Chemistry,” synthetic chemicals were 
going to be literally everywhere. We were going to be wearing them, 
sleeping on them, washing our clothes, our hair, our dishes, and our homes 
with them, bathing in them, insulating our houses with them, carpeting our 
floors with them, spraying our crops, our lawns, and our pets with them, 
preserving our food with them, coating our cookware with them, packing 
our groceries in them, moisturizing our skin with them, and perfuming our 
bodies with them. 

The medical profession had two choices. It could have attempted to 
study the health effects, singly and in combination, of the hundreds of 
thousands of new chemicals that were kaleidoscoping over our world, a 
virtually impossible task. The attempt itself would have put the profession 
on a collision course with the mushrooming petrochemical industry, 
threatening the banning of most new chemicals and the strangling of the 
economic boom of the next two decades. 

The other alternative was for the profession to bury its collective head in 
the sand and pretend that the world’s population was not actually going to 
become poisoned. 

Environmental medicine was born as a medical specialty in 1951, 
founded by Dr. Theron Randolph.' It had to be created: the scale of the 
poisoning was too great to go completely ignored. The sheer numbers of 
sickened patients, abandoned by mainstream medicine, produced an urgent 
need for practitioners trained to recognize at least some of the effects of the 
new chemicals and to treat the resulting diseases. But the specialty was 
ignored by the mainstream as though it didn't exist, its practitioners 
ostracized by the American Medical Association. When I attended medical 
school from 1978 to 1982, environmental medicine wasn't even on the 


curriculum. 





Heightened sensitivity to chemicals, we recall, was first described by 
New York physician George Miller Beard, who considered it a symptom of 
a new disease. The initial electrification of society through telegraph wires 
brought with it the constellation of health complaints known as 
neurasthenia, two of which were a tendency to develop allergies and a 
drastically reduced tolerance for alcohol and drugs. 





In 1888, one more drug was added to the list. Sulfonal was a sleeping 
medication that had a reputation for its prompt effect, its non- addictive 
nature, and its relative lack of side effects. There was just one problem, 
which only became widely known after three years of its popularity: it 
killed people. 

But its effects were quirky, unexpected. Nine people could take sulfonal, 
even in large doses and for a long time, with no untoward effects, but the 
tenth person, sometimes after only a few or even one small dose, would 
become critically ill. He or she would typically be confused, so weak as to 
be unable to walk, constipated, with pain in the abdomen, sometimes with a 
skin rash, and reddish urine often described as the color of port wine. The 
reactions were idiosyncratic, liable to affect almost any organ, and the 
patients were apt to die of heart failure without warning. Between four and 
twenty percent of the general population were reported to be subject to such 
side effects from taking sulfonal.? 

During the ensuing decades the chemistry of this surprising disease was 
worked out. 


Porphyrins are light-sensitive pigments that play pivotal roles in the 
economy of both plants and animals, and in the ecology of planet Earth. In 
plants a porphyrin bound to magnesium is the pigment called chlorophyll, 
that makes plants green and is responsible for photosynthesis. In animals an 
almost identical molecule bound to iron is the pigment called heme, the 
essential part of hemoglobin that makes blood red and enables it to carry 
oxygen. It is also the essential part of myoglobin, the protein that makes 
muscles red and delivers oxygen from our blood to our muscle cells. Heme 
is also the central component of cytochrome c and cytochrome oxidase, 
enzymes that are contained in every cell of every plant, animal and 
bacterium, that transport electrons from nutrients to oxygen so that our cells 
can extract energy. And heme is the main component of the cytochrome P- 
450 enzymes in our liver that detoxify environmental chemicals for us by 
oxidizing them. 





Our cells manufacture heme from a series of other porphyrins and 
porphyrin precursors in a series of eight steps, catalyzed by eight different 
enzymes. Like workers on an assembly line, each enzyme has to work at the 
same rate as all the others in order to keep up with the demand for the final 
product, heme. A slowdown by any one enzyme creates a bottleneck, and 
the porphyrins and precursors that accumulate behind the bottleneck get 
deposited all over the body, causing disease. Or if the first enzyme is 
working harder than the rest, it produces precursors faster than the enzymes 
down the line can handle, with the same result. Their accumulation in the 


skin can cause mild to disfiguring skin lesions, and mild to severe light 
sensitivity. Their accumulation in the nervous system causes neurological 
illness, and their accumulation in other organs causes corresponding illness. 
And when excess porphyrins spill into the urine, it takes on the color of port 
wine. 





The enzymes of the heme pathway are among the most sensitive 
elements of the body to environmental toxins. Porphyria, therefore, is a 
response to environmental pollution and was indeed extremely rare in an 
unpolluted world. Except for one severe, disfiguring congenital form, of 
which only a few hundred cases are known in the world, porphyrin enzyme 
deficiencies do not normally cause disease at all. Human beings are 
genetically diverse, and in times past most people with relatively lower 
levels of one or more porphyrin enzymes were simply more sensitive to 
their environment. In an unpolluted world this was a survival advantage, 
allowing the possessors of this trait to easily avoid places and things that 
might do them harm. But in a world in which toxic chemicals are 
inescapable, the porphyrin pathway is to some degree always stressed, and 
only those with high enough enzyme levels tolerate the pollution well. 
Sensitivity has become a curse. 

Because of the way it was discovered, and the lack of synthetic 
chemicals in the environment at that time, porphyria became known as a 
rare disease that was triggered in genetically susceptible people by certain 
drugs, such as sulfonal and barbiturates, which these patients had to avoid. 
It was not until another century had passed, in the early 1990s, that Dr. 
William E. Morton, professor of occupational and environmental medicine 
at Oregon Health Sciences University, realized that because ordinary 


synthetic chemicals were far more widespread in the modern environment 
than pharmaceuticals, they had to be the most common triggers of 
porphyric attacks. 





something no one had attempted before because MCS had never 
before been connected to a testable biological marker.? 





Porphyria, Morton showed, is not the 
extremely rare illness it is currently thought to be, but has to affect at least 
five to ten percent of the world's population.^ 

Morton was courageous, because the rare-disease world of por-phyria 
had come to be dominated by a handful of clinicians who controlled 
virtually all research and scholarship in their small, inbred field. They 
tended to diagnose porphyria only during acute attacks with severe 
neurological symptoms and to exclude cases of milder, smoldering illness. 
They generally would not make the diagnosis unless porphyrin excretion in 
urine or stool was at least five to ten times normal. “This makes no sense,” 
wrote Morton in 1995, *and would be analogous to restricting the diagnosis 
of diabetes mellitus to those who have ketoacidosis or restricting the 
diagnosis of coronary artery disease to those who have myocardial 
infarction."^ 

The higher numbers reported by Morton agree with the numbers 
reported over a century ago—the proportion of the population that became 
ill when they took the sleeping medication sulfonal. They are consistent 
with the finding, in the 1960s, of “mauve factor,” a lavender-staining 
chemical, not only in the urine of patients diagnosed with porphyria, but in 
the urine of five to ten percent of the general population.* Mauve factor was 
eventually identified as a breakdown product of porphobilinogen, one of the 
porphyrin precursors.’ Morton also found, in agreement with recent reports 


from England, the Netherlands, Germany, and Russia, that persistent 
neurological problems occur during the chronic, smoldering phase of every 
type of porphyria—even those types which were previously supposed to 
cause only skin lesions.? 





Morton has brought us back to the 
original view of porphyria: it is not only a fairly common disease but exists 
most often in a chronic form with comparatively mild symptoms. And its 
principal cause is the synthetic chemicals and electromagnetic fields that 
pollute our modern environment. 

Porphyrins are central to our story not only because of a disease named 
porphyria, which affects a few percent of the population, but because of the 
part porphyrins play in the modern epidemics of heart disease, cancer, and 
diabetes, which affect half the world, and because their very existence is a 
reminder of the role of electricity in life itself, a role which a few 
courageous scientists have slowly elucidated. 

Asa child, Albert Szent Györgyi (pronounced approximately like “Saint 
Georgie”) hated books and needed a tutor’s help to pass his exams. But 
later, having graduated from Budapest Medical School in 1917, he went on 
to become one of the world’s greatest geniuses in the field of biochemistry. 
In 1929 he discovered Vitamin C, and during the next few years he worked 
out most of the steps in cellular respiration, a system now known as the 
Krebs cycle. For these two discoveries 
He then spent the next two decades 
figuring out how muscles function. After emigrating to the United States 
and settling at Woods Hole, Massachusetts, he received the Albert Lasker 
Award of the American Heart Association in 1954 for his work on muscles. 









Albert Szent-Gyórgyi, M.D., Ph.D. (1893-1986) 


But perhaps his greatest insight is one for which he is least known, 
although he devoted almost half his life to the subject. For on March 12, 
1941, in a lecture delivered in Budapest, he boldly stood up before his peers 
and suggested to them that the discipline of biochemistry was obsolete and 
should be brought into the twentieth century. Living organisms, he told 
them, were not simply bags of water in which molecules floated like tiny 
billiard balls, forming chemical bonds with other billiard balls with which 
they happened to collide. Quantum theory, he said, had made such old ideas 
invalid; biologists needed to study solid state physics. 

In his own specialty, although he had worked out the structures of the 
molecules involved in muscular contraction, he could not begin to fathom 
why they had those particular structures, nor how the molecules 
communicated with one another to coordinate their activities. He saw such 
unsolved problems everywhere he looked in biology. “One of my 
difficulties within protein chemistry,” he bluntly told his colleagues, “was 
that I could not imagine how such a protein molecule can ‘live.’ Even the 
most involved protein structural formula looks ‘stupid,’ if I may say so.” 

The phenomena that had forced Szent-Gyórgyi to face these questions 
were the porphyrin-based systems of life. He pointed out that in plants, 
2,500 chlorophyll molecules form a single functional unit, and that in dim 
light at least 1,000 chlorophyll molecules have to cooperate simultaneously 


in order to split one molecule of carbon dioxide and create one molecule of 
oxygen. 

He spoke about the *enzymes of oxidation"—the cytochromes in our 
cells—and wondered, again, how the prevailing model could be correct. 
How could a whole series of large protein molecules be arranged 
geometrically so that electrons could wander directly from one to the other 
in a precise sequence? “Even if we could devise such an arrangement,” he 
said, “it would still be incomprehensible how the energy liberated by the 
passing of an electron from one substance to the other, viz., from one iron 
atom to the other, could do anything useful.” 











Szent-Gyórgyi's sin was not that he was incorrect. He wasn't. It was his 
failure to respect the old animosity. Electricity and life were long divorced; 
the industrial revolution had been running full bore for a century and a half. 
Millions of miles of electric wires clothed the earth, exhaling electric fields 
that permeated all living things. Thousands of radio stations blanketed the 
very air with electromagnetic oscillations that one could not avoid. Skin and 
bones, nerves and muscles were not allowed to be influenced by them. 
The threat to industry, 





economics, and modern culture would be too great. 








They even thought of the nervous system this 
way. When forced to, they admitted parts of quantum theory, but only on a 
limited basis. Biological molecules were still only permitted to interact with 
their immediate neighbors, not to act at a distance. It was okay to 
acknowledge modern physics only that much, like opening a small hole in a 


dam for knowledge to leak through one drop at a time, while the main 
structure is reinforced lest a flood demolish it. 

Old knowledge about chemical bonds and enzymes in a water solution 
must now coexist with new models of electron transport chains. It was 
necessary to invent these to explain phenomena that were most central to 
life: photosynthesis and respiration. Large porphyrin-containing protein 
molecules no longer had to move and physically interact with one another 
in order for anything useful to happen. These molecules could stay put and 
electrons could shuttle between them instead. Biochemistry was becoming 
that much more alive. But it still had a long way to go. For even in the new 
models, electrons were constrained to move only, like little messenger boys, 
between one protein molecule and its immediate neighbor. They could cross 
the street, so to speak, but they couldn't travel down a highway to a distant 
town. Organisms were still pictured essentially as bags of water containing 
very complex solutions of chemicals. 

The laws of chemistry had explained a lot about metabolic processes, 
and electron transport now explained even more, but there was not yet an 
organizing principle. Elephants grow from tiny embryos, which grow from 
single brainless cells. Salamanders regenerate perfect limbs. When we are 
cut, or break a bone, cells and organs throughout our body mobilize and 
coordinate their activities to repair the damage. How does the information 
travel? How, borrowing Szent-Gyórgyi's words, do protein molecules 
“live”? 

Despite Szent-Gyórgyi's sin, his predictions have proven correct. 
Molecules in cells do not drift at random to collide with one another. Most 
are firmly anchored to membranes. The water inside cells is highly 
structured and does not resemble the free-flowing liquid that sloshes around 
in a glass before you drink it. Piezoelectricity, a property of crystals that 
makes them useful in electronic products, that transforms mechanical stress 
into electrical voltages and vice versa, has been found in cellulose, 
collagen, horn, bone, wool, wood, tendon, blood vessel walls, muscle, 
nerve, fibrin, DNA, and every type of protein examined.!° In other words— 
something most biologists have been denying for two centuries—electricity 
is essential to biology. 


Szent-Györgyi was not the first to challenge conventional thinking. It 
was Otto Lehmann, already in 1908, who, noticing the close resemblance 
between the shapes of known liquid crystals and many biological structures, 
proposed that the very basis of life was the liquid crystalline state. Liquid 
crystals, like organisms, had the ability to grow from seeds; to heal wounds; 
to consume other substances, or other crystals; to be poisoned; to form 
membranes, spheres, rods, filaments and helical structures; to divide; to 
*mate" with other forms, resulting in offspring that had characteristics of 
both parents; to transform chemical energy into mechanical motion. 

After Szent-Gyórgyi's daring Budapest lecture, others pursued his ideas. 
In 1949, Dutch researcher E. Katz explained how electrons could move 
through a semiconducting chlorophyll crystal during photosynthesis. In 
1955, James Bassham and Melvin Calvin, working for the U.S. Atomic 
Energy Commission, elaborated on this theory. In 1956, William Arnold, at 
Oak Ridge National Laboratory, confirmed experimentally that dried 
chloroplasts—the particles in green plants that contain chlorophyll—have 
many of the properties of semiconductors. In 1959, Daniel Eley, at 
Nottingham University, proved that dried proteins, amino acids, and 
porphyrins are indeed semiconductors. 





In 1970, Alan Adler, at the New England Institute, showed 
that thin films of porphyrins do also. In the 1970s, biochemist Freeman 
Cope, at the United States Naval Air Development Center in Warminster, 
Pennsylvania, emphasized the importance of solid state physics for a true 
understanding of biology, as did biologist Allan Frey, the most active 
American researcher into the effects of microwave radiation on the nervous 
system at that time. 





said that the equivalent circuitry “can be found in any electronics book 
today,” and that “one can easily derive the nerve behavior from 
semiconductor physics.” When he did so, his equations predicted some of 
the properties of nerves that were, and still are, puzzling to physiologists. 


In 1979, a young professor of bioelectronics at the University of 
Edinburgh published a book titled Dielectric and Electronic Properties of 
Biological Materials. The earlier work of Eley and Arnold had been 
criticized because the activation energies they had measured—the amount 
of energy necessary to make proteins conduct electricity—seemed to be too 
large. Supposedly there was not enough energy available in living 
organisms to lift electrons into the conduction band. Proteins might be made 
to conduct electricity in the laboratory, said the critics, but this could not 
happen in the real world. Eley and Arnold, however, had done all their work 
on dried proteins, not living ones. 





The electronic role of living water had already been noted by others. 
Physiologist Gilbert Ling, realizing that cell water is a gel and not a liquid, 
developed his theory of the electronic nature of cells in 1962. More 
recently, Gerald Pollack, professor of bioengineering at the University of 
Washington, has taken up this line of investigation. He was inspired by Ling 
when they met at a conference in the mid-1980s. Pollack's most recent 
book, The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor, was 
published in 2011. 

The late geneticist Mae-Wan Ho, in London, has clothed Szent- 
Gyórgyi's ideas in garments that all can see. She developed a technique 
using a polarizing microscope that displayed, in vivid color, the interference 
patterns generated by the liquid crystalline structures that make up living 
creatures. The first animal she put under her microscope was a tiny worm— 
a fruit fly larva. “As it crawls along, it weaves its head from side to side 
flashing jaw muscles in blue and orange stripes on a magenta background,” 
she wrote in 1993 in her book, The Rainbow and the Worm: The Physics of 
Organisms. She and many others have urged that the liquid crystalline 
properties of our cells and tissues not only teach us about our chemistry, but 
have something special to tell us about life itself. 


Wiodzimierz Sedlak, pursuing Szent-Gyórgyi's ideas in Poland, 
developed the discipline of bioelectronics within the Catholic University of 
Lublin during the 1960s. Life, he said, is not only a collection of organic 
compounds undergoing chemical reactions, but those chemical reactions are 
coordinated with electronic processes that take place in an environment of 
protein semiconductors. Other scientists working at the same university are 
continuing to develop this discipline theoretically and experimentally today. 
Marian Wnuk has focused on porphyrins as key to the evolution of life. He 
states that the principal function of porphyrin systems is an electronic one. 
Józef Zon, head of the Department of Theoretical Biology at the University, 
has focused on the electronic properties of biological membranes. 

Oddly enough, the use of porphyrins in electronic products instructs us 
about biology. Adding thin films of porphyrins to commercially available 
photovoltaic cells increases the voltage, current, and total power output.!! 
Prototype solar cells based on porphyrins have been produced,? as have 
organic transistors based on porphyrins.'? 

The properties that make porphyrins suitable in electronics are the same 
properties that make us alive. As everyone knows, playing with fire is 
dangerous; oxidation releases tremendous energy quickly and violently. 
How, then, do living organisms make use of oxygen? How do we manage to 
breathe and metabolize our food without being destroyed in a 
conflagration? The secret lies in the highly pigmented, fluorescent molecule 
called porphyrin. Strong pigments are always efficient energy absorbers, 
and if they are also fluorescent, they are also good energy transmitters. As 
Szent-Györgyi taught us in his 1957 book, Bioenergetics, “fluorescence 
thus tells us that the molecule is capable of accepting energy and does not 
dissipate it. These are two qualities any molecule must have to be able to 
act as an energy transmitter." 

Porphyrins are more efficient energy transmitters than any other of life’s 
components. In technical terms, their ionization potential is low, and their 
electron affinity high. They are therefore capable of transmitting large 
amounts of energy rapidly in small steps, one low-energy electron at a time. 
They can even transmit energy electronically from oxygen to other 
molecules, instead of dissipating that energy as heat and burning up. That’s 





Porphyrins, the Nervous System, and the Environment 
There is one more place these surprising molecules are found: 









porphyrins, too, perform a function that is basic to life. They occur, 
however, in a location where one might least expect to find them—not in 
the neurons themselves, the cells that carry messages from our five senses 
to our brain, 





It was orthopedic 
surgeon Robert O. Becker who, in the 1970s, discovered that myelin 
sheaths are really electrical transmission lines. 

In a state of health the myelin sheaths contain primarily two types of 
porphyrins—coproporphyrin III and protoporphyrin—in a ratio of two to 
one, complexed with zinc. The exact composition is crucial. When 
environmental chemicals poison the porphyrin pathway, excess porphyrins, 
bound to heavy metals, build up in the nervous system as in the rest of the 
body. This disrupts the myelin sheaths and changes their conductivity 
which, in turn, alters the excitability of the nerves they surround. The entire 
nervous system becomes hyperreactive to stimuli of all kinds, including 
electromagnetic fields. 

The cells surrounding our nerves were hardly even studied until 
recently. In the nineteenth century, anatomists, finding no apparent function 
for them, supposed that they must have only a “nutritive” and “supportive” 
role, protecting the “real” nerves that they surrounded. They named them 
glial cells after the Greek word for “glue.” The discovery of the action 
potential, which transmits signals along each neuron, and of 
neurotransmitters, the chemicals that carry signals from one neuron to the 


next, had ended the discussion. From then on, glial cells were thought to be 
little more than packing material. Most biologists ignored the fact, 
discovered by German physician Rudolf Virchow in 1854, that myelin is a 
liquid crystal. They did not think it was relevant. 

However, working from the 1960s to the early 1980s and author, in 
1985, of The Body Electric, Becker found quite another function for the 
myelin-containing cells and took another step toward restoring electricity to 
its proper role in the functioning of living things. 

When he began his research in 1958, Becker was simply looking for a 
solution to orthopedists’ greatest unsolved problem: nonunion of fractures. 
Occasionally, despite the best medical care, a bone would refuse to heal. 
Surgeons, believing that only chemical processes were at work, simply 
scraped the fracture surfaces, devised complicated plates and screws to hold 
the bone ends rigidly together, and hoped for the best. Where this did not 
work, limbs had to be amputated. “These approaches seemed superficial to 
me,” Becker recalled. “I doubted that we would ever understand the failure 
to heal unless we truly understood healing itself."!5 

Becker began to pursue the ideas of Albert Szent-Gyórgyi, thinking that 
if proteins were semiconductors, maybe bones were too, and maybe 
electron flow was the secret to the healing of fractures. Ultimately he 
proved that this was correct. Bones were not just made of collagen and 
appatite, as he was taught in medical school; they were also doped with tiny 
amounts of copper, much as silicon wafers in computers are doped with tiny 
amounts of boron or aluminum. The presence of greater or lesser amounts 
of metal atoms regulates the electrical conductivity of the circuitry—in 
bones as in computers. With this understanding, Becker designed machines 
that delivered miniscule electric currents—as small as 100 trillionths of an 
ampere—to fractured bones to stimulate the healing process, with great 
success: his devices were the forerunners of machines that are used today 
by orthopedic surgeons in hospitals throughout the world. 

Becker's work on the nervous system is less well known. As already 
mentioned, the functioning of neurons had been worked out, up to a point, 
in the nineteenth century. They transmit enormous amounts of information 
to and from the brain at high speed, including data about one's 


environment, and instructions to one's muscles. They do this via the 
familiar action potential and neurotransmitters. And since the action 
potential is an all-or-nothing event, neuron signaling is an on-off digital 
system like today's computers. But Becker thought that this could not 
explain the most important properties of life; there had to be a slower, more 
primitive, and more sensitive analog system that regulates growth and 
healing, that we inherited from lower forms of life—a system that might be 
related to the acupuncture meridians of Chinese medicine, which western 
medicine also made no attempt to understand. 

A number of researchers before Becker, among them Harold Saxton 
Burr at Yale, Lester Barth at Columbia, Elmer Lund at the University of 
Texas, Ralph Gerard and Benjamin Libet at the University of Chicago, 
Theodore Bullock at U.C.L.A., and William Burge at the University of 
Illinois, had measured DC voltages on the surfaces of living organisms, 
both plants and animals, and embryos. Most biologists paid no attention. 
After all, certain DC currents, called “currents of injury,” were well known, 
and were thought to be well understood. They had been discovered by Carlo 
Matteucci as long ago as the 1830s. Biologists had assumed, for a century, 
that these currents were meaningless artifacts, caused simply by ions 
leaking out of wounds. But when, in the 1930s and 1940s, a growing 
number of scientists, using better techniques, began to find DC voltages on 
all surfaces of all living things, and not just on the surfaces of wounds, a 
few began to wonder whether those “currents of injury” just might be a bit 
more important than they had learned in school. 

The accumulated work of these scientists showed that trees,!6 and 
probably all plants, are polarized electrically, positive to negative, from 
leaves to roots, and that animals are similarly polarized from head to feet. In 
humans potential differences of up to 150 millivolts or more could 
sometimes be measured between one part of the body and another. 

Becker was the first to map the charge distribution in an animal in some 
detail, accomplishing this with salamanders in 1960. The places of greatest 
positive voltage, he found, as measured from the back of the animal, were 
the center of the head, the upper spine over the heart, and the lumbosacral 
plexus at the lower end of the spine, while the places of greatest negative 


voltage were the four feet and the end of the tail. In addition, the head of an 
alert animal was polarized from back to front, as though an electric current 
were always flowing in one direction through the middle of its brain. 
However, when an animal was anesthetized the voltage diminished as the 
anesthetic took effect, and then the head reversed polarity when the animal 
lost consciousness. This suggested to him a novel method of inducing 
anesthesia, and when Becker tried it, it worked like a charm. In the 
salamander, at least, passing an electric current of only 30 millionths of an 
ampere from front to back through the center of its head caused the animal 
to become immediately unconscious and unresponsive to pain. When the 
current was turned off, the animal promptly woke up. He observed the same 
back-to-front polarity in alert humans, and the same reversal during sleep 
and anesthesia.!? 

While Becker did not try it himself, even tinier electric currents have 
been used in psychiatry to put humans to sleep since about 1950 in Russia, 
Eastern Europe, and Asian countries that were once part of the Soviet 
Union. In these treatments, current is sent from front to back through the 
midline of the head, reversing the normal polarity of the brain, just as 
Becker did with his salamanders. The first publications describing this 
procedure specified short pulses of 10 to 15 microamperes each, 5 to 25 
times per second, which gave an average current of only about 30 billionths 
of an ampere. Although larger currents will cause immediate 
unconsciousness in a human, just like in a salamander, 





By the 1970s it had become clear to the researchers who were looking 
into such things that the DC potentials they were measuring played a key 


role in organizing living structures. They were necessary for growth and 
development.?' They were also needed for regeneration and healing. 

Tweedy John Todd demonstrated as long ago as 1823 that a salamander 
cannot regenerate a severed leg if you destroy that leg's nerve supply. So for 
a century and a half, scientists searched for the chemical signal that must be 
transmitted by nerves to trigger growth. No one ever found one. Finally, 
embryologist Sylvan Meryl Rose, in the mid-1970s at Tulane University, 
proposed that maybe there was no such chemical, and that the long-sought 
signal was purely electrical. Could the currents of injury, he asked, that had 
previously been considered mere artifacts, themselves play a central role in 
healing? 

Rose found that they did. He recorded the patterns of the currents in the 
wound stumps of salamanders as they regenerated their severed limbs. The 
end of the stump, he found, was always strongly positive during the first 
few days after injury, then reversed polarity to become strongly negative for 
the next couple of weeks, finally reestablishing the weakly negative voltage 
found on all healthy salamander legs. Rose then found that salamanders 
would regenerate their legs normally, even without a nerve supply, provided 
he carefully duplicated, with an artificial source of current, the electrical 
patterns of healing that he had observed. 






Once having established that the signals that trigger regeneration are 
electrical and not chemical in nature, these scientists were in for yet another 
surprise. For the DC potentials of the body that, as we have seen, are 
necessary not just for regeneration but for growth, healing, pain perception, 
and even consciousness, seemed to be generated not in the “real” nerves but 
in the myelin-containing cells that surround them—the cells that also 
contain porphyrins. Proof came by accident while Becker was again 
working on the problem of why some bone fractures fail to mend. Since he 
had already learned that nerves were essential to healing, he tried, in the 
early 1970s, to create an animal model for fractures that do not heal by 
severing the nerve supply to a series of rats’ legs before breaking them. 

To his surprise, the leg bones still healed normally—with a six-day 
delay. Yet six days was not nearly enough time for a rat to regenerate a 


severed nerve. Could bones be an exception, he wondered, to the rule that 
nerves are needed for healing? *Then we took a more detailed look at the 
specimens," wrote Becker. *We found that the Schwann cell sheaths were 
growing across the gap during the six-day delay. As soon as the perineural 
sleeve was mended, the bones began to heal normally, indicating that at 
least the healing, or output, signal, was being carried by the sheath rather 
than the nerve itself. The cells that biologists had considered merely 
insulation turned out to be the real wires."? It was the Schwann cells, 
Becker concluded—the myelin-containing glial cells—and not the neurons 
they surrounded, that carried the currents that determined growth and 
healing. And in a much earlier study Becker had already shown that the DC 
currents that flow along salamander legs, and presumably along the limbs 
and bodies of all higher animals, are of semiconducting type.” 

Which brings us full circle. The myelin sheaths—the liquid crystalline 
sleeves surrounding our nerves—contain semiconducting porphyrins,” 
doped with heavy metal atoms, probably zinc.?» It was Harvey Solomon and 
Frank Figge who, in 1958, first proposed that these porphyrins must play an 
important role in nerve conduction. The implications of this are especially 
important for people with chemical and electromagnetic sensitivities. Those 
of us who, genetically, have relatively less of one or more porphyrin 
enzymes, may have a “nervous temperament” because our myelin is doped 
with slightly more zinc than our neighbors’ and is more easily disturbed by 
the electromagnetic fields (EMFs) around us. Toxic chemicals and EMFs 
are therefore synergistic: exposure to toxins further disrupts the porphyrin 
pathway, causing the accumulation of more porphyrins and their precursors, 
rendering the myelin and the nerves they surround still more sensitive to 
EMFs. According to more recent research, a large excess of porphyrin 
precursors can prevent the synthesis of myelin and break apart the myelin 
sheaths, leaving the neurons they surround naked and exposed.”6 

The true situation is undoubtedly more complex than this, but to put all 
the pieces correctly together will require researchers who are willing to step 
outside our cultural blinders and acknowledge the existence of electrical 
transmission lines in the nervous systems of animals. Already, mainstream 
science has taken the first step by finally acknowledging that glial cells are 


much more than packing material." In fact, a discovery by a team of 
researchers at the University of Genoa is currently revolutionizing 
neurology. Their discovery is related to breathing .?? 

Everyone knows that the brain consumes more oxygen than any other 
organ, and that if a person stops breathing, the brain is the first organ to die. 
What the Italian team confirmed in 2009 is that as much as ninety percent 
of that oxygen is consumed not by the brain's nerve cells, but by the myelin 
sheaths that surround them. Traditional wisdom has it that the consumption 
of oxygen for energy takes place only in tiny bodies inside cells called 
mitochondria. That wisdom has now been turned on its head. In the nervous 
system, at least, most of the oxygen appears to be consumed in the multiple 
layers of fatty substance called myelin, which contain no mitochondria at 
all, but which forty-year-old research showed contains non-heme 
porphyrins and is semiconducting. Some scientists are even beginning to 
say that the myelin sheath is, in effect, itself a giant mitochondrion, without 
which the huge oxygen needs of our brain and nervous system could never 
be met. But to truly make sense of this collection of facts will also require 
the recognition that both the neurons, as Ling Wei proposed, and the myelin 
sheaths that envelop them, as Robert Becker proposed, work together to 
form a complex and elegant electrical transmission line system, subject to 
electrical interference just like transmission lines built by human engineers. 

The exquisite sensitivity of even the normal nervous system to 
electromagnetic fields was proven in 1956 by zoologists Carlo Terzuolo and 
Theodore Bullock—and then ignored by everyone since. In fact, even 
Terzuolo and Bullock were astonished by the results. Experimenting on 
crayfish, they found that although a substantial amount of electric current 
was needed to cause a previously silent nerve to fire, incredibly tiny 
currents could cause an already firing nerve to alter its firing rate 
tremendously. A current of only 36 billionths of an ampere was enough to 
increase or decrease a nerve's rate of firing by five to ten percent. And a 
current of 150 billionths of an ampere—thousands of times less than is 
widely assumed, still today, by developers of modern safety codes, to have 
any biological effect whatever—would actually double the rate of firing, or 
silence the nerve altogether. Whether it increased or decreased the activity 


of the nerve depended only on the direction in which the current was 
applied to the nerve. 


The Zinc Connection 

The role of zinc was discovered in the 1950s by Henry Peters, a 
porphyrinologist at the University of Wisconsin Medical School. Like 
Morton after him, Peters was impressed by the number of people who 
seemed to have mild or latent porphyria, and thought the trait was far more 
prevalent that was commonly believed.?? 

Peters discovered that his porphyria patients who had neurological 
symptoms were excreting very large amounts of zinc in their urine—up to 
36 times normal. In fact, their symptoms correlated better with the levels of 
zinc in their urine than with the levels of porphyrins they were excreting. 
With this information, Peters did the most logical thing: in scores of 
patients, he tried chelation to reduce the body's load of zinc, and it worked! 
In patient after patient, when courses of treatment with BAL or EDTA had 
reduced the level of zinc in their urine to normal, their illness resolved, and 
the patient remained symptom-free for up to several years.? Contrary to 
conventional wisdom, which assumes that zinc deficiency is common and 
should be supplemented, Peters’ patients, because of their genetics and their 
polluted environment, were actually zinc-poisoned—as at least five to ten 
percent of the population, with hidden porphyria, may also be. 

For the next forty years Peters found tremendous resistance to his idea 
that zinc toxicity was at all common, but growing evidence is now 
accumulating that this is so. Large amounts of zinc are in fact entering our 
environment, our homes, and our bodies from industrial processes, 
galvanized metals, and even the fillings in our teeth. Zinc is in denture 
cream and in motor oil. There is so much zinc in automobile tires that their 
constant erosion makes zinc one of the main components of road dust— 
which washes into our streams, rivers, and reservoirs, eventually getting 
into our drinking water.*! Wondering whether this was perhaps poisoning us 
all, a group of scientists from Brookhaven National Laboratory, the United 
States Geological Survey, and several universities raised rats on water 
supplemented with a low level of zinc. By three months of age, the rats 


o 


o 


already had memory deficits. By nine months of age, they had elevated 
levels of zinc in their brains.? In a human experiment, pregnant women in a 
slum area of Bangladesh were given 30 milligrams of zinc daily, in the 
expectation that this would benefit the mental development and motor skills 
of their babies. The researchers found just the opposite.? In a companion 
experiment, a group of Bangladeshi infants were given 5 milligrams of zinc 
daily for five months, with the same surprising result: the supplemented 
infants scored more poorly on standard tests of mental development.*4 And 
a growing body of literature shows that zinc supplements worsen 
Alzheimer’s disease, 





Nutritionists have long been misled by using blood tests to judge the 
body’s stores of zinc; scientists are finding out that blood levels are not 
reliable, and that unless you are severely malnourished there is no relation 
between the amount of zinc in your diet and the level of zinc in your 
blood. In some neurological diseases, including Alzheimer's disease, it is 
common to have high levels of zinc in the brain while having normal or low 
levels of zinc in the blood.? In a number of diseases including diabetes and 
cancer, urinary zinc is high while blood zinc is low.^ It appears that the 
kidneys respond to the body's total load of zinc, and not to the levels in the 
blood, so that blood levels can become low, not because of a zinc deficiency 
but because the body is overloaded with zinc and the kidneys are removing 
it from the blood as fast as they can. It also appears to be much more 
difficult than we used to think for people to become deficient by eating a 
zinc-poor diet; the body is amazingly capable of compensating for even 
extremely low levels of dietary zinc by increasing intestinal absorption and 
decreasing excretion through urine, stool, and skin." "While the 
recommended dietary allowance for adult males is 11 milligrams per day, a 
man can take in as little as 1.4 milligrams of zinc a day and still maintain 
homeostasis and normal levels of zinc in the blood and tissues.? But a 


person who increases his or her daily intake beyond 20 milligrams may risk 
toxic effects in the long term. 


Canaries in the Mine 
In our cells, the manufacture of heme from porphyrins can be inhibited by a 
large variety of toxic chemicals, and not—so far as we know—by 
electricity. But we will see in the coming chapters that electromagnetic 
fields interfere with the most important job that this heme is supposed to do 





There is no escape. Regardless of diet, exercise, lifestyle, and 
genetics, the risk of developing these diseases is greater for every human 
being and every animal than it was a century and a half ago. People with a 
genetic predisposition simply have a greater risk than everyone else, 
because they have a bit less heme in their mitochondria to start with. 

In France, liver cancer was found to be 36 times as frequent in people 
carrying a gene for porphyria as in the general population.? In Sweden and 
Denmark the rate was 39 times as high, and the lung cancer rate triple the 
general rate.^ Chest pain, heart failure, high blood pressure, and EKGs 
suggestive of oxygen starvation are well known in porphyria.^ Porphyria 
patients with normal coronary arteries often die of heart arrhythmias^ or 
heart attacks." Glucose tolerance tests and insulin levels are usually 
abnormal.^ In one study, 15 of 36 porphyria patients had diabetes.^ The 
protean manifestations of this disease, capable of affecting almost any 
organ, are widely blamed on impaired cellular respiration due to a 


deficiency of heme.» Indeed, no porphyrin expert has offered a better 
explanation. 

The five to ten percent of the population who have lower porphyrin 
enzyme levels are the so-called canaries in the coal mine, whose songs of 
warning, however, have been tragically ignored. They are the people who 
came down with neurasthenia in the last half of the nineteenth century when 
telegraph wires swept the world; the victims of sleeping pills in the late 
1880s, of barbiturates in the 1920s, and of sulfa drugs in the 1930s; the 
men, women, and children with multiple chemical sensitivity, poisoned by 
the soup of chemicals that have rained on us since World War II; the 
abandoned souls with electrical sensitivity left behind by the computer age, 
forced into lonely exile by the inescapable radiation of the wireless 
revolution. 

In Part Two of this book we will see just how extensively the general 
population of the world has been affected as a result of the failure to heed 
their warnings. 


PART TWO 








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11. Irritable Heart 


ON THE FIRST DAY OF AUTUMN, 1998, Florence Griffith Joyner, 
former Olympic track gold medalist, died in her sleep at the age of thirty- 
eight when her heart stopped beating. That same fall, Canadian ice hockey 
player Stéphane Morin, age twenty-nine, died of sudden heart failure during 
a hockey game in Germany, leaving behind a wife and newborn son. Chad 
Silver, who had played on the Swiss national ice hockey team, also age 
twenty-nine, died of a heart attack. Former Tampa Bay Buccaneers nose 
tackle Dave Logan collapsed and died from the same cause. He was forty- 
two. None of these athletes had any history of heart disease. 

A decade later, responding to mounting alarm among the sports 
community, the Minneapolis Heart Institute Foundation created a National 
Registry of Sudden Deaths in Athletes. After combing through public 
records, news reports, hospital archives, and autopsy records, the 
Foundation identified 1,049 American athletes in thirtyeight competitive 
sports who had suffered sudden cardiac arrest between 1980 and 2006. The 
data confirmed what the sports community already knew. In 1980, heart 
attacks in young athletes were rare: only nine cases occurred in the United 
States. The number rose gradually but steadily, increasing about ten percent 
per year, until 1996, when the number of cases of fatal cardiac arrest among 
athletes suddenly doubled. There were 64 that year, and 66 the following 
year. In the last year of the study, 76 competitive athletes died when their 
hearts gave out, most of them under eighteen years of age.! 

The American medical community was at a loss to explain it. But in 
Europe, some physicians thought they knew the answer, not only to the 
question of why so many young athletes’ hearts could no longer stand the 
strain of exertion, but to the more general question of why so many young 
people were succumbing to diseases from which only old people used to 


die. On October 9, 2002, an association of German doctors specializing in 
environmental medicine began circulating a document calling for a 
moratorium on antennas and towers used for mobile phone 
communications. Electromagnetic radiation, they said, was causing a drastic 
rise in both acute and chronic diseases, prominent among which were 
“extreme fluctuations in blood pressure,” “heart rhythm disorders,” and 
“heart attacks and strokes among an increasingly younger population.” 





Although I knew about the Freiburger Appeal and the profound effects 
electricity could have on the heart, when I first conceived this book I did 
not intend to include a chapter on heart disease, for I was still in denial 
despite the abundant evidence. 

We recall from chapter 8 that Marconi, the father of radio, had ten heart 
attacks after he began his world-changing work, including the one that 
killed him at the young age of 63. 

“Anxiety disorder,” which is rampant today, is most often diagnosed 
from its cardiac symptoms. Many suffering from an acute “anxiety attack” 
have heart palpitations, shortness of breath, and pain or pressure in the 
chest, which so often resemble an actual heart attack that hospital 
emergency rooms are visited by more patients who turn out to have nothing 
more than “anxiety” than by patients who prove to have something wrong 
with their hearts. And yet we recall from chapter 6 that “anxiety neurosis” 
was an invention of Sigmund Freud, a renaming of a disease formerly 
called neurasthenia, that became prevalent only in the late nineteenth 
century following the building of the first electrical communication 
systems. 

Radio wave sickness, described by Russian doctors in the 1950s, 
includes cardiac disturbances as a prominent feature. 


Not only did I know all this, but I myself have suffered for thirty- five 
years from palpitations, abnormal heart rhythm, shortness of breath, and 
chest pain, related to exposure to electricity. 

Yet when my friend and colleague Jolie Andritzakis suggested to me 
that heart disease itself had appeared in the medical literature for the first 
time at the beginning of the twentieth century and that I should write a 
chapter about it, I was taken by surprise. In medical school I had had it so 
thoroughly drilled into me that cholesterol is the main cause of heart disease 
that I had never before questioned the wisdom that bad diet and lack of 
exercise are the most important factors contributing to the modern 
epidemic. 





I decided to dive in. 


I first became aware of Milham's work in 1996, when I was asked to help 
with a national lawsuit against the Federal Communications Commission. I 
was still living in Brooklyn, and knew only that the telecommunications 
industry was promising a “wireless revolution." The industry wanted to 
place a cell phone in the hands of every American, and in order to make 
those devices work in the urban canyons of my home town they were 
applying for permission to erect thousands of microwave antennas close to 
street level throughout New York. Advertisements for the newfangled 
phones were beginning to appear on radio and television, telling the public 
why they needed such things and that they would make ideal Christmas 
gifts. I did not have any idea how radically the world was about to change. 
Then came a phone call from David Fichtenberg, a statistician in 
Washington State, who told me the FCC had just released human exposure 
guidelines for microwave radiation, and asked if I wanted to join a 


nationwide legal challenge against them. The new guidelines, I came to find 
out, had been written by the cell phone industry itself and did not protect 
people from any of the effects of microwave radiation except one: being 
cooked like a roast in a microwave oven. None of the known effects of such 
radiation, apart from heat—effects on the heart, nervous system, thyroid 
gland, and other organs—were taken into consideration. 

Worse, Congress had passed a law that January that actually made it 
illegal for cities and states to regulate this new technology on the basis of 
health. President Clinton had signed it on February 8. The industry, the 
FCC, Congress, and the President were conspiring to tell us that we should 
all feel comfortable holding devices that emit microwave radiation directly 
against our brains, and that we should all get used to living in close quarters 
with microwave towers, because they were coming to a street near you 
whether you liked it or not. A giant biological experiment had been 
launched, and we were all going to be unwitting guinea pigs. 

Except that the outcome was already known. The research had been 
done, and the scientists who had done it were trying to tell us what the new 
technology was going to do to the brains of cell phone users, and to the 
hearts and nervous systems of people living in the vicinity of cell towers— 
which one day soon was going to be everybody. 
was one of those researchers. He had not done any 
of the clinical or experimental research on individual humans or animals; 
such work had been done by others in previous decades. Milham is an 
epidemiologist, a scientist who proves that the results obtained by others in 
the laboratory actually happen to masses of people living in the real world. 








He knew that the new FCC 
standards were inadequate, and he made himself available as a consultant to 
those who were challenging them in court. 





Samuel Milham, M.D., M.P.H 


In recent years, Milham turned his skills to the examination of vital 
statistics from the 1930s and 1940s, when the Roosevelt administration 
made it a national priority to electrify every farm and rural community in 
America. What Milham discovered surprised even him. Not only cancer, he 
found, but also diabetes and heart disease seemed to be directly related to 
residential electrification. Rural communities that had no electricity had 
little heart disease—until electric service began. In fact, in 1940, country 
folk in electrified regions of the country were suddenly dying of heart 
disease four to five times as frequently as those who still lived out of 
electricity’s reach. “It seems unbelievable that mortality differences of this 
magnitude could go unexplained for over 70 years after they were first 
reported," wrote Milham.? He speculated that early in the twentieth century 
nobody was looking for answers. 

But when I began reading the early literature I found that everyone was 
looking for answers. Paul Dudley White, for example, a well-known 
cardiologist associated with Harvard Medical School, puzzled over the 
problem in 1938. In the second edition of his textbook, Heart Disease, he 
wrote in amazement that Austin Flint, a prominent physician practicing 
internal medicine in New York City during the last half of the nineteenth 
century, had not encountered a single case of angina pectoris (chest pain 
due to heart disease) for one period of five years. White was provoked by 
the tripling of heart disease rates in his home state of Massachusetts since 


he had begun practicing in 1911. “As a cause of death,” he wrote, “heart 
disease has assumed greater and greater proportions in this part of the world 
until now it leads all other causes, having far outstripped tuberculosis, 
pneumonia, and malignant disease.” 





the first 100 papers I published,” he wrote, “only two, at the end of the 100, 
were concerned with coronary heart disease."? 

Heart disease had not, however, sprung full-blown from nothing at the 
turn of the twentieth century. It had been relatively uncommon but not 
unheard of. The vital statistics of the United States show that rates of heart 
disease had begun to rise long before White graduated from medical school. 
The modern epidemic actually began, quite suddenly, in the 1870s, at the 
same time as the first great proliferation of telegraph wires. But that is to 
jump ahead of myself. For the evidence that heart disease is caused 
primarily by electricity is even more extensive than Milham suspected, and 
the mechanism by which electricity damages the heart is known. 


To begin with, we need not rely only on historical data for evidence 
supporting Milham's proposal, for electrification is still going on in a few 
parts of the world. 

From 1984 to 1987, scientists at the Sitaram Bhartia Institute of Science 
and Research decided to compare rates of coronary heart disease in Delhi, 
India, which were disturbingly high, with rates in rural areas of Gurgaon 
district in Haryana state 50 to 70 kilometers away. Twenty-seven thousand 
people were interviewed, and as expected, the researchers found more heart 
disease in the city than in the country. But they were surprised by the fact 
that virtually all of the supposed risk factors were actually greater in the 
rural districts. 

City dwellers smoked much less. They consumed fewer calories, less 
cholesterol, and much less saturated fat than their rural counterparts. Yet 
they had five times as much heart disease. *It is clear from the present 


study,” wrote the researchers, “that the prevalence of coronary heart disease 
and its urban-rural differences are not related to any particular risk factor, 
and it is therefore necessary to look for other factors beyond the 
conventional explanations."^ The most obvious factor that these researchers 
did not look at was electricity. For in the mid-1980s the Gurgaon district 
had not yet been electrified.® 

In order to make sense of these kinds of data it is necessary to review 
what is known—and what is still not known—about heart disease, 
electricity, and the relationship between the two. 


My Hungarian grandmother, who was the main cook in my family while I 
was growing up, had arteriosclerosis (hardening of the arteries). She fed us 
the same meals she cooked for herself and, at the advice of her doctor, they 
were low in fat. She happened to be a marvelous cook, so after I left home I 
continued eating in a similar style because I was hooked on the taste. For 
the past thirty-eight years I have also been a vegetarian. I feel healthiest 
eating this way, and I believe that it is good for my heart. 

However, soon after I began to do research for this chapter, a friend 
gave me a book to read titled The Cholesterol Myths. It was published in 
2000 by Danish physician Uffe Ravnskov, a specialist in internal medicine 
and kidney disease and a retired family practice doctor living in Lund, 
Sweden. I resisted reading it, because Ravnskov is not unbiased: he thinks 
vegetarians are pleasure-avoiding stoics who heroically deny themselves 
the taste of proper food in the mistaken belief that this will make them live 
longer. 

Ignoring his prejudices, I eventually read Ravnskov's book and found it 
well-researched and thoroughly referenced. It demolishes the idea that 
people are having more heart attacks today because they are stuffing 
themselves with more animal fat than their ancestors did. On its surface, his 
thesis is contrary to what I was taught as well as to my own experience. So I 
obtained copies of many of the studies he quoted, and read them over and 
over until they finally made sense in light of what I knew about electricity. 
The most important thing to keep in mind is that the early studies did not 
have the same outcome as research being done today, and that there is a 


reason for this difference. Even recent studies from different parts of the 
world do not always agree with each other, for the same reason. 

Ravnskov, however, has become something of an icon among portions 
of the alternative health community, including many environmental 
physicians who are now prescribing high-fat diets—emphasizing animal 
fats—to their severely ill patients. They are misreading the medical 
literature. The studies that Ravnskov relied on show unequivocally that 
some factor other than diet is responsible for the modern scourge of heart 
disease, but they also show that cutting down on dietary fat in today’s world 
helps to prevent the damage caused by that other factor. Virtually every 
large study done since the 1950s in the industrialized world—agreeing with 
what I was taught in medical school—has shown a direct correlation 
between cholesterol and heart disease. And every study comparing 
vegetarians to meat eaters has found that vegetarians today have both lower 
cholesterol levels and a reduced risk of dying from a heart attack." 

Ravnskov speculated that this is because people who eat no meat are 
also more health-conscious in other ways. But the same results have been 
found in people who are vegetarians only for religious reasons. Seventh 
Day Adventists all abstain from tobacco and alcohol, but only about half 
abstain from meat. A number of large long-term studies have shown that 
Adventists who are also vegetarians are two to three times less likely to die 
from heart disease.? 

Perplexingly, the very early studies—those done in the first half of the 
twentieth century—did not give these kinds of results and did not show that 
cholesterol was related to heart disease. To most researchers, this has been 
an insoluble paradox, contradicting present ideas about diet, and has been a 
reason for the mainstream medical community to dismiss the early research. 

For example, people with the genetic trait called familial 
hypercholesterolemia have extremely high levels of cholesterol in their 
blood—so high that they sometimes have fatty growths on their joints and 
are prone to gout-like attacks in toes, ankles, and knees caused by 
cholesterol crystals. In today’s world these people are prone to dying young 
of coronary heart disease. However, this was not always so. Researchers at 
Leiden University in the Netherlands traced the ancestors of three present- 


day individuals with this disorder until they found a pair of common 
ancestors who lived in the late eighteenth century. Then, by tracing all 
descendants of this pair and screening all living descendants for the 
defective gene, they were able to identify 412 individuals who either had 
definitely carried the gene and passed it on, or who were siblings who had a 
fifty percent chance of carrying it. They found, to their amazement, that 
before the 1860s people with this trait had a fifty percent lower mortality 
rate than the general population. In other words, cholesterol seemed to have 
had protective value and people with very high cholesterol levels lived 
longer than average. Their mortality rate, however, rose steadily during the 
late nineteenth century until it equaled the rate of the general population in 
about 1915. The mortality of this subgroup continued rising during the 
twentieth century, reaching double the average during the 1950s and then 
leveling off somewhat.? One can speculate, based on this study, that before 
the 1860s cholesterol did not cause coronary heart disease, and there is 
other evidence that this is so. 

In 1965, Leon Michaels, working at the University of Manitoba, decided 
to see what historical documents revealed about fat consumption in 
previous centuries when coronary heart disease was extremely rare. What 
he found also contradicted current wisdom and convinced him that there 
must be something wrong with the cholesterol theory. One author in 1696 
had calculated that the wealthier half of the English population, or about 2.7 
million people, ate an amount of flesh yearly averaging 147.5 pounds per 
person—more than the national average for meat consumption in England 
in 1962. Nor did the consumption of animal fats decline at any time before 
the twentieth century. Another calculation made in 1901 had shown that the 
servant-keeping class of England consumed, on average, a much larger 
amount of fat in 1900 than they did in 1950. Michaels did not think that 
lack of exercise could explain the modern epidemic of heart disease either, 
because it was among the idle upper classes, who had never engaged in 
manual labor, and who were eating much less fat than they used to, that 
heart disease had increased the most. 

Then there was the incisive work of Jeremiah Morris, Professor of 
Social Medicine at the University of London, who observed that in the first 


half of the twentieth century, coronary heart disease had increased while 
coronary atheroma—cholesterol plaques in the coronary arteries—had 
actually decreased. Morris examined the autopsy records at London 
Hospital from the years 1908 through 1949. In 1908, 30.4 percent of all 
autopsies in men aged thirty to seventy showed advanced atheroma; in 
1949, only 16 percent. In women the rate had fallen from 25.9 percent to 
7.5 percent. In other words, cholesterol plaques in coronary arteries were 
far less common than before, but they were contributing to more disease, 
more angina, and more heart attacks. By 1961, when Morris presented a 
paper about the subject at Yale University Medical School, studies 
conducted in Framingham, Massachusetts? and Albany, New York" had 
established a connection between cholesterol and heart disease. Morris was 
sure that some other, unknown environmental factor was also important. “It 
is tolerably certain,” he told his audience, “that more than fats in the diet 
affect blood lipid levels, more than blood lipid levels are involved in 
atheroma formation, and more than atheroma is needed for ischemic heart 
disease.” 





Whatever environmental factor was affecting human beings in America 
during the 1930s and 1940s was also affecting all the animals in the 
Philadelphia Zoo. 

The Laboratory of Comparative Pathology was a unique facility founded 
at the zoo in 1901. And from 1916 to 1964, laboratory director Herbert Fox 
and his successor, Herbert L. Ratcliffe, kept complete records of autopsies 
performed on over thirteen thousand animals that had died in the zoo. 

During this period, arteriosclerosis increased an astonishing ten- to 
twenty-fold among all species of mammals and birds. In 1923, Fox had 
written that such lesions were “exceedingly rare,” occurring in less than two 
percent of animals as a minor and incidental finding at autopsy.? The 
incidence rose rapidly during the 1930s, and by the 1950s arteriosclerosis 
was not only occurring in young animals, but was often the cause of their 


death rather than just a finding on autopsy. By 1964, the disease occurred in 
one-quarter of all mammals and thirty-five percent of all birds. 

Coronary heart disease appeared even more suddenly. In fact, before 
1945 the disease did not exist in the zoo.? And the first heart attacks ever 
recorded in zoo animals occurred ten years later, in 1955. Arteriosclerosis 
had been occurring with some regularity since the 1930s in the aorta and 
other arteries, but not in the coronary arteries of the heart. But sclerosis of 
the coronary arteries now increased so rapidly among both mammals and 
birds that by 1963, over 90 percent of all mammals and 72 percent of all 
birds that died in the zoo had coronary disease, while 24 percent of the 
mammals and 10 percent of the birds had had heart attacks. And a majority 
of the heart attacks were occurring in young animals in the first half of their 
expected life spans. Arteriosclerosis and heart disease were now occurring 
in 45 families of mammals and 65 families of birds residing in the zoo—in 
deer and in antelope; in prairie dogs and squirrels; in lions, and tigers, and 
bears; and in geese, storks, and eagles. 

Diet had nothing to do with these changes. The increase in 
arteriosclerosis had begun well before 1935, the year that more nutritious 
diets were introduced throughout the zoo. And coronary disease did not 
make its appearance until ten years later, yet the animals’ diets were the 
same at all times between 1935 and 1964. The population density, for 
mammals at least, remained about the same during all fifty years, as did the 
amount of exercise they got. Ratcliffe tried to find the answer in social 
pressures brought about by breeding programs that were begun in 1940. He 
thought that psychological stresses must be affecting the animals’ hearts. 
But he could not explain why, more than two decades later, coronary 
disease and heart attacks were continuing to increase, spectacularly, 
throughout the zoo, and among all species, whether or not they were being 
bred. Nor could he explain why sclerosis of artieries outside the heart had 
increased during the 1930s, nor why, thousands of miles away, researchers 
were finding arteriosclerosis in 22 percent of the animals in the London Zoo 
in 1960," and a similar number in the Zoo of Antwerp, Belgium in 1962.5 


The element that increased most spectacularly in the environment during 
the 1950s when coronary disease was exploding among humans and 
animals was radio frequency (RF) radiation. Before World War II, radio 
waves had been widely used for only two purposes: radio communication, 
and diathermy, which is their therapeutic use in medicine to heat parts of 
the body. 

Suddenly the demand for RF generating equipment was unquenchable. 
While the use of the telegraph in the Civil War had stimulated its 
commercial development, and the use of radio in World War I had done the 
same for that technology, the use of radar in World War II spawned scores 
of new industries. RF oscillators were being mass produced for the first 
time, and hundreds of thousands of people were being exposed to radio 
waves on the job—radio waves that were now used not only in radar, but in 
navigation; radio and television broad- casting; radio astronomy; heating, 
sealing and welding in dozens of industries; and “radar ranges” for the 
home. Not only industrial workers, but the entire population, were being 
exposed to unprecedented levels of RF radiation. 

For reasons having more to do with politics than science, history took 
opposite tracks on opposite sides of the world. In Western Bloc countries, 
science went deeper into denial. It had buried its head, ostrich-like, in the 
year 1800, as we saw in chapter 4, and now simply piled on more sand. 
When radar technicians complained of headaches, fatigue, chest discomfort, 
and eye pain, and even sterility and hair loss, they were sent for a quick 
medical exam and some blood work. When nothing dramatic turned up, 
they were ordered back to work.!'5 The attitude of Charles I. Barron, medical 
director of the California division of Lockheed Aircraft Corporation, was 
typical. Reports of illness from microwave radiation “had all too often 
found their way into lay publications and newspapers,” he said in 1955. He 
was addressing representatives of the medical profession, the armed forces, 
various academic institutions, and the airline industry at a meeting in 
Washington, DC. “Unfortunately,” he added, “the publication of this 
information within the past several years coincided with the development of 
our most powerful airborne radar transmitters, and considerable 
apprehension and misunderstanding has arisen among engineering and 


radar test personnel." He told his audience that he had examined hundreds 
of Lockheed employees and found no difference between the health of 
those exposed to radar and those not exposed. However, his study, which 
was subsequently published in the Journal of Aviation Medicine, was 
tainted by the same see-no-evil attitude. His “unexposed” control 
population were actually Lockheed workers who were exposed to radar 
intensities of less than 3.9 milliwatts per square centimeter—a level that is 
almost four times the legal limit for exposure of the general public in the 
United States today. Twenty-eight percent of these “unexposed” employees 
suffered from neurological or cardiovascular disorders, or from jaundice, 
migraines, bleeding, anemia, or arthritis. And when Barron took repeated 
blood samples from his “exposed” population—those who were exposed to 
more than 3.9 milliwatts per square centimeter—the majority had a 
significant drop in their red cell count over time, and a significant increase 
in their white cell count. Barron dismissed these findings as “laboratory 
errors.” !” 

The Eastern Bloc experience was different. Workers’ complaints were 
considered important. Clinics dedicated entirely to the diagnosis and 
treatment of workers exposed to microwave radiation were established in 
Moscow, Leningrad, Kiev, Warsaw, Prague, and other cities. On average, 
about fifteen percent of workers in these industries became sick enough to 
seek medical treatment, and two percent became permanently disabled. !® 

The Soviets and their allies recognized that the symptoms caused by 
microwave radiation were the same as those first described in 1869 by 
American physician George Beard. Therefore, using Beard’s terminology, 
they called the symptoms "neurasthenia," while the disease that caused 
them was named “microwave sickness” or “radio wave sickness.” 

Intensive research began at the Institute of Labor Hygiene and 
Occupational Diseases in Moscow in 1953. By the 1970s, the fruits of such 
investigations had produced thousands of publications.!9 Medical textbooks 
on radio wave sickness were written, and the subject entered the curriculum 
of Russian and Eastern European medical schools. Today, Russian 
textbooks describe effects on the heart, nervous system, thyroid, adrenals, 
and other organs.? Symptoms of radio wave exposure include headache, 


fatigue, weakness, dizziness, nausea, sleep disturbances, irritability, 
memory loss, emotional instability, depression, anxiety, sexual dysfunction, 
impaired appetite, abdominal pain, and digestive disturbances. Patients have 
visible tremors, cold hands and feet, flushed face, hyperactive reflexes, 
abundant perspiration, and brittle fingernails. Blood tests reveal disturbed 
carbohydrate metabolism and elevated triglycerides and cholesterol. 

Cardiac symptoms are prominent. They include heart palpitations, 
heaviness and stabbing pains in the chest, and shortness of breath after 
exertion. The blood pressure and pulse rate become unstable. Acute 
exposure usually causes rapid heartbeat and high blood pressure, while 
chronic exposure causes the opposite: low blood pressure and a heartbeat 
that can be as slow as 35 to 40 beats per minute. The first heart sound is 
dulled, the heart is enlarged on the left side, and a murmur is heard over the 
apex of the heart, often accompanied by premature beats and an irregular 
rhythm. The electrocardiogram may reveal a blockage of electrical 
conduction within the heart, and a condition known as left axis deviation. 
Signs of oxygen deprivation to the heart muscle—a flattened or inverted T 
wave, and depression of the ST interval—are extremely frequent. 
Congestive heart failure is sometimes the ultimate outcome. In one medical 
textbook published in 1971, the author, Nikolay Tyagin, stated that in his 
experience only about fifteen percent of workers exposed to radio waves 
had normal EKGs.?! 

Although this knowledge has been completely ignored by the American 
Medical Association and is not taught in any American medical school, it 
has not gone unnoticed by some American researchers. 


Trained as a biologist, Allan H. Frey became interested in microwave 
research in 1960 by following his curiosity. Employed at the General 
Electric Company’s Advanced Electronics Center at Cornell University, he 
was already exploring how electrostatic fields affect an animal’s nervous 
system, and he was experimenting with the biological effects of air ions. 
Late that year, while attending a conference, he met a technician from GE's 
radar test facility at Syracuse, who told Frey that he could hear radar. *He 
was rather surprised," Frey later recalled, *when I asked if he would take 


me to a site and let me hear the radar. It seemed that I was the first person 
he had told about hearing radars who did not dismiss his statement out of 
hand.”?? The man took Frey to his work site near the radar dome at 
Syracuse. “And when I walked around there and climbed up to stand at the 
edge of the pulsating beam, I could hear it, too," Frey remembers. *I could 
hear the radar going zip-zip-zip.”° 

This chance meeting determined the future course of Frey’s career. He 
left his job at General Electric and began doing full-time research into the 
biological effects of microwave radiation. In 1961, he published his first 
paper on “microwave hearing,” a phenomenon that is now fully recognized 
although still not fully explained. He spent the next two decades 
experimenting on animals to determine the effects of microwaves on 
behavior, and to clarify their effects on the auditory system, the eyes, the 
brain, the nervous system, and the heart. He discovered the blood-brain 
barrier effect, an alarming damage to the protective shield that keeps 
bacteria, viruses, and toxic chemicals out of the brain—damage that occurs 
at levels of radiation that are much lower than what is emitted by cell 
phones today. He proved that nerves, when firing, emit pulses of radiation 
themselves, in the infrared spectrum. All of Frey’s pioneering work was 
funded by the Office of Naval Research and the United States Army. 

When scientists in the Soviet Union began reporting that they could 
modify the rhythm of the heart at will with microwave radiation, Frey took 
a special interest. N. A. Levitina, in Moscow, had found that she could 
either speed up an animal’s heart rate or slow it down, depending on which 
part of the animal’s body she irradiated. Irradiating the back of an animal’s 
head quickened its heart rate, while irradiating the back of its body, or its 
stomach, slowed it down.”4 

Frey, in his laboratory in Pennsylvania, decided to take this research one 
step farther. Based on the Russian results and his knowledge of physiology 
he predicted that if he used brief pulses of microwave radiation, 
synchronized with the heartbeat and timed to coincide precisely with the 
beginning of each beat, he would cause the heart to speed up, and might 
disrupt its rhythm. 


It worked like magic. He first tried the experiment on the isolated hearts 
of 22 different frogs. The heart rate increased every time. In half the hearts, 
arrhythmias occurred, and in some of the experiments the heart stopped. 
The pulse of radiation was most damaging when it occurred exactly one- 
fifth of a second after the beginning of each beat. The average power 
density was only six-tenths of a microwatt per square centimeter—roughly 
ten thousand times weaker than the radiation that a person's heart would 
absorb today if he or she kept a cell phone in a shirt pocket while making a 
call. 

Frey conducted the experiments with isolated hearts in 1967. Two years 
later, he tried the same thing on 24 live frogs, with similar though less 
dramatic results. No arrhythmias or cardiac arrests occurred, but when the 
pulses of radiation coincided with the beginning of each beat, the heart 
speeded up significantly.?* 





hese cellular effects were discovered, oddly 
enough, by a team that included Paul Dudley White. In the 1940s and 
1950s, while the Soviets were beginning to describe how radio waves cause 
neurasthenia in workers, the United States military was investigating the 
same disease in military recruits. 


The job that was assigned to Dr. Mandel Cohen and his associates in 1941 
was to determine why so many soldiers fighting in the Second World War 
were reporting sick because of heart symptoms. Although their research 
spawned a number of shorter articles in medical journals, the main body of 
their work was a 150-page report that has been long forgotten. It was 
written for the Committee of Medical Research of the Office of Scientific 
Research and Development—the office that was created by President 
Roosevelt to coordinate scientific and medical research related to the war 
effort. The only copy I located in the United States was on a single 


deteriorating roll of microfilm buried in the Pennsylvania storage facility of 
the National Library of Medicine.?6 

Unlike their predecessors since the time of Sigmund Freud, this medical 
team not only took these anxiety-like complaints seriously, but looked for 
and found physical abnormalities in the majority of these patients. They 
preferred to call the illness “neurocirculatory asthenia,” rather than 
“neurasthenia,” “irritable heart,” “effort syndrome,” or “anxiety neurosis,” 
as it had variously been known since the 1860s. But the symptoms 
confronting them were the same as those first described by George Miller 
Beard in 1869 (see chapter 5). Although the focus of this team was the 
heart, the 144 soldiers enrolled in their study also had respiratory, 
neurological, muscular, and digestive symptoms. Their average patient, in 
addition to having heart palpitations, chest pains, and shortness of breath, 
was nervous, irritable, shaky, weak, depressed, and exhausted. He could not 
concentrate, was losing weight, and was troubled by insomnia. He 
complained of headaches, dizziness, and nausea, and sometimes suffered 
from diarrhea or vomiting. Yet standard laboratory tests—blood work, 
urinalysis, X-rays, electrocardiogram, and electroencephalogram—were 
usually “within normal limits.” 

Cohen, who directed the research, brought to it an open mind. Raised in 
Alabama and educated at Yale, he was then a young professor at Harvard 
Medical School who was already challenging delivered wisdom and 
lighting one of the earliest sparks of what would eventually be a revolution 
in psychiatry. For he had the courage to call Freudian psychoanalysis a cult 
back in the 1940s when its practitioners were asserting control in every 
academic institution, capturing the imagination of Hollywood, and touching 
every aspect of American culture.” 


33) && 





Mandel Ettelson Cohen (1907-2000) 


Paul White, one of the two chief investigators—the other was 
neurologist Stanley Cobb—was already familiar with neurocirculatory 
asthenia from his civilian cardiology practice, and thought, contrary to 
Freud, that it was a genuine physical disease. Under the leadership of these 
three individuals, the team confirmed that this was indeed the case. Using 
the techniques that were available in the 1940s, they accomplished what no 
one in the nineteenth century, when the epidemic began, had been able to 
do: 





It has long been known that people with disorders of circulation have 
abnormal capillaries that can be most easily seen in the nail fold—the fold 
of skin at the base of the fingernails. White’s team routinely found such 
abnormal capillaries in their patients with neurocirculatory asthenia. 

They found that these patients were hypersensitive to heat, pain and, 
significantly, to electricity—they reflexively pulled their hands away from 
electric shocks of much lower intensity than did normal healthy individuals. 


When asked to run on an inclined treadmill for three minutes, the 
majority of these patients could not do it. On average, they lasted only a 
minute and a half. Their heart rate after such exercise was excessively fast, 
their oxygen consumption during the exercise was abnormally low and, 
most significantly, their ventilatory efficiency was abnormally low. This 
means that they used less oxygen, and exhaled less carbon dioxide, than a 
normal person even when they breathed the same amount of air. To 
compensate, they breathed more air more rapidly than a healthy person and 
were still not able to continue running because their bodies were still not 
using enough oxygen. 

A fifteen-minute walk on the same treadmill gave similar results. All 
subjects were able to complete this easier task. However, on average, the 
patients with neurocirculatory asthenia breathed fifteen percent more air per 
minute than healthy volunteers in order to consume the same amount of 
oxygen. And although, by breathing faster, the patients with 
neurocirculatory asthenia managed to consume the same amount of oxygen 
as the healthy volunteers, they had twice as much lactic acid in their blood, 
indicating that their cells were not using that oxygen efficiently. 

Compared to healthy individuals, people with this disorder were able to 
extract less oxygen from the same amount of air, and their cells were able to 
extract less energy from the same amount of oxygen. The researchers 
concluded that these patients suffered from a defect of aerobic metabolism. 
In other words, something was wrong with their mitochondria—the 
powerhouses of their cells. The patients correctly complained that they 
could not get enough air. This was starving all of their organs of oxygen and 
causing both their heart symptoms and their other disabling complaints. 
Patients with neurocirculatory asthenia were consequently unable to hold 
their breath for anything like a normal period of time, even when breathing 
oxygen.78 

During the five years of Cohen’s team’s study, several types of treatment 
were attempted with different groups of patients: oral testosterone; massive 
doses of vitamin B complex; thiamine; cytochrome c; psychotherapy; and a 
course of physical training under a professional trainer. None of these 
programs produced any improvement in symptoms or endurance. 


“We conclude,” wrote the team in June 1946, “that neurocirculatory 
asthenia is a condition that actually exists and has not been invented by 
patients or medical observers. It is not malingering or simply a mechanism 
aroused during war time for purposes of evading military service. The 
disorder is quite common both as a civilian and as a service problem.”2° 
They objected to Freud’s term “anxiety neurosis” because anxiety was 
obviously a result, and not a cause, of the profound physical effects of not 
being able to get enough air. 

In fact, these researchers virtually disproved the theory that the disease 
was caused by “stress” or “anxiety.” It was not caused by 
hyperventilation.?^ Their patients did not have elevated levels of stress 
hormones—17-ketosteroids—in their urine. A twenty-year follow-up study 
of civilians with neurocirculatory asthenia revealed that these people 
typically did not develop any of the diseases that are supposed to be caused 
by anxiety, such as high blood pressure, peptic ulcer, asthma, or ulcerative 
colitis. However, they did have abnormal electrocardiograms that 
indicated that the heart muscle was being starved of oxygen, and that were 
sometimes indistinguishable from the EKGs of people who had actual 
coronary artery disease or actual structural damage to the heart.? 

The connection to electricity was provided by the Soviets. Soviet 
researchers, during the 1950s, 1960s, and 1970s, described physical signs 
and symptoms and EKG changes, caused by radio waves, that were 
identical to those that White and others had first reported in the 1930s and 


1940s. 
The Soviet scientists—in agreement with Cohen 


and White’s team—concluded that 

Something was wrong with the mitochondria 
in their cells. And they discovered what that defect was. Scientists that 
included Yury  Dumanskiy, Mikhail  Shandala, and Lyudmila 
Tomashevskaya, working in Kiev, and F. A. Kolodub, N. P. Zalyubovskaya 
and R. I. Kiselev, working in Kharkov, proved that the activity of the 
electron transport chain—the mitochondrial enzymes that extract energy 
from our food—is diminished not only in animals that are exposed to radio 


waves,?^ but in animals exposed to magnetic fields from ordinary electric 
power lines.? 


The first war in which the electric telegraph was widely used—the 
American Civil War—was also the first in which “irritable heart” was a 
prominent disease. A young physician named Jacob M. Da Costa, visiting 
physician at a military hospital in Philadelphia, described the typical 
patient. 

“A man who had been for some months or longer in active service,” he 
wrote, “would be seized with diarrhoea, annoying, yet not severe enough to 
keep him out of the field; or, attacked with diarrhoea or fever, he rejoined, 
after a short stay in hospital, his command, and again underwent the 
exertions of a soldier’s life. He soon noticed that he could not bear them as 
formerly; he got out of breath, could not keep up with his comrades, was 
annoyed with dizziness and palpitation, and with pain in his chest; his 
accoutrements oppressed him, and all this though he appeared well and 
healthy. Seeking advice from the surgeon of the regiment, it was decided 
that he was unfit for duty, and he was sent to a hospital, where his 
persistently quick acting heart confirmed his story, though he looked like a 
man in sound condition."?6 

Exposure to electricity in this war was universal. When the Civil War 
broke out in 1861, the east and west coasts had not yet been linked, and 
most of the country west of the Mississippi was not yet served by any 
telegraph lines. But in this war, every soldier, at least on the Union side, 
marched and camped near such lines. From the attack on Fort Sumter on 
April 12, 1861, until General Lee's surrender at Appomattux, the United 
States Military Telegraph Corps rolled out 15,389 miles of telegraph lines 
on the heels of the marching troops, so that military commanders in 
Washington could communicate instantly with all of the troops at their 
encampments. After the war all of these temporary lines were dismantled 
and disposed of.* 

“Hardly a day intervened when General Grant did not know the exact 
state of facts with me, more than 1,500 miles off as the wires ran," wrote 
General Sherman in 1864. “On the field a thin insulated wire may be run on 


improvised stakes, or from tree to tree, for six or more miles in a couple of 
hours, and I have seen operators so skillful that by cutting the wire they 
would receive a message from a distant station with their tongues."*? 

Because the distinctive symptoms of irritable heart were encountered in 
every army of the United States, and attracted the attention of so many of its 
medical officers, Da Costa was puzzled that no one had described such a 
disease in any previous war. But telegraphic communications were never 
before used to such an extent in war. In the British Blue Book of the 
Crimean War, a conflict which lasted from 1853-56, Da Costa found two 
references to some troops being admitted to hospitals for “palpitations,” and 
he found possible hints of the same problem reported from India during the 
Indian Rebellion of 1857-58. These were also the only two conflicts prior to 
the American Civil War in which some telegraph lines were erected to 
connect command headquarters with troop units.? Da Costa wrote that he 
searched through medical documents from many previous conflicts and did 
not find even a hint of such a disease prior to the Crimean War. 

During the next several decades, irritable heart attracted relatively little 
interest. It was reported among British troops in India and South Africa, and 
occasionally among soldiers of other nations.^ But the number of cases was 
small. Even during the Civil War, what Da Costa considered *common" did 
not amount to many cases by today's standards. In his day, when heart 
disease was practically non-existent, the appearance of 1,200 cases of chest 
pain among two million young soldiers^ caught his attention like an 
unfamiliar reef, suddenly materialized in a well-traveled shipping lane 
across an otherwise calm sea—a sea that was not further disturbed until 
1914. 





Most of these men had 
irritable heart, also called “Da Costa’s syndrome,” or “effort syndrome.” In 


the United States Army such cases were all listed under *Valvular Disorders 
of the Heart," and were the third most common medical cause for discharge 
from the Army.* The same disease also occurred in the Air Force, but was 
almost always diagnosed as “flying sickness,” thought to be cause by 
repeated exposure to reduced oxygen pressure at high altitudes.^ 

Similar reports came from Germany, Austria, Italy, and France.^ 

So enormous was the problem that the United States Surgeon-General 
ordered four million soldiers training in the Army camps to be given 
cardiac examinations before being sent overseas. Effort syndrome was “far 
away the commonest disorder encountered and transcended in interest and 
importance all the other heart affections combined,” said one of the 
examining physicians, Lewis A. Conner.^6 

Some soldiers in this war developed effort syndrome after shell shock, 
or exposure to poison gas. Many more had no such history. All, however, 
had gone into battle using a newfangled form of communication. 

The United Kingdom declared war on Germany on August 4, 1914, two 
days after Germany invaded its ally, France. The British army began 
embarking for France on August 9, and continued on to Belgium, reaching 
the city of Mons on August 22, without the aid of the wireless telegraph. 
While in Mons, a 1500-watt mobile radio set, having a range of 60 to 80 
miles, was supplied to the British army signal troops.^ It was during the 
retreat from Mons that many British soldiers first became ill with chest 
pain, shortness of breath, palpitations, and rapid heart beat and were sent 
back to England to be evaluated for possible heart disease.^ 

Exposure to radio was universal and intense. A knapsack radio with a 
range of five miles was used by the British army in all trench warfare on the 
front lines. Every battalion carried two such sets, each having two 
operators, in the front line with the infantry. One or two hundred yards 
behind, back with the reserve, were two more sets and two more operators. 
A mile further behind at Brigade Headquarters was a larger radio set, two 
miles back at Divisional Headquarters was a 500-watt set, and six miles 
behind the front lines at Army Headquarters was a 1500-watt radio wagon 
with a 120-foot steel mast and an umbrella-type aerial. Each operator 
relayed the telegraph messages received from in front of or behind him.^ 


All cavalry divisions and brigades were assigned radio wagons and 
knapsack sets. Cavalry scouts carried special sets right on their horses, that 
were Called “whisker wireless” because of the antennae that sprouted from 
the horses’ flanks like the quills of a porcupine.°° 

Most aircraft carried lightweight radio sets, using the metal frame of the 
airplane as the antenna. German war Zeppelins and French dirigibles 
carried much more powerful sets, and Japan had wireless sets in its war 
balloons. Radio sets on ships made it possible for naval battle lines to be 
spread out in formations 200 or 300 miles long. Even submarines, while 
cruising below the surface, sent up a short mast, or an insulated jet of water, 
as an antenna for the coded radio messages they broadcast and received.*! 





Radar joined radio for the first time in 
this war, and it too was universal and intense. Like children with a new toy, 
every nation devised as many uses for it as possible. Britain, for example, 
peppered its coastline with hundreds of early warming radars emitting more 
than half a million watts each, and outfitted all its airplanes with powerful 
radars that could detect objects as small as a submarine periscope. More 
than two thousand portable radars, accompanied by 105-foot-tall portable 
towers, were deployed by the British army. Two thousand more “gun- 
laying” radars assisted anti-aircraft guns in tracking and shooting down 
enemy aircraft. The ships of the Royal Navy sported surface radars with a 
power of up to one million watts, as well as air search radars, and 
microwave radars that detected submarines and were used for navigation. 

The Americans deployed five hundred early-warning radars on board 
ships, and additional early-warning radars on aircraft, each having a power 
of one million watts. They used portable radar sets at beachheads and 
airfields in the South Pacific, and thousands of microwave radars on ships, 
aircraft, and Navy blimps. From 1941 to 1945 the Radiation Laboratory at 
the Massachusetts Institute of Technology was kept busy by its military 
masters developing some one hundred different types of radar for various 
uses in the war. 

The other powers fielded radar installations with equal vigor on land, at 
sea, and in air. Germany deployed over one thousand ground-based early 


warning radars in Europe, as well as thousands of shipborne, airborne, and 
gun-laying radars. The Soviet Union did likewise, as did Australia, Canada, 
New Zealand, South Africa, the Netherlands, France, Italy, and Hungary. 
Wherever a soldier was asked to fight he was bathed in an ever-thickening 
soup of pulsed radio wave and microwave frequencies. And he succumbed 
in large numbers, in the armies, navies, and air forces of every nation.? 

It was during this war that the first rigorous program of medical research 
was conducted on soldiers with this disease. By this time Freud's proposed 
term "anxiety neurosis" had taken firm hold among army doctors. Members 
of the Air Force who had heart symptoms were now receiving a diagnosis 
of “L.M.F.,” standing for “lack of moral fiber.” Cohen’s team was stacked 
with psychiatrists. But to their surprise, and guided by cardiologist Paul 
White, they found objective evidence of a real disease that they concluded 
was not caused by anxiety. 

Largely because of the prestige of this team, research into 
neurocirculatory asthenia continued in the United States throughout the 
1950s; in Sweden, Finland, Portugal, and France into the 1970s and 1980s; 
and even, in Israel and Italy, into the 1990s. But a growing stigma was 
attached to any doctor who still believed in the physical causation of this 
disease. Although the dominance of the Freudians had waned, they left an 
indelible mark not only on psychiatry but on all of medicine. Today, in the 
West, only the “anxiety” label remains, and people with the symptoms of 
neurocirculatory asthenia are automatically given a psychiatric diagnosis 
and, very likely, a paper bag to breathe into. Ironically, Freud himself, 
although he coined the term “anxiety neurosis,” thought that its symptoms 
were not mentally caused, “nor amenable to psychotherapy.” 

Meanwhile, an unending stream of patients continued to appear in 
doctors’ offices suffering from unexplained exhaustion, often accompanied 
by chest pain and shortness of breath, and a few courageous doctors 
stubbornly continued to insist that psychiatric problems could not explain 
them all. In 1988, the term “chronic fatigue syndrome” (CFS) was coined 
by Gary Holmes at the Centers for Disease Control, and it continues to be 
applied by some doctors to patients whose most prominent symptom is 
exhaustion. Those doctors are still very much in the minority. Based on 


their reports, the CDC estimates that the prevalence of CFS is between 0.2 
percent and 2.5 percent of the population, while their counterparts in the 
psychiatric community tell us that as many as one person in six, suffering 
from the identical symptoms, fits the criteria for "anxiety disorder" or 
"depression." 

To confuse the matter still further, the same set of symptoms was called 
myalgic encephalomyelitis (ME) in England as early as 1956, a name that 
focused attention on muscle pains and neurological symptoms rather than 
fatigue. Finally, in 2011, doctors from thirteen countries got together and 
adopted a set of "International Consensus Criteria" that recommends 
abandoning the name “chronic fatigue syndrome” and applying “myalgic 
encephalomyelitis” to all patients who suffer from “post-exertional 
exhaustion” plus specific neurological, cardiovascular, respiratory, immune, 
gastrointestinal, and other impairments.°° 

This international “consensus” effort, however, is doomed to failure. It 
completely ignores the psychiatric community, which sees far more of these 
patients. And it pretends that the schism that emerged from World War II 
never occurred. In the former Soviet Union, Eastern Europe, and most of 
Asia, the older term “neurasthenia” persists today. That term is still widely 
applied to the full spectrum of symptoms described by George Beard in 
1869. In those parts of the world it is generally recognized that exposure to 
toxic agents, both chemical and electromagnetic, often causes this disease. 


According to published literature, all of these diseases—neurocirculatory 
asthenia, radio wave sickness, anxiety disorder, chronic fatigue syndrome, 
and myalgic encephalomyelitis—predispose to elevated levels of blood 
cholesterol, and all carry an increased risk of death from heart disease." So 
do porphyria and oxygen deprivation.? The fundamental defect in this 
disease of many names is that although enough oxygen and nutrients reach 
the cells, the mitochondria—the powerhouses of the cells—cannot 
efficiently use that oxygen and those nutrients, and not enough energy is 
produced to satisfy the requirements of heart, brain, muscles, and organs. 
This effectively starves the entire body, including the heart, of oxygen, and 
can eventually damage the heart. In addition, neither sugars nor fats are 


efficiently utilized by the cells, causing unutilized sugar to build up in the 
blood—leading to diabetes—as well as unutilized fats to be deposited in 
arteries. 

And we have a good idea of precisely where the defect is located. 
People with this disease have reduced activity of a porphyrin-containing 
enzyme called cytochrome oxidase, which resides within the mitochondria, 
and delivers electrons from the food we eat to the oxygen we breathe. Its 
activity is impaired in all the incarnations of this disease. Mitochondrial 
dysfunction has been reported in chronic fatigue syndrome® and in anxiety 
disorder. Muscle biopsies in these patients show reduced cytochrome 
oxidase activity. Impaired glucose metabolism is well known in radio wave 
sickness, as is an impairment of cytochrome oxidase activity in animals 
exposed to even extremely low levels of radio waves. And the 
neurological and cardiac symptoms of porphyria are widely blamed on a 
deficiency of cytochrome oxidase and cytochrome c, the heme-containing 
enzymes of respiration.® 





The 
concentration of total carbohydrates in their hemolymph, which is what 
bees’ blood is called, rose from 1.29 to 1.5 milligrams per milliliter. After 
twenty minutes it rose to 1.73 milligrams per milliliter. The glucose content 
rose from 0.218 to 0.231 to 0.277 milligrams per milliliter. Total lipids rose 
from 2.06 to 3.03 to 4.50 milligrams per milliliter. Cholesterol rose from 
0.230 to 1.381 to 2.565 milligrams per milliliter. Total protein rose from 
0.475 to 0.525 to 0.825 milligrams per milliliter. 





In the twentieth century, particularly after World War II, a barrage of 
toxic chemicals and electromagnetic fields (EMFs) began to significantly 
interfere with the breathing of our cells. We know from work at Columbia 
University that even tiny electric fields alter the speed of electron transport 


from cytochrome oxidase. Researchers Martin Blank and Reba Goodman 
thought that the explanation lay in the most basic of physical principles. 









Scientists at the Environmental Protection 
Agency—John Allis and William Joines—finding a similar effect from 
radio waves, developed a variant theory along the same lines. They 
speculated that the iron atoms in the porphyrin-containing enzymes were set 
into motion by the oscillating electric fields, interfering with their ability to 
transport electrons.“ 

It was the English physiologist John Scott Haldane who first suggested, 
in his classic book, Respiration, that “soldier’s heart” was caused not by 
anxiety but by a chronic lack of oxygen. Mandel Cohen later proved that 
the defect was not in the lungs, but in the cells. These patients continually 
gulped air not because they were neurotic, but because they really could not 
get enough of it. You might as well have put them in an atmosphere that 
contained only 15 percent oxygen instead of 21 percent, or transported them 
to an altitude of 15,000 feet. Their chests hurt, and their hearts beat fast, not 
because of panic, but because they craved air. And their hearts craved 
oxygen, not because their coronary arteries were blocked, but because their 
cells could not fully utilize the air they were breathing. 

These patients were not psychiatric cases; they were warnings for the 
world. For the same thing was also happening to the civilian population: 

and the pandemic of heart disease 
that was well underway in the 1950s was one result. Even in people who 
did not have a porphyrin enzyme deficiency, the mitochondria in their cells 
were still struggling, to some smaller degree, to metabolize carbohydrates, 
fats, and proteins. Unburned fats, together with the cholesterol that 
transported those fats in the blood, were being deposited on the walls of 
arteries. 





The real story is told by the astonishing statistics. 


When I began my research, I had only Samuel Milham's data. Since he 
found such a large difference in rural disease rates in 1940 between the five 
least and five most electrified states, I wanted to see what would happen if I 
calculated the rates for all forty-eight states and plotted the numbers on a 
graph. I looked up rural mortality rates in volumes of the Vital Statistics of 
the United States. I calculated the percent of electrification for each state by 
dividing the number of its residential electric customers, as published by the 
Edison Electric Institute, by the total number of its households, as published 
by the United States Census. 

The results, for 1931 and 1940, are pictured in figures 1 and 2. Not only 
is there a five- to six-fold difference in mortality from rural heart disease 
between the most and least electrified states, but all of the data points come 
very close to lying on the same line. 





Figure 1 — Rate of Rural Heart Disease in 1931 


Percent electrification 1931 


30 


20 


10 


60 80 





100 120 140 160 180 200 220 240 260 280 300 320 340 360 


Rate of rural heart disease (1931) 
(mortality per 100,000 population) 


Table 2 











*/» electrification Rural heart disease 1931 °% electrification Rural heart disease 1940 
(1931) (deaths per 100,000) (1940) (deaths per 100,000) 
AL 25.7 98.8 34.7 147 
AZ 62.5 61.4 56.1 87 
AR 22.1 84.6 27.3 109 
CA 92.5 250.3 75.6 305 
co 61.5 137.4 56.9 188 
CT 94.9 255.7 90.5 328 
DE 644 277.5 66.1 364 
FL 53.8 124.0 50.7 186 
GA 28.4 (missing) 36.5 144 
ID 48.2 106.5 64.5 187 
IL 82.5 259.9 79.4 330 
IN 70.0 241.8 74.9 311 
IA 61.4 148.3 65.3 234 
KS 594 157.8 60.2 246 
KY 38.0 (missing) 41.6 177 
LA 34.1 118.7 41.5 189 
ME 77.5 258.5 70.5 344 
MD 72.3 219.2 65,2 312 
MA 98.5 357.0 91.9 479 
MI 78.4 267.4 81.3 339 
MN 64.2 156.3 634 225 
MS 16.5 81.2 22.7 149 
MO 59.1 166.3 583 241 
Mr 48.9 131.4 56.8 217 
NE 60.0 138.5 62.1 208 
NV 54.8 150.0 58.3 370 
NH 86.3 327.4 78.7 428 
NJ 97.7 313.2 87.0 423 
NM 27.3 64.8 26.5 88 
NY 98.1 360.3 83.9 465 
NC 32.4 120.8 43.7 152 
ND 34.5 94.1 40.5 190 
OH 77.0 240.1 82.5 323 
OK 392 59.9 41.3 127 
OR 68.8 168.5 67.7 220 
PA 78.5 234.2 80.4 331 
RI 98.2 289.8 91.0 404 
sc 25.6 136.8 32.1 165 
SD 41.0 106.0 43.0 188 
TN 34.0 100.1 42.1 154 
TX 39.5 97.9 43.5 144 
UT 71.8 103.9 75.2 198 
VT 71.9 (missing) 71.5 367 
VA 41.7 181.6 53.1 231 
WA 78.7 166.6 73.8 230 
wy 41.0 94.7 53.4 146 
WI 74.7 198.0 $4.2 282 
WY 49.5 95.1 50.8 170 





Figure 2 — Rate of Rural Heart Disease in 1940 


Percent electrification 1940 





80 120 160 200 240 280 320 360 400 440 480 


Rate of rural heart disease (1940) 
(mortality per 100,000 population) 


What is even more remarkable is that the death rates from heart disease 
in unelectrified rural areas of the United States in 1931, before the Rural 
Electrification Program got into gear, were still as low as the death rates for 
the whole United States prior to the beginning of the heart disease epidemic 
in the nineteenth century. 

In 1850, the first census year in which mortality data were collected, a 
total of 2,527 deaths from heart disease were recorded in the nation. Heart 
disease ranked twenty-fifth among causes of death in that year. About as 
many people died from accidental drowning as from heart disease. Heart 
disease was something that occurred mainly in young children and in old 
age, and was predominantly a rural rather than an urban disease because 
farmers lived longer than city-dwellers. 

In order to realistically compare nineteenth century statistics with those 
of today, I had to make some adjustments to the Census figures. The census 
enumerators for 1850, 1860, and 1870 had only the numbers reported to 
them from memory by the households they visited as to who had died 


during the previous year and from what causes. These numbers were 
estimated by the Census Office to be deficient, on average, by about 40 
percent. In the census for 1880, the numbers were supplemented by reports 
from physicians and averaged only 19 percent short of the truth. By 1890 
eight northeastern states plus the District of Columbia had passed laws 
requiring the official registration of all deaths, and the statistics for those 
registration states were considered accurate to within two to three percent. 
By 1910 the registration area had expanded to 23 states, and by 1930 only 
Texas did not require registration of deaths. 

Another complicating factor is that heart failure was sometimes not 
evident except for the edema it caused, and therefore edema, then called 
“dropsy,”5 was sometimes reported as the only cause of death, although the 
death was most likely to have been caused by either heart or kidney disease. 
Yet a further complication is the appearance of “Bright’s disease” for the 
first time in the tables for 1870. This was the new term for the type of 
kidney disease that caused edema. Its prevalence in 1870 was reported to be 
4.5 cases per 100,000 population. 

With these complexities in mind, I have calculated the approximate rates 
of death from cardiovascular disease for each decade from 1850 to 2010, 
adding the figures for “dropsy” when that term was still in use (until 1900), 
and subtracting 4.5 per 100,000 for the years 1850 and 1860. I added a 
correction factor of 40 percent for 1850, 1860 and 1870, and 19 percent for 
1880. I included reports of deaths from all diseases of the heart, arteries, 
and blood pressure. Beginning with 1890 I used only the figures for the 
death registration states, which by 1930 included the entire country except 
for Texas. The results are as follows: 


Death Rates from Cardiovascular Disease (per 100,000 population) 


1850 A 
1860 78 
1870 78 
1880 102 
1890 145 


1890 (Indians on reservations) 60 


1900 154 


1910 183 
1920 187 
1930 235 
1940 291 
1950 384 
1960 396 
1970 394 
1980 361 
1990 310 
2000 280 
2010 210 
2017 214 


1910 was the first year in which the mortality in cities surpassed that in 
the countryside. But the greatest disparities emerged in the countryside. In 
the northeastern states, which in 1910 had the greatest use of telegraphs, 
telephones, and now electric lights and power, and the densest networks of 
wires crisscrossing the land, the rural areas had as much mortality from 
cardiovascular disease, or more, than the cities. The rural mortality rate of 
Connecticut was then 234, of New York 279, and of Massachusetts 296. By 
contrast Colorado's rural rate was still 100, and Washington's 92. 
Kentucky's rural rate, at 88.5, was only 44 percent of its urban rate, which 
was 202. 

Heart disease rose steadily with electrification, as we saw in figures 1 
and 2, and reached a peak when rural electrification approached 100 percent 
during the 1950s. Rates of heart disease then leveled off for three decades 
and began to drop again—or so it seems at first glance. A closer look, 
however, shows the true picture. These are just the mortality rates. The 
number of people walking around with heart disease—the prevalence rate— 
actually continued to rise, and is still rising today. Mortality stopped rising 
in the 1950s because of the introduction of anticoagulants like heparin, and 
later aspirin, both to treat heart attacks and to prevent them.® In the 
succeeding decades the ever more aggressive use of anticoagulants, drugs to 
lower blood pressure, cardiac bypass surgery, balloon angioplasty, coronary 


stents, pacemakers, and even heart transplants, has simply allowed an ever 
growing number of people with heart disease to stay alive. But people are 
not having fewer heart attacks. They are having more. 

The Framingham Heart Study showed that at any given age the chance 
of having a first heart attack was essentially the same during the 1990s as it 
was during the 1960s.°° This came as something of a surprise. By giving 
people statin drugs to lower their cholesterol, doctors thought they were 
going to save people from having clogged arteries, which was supposed to 
automatically mean healthier hearts. It hasn’t turned out that way. And in 
another study, scientists involved in the Minnesota Heart Survey discovered 
in 2001 that although fewer hospital patients were being diagnosed with 
coronary heart disease, more patients were being diagnosed with heart- 
related chest pain. In fact, between 1985 and 1995 the rate of unstable 
angina had increased by 56 percent in men and by 30 percent in women.” 

The number of people with congestive heart failure has also continued 
steadily to rise. Researchers at the Mayo Clinic searched two decades of 
their records and discovered that the incidence of heart failure was 8.3 
percent higher during the period 1996-2000 than it had been during 1979- 
1984.7! 

The true situation is much worse still. Those numbers reflect only 
people newly diagnosed with heart failure. The increase in the total number 
of people walking around with this condition is astonishing, and only a 
small part of the increase is due to the aging of the population. Doctors 
from Cook County Hospital, Loyola University Medical School, and the 
Centers for Disease Control examined patient records from a representative 
sample of American hospitals and found that the numbers of patients with a 
diagnosis of heart failure more than doubled between 1973 and 1986.” A 
later, similar study by scientists at the Centers for Disease Control found 
that this trend had continued. The number of hospitalizations for heart 
failure tripled between 1979 and 2004, the age-adjusted rate doubled, and 
the greatest increase occurred in people under 65 years of age. A similar 
study of patients at Henry Ford Hospital in Detroit showed that the annual 
prevalence of congestive heart failure had almost quadrupled from 1989 to 
1999.^ 


Young people, as the 3,000 alarmed doctors who signed the Freiburger 
Appeal affirmed, are having heart attacks at an unprecedented rate. In the 
United States, as great a percentage of forty-year-olds today have 
cardiovascular disease as the percentage of seventy-year-olds that had 
cardiovascular disease in 1970. Close to one-quarter of Americans aged 
forty to forty-four today have some form of cardiovascular disease. And 
the stress on even younger hearts is not confined to athletes. In 2005, 
researchers at the Centers for Disease Control, surveying the health of 
adolescents and young adults, aged 15 to 34, found to their surprise that 
between 1989 and 1998 rates of sudden cardiac death in young men had 
risen 11 percent, and in young women had risen 30 percent, and that rates of 
mortality from enlarged heart, heart rhythm disturbances, pulmonary heart 
disease, and hypertensive heart disease had also increased in this young 
population.7* 

In the twenty-first century this trend has continued. The number of heart 
attacks in Americans in their twenties rose by 20 percent between 1999 and 
2006, and the mortality from all types of heart disease in this age group rose 
by one-third." In 2014, among patients between the ages of 35 and 74 who 
were hospitalized with heart attacks, one-third were below the age of 54.7 

Developing countries are no better off. They have already followed the 
developed countries down the primrose path of electrification, and they are 
following us even faster to the wholesale embrace of wireless technology. 
The consequences are inevitable. Heart disease was once unimportant in 
low-income nations. It is now the number one killer of human beings in 
every region of the world except one. Only in sub-Saharan Africa, in 2017, 
was heart disease still outranked by diseases of poverty—AIDS and 
pneumonia—as a cause of mortality. 





12. The Transformation of Diabetes 


IN 1859, AT THE AGE OF TWELVE, the son of a lumber and grain 
merchant in Port Huron, Michigan strung a telegraph line one mile long 
between his house and a friend's, placing the two into electrical 
communication. From that day forward Thomas Alva Edison was intimate 
with the mysterious forces of electricity. He worked as an itinerant 
telegraph operator from the age of fifteen until he went into business for 
himself in Boston at age twenty-one, providing private-line telegraph 
service for Boston firms, stringing the wires from downtown offices, along 
the rooftops of houses and buildings, to factories and warehouses on the 
outskirts of the city. By the time he was twenty-nine, when he moved his 
laboratory to a small hamlet in New Jersey, he had made improvements to 
telegraph technology and was engaged in perfecting the newly invented 
telephone. The *Wizard of Menlo Park" became world famous in 1878 for 
his invention of the phonograph. He then set himself a much more 
ambitious task: he dreamed of lighting people's homes with electricity, and 
displacing the hundred-fifty-million-dollar-a-year gas lighting industry. 
Before he was done, 





Another young man, who grew up in Scotland, was teaching elocution at a 
school in Bath in 1866 when he hooked up a homemade telegraph system 
between his house and a neighbor's. Five years later he found himself 
teaching the deaf to speak in Boston, where he was also a professor of 


elocution at Boston University. But he did not give up his lifelong affair 
with electricity. One of his deaf students, with whose family he boarded, 
glanced one day into his bedroom. “I found the floor, the chairs, the table, 
and even the dresser covered with wires, batteries, coils, cigar boxes, and an 
indescribable mass of miscellaneous equipment," the man recalled many 
years later. “The overflow was already in the basement, and it wasn't many 
months before he had expanded into the carriage house.” 





To begin to get a sense of just how rare diabetes once was, I searched the 
antique books in my medical library. I first looked in the Works of Robert 
Whytt, a Scottish physician of the early and mid-eighteenth century. I did 
not find diabetes mentioned in the 750-page volume. 

American physician John Brown, at the end of the eighteenth century, 
devoted two paragraphs to the disorder in his Elements of Medicine. In the 
Works of Thomas Sydenham, who practiced in the seventeenth century and 
is known as the Father of English Medicine, I found a single page on 
diabetes. It set forth a sparse description of the disease, recommended an 
all-meat diet, and prescribed an herbal remedy. 

I opened Benjamin Ward Richardson’s 500-page work, Diseases of 
Modern Life, published in New York in 1876, a time when Edison and Bell 
were experimenting intensively with electricity. Four pages were devoted to 
diabetes. Richardson considered it a modern disease caused by exhaustion 
from mental overwork or by some shock to the nervous system. But it was 
still uncommon. 

Then I consulted my “bible” of diseases of the nineteenth century, the 
Handbook of Geographical and Historical Pathology, published in stages 
between 1881 and 1886 in German and English. In this massive three- 


volume scholarly work, August Hirsch compiled the history of known 
diseases, along with their prevalence and distribution throughout the world. 
Hirsch spared six pages for diabetes, noting primarily that it was rare and 
that little information about it was known. In ancient Greece, he wrote, in 
the fourth century B.C., Hippocrates never mentioned it. In the second 
century A.D., Galen, a Greek-born physician practicing in Rome, devoted 
some passages to diabetes, but stated that he himself had seen only two 
cases. 

The first book on diabetes had actually been written in 1798, but its 
author, John Rollo of England, had only seen three cases of it himself in his 
twenty-three years of practicing medicine. 

The statistics Hirsch gathered from around the world confirmed to him 
that the disease “is one of the rarest.”? About 16 people per year died of it in 
Philadelphia, 3 in Brussels, 30 in Berlin, and 550 in all of England. 
Occasional cases were reported in Turkey, Egypt, Morocco, Mexico, 
Ceylon, and certain parts of India. But an informant in St. Petersburg had 
not seen a case in six years. Practitioners in Senegambia and the Guinea 
Coast had never seen a case, nor was there any record of it occurring in 
China, Japan, Australia, the islands of the Pacific, Central America, the 
West Indies, Guiana, or Peru. One informant had never seen a case of 
diabetes during a practice of many years in Rio de Janeiro. 

How, then, did diabetes come to be one of the major killers of 
humanity? In today's world, as we will see, limiting one's intake of sugar 
plays an important role in the prevention and control of this disease. But, as 
we will also see, blaming the rise of diabetes on dietary sugars is as 
unsatisfactory as blaming the rise of heart disease on dietary fats. 

In 1976, I was living in Albuquerque when a friend placed a newly 
published book in my hands that changed the way I ate and drank. 

had done his homework thoroughly. He 





convinced me that 


He further blamed 
four centuries of the African slave trade largely on the need to feed a sugar 
habit that had been acquired by the Crusaders during the twelfth and 





thirteenth centuries. Europeans, he said, had wrested control of the world 
sugar trade from the Arab Empire, and needed a steady supply of labor to 
tend their sugar plantations. His claim that sugar was “more intoxicating 
than beer or wine and more potent than many drugs" was supported by an 
entertaining tale that he spun about his own perplexing illnesses and his 
heroic efforts to kick the sugar habit, which finally succeeded. Migraine 
headaches, mysterious fevers, bleeding gums, hemorrhoids, skin eruptions, 
a tendency to gain weight, chronic fatigue, and an impressive assortment of 
aches and pains that had tormented him for fifteen years vanished within 
twenty-four hours, he said, and did not return. 

Dufty also explained why sugar causes diabetes. Our cells, especially 
our brain cells, get their energy from a steady supply of a simple sugar 
called glucose, which is the end product of digesting the carbohydrates we 
eat. “The difference between feeling up or down, sane or insane, calm or 
freaked out, inspired or depressed depends in large measure upon what we 
put in our mouth,” he wrote. 





If not enough insulin is 
secreted by the pancreas after a meal, glucose builds up to a toxic level in 
the blood and we begin excreting it in our urine. If too much insulin is 
produced, blood glucose levels drop dangerously low. 

The problem with eating pure sugar, wrote Dufty, is that it doesn’t need 
to be digested and is absorbed into the blood much too fast. Eating complex 
carbohydrates, fats, and proteins requires the pancreas to secrete an 
assortment of digestive enzymes into the small intestine so that these foods 
can be broken down. This takes time. The glucose level in the blood rises 
gradually. However, when we eat refined sugar it is turned into glucose 
almost immediately and passes directly into the blood, Dufty explained, 
“where the glucose level has already been established in precise balance 
with oxygen. The glucose level in the blood is thus drastically increased. 
Balance is destroyed. The body is in crisis.” 

A year after reading this book I decided to apply to medical school, and 
had to first take basic courses in biology and chemistry that I did not take in 


college. My biochemistry professor at the University of California, San 
Diego essentially confirmed what I had learned from reading Sugar Blues. 
We evolved, said my professor, eating foods like potatoes that have to be 
digested gradually. The pancreas automatically secretes insulin at a rate that 
exactly corresponds to the rate at which glucose—over a considerable 
period of time after a meal—enters the bloodstream. Although this 
mechanism works perfectly if you eat meat, potatoes, and vegetables, a 
meal containing refined sugar creates a disturbance. The entire load of 
sugar enters the bloodstream at once. The pancreas, however, hasn’t learned 
about refined sugar and “thinks” that you have just eaten a meal containing 
a tremendous amount of potatoes. A lot more glucose should be on its way. 
The pancreas therefore manufactures an amount of insulin that can deal 
with a tremendous meal. This overreaction by the pancreas drives the blood 
glucose level too low, starving the brain and muscles—a condition known 
as hypoglycemia.^ After years of such overstimulation the pancreas may 
become exhausted and stop producing enough insulin or produce none at 
all. This condition is called diabetes and requires the person to take insulin 
or other drugs to maintain his or her energy balance and stay alive. 

Many besides Dufty have pointed out that an extraordinary rise in sugar 
consumption has accompanied the equally extraordinary rise in diabetes 
rates over the past two hundred years. Almost a century ago Dr. Elliott P. 
Joslin, founder of Boston’s Joslin Diabetes Center, published statistics 
showing that yearly sugar consumption per person in the United States had 
increased eightfold between 1800 in 1917.° 

But this model of diabetes is missing an important piece. It teaches us 
how to avoid getting diabetes in the twenty-first century: don’t eat highly 
refined foods, especially sugar. But it completely fails to explain the terrible 
prevalence of diabetes in our time. Sugar or no sugar, diabetes was once an 
impressively rare disease. The vast majority of human beings were once 
able to digest and metabolize large quantities of pure sugar without 
eliminating it in their urine and without wearing out their pancreas. Even 
Joslin, whose clinical experience led him to suspect sugar as a cause of 
diabetes, pointed out that the consumption of sugar in the United States had 
increased by only 17 percent between 1900 and 1917, a period during 


which the death rate from diabetes had nearly doubled. And he 
underestimated sugar use in the nineteenth century because his statistics 
were for refined sugar only. They did not include maple syrup, honey, 
sorghum syrup, cane syrup, and especially molasses. Molasses was cheaper 
than refined sugar, and until about 1850 Americans consumed more 
molasses than refined sugar. The following graph® shows actual sugar 
consumption during the past two centuries, including the sugar content of 
syrups and molasses, and it does not fit the dietary model of this disease. In 
fact, per capita sugar consumption did not rise at all between 1922 and 
1984, yet diabetes rates soared tenfold. 


U.S. Consumption of Sugar 
and Other Caloric Sweeteners, 1822-2014 


150 


pounds per person per year 
S à 8 D 


N 
tn 





0 
1820 1840 1860 1880 1900 1920 1940 1960 1980 2000 


That diet alone is not responsible for the modern pandemic of diabetes is 
clearly shown by the histories of three communities at opposite ends of the 
world from one another. One has the highest rates of diabetes in the world 
today. The second is the largest consumer of sugar in the world. And the 
third, which I will examine in some detail, is the most recently electrified 
country in the world. 


American Indians 


The poster child for the diabetes story is supposed to be the American 
Indian. Supposedly—according to the American Diabetes Association— 
people today are just eating too much food and not getting enough exercise 
to burn off all the calories. This causes obesity, which, it is believed, is the 
real cause of most diabetes. Indians, so the story goes, are genetically 
predisposed to diabetes, and this predisposition has been triggered by the 
sedentary lifestyle imposed on them when they were confined to 
reservations, as well as by an unhealthy diet containing large amounts of 
white flour, fat, and sugar that have replaced traditional foods. And indeed, 
today, Indians on most reservations in the United States and Canada have 
rates of diabetes that are the highest in the world. 

Yet this does not explain why, since all Indian reservations were created 
by the end of the nineteenth century, and Indian fry bread, consisting of 
white flour deep fried in lard and eaten with sugar, became a staple food on 
most reservations at that time, diabetes nevertheless did not exist among 
Indians until the latter half of the twentieth century. Before 1940 the Indian 
Health Service had never listed diabetes as a cause of death for a single 
Indian. And as late as 1987, surveys done by the Indian Health Service in 
the United States and the Department of National Health and Welfare in 
Canada revealed differences in diabetes rates between different populations 
of Indians that were extreme: 7 cases of diabetes per 1,000 population in the 
Northwest Territories, 9 in the Yukon, 17 in Alaska, 28 among the 
Cree/Ojibwa of Ontario and Manitoba, 40 on the Lummi Reservation in 
Washington, 53 among the Micmac of Nova Scotia and the Makah of 
Washington, 70 on the Pine Ridge Reservation in South Dakota, 85 on the 
Crow Reservation in Montana, 125 on the Standing Rock Sioux 
Reservation in the Dakotas, 148 on the Chippewa Reservation in Minnesota 
and North Dakota, 218 on the Winnebago/Omaha Reservation in Nebraska, 
and 380 on the Gila River Reservation in Arizona." 

In 1987, neither diet nor lifestyle in the various communities was 
different enough to account for a fifty-fold difference in diabetes rates. But 
one environmental factor could account for the disparities. Electrification 
came to most Indian reservations later than it came to most American 
farms. Even in the late twentieth century some reservations were still not 


electrified. This included most Indian reserves in the Canadian Territories 
and most native villages in Alaska. 


he Gila River Reservation is located 
on the outskirts of Phoenix. Not only is it traversed by high voltage power 
lines serving a metropolis of four million, but the Gila River Indian 
Community operates its own electric utility and its own telecommunications 
company. The Pima and Maricopa on this small reservation are exposed to a 
greater concentration of electromagnetic fields than any other Indian tribes 
in North America. 





Brazil 

Brazil, which has grown sugar cane since 1516, has been the largest 
producer and consumer of that commodity since the seventeenth century. 
Yet in the 1870s, when diabetes was beginning to be noticed as a disease of 
civilization in the United States, that disease was completely unknown in 
the sugar capital of the world, Rio de Janeiro. 

Brazil today produces over 30 million metric tons of sugar per year and 
consumes over 130 pounds of white sugar per person, more than the United 
States. Analyses of the diets of the two countries—Brazil in 2002-2003, 
and the United States from 1996—2006— revealed that the average Brazilian 
obtained 16.7 percent of his or her calories from table sugar or sugar added 
to processed foods, while Americans consumed only 15.7 percent of their 
calories from refined sugars. Yet the United States had more than two and a 
half times the rate of diabetes as Brazil.? 


Bhutan 

Sandwiched between the mountainous borders of India and China, the 
isolated Himalayan kingdom of Bhutan may be the last country in the world 
to be electrified. Until the 1960s, Bhutan had no banking system, no 
national currency, and no roads. In the late 1980s, I learned something 
about this Buddhist country, thought by some to be the model for James 
Hilton's Shangri-La, when I made the acquaintance of a Canadian woman 
who worked for CUSO International, the Canadian version of the United 
States Peace Corps. She had just returned from a four-year stint in a small 


Bhutanese village, where she taught English to the local children. Bhutan is 
somewhat larger, in area, than the Netherlands, and has a population just 
over 750,000. The road system at the time was still extremely limited, and 
most travel outside the immediate vicinity of the small capital, Thimphu, 
including travel to my friend's village, was by foot or horseback. She felt 
privileged to be able to live in that country at all, because outside visitors to 
Bhutan were limited to 1,000 per year. The woven baskets and other 
handcrafts that she brought back were intricate and beautiful. 





As recently as 2002, fuel wood provided virtually one hundred percent 
of all non-commercial energy consumption. Fuel wood consumption, at 
1.22 tons per capita, was one of the highest, if not the highest, in the world. 
Bhutan was an ideal laboratory in which to monitor the effects of electricity, 
because that country was about to be transformed from near zero percent 
electrification to one hundred percent electrification in a little over a 
decade. 

In 1998, King Jigme Singye Wangchuk ceded some of his powers to a 
democratic assembly, which wanted to modernize the country. The 
Department of Energy and the Bhutan Electricity Authority were created on 
July 1, 2002. That same day the Bhutan Power Corporation was launched. 
With 1,193 employees, it immediately became the largest corporation in the 
kingdom. Its mandate was to generate and distribute electricity throughout 
the kingdom, with a target of full electrification of the country within ten 
years. 





The next 
year, 944. The year after that, 1,470. The following year, 1,732. The next 
year, 2,541, with 15 deaths.'!° In 2010, there were 91 deaths and diabetes 
mellitus was already the eighth most common cause of mortality in the 
kingdom. Coronary heart disease was number one. Only 66.5 percent of the 
population had normal blood sugar." This sudden change in the health of 
the population, especially the rural population, was being blamed, 
incredibly, on the traditional Bhutanese diet which, however, had not 


changed. *Bhutanese have a penchant for fat-rich foods," reported Jigme 
Wangchuk in the Bhutan Observer. “All Bhutanese delicacies are fat-rich. 
Salty and fatty foods cause hypertension. Today, one of the main causes of 
ill-health in Bhutan is hypertension caused by oil-rich and salty traditional 
Bhutanese diet.” Rice, the article continued, which is the staple food of the 
Bhutanese, is rich in carbohydrates, which turns into fat unless there is 
physical activity; perhaps the Bhutanese are not getting enough exercise. 
Two-thirds of the population, the author complained, are not eating enough 
fruits and vegetables. 

But the Bhutanese diet has not altered. The Bhutanese people are poor. 
Their country is mountainous with few roads. They have not all gone out 
and suddenly bought automobiles, refrigerators, washing machines, 
televisions, and computers, and become a lazy, inactive people. Yet rates of 
diabetes quadruple in four years. Bhutan now ranks eighteenth in the world 
in its mortality rate from heart disease. 





We recall from the last chapter that exposure to electromagnetic fields 
interferes with basic metabolism. The power plants of our cells, the 
mitochondria, become less active, slowing the rate at which our cells can 
burn glucose, fats, and protein. Instead of being taken up by our cells, 
excess fats accumulate in our blood and are deposited on the walls of our 
arteries along with the cholesterol that transports them, forming plaques and 
causing coronary heart disease. This can be prevented by eating a low-fat 
diet. 

In the same way, excess glucose, instead of being taken up by our cells, 
also backs up and accumulates in our blood. This increases the secretion of 
insulin by our pancreas. Normally, insulin lowers blood sugar by increasing 
its uptake by our muscles. 





have Type 1 diabetes. If your pancreas is producing enough, or too much 
insulin, but your muscles are unable to use glucose quickly enough, this is 
interpreted as “insulin resistance” and you have Type 2 diabetes. 

Eating a diet free of highly refined, quickly digested foods, especially 
sugar, can prevent this. In fact, before the discovery of insulin in 1922, 
some doctors, including Elliott Joslin, successfully treated severe cases of 
diabetes with a near-starvation diet.7 They radically restricted their 
patients? intake of not just sugar, but all calories, thus ensuring that glucose 
entered the bloodstream at a rate no faster than the cells could deal with. 
After a several days' fast normalized the blood glucose, first carbohydrates, 
then proteins, then fats were gradually reintroduced into the patient's diet. 
Sugar was eliminated. This saved many people who would have died within 
a year or two. 

But in Joslin's time the very nature of this disease underwent a 
mysterious transformation. 

Insulin resistance—which accounts for the vast majority of diabetes in 
the world today—did not exist before the late nineteenth century. Neither 
did obese diabetic patients. Almost all people with diabetes were insulin- 
deficient, and they were universally thin: since insulin is needed in order for 
muscle and fat cells to absorb glucose, people with little or no insulin will 
waste away. They pee away their glucose instead of using it for energy, and 
survive by burning their stores of body fat. 

In fact, overweight diabetics were at first so unusual that late- 
nineteenth-century doctors couldn't quite believe the change in the disease 
—and some of them didn't. One of these, John Milner Fothergill, a 
prominent London physician, wrote a letter to the Philadelphia Medical 
Times in 1884, in which he stated: *When a corpulent, florid- complexioned 
man, well-fed and vigorous, passes sugar in his urine, only a tyro would 
conjecture that he was the victim of classical diabetes, a formidable wasting 
disease."?? Dr. Fothergill, as it turned out, was in denial. A corpulent, florid- 
complexioned man himself, Fothergill died of diabetes five years later. 

Today the disease has changed entirely. Even children with Type 1, 
insulin-deficient diabetes tend to be overweight. They are overweight 
before they become diabetic because of their cells' reduced ability to 





Diabetes Is Also a Disorder of Fat Metabolism 

Nowadays, all blood that is drawn from a patient is sent right off to a 
laboratory to be analyzed. The doctor rarely looks at it. But a hundred years 
ago the quality and consistency of the blood were valuable guides to 
diagnosis. Doctors knew that diabetes involved an inability to metabolize 
not just sugar but fat, because blood drawn from a diabetic's vein was 
milky, and when it was allowed to stand, a thick layer of *cream" invariably 
floated to the top. 

In the early years of the twentieth century, when diabetes had become 
epidemic and was not yet controllable with any medication, it was not 
unusual for a diabetic's blood to contain 15 to 20 percent fat. Joslin even 
found that blood cholesterol was a more reliable measure of the severity of 
the disease than blood sugar. He disagreed with those of his contemporaries 
who were treating diabetes with a low-carbohydrate, high-fat diet. ^The 
importance of the modification of the treatment to include control of the fat 
of the diet is obvious," he wrote. He issued a warning, appropriate not only 
for his contemporaries but for the future: “When fat ceases to be 
metabolized in a normal manner no striking evidence of it is afforded, and 
both patient and doctor continue to journey along in innocent oblivion of its 
existence, and hence fat is often a greater danger to a diabetic than 
carbohydrate.” 4 

The linked failure of both carbohydrate and fat metabolism is a sign of 
disordered respiration in the mitochondria, and the mitochondria, we have 
seen, are disturbed by electromagnetic fields. Under the influence of such 
fields, respiratory enzyme activity is slower. After a meal, the cells cannot 
oxidize the breakdown products of the proteins, fats, and sugars that we eat 
as quickly as they are being supplied by the blood. Supply outstrips 
demand. Recent research has shown exactly how this happens. 

Glucose and fatty acids, proposed University of Cambridge biochemist 
Philip J. Randle in 1963, compete with each other for energy production. 


This mutual competition, he said, operates independently of insulin to 
regulate glucose levels in the blood. In other words, high fatty acid levels in 
the blood inhibit glucose metabolism, and vice versa. Evidence in support 
appeared almost immediately. Jean-Pierre Felber and Alfredo Vannotti at 
the University of Lausanne gave a glucose tolerance test to five healthy 
volunteers, and then another one a few days later to the same individuals 
while they were receiving an intravenous infusion of lipids. Every person 
responded to the second test as though they were insulin resistant. Although 
their insulin levels remained the same, they were unable to metabolize the 
glucose as quickly in the presence of high levels of fatty acids in their 
blood, competing for the same respiratory enzymes. These experiments 
were easy to repeat, and overwhelming evidence confirmed the concept of 
the *glucose-fatty acid cycle." Some evidence also supported the idea that 
not only fats, but amino acids as well, competed with glucose for 
respiration. 

Randle had not been thinking in terms of mitochondria, much less what 
could happen if an environmental factor restricted the ability of the 
respiratory enzymes to work at all. But during the last decade and a half, 
finally some diabetes researchers have begun focusing specifically on 
mitochondrial function. 

Remember that our food contains three main types of nutrients— 
proteins, fats, and carbohydrates—that are broken down into simpler 
substances before being absorbed into our blood. Proteins become amino 
acids. Fats become triglycerides and free fatty acids. Carbohydrates become 
glucose. Some portion of these is used for growth and repair and becomes 
part of the structure of our body. The rest is burned by our cells for energy. 

Within our cells, inside tiny bodies called mitochondria, amino acids, 
fatty acids, and glucose are all further transformed into even simpler 
chemicals that feed into a common cellular laboratory called the Krebs 
cycle, which breaks them down the rest of the way so that they can combine 
with the oxygen we breathe to produce carbon dioxide, water, and energy. 
The last component in this process of combustion, the electron transport 
chain, receives electrons from the Krebs cycle and delivers them, one at a 
time, to molecules of oxygen. If the speed of those electrons is modified by 


external electromagnetic fields, as suggested by Blank and Goodman, or if 
the functioning of any of the elements of the electron transport chain is 
otherwise altered, the final combustion of our food is impaired. Proteins, 
fats, and carbohydrates begin to compete with each other and back up into 
the bloodstream. Fats are deposited in arteries. Glucose is excreted in urine. 
The brain, heart, muscles, and organs become oxygen-deprived. Life slows 
down and breaks down. 

Only recently was it proven that this actually happens in diabetes. For a 
century, scientists had assumed that because most diabetics were fat, 
obesity causes diabetes, But in 1994, David E. Kelley at the University of 
Pittsburgh School of Medicine, in collaboration with Jean-Aimé Simoneau 
at Laval University in Quebec, decided to find out exactly why diabetics 
have such high fatty acid levels in their blood. Seventy-two years after 
insulin was discovered, Kelley and Simoneau were among the first to 
measure cellular respiration in detail in this disease. To their surprise, the 
defect turned out not to be in the cells’ ability to absorb lipids but in their 
ability to burn them for energy. Large amounts of fatty acids were being 
absorbed by the muscles and not metabolized. This led to intensive research 
into all aspects of respiration at the cellular level in diabetes mellitus. 
Important work continues to be done at the University of Pittsburgh, as well 
as at the Joslin Diabetes Center, RMIT University in Victoria, Australia, 
and other research centers.!^ 

What has been discovered is that cellular metabolism is reduced at all 
levels. The enzymes that break down fats and feed them into the Krebs 
cycle are impaired. The enzymes of the Krebs cycle itself, which receives 
the breakdown products of fats, sugars, and proteins, are impaired. The 
electron transport chain is impaired. The mitochondria are smaller and 
reduced in number. Consumption of oxygen by the patient during exercise 
is reduced. The more severe the insulin resistance—i.e., the more severe the 
diabetes—the greater the reductions in all these measures of cellular 
respiratory capacity. 

In fact, Clinton Bruce and his colleagues in Australia found that the 
oxidative capacity of the muscles was a better indicator of insulin resistance 
than their fat content—which threw into question the traditional wisdom 


that obesity causes diabetes. Perhaps, they speculated, obesity is not a cause 
but an effect of the same defect in cellular respiration that causes diabetes. 
A study involving lean, active young African-American women in 
Pittsburgh, published in 2014, seemed to confirm this. Although the women 
were somewhat insulin resistant, they were not yet diabetic, and the medical 
team could find no other physiological abnormalities in the group except 
two: their oxygen consumption during exercise was reduced, and 
mitochondrial respiration in their muscle cells was reduced.!5 

In 2009, the Pittsburgh team made an extraordinary finding. If the 
electrons in the electron transport chain are being disturbed by an 
environmental factor, then one would expect that diet and exercise might 
improve all components of metabolism except the last, energy-producing 
step involving oxygen. That is exactly what the Pittsburgh team found. 
Placing diabetic patients on calorie restriction and a strict exercise regime 
was beneficial in many respects. It increased the activity of the Krebs cycle 
enzymes. It reduced the fat content of muscle cells. It increased the number 
of mitochondria in the cells. These benefits improved insulin sensitivity and 
helped control blood sugar. But although the number of mitochondria 
increased, their efficiency did not. The electron transport enzymes in dieted, 
exercised diabetic patients were still only half as active as the same 
enzymes in healthy individuals." 

In June 2010, Mary-Elizabeth Patti, a professor at Harvard Medical 
School and researcher at the Joslin Diabetes Center, and Silvia Corvera, a 
professor at the University of Massachusetts Medical School in Worcester, 
published a comprehensive review of existing research on the role of 
mitochondria in diabetes. They were forced to conclude that a defect of 
cellular respiration may be the basic problem behind the modern epidemic. 
Due to "failure of mitochondria to adapt to higher cellular oxidative 
demands," they wrote, *a vicious cycle of insulin resistance and impaired 
insulin secretion can be initiated." 

But they were not willing to take the next step. No diabetes researchers 
today are looking for an environmental cause of this “failure to adapt" of so 
many people's mitochondria. They are still, in the face of evidence refuting 
it, blaming this disease on faulty diet, lack of exercise, and genetics. This in 


spite of the fact that, as Dan Hurley noted in his 2011 book, Diabetes 
Rising, human genetics has not changed and neither diet, exercise, nor 
drugs has put a dent in the escalation of this disease during the ninety years 
since insulin was discovered. 


Diabetes in Radio Wave Sickness 
In 1917, when Joslin was publishing the second edition of his book on 
diabetes, radio waves were being massively deployed on and off the 
battlefield in the service of war. At that point, as we saw in chapter 8, radio 
waves joined power distribution as a leading source of electromagnetic 
pollution on this planet. Their contribution has steadily grown until today 
when radio, television, radar, computers, cell phones, satellites, and millions 
of transmission towers have made radio waves by far the predominant 
source of electromagnetic fields bathing living cells. 





But some of it has, thanks to the United States military, in documents 
that have not been widely circulated, and thanks to a few international 
conferences. 

During the Cold War, from the late 1950s through the 1980s, the United 
States Army, Navy, and Air Force were developing and building 
enormously powerful early warning radar stations to protect against the 
possibility of nuclear attack. In order to stand sentinel over the air spaces 
surrounding the United States, these stations were going to monitor the 
entire coastline and the borders with Mexico and Canada. This meant that a 
strip of the American border up to hundreds of miles wide—and everyone 
who lived there—was going to be continuously bombarded with radio 
waves at power levels that were unprecedented in human history. Military 
authorities needed to review all ongoing research into the health effects of 
such radiation. In essence, they wanted to know what were the maximum 


levels of radiation to which they could get away with exposing the 
American population. And so one of the functions of the Joint Publications 
Research Service, a federal agency established during the Cold War to 
translate foreign documents, 





In the late 1950s, in Moscow, Maria Sadchikova gave glucose tolerance 
tests to 57 workers exposed to UHF radiation. The majority had altered 
sugar curves: their blood sugar remained abnormally high for over two 
hours after an oral dose of glucose. And a second dose, given after one 
hour, caused a second spike in some patients, indicating a deficiency of 
insulin.!? 

In 1964, V. BartoníCek, in Czechoslovakia, gave glucose tolerance tests 
to 27 workers exposed to centimeter waves—the type of waves we are all 
heavily exposed to today from cordless phones, cell phones, and wireless 
computers. Fourteen of the workers were prediabetic and four had sugar in 
their urine. This work was summarized by Christopher Dodge in a report he 
prepared at the United States Naval Observatory and read at a symposium 
held in Richmond, Virginia in 1969. 

In 1973, Sadchikova attended a symposium in Warsaw on the Biologic 
Effects and Health Hazards of Microwave Radiation. She was able to report 
on her research team's observations of 1,180 workers exposed to radio 
waves over a twenty-year period, of whom about 150 had been diagnosed 
with radio wave sickness. Both prediabetic and diabetic sugar curves, she 
said, “accompanied all clinical forms of this disease.” 

Eliska Klimkova-Deutschova of Czechoslovakia, at the same 
symposium, reported finding an elevated fasting blood sugar in fully three- 
quarters of all individuals exposed to centimeter waves. 

Valentina Nikitina, who was involved in some of the Soviet research and 
was continuing to do such research in modern Russia, attended an 
international conference in St. Petersburg in 2000. She reported that people 
who maintained and tested radio communication equipment for the Russian 
Navy—even people who had ceased such employment five to ten years 


previously—had, on average, higher blood glucose levels than unexposed 
individuals. 

Attached to the same medical centers at which Soviet doctors were 
examining patients were laboratories where scientists were exposing 
animals to the very same types of radio waves. They, too, reported seriously 
disturbed carbohydrate metabolism. They found that the activity of the 
enzymes in the electron transport chain, including the last enzyme, 
cytochrome oxidase, is always inhibited. This interferes with the oxidation 
of sugars, fats and proteins. To compensate, anaerobic (non-oxygen using) 
metabolism increases, lactic acid builds up in the tissues, and the liver 
becomes depleted of its energy-rich stores of glycogen. Oxygen 
consumption declines. The blood sugar curve is affected, and the fasting 
glucose level rises. The organism craves carbohydrates, and the cells 
become oxygen starved.!? 

These changes happen rapidly. As early as 1962, V. A. Syngayevskaya, 
working in Leningrad, exposed rabbits to low level radio waves and found 
that the animals' blood sugar rose by one-third in less than an hour. In 1982, 
Vasily Belokrinitskiy, working in Kiev, reported that the amount of sugar in 
the urine was in direct proportion to the dose of radiation and the number of 
times the animal was exposed. Mikhail Navakatikian and Lyudmila 
Tomashevskaya reported in 1994 that insulin levels decreased by 15 percent 
in rats exposed for just half an hour, and by 50 percent in rats exposed for 
twelve hours, to pulsed radiation at a power level of 100 microwatts per 
square centimeter. 





If there wasn't a public outcry when most of this information was 
concealed in foreign alphabets, there should be one now, because it has 
become possible to confirm directly, in human beings, the degree to which 
cell phones interfere with glucose metabolism, and the outcomes of such 
studies are being published in English. Finnish researchers reported their 
alarming findings in the Journal of Cerebral Blood Flow and Metabolism in 
2011. Using positron emission tomography (PET) to scan the brain, they 


found that glucose uptake is considerably reduced in the region of the brain 
next to a cell phone.”° 

Even more recently, researchers at Kaiser Permanente in Oakland, 
California, confirmed that electromagnetic fields cause obesity in children. 
They gave pregnant women meters to wear for 24 hours to measure their 
exposure to magnetic fields during an average day. The children of those 
women were more than six times as likely to be obese when they were 
teenagers if their mothers’ average exposure during pregnancy had 
exceeded 2.5 milligauss. Of course, the children were exposed to the same 
high fields while growing up, so what the study really proved is that 
magnetic fields cause obesity in chidren.?! 


Vital Statistics 

As with heart disease, rural mortality from diabetes in the 1930s 
corresponded closely with rates of rural electrification, and varied as much 
as tenfold between the least and the most electrified states. This is 
graphically illustrated in figures 3 and 4. 


Figure 3 — Rate of Rural Diabetes in 1931 


Percent electrification 1931 


80 


70 


60 


50 


20 


10 


8 10 12 14 16 18 


Rate of rural diabetes (1931) 
(mortality per 100,000 population) 


Table 3 













































% electrification Rural diabetes 1931 % electrification Rural diabetes 1940 
(1931) (deaths per 100,000) (1940) (deaths per 100,000) 

AL 25.7 &.9 34.7 9.8 
AZ 62.5 1.7 56.1 49 
AR 22.1 6.5 27.3 7.8 
CA 92.5 13.7 75.6 18.0 
co 61.5 12.2 56.9 11.6 
GT 94.9 18.2 90.5 29.0 
DE 64.4 14.6 66.1 21.2 
FL 53.8 9.4 30.7 11.5 
GA 28.4 (missing) 36.5 9.8 
ID 48.2 10.8 64.5 13.5 
IL 82.5 20.3 79.4 284 
IN 70.0 20.3 74.9 25.8 
1A 61.4 15.0 65.5 24.7 
KS 59,4 18.1 60.2 25.1 
KY 38.0 (missing) 41.6 11.9 
LA 34.1 6.9 41.5 12.1 
ME TS 22.1 70.5 294 
MD 72.3 12.2 65.2 23.6 
MA 98.5 23.7 91.9 42.9 
MI 78.4 20.6 81.3 26.4 
MN 64.2 13.6 63.4 24.6 
MS 16.5 8.9 22.7 11.3 
MO 59.1 14.0 583 19.4 
MT 48.9 12.4 56.8 16.7 
NE 60.0 19.0 62.1 27.8 
NV 54.8 3.6 58.3 17.9 
NH 86.3 20.9 78.7 40.8 
NJ 97.7 21.4 87.0 35.9 
NM 273 53 26.5 48 
NY 98.1 25.2 83.9 37.4 
NC 32.4 8.2 43.7 12.1 
ND 34.5 14.3 40.5 235 
OH 77.0 18.5 82.5 27.3 
OK 39.2 62 41.3 117 
OR 68.8 11.8 67.7 16.3 
PA 78.5 20.1 80.4 a d 
RI 98.2 36.7 91.0 48.4 
sc 25.6 8.9 32.1 9.1 
sD 41.0 15.8 43.0 214 
TN 34.0 7.8 42.1 10.8 
IX 39.5 8.4 43.5 10.6 
UT 71.8 9.6 752 13.9 
VT 71.9 (missing) 71.5 32.2 
VA 41.7 10.9 53.1 16.6 
WA 78.7 13.2 73.8 19.3 
wv 41.0 8.8 534 12.4 
WI 74.7 18.7 

WY 49.5 8.3 





Figure 4 — Rate of Rural Diabetes in 1940 


MA. (R—- 
48.4) 


Percent electrification 1940 





4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 
Rate of rural diabetes (1940) 
(mortality per 100,000 population) 


The overall history of diabetes in the United States is similar to that of 
heart disease. 


Death Rate from Diabetes in the United States (per 100,000 population) 


1850 1.4 
1860 1.7 
1870 3.0 
1880 3.4 
1890 6.4 
1900 10.6 
1910 15.0 
1920 16.2 
1930 19.0 
1940 26.6 
1950 16.2 
1960 16.7 
1970 18.9 


1980 15.4 


1990 19.2 


2000 25.2 
2010 22.3 
2017 25.7 





Beginning in 1949, those deaths were reported as due to heart disease, 
diminishing the reported mortality from diabetes by about 40 percent. In the 
late 1950s, Orinase, Diabinase, and Phenformin were brought to market, the 
first of many oral medications that helped control the blood sugar of people 
with “insulin-resistant” diabetes for whom insulin was of limited use. These 
drugs have restrained, but not reduced the mortality from this disease. 
Meanwhile the number of diagnosed cases of diabetes in the United States 
has steadily increased: 


Year Cases per 1,000 population 
1917 1.92 
1944 5.7 
1958 9.3 
1963 11.5 
1968 16.2 
1973 20.4 
1978 23.7 
1983 24.5 
1988 25.6 
1990 25.2 
1992 29.3 
1994 29.8 
1996 28.9 
1997 38.0 
1998 39.0 


1999 40.0 


2000 44.0 


2001 47.5 
2002 48.4 
2003 49.3 
2004 52.9 
2005 56.1 
2006 59.0 
2007 58.6 
2008 62.9 
2009 68.6 
2010 69.6 
2011 67.8 
2012 69.6 
2013 71.8 
2014 70.1 
2015 72.0 

70 

62 


Yearly Prevalence of Diabetes 
54 (cases per 1,000 population) 


Number of Cases 





C~ = 900 e^ W A o0 M 96 r4 S c 4 e foc 
= = wA S Ss ct y SA A CO UC GO = ce 
2 a eS A C c ce > a Aas, c coco 
= = = å = n cn ocn ol ol—c uu 1 N A N 





Levels between 140 and 200, which may not cause sugar in the urine, are 
now called “prediabetes.” 

A sudden spike in diabetes cases occurred nationwide in 1997—a 31 
percent increase in a single year. No one was able to explain why. But that 
was the year the telecommunications industry introduced digital cell phones 
en masse to the United States. The first such phones went on sale in dozens 
of American cities during the Christmas season of 1996. Construction of 
cell towers began in those cities during 1996, but 1997 was the year that 
battalions of towers, previously confined to metropolises, marched out over 
the rural landscapes to occupy previously virgin territory. That was the year 
cell phones were transformed from a rich person’s luxury to the common 
person’s soon-to-be necessity—the year microwave radiation from towers 
and antennas became inescapable over large parts of the United States. 

The situation today is out of control. The Centers for Disease Control 
estimates that in addition to the 21 million American adults over the age of 
twenty who have diagnosed diabetes, 8 million have undiagnosed diabetes, 
and 86 million have prediabetes. Adding these numbers together gives the 
shocking statistic that 115 million Americans, or more than half of all 
adults, have elevated levels of sugar in their blood. 

Worldwide, it was estimated that more than 180,000,000 adults had 
diabetes in 2000. In 2014, the estimate was 387,000,000. In no country on 
earth is the rate of diabetes, or of obesity, decreasing. 

Like diabetes, obesity has tracked exposure to electromagnetic fields. 
The first official statistics in the United States date from 1960, showing that 
one-quarter of adults were overweight. That number did not change for 
twenty years. The fourth survey, however, conducted during 1988-1991, 
revealed something alarming: fourteen million additional Americans had 
become fat. 


Overweight in the United States (percent of adults 20 through 74 years of 
age) 
1960-1962 24.3 


1971-1974 25.0 
1976-1980 25.4 


1988-1991 33.3 


The authors, writing in the Journal of the American Medical 
Association, commented that studies in Hawaii and England had found 
similar rises in overweight during the 1980s across the board throughout the 
population in both sexes and at all ages. They speculated about “dietary 
knowledge, attitudes, and practices, physical activity levels, and perhaps 
social, demographic, and health behavior factors” that might have changed, 
although they did not point to a single piece of evidence that any of those 
things had changed.” In rebuttal, British physician Jeremiah Morris noted 
in a letter to the British Medical Journal that the average lifestyle had 
improved during this time, not worsened. More people in England were 
cycling, walking, swimming, and doing aerobics than ever before. Average 
daily food consumption, even after adjusting for meals eaten outside the 
home, had declined by 20 percent between 1970 and 1990. 

However, in 1977, Apple had marketed its first personal computer, and 
during the 1980s the majority of people in both the United States and 
England, either at home or at work or both, were suddenly—and for the first 
time in history—exposed to high frequency electromagnetic fields 
continuously for hours everyday. 

The problem became so huge that in 1991 the Centers for Disease 
Control began retroactively tracking not just overweight but obesity. For an 
American man or woman of average height this is defined as being more 
than about 30 pounds overweight. 


Obesity in the United States?^ (percent of adults over 20 years of age) 


1960-1962 13.4 
1971-1974 14.4 
1976-1980 14.7 
1988-1991 22.3 
1999-2000 30.5 
2009-2010 35.7 


2015-2016 39.6 


Grade III obesity, called “morbid obesity,” has also been rising since 
1980. This is defined as being more than about 100 pounds overweight. 


Grade III Obesity in the United States (percent of adults over 20 years of 


age) 
1960-1962 0.8 
1971-1974 1.3 
1976-1980 1.3 
1988-1991 2.8 
1999-2000 4.7 
2009-2010 6.3 
2015-2016 7.7 


More than two-thirds of all adults today—about 150 million Americans 
—are overweight. Eighty million are obese, as are twelve and a half million 
children, including one and a half million children aged two to five.» 
Twelve and a half million adults are more than 100 pounds overweight. The 
experts at the Centers for Disease Control have been able to do little more 
than shout that similar trends are being reported elsewhere—more than half 
a billion adults worldwide are obese—and to throw up their hands and say, 
“We do not know the causes of these increases in overweight and obesity."? 


Obesity in Wild and Domestic Animals 
If obesity is caused by an environmental factor, then it should be occurring 
in animals too. And it is so. 

A few years ago David B. Allison, professor of biostatistics at the 
University of Alabama School of Public Health, was looking over data on 
small primates called marmosets from the Wisconsin Non-Human Primate 
Center, when he noticed that the average weight of the animals had 
increased remarkably over time. Mystified, he checked with the center, but 
could find no convincing reason for weight gain in this large population of 
animals living in a fixed laboratory environment on a controlled diet. 

Intrigued, Allison searched online for previous studies of mammals that 
had lasted at least a decade and contained information about the animals’ 
weight. He involved colleagues at primate centers, toxicology programs, pet 


food companies, and veterinary programs. The final paper, published in 
2010 in the Proceedings of the Royal Society B, had eleven coauthors from 
Alabama, Florida, Puerto Rico, Maryland, Wisconsin, North Carolina, and 
California, and analyzed data on over 20,000 animals from twenty-four 
populations representing eight species, including laboratory animals, house 
pets, and feral rats, both rural and urban. In all twenty-four populations, the 
average weight of the animals rose over time. The odds of this happening 
by chance were less than ten billion to one. 


Animal population Average weight gain per 
decade 

macaques, 1971 to 2006 5.396 
(Wisconsin Primate Center) 

macaques, 1981 to 1993 9.696 
(Oregon Primate Center) 

macaques, 1979 to 1992 11.596 
(California Primate Center) 

chimpanzees, 1985 to 2005 33.696 
(Yerkes Primate Center, 
Atlanta) 

vervets, 1990 to 2006 8.896 
(UCLA Vervet Research 
Center) 

marmosets, 1991 to 2006 9.396 
(Wisconsin Primate Center) 

laboratory mice, 1982 to 2005 3.496 

domestic dogs, 1989 to 2001 2.996 

domestic cats, 1989 to 2001 9.796 

feral rats, 1948 to 2006 (urban) 6.996 


feral rats, 1948 to 1986 (rural) 4.8% 


Chimpanzees gained the most weight: they were twenty-nine times as 
likely to be obese in 2005 as they were in 1985. But even among country 
rats there was 15 percent more obesity every decade, consistently for four 
decades. The authors found similar studies with the same results elsewhere: 
19 percent of light breed horses in Virginia were obese in 2006, versus 5 
percent in 1998;? laboratory rats in France, under identical conditions, had 
increased in weight between 1979 and 1991. 





13. Cancer and the Starvation of Life 


At the commencement of the twentieth century the great 
problem of the causation of tumours, like a giant sphinx, 
looms large on the medical horizon. 


W. ROGER WILLIAMS, Fellow of the Royal College of 
Surgeons, England, 1908 





nd for decades, residents in those communities had been 
screaming that the transmissions were destroying their health as well as 
causing an epidemic of childhood leukemia. At the request of the Public 
Prosecutor's office in Rome, which was considering bringing charges 
against the Vatican for negligent homicide, Judge Zaira Secchi ordered an 
official investigation by the National Cancer Institute of Milan. The results, 
released November 13, 2010, were shocking. 








Photo by Angelo Franceschi 


in his 
laboratory over one hundred years ago. He was a native of the same city 
where, a century later, three thousand doctors were to sign an appeal to the 
world stating, among other things, that radio waves cause leukemia. 

On October 8, 1883, a son was born to Emil Warburg, a prominent 
Jewish physicist in Freiburg, Germany. When he was thirteen, the family 
moved to Berlin, where visitors to his parents’ home included some of the 
giants of the natural sciences—chemist Emil Fischer, physical chemist 
Walter Nernst, physiologist Theodor Wilhelm Engelmann. Later, when 
Albert Einstein moved to Berlin, the great scientist used to come over to 
play chamber music with his father—Einstein on violin and Emil Warburg 
on piano. No one was surprised when young Otto, growing up in such an 
atmosphere, enrolled in the University of Freiburg to study chemistry. 

But by the time he received his Ph.D. in 1906, a growing disease 
epidemic had caught the attention of this ambitious young man. His was the 





first generation seriously to be affected by it. Cancer rates all over Europe 
had doubled since he was born, and he determined to devote his life to 
finding the reason and, hopefully, a cure. With this in mind he returned to 
school, receiving his M.D. from the University of Heidelberg in 1911. 

What fundamental changes, he wondered, take place in the tissue when 
a normal cell becomes cancerous? *Does the metabolism of tumours," he 
asked, “growing in a disorganized manner, differ from the metabolism of 
orderly cells growing at the same rate?”! Impressed that both tumors and 
early embryos consist of undifferentiated cells that multiply rapidly, Otto 
Warburg began his life’s work by studying fertilized eggs. Perhaps, he 
speculated, cancer cells are just normal cells that have reverted to an 
embryonic pattern of growth. He chose the sea urchin egg to study because 
its embryo is large and grows particularly fast. His first major work, 
published while he was still in medical school, showed that on fertilization 
the rate of oxygen consumption of an egg rises sixfold.” 





Otto Heinrich Warburg, M.D., Ph.D. (1883-1970) 


But in 1908, he could pursue his ambition no further because the 
chemical reactions within cells that involve oxygen were completely 
unknown. Spectrophotometry—the identification of chemicals from the 
frequencies of light they absorb—was new, and had not yet been applied to 
living systems. Existing techniques for culturing cells and measuring gas 
exchange were primitive. Warburg realized that before any real progress 


could be made in elucidating the metabolism of cancer, fundamental 
research on the metabolism of normal cells would have to be done. Cancer 
research would have to wait. 

During the coming years—with a break during which he served in the 
World War—Warburg, using techniques that he developed, proved that 
respiration in a cell took place in tiny structures that he called “grana” and 
that we now call mitochondria. He experimented with the effects of 
alcohols, cyanide, and other chemicals on respiration and concluded that the 
enzymes in the “grana” must contain a heavy metal that he suspected, and 
later proved, was iron. He conducted landmark experiments using 
spectrophotometry that proved that the portion of the enzyme that reacts 
with oxygen in a cell is identical with the portion of hemoglobin that binds 
oxygen in the blood. That chemical, called heme, is a porphyrin bonded to 
iron, and the enzyme containing it, which exists in every cell and makes 
breathing possible, is known today as cytochrome oxidase. For this work 
Warburg was awarded the Nobel Prize in Physiology or Medicine in 1931. 

Meanwhile, in 1923, Warburg resumed his research on cancer, picking 
up where he had left off fifteen years earlier. “The starting point,” he wrote, 
“has been the fact that the respiration of sea urchin eggs increases six-fold 
at the moment of fertilization,” i.e. at the moment that it changes from a 
State of rest to a state of growth. He expected to find a similar increase of 
respiration in cancer cells. But to his amazement, he found just the opposite. 
The rat tumor he was working with used considerably less oxygen than 
normal tissues from healthy rats. 

“This result seemed so startling,” he wrote, “that the assumption seemed 
justified that the tumor lacked suitable material for combustion.” So 
Warburg added various nutrients to the culture medium, still expecting to 
see a dramatic rise in oxygen use. Instead, when he added glucose, the 
tumor’s respiration ceased completely! And in trying to discover why this 
happened, he found that tremendous amounts of lactic acid were 
accumulating in the culture medium. The tumor, in fact, was producing 
fully twelve percent of its weight in lactic acid per hour. Per unit time, it 
was producing 124 times as much lactic acid as blood, 200 times as much 
as a frog’s muscle at rest, and eight times as much as a frog’s muscle 


working to the limit of its capacity. The tumor was consuming the glucose, 
all right, but it was not making use of oxygen to do it. 

In additional experiments on other types of cancers in animals and 
humans, Warburg found that this was generally true of all cancer cells, and 
of no normal cells. This singular fact impressed Warburg as of utmost 
importance and the key to the causation of this disease. 

The extraction of energy from glucose without using oxygen, a type of 
metabolism called anaerobic glycolysis—also called fermentation—is a 
highly inefficient process that takes place to a small extent in most living 
cells but only becomes important when not enough oxygen is available. For 
example, runners, during a sprint, push their muscles to use energy faster 
than their lungs can deliver oxygen to them. Their muscles temporarily 
produce energy anaerobically (without oxygen), incurring an oxygen debt 
that is repaid when they end their sprint and stop to gulp air. Although 
capable of supplying energy rapidly in an emergency, anaerobic glycolysis 
produces much less energy for the same amount of glucose, and deposits 
lactic acid in the tissues that has to be disposed of. 

Fermentation is a very old form of metabolism from which all forms of 
life obtained their energy for billions of years, before green plants appeared 
on earth and filled the atmosphere with oxygen. Some primitive forms of 
life today—many bacteria and yeasts, for example—still rely on it, but all 
complex organisms have abandoned that way of making a living. 





Warburg reasonably believed he had discovered the cause of cancer. 
Evidently, in cancer, the respiratory mechanism has been damaged and has 
lost control over the metabolism of the cell. Unrestrained glycolysis—and 


unrestrained growth—are the result. In the absence of normal metabolic 
control the cell reverts to a more primitive state. All complex organisms, 
proposed Warburg, must have oxygen in order to maintain their highly 
differentiated forms. Without oxygen, they will revert to a more 
undifferentiated, simple form of growth, such as existed exclusively on this 
planet before there was oxygen in the air. 





When cells are deprived of oxygen only temporarily, glycolysis takes over 
during the emergency, but ceases again when oxygen is once more 
available. But when cells are repeatedly or chronically deprived of oxygen, 
he said, respiratory control is eventually damaged and glycolysis becomes 
independent. “If respiration of a growing cell is disturbed,” wrote Warburg 
in 1930, “as a rule the cell dies. If it does not die, a tumour cell results.”5 

Warburg's hypothesis was first brought to my attention in the mid-1990s 
by Dr. John Holt, a colorful figure in Australia who was treating cancer 
with microwave radiation, and who warned his colleagues that the same 
radiation could convert normal cells into cancerous ones. I didn't fully 
understand the connection of Warburg's work on cancer to my work on 
electricity, so I filed away the research papers Holt sent me for future 
reference. 


If Warburg was correct, and chronic 
lack of oxygen causes cancer, then one need look no further than 
electrification for the origin of the modern pandemic. 

Warburg's theory was controversial from the beginning. Hundreds of 
different kinds of cancers were known in the 1920s, triggered by thousands 








of kinds of chemical and physical agents. 


Although they didn’t necessarily accept Warburg’s theory of causation, 
other researchers lost little time confirming the Warburg effect. Tumors did, 
universally, have the ability to grow without oxygen. By 1942, Dean Burk 
at the National Cancer Institute was able to report that this was true of over 
95 percent of the cancerous tissues he had examined. 

Then, in the early 1950s, Harry Goldblatt and Gladys Cameron, at the 
Institute for Medical Research at Cedars of Lebanon Hospital in Los 
Angeles, reported to a skeptical public that they had succeeded in 
transforming normal cells—cultured fibroblasts from the heart of a five- 
day-old rat—into cancer cells merely by repeatedly depriving them of 
oxygen. 

In 1959, Paul Goldhaber gave further support to Warburg’s hypothesis 
when he discovered that some types of Millipore diffusion chambers, but 
not others, when implanted under the skin of mice, caused large tumors to 
grow around them. Diffusion chambers were used to sample tissue fluid in 
many kinds of animal experiments. Their ability to cause cancer turned out 
to depend not on the type of plastic they were made of, but on the size of 
the pores that allowed fluid to flow through them. Only one animal out of 
39 developed a tumor when the pores were 450 millimicrons in diameter. 
But 9 out of 34 developed tumors when the pore size was 100 millimicrons, 
and 16 out of 35—close to half—developed tumors when the pore size was 
only 50 millimicrons. The interference with free fluid circulation when the 
pore size was too small apparently deprived the tissues next to the chamber 
walls of oxygen. 

In 1967, Burk’s team proved that the more malignant a tumor is, the 
higher its rate of glycolysis, the more glucose it consumes, and the more 
lactic acid it produces. “The extreme forms of rapidly growing ascites 
cancer cells,” Burk reported, “can produce lactic acid from glucose 
anaerobically at a sustained rate probably faster than any other living 
mammalian tissue—up to half the tissue dry weight per hour. Even a 
hummingbird, whose wings may beat up to at least one hundred times a 
second, consumes at best only half its dry weight of glucose equivalent per 
day.” 


Because he insisted that the origin of cancer was known, Warburg 
thought that *one could prevent about 80 percent of all cancers if one could 
keep out the known carcinogens.”’ He therefore advocated, in 1954, for 
restrictions on cigarette smoking, pesticides, food additives, and air 
pollution by car exhaust? His incorporation of these attitudes into his 
personal life earned him a reputation as an eccentric. Long before 
environmentalism was popular, Warburg had a one-acre organic garden, 
obtained milk from an organically maintained herd, and purchased French 
butter because in France the use of herbicides and pesticides was more 
strictly controlled than in Germany. 

Otto Warburg passed away in 1970 at the age of 83—the same year the 
first oncogene was discovered. An oncogene is an abnormal gene, thought 
to be caused by mutation, that is associated with the development of cancer. 
The discovery of oncogenes and tumor suppressor genes promoted a 
widespread belief that cancer was caused by genetic mutations and not by 
altered metabolism. Warburg’s hypothesis, controversial from the start, was 
largely abandoned for three decades. 

But the widespread use of PET scanning for diagnosing and staging 
human cancers has catapulted the Warburg effect back onto the main stage 
of cancer research. No one can now deny that cancers live in anaerobic 
environments, and that they rely on anaerobic metabolism in order to grow. 
Even molecular biologists, who once focused exclusively on the oncogene 
theory, are discovering, after all, that there is a connection between lack of 
oxygen and cancer. A protein has been discovered that exists in all cells— 
hypoxia-inducible factor (HIF)—that is activated under conditions of low 
oxygen, and that in turn activates many of the genes necessary for cancer 
growth. HIF activity has been found to be elevated in colon, breast, gastric, 
lung, skin, esophageal, uterine, ovarian, pancreatic, prostate, renal, stomach, 
and brain cancers.? 

Cellular changes that indicate damaged  respiration—including 
reductions in the number and size of mitochondria, abnormal structure of 
mitochondria, lessened activity of Krebs cycle enzymes, lessened activity of 
the electron transport chain, and mutations of mitochondrial genes—are 
being routinely found in most types of cancer. Even in tumors caused by 


o 


| cc 


Experimentally inhibiting the respiration of cancer cells, or simply 
depriving them of oxygen, has been shown to alter the expression of 
hundreds of genes that are involved in malignant transformation and cancer 
growth. Damaging respiration makes cancer cells more invasive; restoring 
normal respiration makes them less invasive. !° 

A consensus is forming among cancer researchers: tumors can only 
develop if cellular respiration is diminished.” In 2009, a book dedicated to 
Otto Warburg was published titled “Cellular Respiration and 
Carcinogenesis.” Addressing all aspects of this question, it contains 
contributions from leading cancer researchers from the United States, 
Germany, France, Italy, Brazil, Japan, and Poland.” In the foreword, Gregg 
Semenza wrote: “Warburg invented a device, now known as the Warburg 
manometer, with which he demonstrated that tumor cells consume less 
oxygen (and produce more lactate) than do normal cells under the same 
ambient oxygen concentrations. A century later, the struggle to understand 
how and why metastatic cancer cells manifest the Warburg effect is still 
ongoing, and 12 rounds of this heavyweight fight await the reader beyond 
this brief introduction.” 





Diabetes and Cancer 





The first person to confirm a connection between the two diseases was 
South African physician George Darell Maynard in 1910. Unlike almost all 
other diseases, rates of both cancer and diabetes were steadily rising. 
Thinking that they might have a common cause, he analyzed mortality 
statistics from the 15 death registration states in the 1900 Census of the 
United States. And he found, after correcting for population and age, that 
the two diseases were strongly related. States that had higher incidences of 
one also had higher incidences of the other. He proposed that electricity 
might be that common cause: 

“Only one cause, it seems to me, will fit the facts as we know them, viz.: 
the pressure of modern civilisation and the strain of modern competition, or 
some factor closely associated with these. Radio-activity and various 
electric phenomenon have from time to time been accused of producing 
cancer. The increased use of high tension currents is an undoubted fact in 
modern city life." 

A century later, it is an accepted fact that diabetes and cancer occur 
together. More than 160 epidemiological studies have investigated this 
question worldwide, and the majority have confirmed a link between the 
two diseases. Diabetics are more likely than non-diabetics to develop, and 
to die from, cancers of the liver, pancreas, kidney, endometrium, colon, 
rectum, bladder, and breast, as well as non-Hodgkin's lymphoma.?^ In 
December 2009, the American Diabetes Association and American Cancer 
Society convened a joint conference. 





Cancer in Animals 

We recall from chapter 11 that complete autopsy records of the Philadelphia 
Z00, kept since 1901, showed an increase in heart disease that accelerated 
during the 1930s and 1940s, and that affected all species of animals and 
birds at the zoo. An equivalent increase occurred in rates of cancer. The 


1959 report from the Penrose Research Laboratory at the zoo" divided the 
autopsies into two time periods: 1901-1934 and 1935-1955. The rate of 
malignant tumors among nine families of mammals increased between two- 
and twenty-fold from the earlier to the later time period. The rate of benign 
tumors increased even more. Only 3.6 percent of felines, for example, had 
benign or malignant tumors at autopsy during the earlier period, compared 
to 18.1 percent during the later period; 7.8 percent of ursines (bears) had 
tumors during the earlier period, compared to 47 percent during the later 
period. 

The autopsy records of 7,286 birds at the zoo, encompassing four 
different orders, showed that malignant tumors increased two-and-a-half- 
fold, and benign tumors eightfold. 


Vital Statistics 
The real story, again, is revealed by the historical records. 

The increase in cancer began slightly before heart disease and diabetes 
began to rise. Early records from England show that cancer deaths were 
rising as early as 1850:18 


Year Cancer deaths, England 
(per 100,000 population) 

1840 17.7 

1850 27.9 

1855 31.9 

1860 34.3 

1865 37.2 

1870 42.4 

1875 47.1 

1880 50.2 

1885 57.2 

1890 67.6 

1895 75.5 

1900 82.8 


1905 88.5 


Cooke and Wheatstone's first telegraph line, running from London to 
West Drayton, opened for business on July 9, 1839. By 1850, over two 
thousand miles of wire ran the length and breadth of England. While we 
don't have earlier statistics from England to prove that cancer rates first 
began rising between 1840 and 1850, or comparable data from any other 
national government, we do have them for the parish of Fellingsbro, a small 
well-to-do rural district 90 miles west of Stockholm, Sweden. We have 
them because in 1902, Swedish physician Adolf Ekblom, in an effort to 
discover whether cancer rates had really risen during the previous century, 
consulted the “death and burial book” kept by the clergy of Fellingsbro 
parish. These are the numbers that he compiled from that book: 


Years Average yearly cancer mortality 
(Fellingsbro, per 100,000 population) 

1801-1810 2.1 
1811-1820 6.5 
1821-1830 8.1 
1831-1840 3.5 
1841-1850 6.6 
1851-1860 14.0 

2K KK 2K KK 
1885-1894 72.5 
1895-1900 141.0 


The records were incomplete from 1863 to 1884. But the records that 
survive tell the story that we seek. 

The population of Fellingsbro was 4,608 at the beginning of the 
nineteenth century, and 7,104 at the end of it. One person died of cancer 
about every three years between 1801 and 1850. Then, in 1853, the first 
telegraph wire in Sweden was strung between Stockholm, the capital, and 
Uppsala, a city 37 miles north. The following year a line was run 
southwestward from Uppsala, via Vasteras, to Orebro. This line ran right 
through the middle of Fellingsbro parish. At that time the cancer rate in 
Fellingsbro began to rise.'? By the turn of the twentieth century, the country 
folk in Fellingsbro were dying of cancer faster than the average residents of 
London. 


In 1900, annual cancer deaths around the world, per 100,000 population, 
were: 


Switzerland 127 
Holland 92 
Norway 91 
England and Wales 83 
Scotland 79 
Bermuda 75 
Germany 72 
Austria 71 
France 65 
USA 64 
Australia 63 
Ireland 61 
New Zealand 56 
Belgium 56 
Italy 52 
Uruguay 50 
Japan 46 
Spain 39 
Hungary 33 
Cuba 29 
Chile 27 
British Guiana 24 
Portugal 22 
Windward and Leeward Islands 22 
Costa Rica 20 
British Honduras 19 
Jamaica 16 
St. Kitts 13 
Trinidad 12 
Mauritius 12 
Serbia 9 

Ceylon 5.5 
Hong Kong 4.5 


Brazil 4.5 


Guatemala 4 


La Paz, Bolivia 3.4 
Bahamas 1.8 
Fiji 1.7 
New Guinea, Borneo, Java, Sumatra, Philippines, most of non- 
Africa, Macao existent 


Every historical source shows that cancer always accompanied 
electricity. In 1914, among about 63,000 American Indians living on 
reservations, none of which had electricity, there were only two deaths from 
cancer. The cancer mortality in the United States as a whole was 25 times as 
high. 

An unusual one-year rise in cancer mortality of from 3 to 10 percent 
occurred in every modernizing country in 1920 or 1921. This corresponded 
to the beginning of commercial AM radio broadcasting. In 1920, cancer 
deaths rose 8 percent in Norway, 7 percent in South Africa and France, 5 
percent in Sweden, 4 percent in the Netherlands, and 3 percent in the United 
States. In 1921, cancer deaths rose 10 percent in Portugal, 5 percent in 
England, Germany, Belgium, and Uruguay, and 4 percent in Australia. 

Lung cancer, breast cancer, and prostate cancer rates rose spectacularly 
throughout the first half of the twentieth century in every country for which 
we have good data. The number of deaths from breast cancer quintupled in 
Norway, sextupled in the Netherlands, and increased sixteen-fold in the 
United States. Lung cancer deaths increase twenty-fold in England. Prostate 
cancer deaths increased eleven-fold in Switzerland, twelve-fold in 
Australia, and thirteen-fold in England. 

Lung cancer was once so uncommon that it was not even listed 
separately in most countries until 1929. In the few countries that tracked it, 
it did not start its dramatic rise until about 1920. Benjamin Ward 
Richardson, in his 1876 book, Diseases of Modern Life, is surprising to a 
modern reader in this respect. His chapter on “Cancer from Smoking” 
discusses the controversy over whether tobacco smoking caused cancer of 
the lip, tongue, or throat, but cancer of the lung is not even mentioned. 
Lung cancer was still rare in 1913, the year when the American Society for 
the Control of Cancer was founded. Out of 2,641 cases of cancer reported to 


the New York State Institute for the Study of Malignant Disease that year, 
there was only a single case of primary lung cancer. Frederick Hoffman, in 
his exhaustive 1915 book, The Mortality From Cancer Throughout the 
World, asserted as a proven fact that smoking caused cancer of the lips, 
mouth, and throat, but like Richardson four decades previously made no 
mention of lung cancer in connection with smoking.?! 

Swedish researchers Orjan Hallberg and Olle Johansson have shown 
that the rates of lung, breast, and prostate cancer continued to rise, just as 
spectacularly, in the second half of the twentieth century in forty countries, 
along with malignant melanoma and cancers of the bladder and colon—and 
that the overall rate of cancer changed precisely with changes in the 
exposure of the population to radio waves. The rate of increase in cancer 
deaths in Sweden accelerated in 1920, 1955, and 1969, and took a downturn 
in 1978. “In 1920 we got AM radio, in 1955 we got FM radio and TV1, in 
1969-70 we got TV2 and colour TV and in 1978 several of the old AM 
broadcasting transmitters were disrupted,” 





The same authors have focused on FM radio exposure in connection 
with malignant melanoma, following up on the findings of Helen Dolk at 
the London School of Hygiene and Tropical Medicine. In 1995, Dolk and 
her colleagues had shown that the incidence of skin melanoma declined 
with distance from the powerful television and FM radio transmitters at 
Sutton Coldfield in The West Midlands, England. Noting that the FM 
frequency range, 85 to 108 MHz, is close to the resonant frequency of the 
human body, Hallberg and Johansson decided to compare melanoma 
incidence with exposure to FM radio waves for all 565 Swedish counties. 
The results are startling. When melanoma incidence is plotted on a graph 
against the average number of FM transmitters to which a municipality is 
exposed, the points fall on a straight line. Counties that get reception from 
4.5 FM stations have a rate of malignant melanoma that is eleven times as 
high as counties that do not get reception from any FM station. 





N 
Cn 








S 
© 20 
e 
e 
= 15 
8 10 
ec 
o 
S 5 
o 
£ 

0 

0 1 2 3 4 5 
Transmitters 


Figure 4, Hallberg & Johansson 2005 


In their article, “Malignant Melanoma of the Skin—Not a Sunshine 
Story,” they refute the notion that the tremendous increase in this disease 
since 1955 is caused primarily by the sun. No increase in ultraviolet 
radiation due to ozone depletion occurred as early as 1955. Nor, until the 
1960s, did Swedes begin to travel to more southerly countries in large 
numbers to soak up the sun. The embarrassing truth is that rates of 
melanoma on the head and feet hardly rose at all between 1955 and 2008, 
while rates for sun-protected areas in the middle of the body increased by a 
factor of twenty. Most moles and melanomas are now occurring not on the 
head, arms, and feet, but in areas of the body that are not exposed to 
sunshine. 





Figure 15, Hallberg & Johansson 2002a 


Elihu Richter, in Israel, has recently published a report on 47 patients, 
treated at Hebrew University-Hadassah School of Medicine, who developed 
cancer after occupational exposure to high levels of electromagnetic fields 
and/or radio waves.? Many of these people—especially the youngest 
people—developed their cancers within a surprisingly short period of time 
— some as short as five or six months after the beginning of their exposure. 
This dispelled the notion that we must wait ten or twenty years to see the 

effects of cell phones on the world's population. Richter's team warns that 
“with the recent introduction of WiFi into schools, personal computers for 
each pupil in many schools, high frequency voltage transients measured in 


schools—as well as the population-wide use of cellphones, cordless phones, 
some exposure to cellphone towers, residential exposure to RF/MW from 
Smart Meters and other 'smart' electronic equipment at the home and 
possibly also ELF exposures to high power generators and transformers— 
young people are no longer free from exposure to EMF.” 

The range of tumors in Richter’s clinic ran the gamut: leukemias, 
lymphomas, and cancers of the brain, nasopharynx, rectum, colon, testis, 
bone, parotid gland, breast, skin, vertebral column, lung, liver, kidney, 
pituitary gland, pineal gland, prostate, and cheek muscle. 


United States 


Year Cancer deaths (per 100,000 population) 
1850 10.3 
1860 14.7 
1870 22.5 
1880 31.0 
1890 46.9 
1900 60.0 
1910 76.2 
1920 83.4 
1930 98.9 
1940 120.3 
1950 139.8 
1960 149.2 
1970 162.8 
1980 183.9 
1990 203.2 
2000 200.9 
2010 185.9 
2017 183.9 


Figures 5 and 6 show the same linear correspondence between cancer 
and electrification in the forty-eight United States in 1931 and 1940 that 
have already been shown for heart disease and diabetes. 


Percent electrification 1931 


100 


90 


80 


70 


60 


50 


CT 
CA 
e AUC f 
WA PA 46H MI 
= ” w 
er on IN 
DE 
MN 
co 4 l 
f N&s uo ^ 
Po N/ 
p X 
ox Wi “So 
LA TN ND 
/ NC 
NM / sc AL 
AR 
MS 


RNJNY (MA— 
197.4) 
NH 
ME 





30 


40 50 60 70 80 90 100 110 


Rate of Rural Cancer (1931) 
(mortality per 100,000 population) 


Figure 5 — Rate of Rural Cancer in 1931 


Table 4 


120 


130 


140 








% electrification Rural cancer 1931 % electrification Rural cancer 1940 
(1931) (deaths per 100,000) (1940) (deaths per 100,000) 
AL 25.7 42.5 34.7 55 
AZ 62.5 234 56.1 43 
AR 22.1 34.5 273 51 
CA 92.5 93.0 75.6 110 
co 61,5 61.5 56.9 80 
CT 94.9 96.6 90.5 137 
DE 64.4 95.4 66.1 98 
FL 53.8 39.6 50.7 68 
GA 28.4 (missing) 36.5 47 
ID 48.2 39.9 64.5 67 
IL 82.5 108.3 79.4 128 
IN 70.0 104.3 74.9 121 
1A 61.4 89.5 65.5 119 
KS 59.4 79.4 60.2 107 
KY 38.0 (missing) 41.6 67 
LA 34.1 39.2 41.5 61 
ME 715 127.0 70.5 153 
MD 72.3 78.9 65.2 112 
MA 98.5 197.4 91.9 177 
MI 784 108.6 81.3 128 
MN 64.2 85.0 63.4 117 
MS 16.5 46.6 22.7 61 
MO 59.1 83.8 58.3 105 
MT 48.9 51.5 56.8 95 
NE 60.0 76.5 62.1 110 
NV 54.8 63.6 583 116 
NH 86,3 143.1 78.7 181 
NJ 91.7 126.8 87.0 123 
NM 273 27.7 26.5 43 
NY 98.1 131.9 83.9 156 
NC 32.4 41.1 43.7 52 
ND 34.5 514 40.5 9] 
OH 77.0 98.6 82.5 126 
OK 39,2 314 41.3 66 
OR 68.8 78.3 67.7 85 
PA 78.5 88.9 80.4 117 
RI 98.2 124.5 91.0 163 
SC 25.6 36.6 32.1 46 
SD 41.0 60.7 43.0 101 
TN 34.0 44.8 42.1 64 
TX 39.5 48.1 43.5 62 
UT 71.8 37.8 75.2 78 
VT 71.9 (missing) 71.5 146 
VA 41.7 59.0 53.1 72 
WA 78.7 71.3 73.8 110 
WV 41.0 41.8 534 64 
WI 74.7 101.2 54.2 122 
WY 49.5 51.7 50.8 66 





Figure 6 — Rate of Rural Cancer in 1940 


100 


90 cT RI E 


NJ 
NY 


o 
80 pa OM - 
UT "UA Wh 
sp VT ME 
Yo OR 
S ID = MDyyA 
E 60 NE 
eO 
B AZ co mt Ms NV 
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= Vi 
H 50 wyi ^ 
3 
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D Ney sD 
= 40-7 uA UR hs 
D 
P GA x, 
as 39-1 95 
AR 
NM 


MS 





40 50 60 70 80 90 100 110 120 130 140 150 160 170 180 
Rate of rural cancer (1940) 


You may notice that the position of Nevada shifted more than any other 
state between 1931 and 1940. For some reason, deaths from heart disease, 
diabetes, and cancer rose dramatically in Nevada while the rate of 
household electrification rose only modestly. I propose that the construction 
of Hoover Dam, completed in 1936, was that reason. The most powerful 
hydroelectric plant in the world at that time, its one billion watt capacity 
supplied Las Vegas, Los Angeles, and most of Southern California via high 
voltage power lines that coursed through southeastern Nevada on their way 
to their destinations, exposing the surrounding area—where most of the 
population of the state lived—to some of the world’s highest levels of 
electromagnetic fields. In June of 1939 the Los Angeles grid was connected 
to Hoover Dam via a 287,000-volt transmission line, also the most powerful 
in the world at that time.?4 





Power lines from Hoover Dam carry electricity to the Los Angeles area. This photo by Charles 
O'Rear is part of the National Archives digital collection. 


Two types of cancer deserve additional comment: lung cancer and brain 
cancer. 

As the following graph shows, the percentage of adults who smoke has 
declined steadily since 1970 among both men and women. Yet lung cancer 
mortality has almost quadrupled in women, and is virtually the same in men 
as it was fifty years ago.25 









male 
smoking 


40 
60 


female 30 


smoking 


t» 


(uone[ndod appe jo 3u2212d) sao30uis 


25 10 


lung cancer mortality (per 100,000 population) 


s female 
20 mortality 


15 








1970 1980 1990 2000 2010 2013 





Brain tumors deserve mention because, obviously, of cell phones. 
Several billion people in the world are exposing their brains for up to hours 
per day to microwave radiation at point blank range—a new situation that 
began in approximately 1996 or 1997 in most countries. Yet honest data on 
brain tumors are difficult to obtain because special interests have controlled 
most of the research funding on brain tumors since the advent of digital cell 
phones two decades ago. As a result, a media war has pitted the 
independent scientists, who report a tripling to quintupling of brain cancer 
rates among those who have used their cell phones for ten years or more, 
against industry scientists who report no increase in cancer at all. 


The problem, as Australian neurosurgeon Charlie Teo tells those who 
will listen, is that all the data on cell phone usage comes from databanks 
controlled by cell phone providers, and *no telcos have allowed scientists 
access to their records for these large studies." 

I found out firsthand how closely not only the telecom providers, but the 
scientists they fund, guard their data, when I requested access to some of it 
in 2006. Yet another industry-funded study was published, this time in 
Denmark, purporting to show not only that cell phones did not cause brain 
cancer, but that cell phone users even had a lower rate of brain cancer than 
everyone else. In other words, those scientists would have the world believe 
that people might actually protect themselves from brain tumors by holding 
a cell phone to their heads for hours per day. The study, published in the 
Journal of the National Cancer Institute, was titled *Cellular Telephone 
Use and Cancer Risks: Update of a Nationwide Danish Cohort."? It 
claimed to come to its conclusions after an examination of the medical 
records of over 420,000 Danish cell phone users and non-users over a 
period of two decades. It was clear to me that something was wrong with 
the statistics. 

Although the study found a lower rate of brain cancer—in men only— 
among cell phone users than non-users, it found a higher rate of exactly 
those cancers that Swedish scientists Hallberg and Johansson had reported 
to be caused by radio waves: bladder cancer, breast cancer, lung cancer, and 
prostate cancer. The Danish study did not report rates of colon cancer or 
melanoma, the other two types of cancer that the Swedish researchers had 
mentioned. However, the Danish study did additionally find that testicular 
cancer in men was higher and that cervical and kidney cancers in women 
were significantly higher among the cell phone users. I sensed manipulation 
of the data, because the only type of cancer for which a “protective” effect 
was reported was the type of cancer these scientists and their funders were 
trying to convince the public that cell phones did not cause: brain cancer. 

It occurred to me that all of the study’s subjects had actually been using 
cell phones for a long time by the year 2004, when the study ended. The 
only difference between “users” and “non-users” was the date of first 
subscription: the “users” first bought a cell phone between 1982 and 1995, 


while the “non-users” didn’t buy one until after 1995. And all the “users” 
were lumped together. The study did not distinguish between people who 
had used cell phones for 9 years and people who had used them for 22 
years. But according to the study, those who subscribed prior to 1994 
tended to be wealthier, and drank and smoked much less, than those who 
first subscribed later. I suspected that controlling for length of use might 
change the results of the study. So I did the natural, normal, accepted thing 
that scientists do when they wish to validate a study that is published in a 
peer-review journal: I requested to look at their data. On December 18, 
2006, I sent an email to the lead author, Joachim Schüz, telling him that I 
had colleagues in Denmark who would like to look at their data. And on 
January 19, 2007, we were cordially refused permission. The letter of 
refusal was signed by three of the study's six authors: Schüz, Christoffer 
Johansen and Jørgen H. Olsen. 

Meanwhile, Teo is sounding the alarm. “I see 10 to 20 new patients each 
week,” he says, “and at least one third of those patients? tumors are in the 
area of the brain around the ear. As a neurosurgeon I cannot ignore this 
fact.” 

Many if not most of us have one or more acquaintances or family 
members who have, or have died from, a brain tumor. My friend Noel 
Kaufmann, who died in 2012 at the age of 46, never used a cell phone, but 
he did use a home cordless phone for years, which emits the same type of 
radiation, and the tumor that killed him was in the part of his brain beneath 
the ear against which he held that phone. All of us have heard about famous 
people who have died of brain tumors—Senator Ted Kennedy, attorney 
Johnnie Cochran, journalist Robert Novak, Vice President Joe Biden’s son 
Beau. I have in my files, sent to me by the director of the California Brain 
Tumor Association, a list of over three hundred celebrities who either have 
a brain tumor or have died from one during the past decade and a half. 
When I was younger I never heard of any celebrity who had brain cancer. 

Yet highly publicized studies assure us that brain tumor rates are not 
increasing. This is certainly not true, and a little investigation shows why 
the data cannot be trusted, in the United States or anywhere else. In 2007, 
researchers at the Swedish National Board of Health and Welfare found out 


that, for some reason, one-third of the cases of brain cancer diagnosed at 
university hospitals, and the majority of cases at county hospitals, were not 
being reported to the Swedish Cancer Registry? AIl other types of cancer 
were being routinely reported, but not brain cancer. 

A. 1994 study revealed that difficulties in brain cancer reporting were 
already occurring in Finland. Although the Finnish cancer registry was 
complete for most types of cancer, it seriously underreported brain tumors.?? 

Here in the United States, severe problems have been found with 
surveillance not just of brain cancer, but across the board. The Surveillance 
Epidemiology and End Results (SEER) program, run by the National 
Cancer Institute, depends on state registries to deliver accurate data. But the 
data are not accurate. American researcher David Harris reported at a 
conference in Berlin in 2008 that state registries cannot keep up with the 
increasing load of cancer cases because they are not receiving enough 
funding to do so. “SEER registries are currently faced with the challenge of 
collecting more cases in less time with often the same limited resources as 
the previous year," he said. This means that the greater the rise in cancer, 
the less it will be reported, barring an improvement in the American 
economy. 

Even worse has been the deliberate refusal by Veterans Administration 
hospitals and military base medical facilities to report cases to the state 
cancer registries. A report by Bryant Furlow that appeared in The Lancet 
Oncology in 2007 noted *a precipitous decline in VA reporting of new cases 
to California cancer registries beginning in late 2004—from 3,000 cases in 
2003 to almost none by the end of 2005." After inquiring in other states, 
Furlow discovered that California was not an exception. The Florida cancer 
registry had never received any VA case reports, and VA facilities in other 
states were dealing with years of backlogged, unreported cancer cases. 
We've been working with the VA for more than 5 years, but it's just got 
worse," Holly Howe told him. She represents the North American 
Association of Central Cancer Registries. As many as 70,000 cases of 
cancer from the VA were not being reported each year. And in 2007, the VA 
made non-reporting official policy when it issued a directive on cancer 
nullifying all existing agreements between state registries and VA facilities. 


Furlow reported that the Department of Defense was also not cooperating 
with the cancer registries. No cancers diagnosed at military base facilities 
had been reported to any state registries for several years. As a result of all 
these failures, Dennis Deapon of the Los Angeles Cancer Surveillance 
Program warned that studies based on the deficient data may be worthless. 
“Research from the mid-2000’s will forever require an asterisk, or perhaps a 
sticker on the cover, to remind researchers and the public that they are not 
correct,” he said. 

Doctors at the Southern Alberta Cancer Research Institute at the 
University of Calgary were shocked when records showed a 30 percent 
increase in malignant brain tumors in Calgary in the single year between 
2012 and 2013,? despite official government statistics proclaiming no rise 
in malignant brain tumor rates at all in either the province of Alberta or the 
nation of Canada. This discrepancy has lit a fire under Faith Davis, 
professor of epidemiology at the University of Alberta's School of Public 
Health. As unreliable as official statistics are for malignant tumors, they are 
even worse for non-malignant tumors: Canada's surveillance system does 
not record them at all. To remedy this incredible situation, the Brain 
Tumour Foundation of Canada announced in July 2015 that it is raising 
money to help Davis create a national brain tumour registry that will finally 
give clinicians and researchers access to accurate information. 

The studies that are assuring us that all is well with cell phones have 
been funded by the telecommunications industry. But, and in spite of severe 
underreporting of brain tumors, independent scientists are confirming the 
impression of brain surgeons and oncologists that their caseloads are 
increasing, as well as the evident fact that many more people that we all 
know and hear about are dying of such tumors than ever before. 








wo thousand hours of cell phone use, according to 
Hardell, triples one's risk. Two thousand hours on a cordless phone more 
than doubles one's risk. First use of a cell phone before the age of twenty 
increases one's overall risk of brain cancer three-fold, the risk of an 
astrocytoma—the most common type of malignant brain tumor—five-fold, 
and the risk of an astrocytoma on the same side of the head as the phone 
eight-fold. First use of a cordless phone before the age of twenty doubles 
the risk of any brain tumor, quadruples the risk of an astrocytoma, and 
increases the risk of an astrocytoma on the same side of the head eight- 
fold.*: 

The literature on cell towers and radio towers is less compromised. 
Almost all of the existing studies, until recently, have been funded by 
independent sources and not by the telecommunications industry, and they 
have yielded consistent results: living near a transmission tower is 
carcinogenic. 

William Morton, at Oregon Health Sciences University, found that 
living near VHF-TV broadcast antennas was a significant risk for leukemia 
and breast cancer in the Portland-Vancouver metropolitan area from 1967 to 
1982. 

In 1986, the Department of Health of the State of Hawaii found that 
residents of Honolulu who lived in census tracts that had one or more 
broadcast towers had a 43 percent increased risk for all types of cancer.? 

In 1996, Bruce Hocking, an occupational physician in Melbourne, 
analyzed the childhood cancer incidence for nine Australian municipalities 
in relation to a group of three high-power television towers. Children who 
lived closer than four kilometers to the towers were almost two and a half 
times more likely to die of leukemia as children in more distant cities. 

In 1997, Helen Dolk and her colleagues found high rates of adult 
leukemia, bladder cancer, and skin melanoma near the Sutton Coldfield 
tower at the northern edge of Birmingham. 






In 2000, Neil Cherry analyzed the childhood cancer rate in San 
Francisco as a function of distance from Sutro Tower. Sutro Tower is almost 
1,000 feet tall, stands on top of a tall hill, and can be seen from all over San 
Francisco. At the time of Cherry's study it was broadcast- ing nearly one 
million watts of VHF-TV and FM radio signals, plus over 18 million watts 
of UHF-TV. The rates of brain cancer, lymphoma, leukemia, and all cancers 
combined, throughout San Francisco, were related to the distance a child 
lived from that tower. 





In 2004, Ronni and Danny Wolf responded to residents in a small 
neighborhood around a single cell tower in south Netanya, Israel. During 
the five years before the tower was erected, two of the 622 residents had 
developed cancer; during the single year after the tower went up, eight more 
developed cancer. This turned a neighborhood with one of the lowest cancer 
rates in the city into a zone where the risk was more than quadruple the 
average for Netanya. 

In the same year, Horst Eger, a physician in Naila, Germany examined 
1,000 patient records in his home town. He found that people who lived 
within 400 meters (1,300 feet) of a cell tower had triple the risk of 
developing cancer, and developed their cancer, on average, when they were 
eight years younger, compared to people who lived further away. 

In 2011, Adilza Dode headed up a team of university scientists and 
government officials of a metropolis in southeastern Brazil that confirmed 
the results of all the previous studies. The risk of cancer for the residents of 
Belo Horizonte decreased uniformly and steadily with distance from a cell 
tower. 





14. Suspended Animation 


We admonish mankind to observe and distinguish between 
what conduces to health, and what to a long life; for some 
things, though they exhilarate the spirits, strengthen the 
faculties, and prevent diseases, are yet destructive to life, 
and, without sickness, bring on a wasting old age; while 
there are others which prolong life and prevent decay, 
though not to be used without danger to health. 


SIR FRANCIS BACON 


Every animal has allotted to it a constant number of 
heartbeats per lifetime. If it lives fast and furiously like a 
shrew or a mouse, it will use up its quota of heartbeats in a 
much shorter time than if its metabolic personality is a 
more temperate one. 


DONALD R. GRIFFIN 
Listening in the Dark 


IN 1880, GEORGE MILLER BEARD wrote his classic medical book on 
neurasthenia, titled A Practical Treatise on Nervous Exhaustion. He made 
an intriguing observation: “Although these difficulties are not directly fatal, 
and so do not appear in the mortality tables; although, on the contrary, they 
may tend to prolong life and to protect the system against febrile and 
inflammatory disease, yet the amount of suffering that they cause is 
enormous.” In American Nervousness: Its Causes and Consequences, 
written a year later for the general public, he reiterated the paradox: “Side 
by side with this increase of nervousness, and partly as a result of it, 
longevity has increased.” Along with migraine headaches, ringing in the 


ears, mental irritability, insomnia, fatigue, digestive disorders, dehydration, 
muscle and joint pains, heart palpitations, allergies, itching, intolerance of 
foods and medications—in addition to this general degradation in the public 
health, the world was witnessing an increase in the human lifespan. Those 
who were suffering the most tended to look young for their age and to live 
longer than average. 

At the end of American Nervousness appears a map showing the 
approximate geographic reach of neurasthenia. It was the same as the reach 
of railroads and telegraphs, being most prevalent in the northeast where the 
electric tangle was densest. *The telegraph is a cause of nervousness the 
potency of which is little understood,” wrote Beard. “Within but thirty years 
the telegraphs of the world have grown to half a million miles of line, and 
over a million miles of wire—or more than forty times the circuit of the 
globe.” Beard also noticed that a rare disease called diabetes was much 
more common among neurasthenes than in the general population.! 

What Beard—an electrotherapist and a friend of Thomas Edison, who 
was shortly to be diagnosed with diabetes—did not figure out was that the 
growing cloud of electromagnetic energy, which permeated air, water, and 
soil wherever telegraph lines advanced, had something to do with the 
growing numbers of neurasthenes and diabetics that sought his 
ministrations. 





Fasting and an austere diet have been recommended since antiquity for 
the rejuvenation of the body. The prolongation of life, said Francis Bacon, 
should be one of the purposes of medicine, along with the preservation of 
health and the cure of diseases. Sometimes, he added, one must make a 
choice: “The same things which conduce to health do not always conduce 
to longevity.” But he laid down one sure rule, for those who wished to 


follow it, that furthered all three goals of the em E 


Three hundred years later Bacon's third arm of medicine was still sorely 
neglected. “What must one do, or rather what must one not do to attain the 
extreme limits of age?” asked Jean Finot in 1906. “What, after all, are the 
boundaries of life? These two series of questions together constitute a 
special science, gerocomy. It exists in name only.” Observing the animal 
world, Finot saw that the length of adolescence had something to do with 
the length of life. A guinea pig’s period of growth endured seven months; 
that of a rabbit, one year; of a lion, four years, of a camel, eight years, of a 
man, twenty years. Human initiative was misguided, said Finot. What 
conduces to health and vigor does not necessarily prolong life. “The 
education and instruction given to children,” he wrote, “are in flagrant 
contradiction to this law of gerocomy. All of our efforts tend towards the 
rapid advancement of physical and intellectual maturity.” To prolong life, it 
would be necessary to do just the opposite. And one method, he suggested, 
was to restrict one’s diet. 

In the early years of the twentieth century, Russell Chittendon at Yale 
University, who is often called the father of American biochemistry, 
experimented on himself and on volunteers at Yale. Over the course of two 
months he gradually eliminated breakfast, settling into a pattern that 
consisted of a substantial midday meal and a light supper at night. Although 
he was eating less than 40 grams of protein daily, one-third the amount then 
recommended by nutritionists, and only 2,000 calories, he not only suffered 
no ill effects but the rheumatism in his knee disappeared, as did his 
migraine headaches and attacks of indigestion. Rowing a boat left him with 
much less fatigue and muscle soreness than before. His weight dropped to 
125 pounds and remained there. After one year on this diet, with funding 
from the Carnegie Institution and the National Academy of Sciences, he 
formally experimented on volunteers. They were: five professors and 
instructors at Yale; thirteen volunteers from the Hospital Corps of the 
Army; and eight students, “all thoroughly trained athletes, some with 
exceptional records in athletic events.” He restricted them to about 2,000 
calories and no more than fifty grams of protein per day. Without exception 


his subjects' health was as good as before or better at the end of half a year, 
with gains in strength, endurance, and well-being. 

While Chittendon proved nothing about lifespan, the ancient 
recommendations have since been thoroughly subjected to the scientific 
method and, in all species of animals from one-celled organisms on up to 
primates, proven accurate. Provided an animal receives the minimal 
nutrients necessary to maintain health, a severe reduction in calories will 
prolong life. And there is no other method known that will reliably do so. 





THESE RATS ARE BOTH 964 DAYS OLD. 


From: C.M. McKay et al., “Retarded growth, life span, ultimate body size and age changes in the 
albino rat after feeding diets restricted in calories.” Journal of Nutrition 18(1): 1-13 (1939). 


A severe restriction in calories will increase the lifespan of rodents by 
60 percent, routinely producing four and five year old mice and rats. 
Calorie restricted rats are not senile. Quite the opposite: they look younger 
and are more vigorous than other animals their age. If they are female they 
reach sexual maturity very late and produce litters at impossibly old ages.” 

The annual fish Cynolebias adloffi lived three times as long when 
restricted in food.3 A wild population of brook trout doubled their lifespan, 
some trout living twenty-four years when food was scarce.4 

Spiders fed three flies a week instead of eight lived an average 139 days 
instead of 30.5 Underfed water fleas lived 60 days instead of 46.6 
Nematodes, a type of worm, more than doubled their lifespan.” The mollusc 
Patella vulgata lives two and a half years when food is abundant, and up to 
sixteen years when it is not.? 


Cows given half the normal amount of feed each winter lived twenty 
months longer. Their breathing rate was also one-third lower, and their heart 
rate ten beats per minute less.? 

During a twenty-five-year-long study at the Wisconsin National Primate 
Research Center, the death rate of fully-fed adult rhesus monkeys from age- 
related causes was three times the death rate of calorie-restricted animals. 
When the study ended in 2013, twice as many diet-restricted monkeys as 
fully fed monkeys were still alive.!? 





It delays or prevents 
heart disease and kidney disease, and drastically decreases the cancer rate: 
in one study, rats that were fed one-fifth as much food had only seven 
percent as many tumors.” In rhesus monkeys it reduces the cancer rate by 
half, heart disease by half, prevents diabetes, prevents atrophy of the brain, 
and reduces the incidence of endometriosis, fibrosis, amyloidosis, ulcers, 
cataracts, and kidney failure.? Older diet-restricted monkeys have less 
wrinkled skin and fewer age spots, and their hair is less gray. 

A natural human experiment exists. In 1977, there lived 888 people over 
one hundred years old in Japan, the greatest concentration of whom lived on 
the southwestern coast and a few islands. The percentage of centenarians on 
Okinawa was the highest in Japan, forty times higher than in the 
northeastern prefectures. Yasuo Kagawa, professor of biochemistry at Jichi 
Medical School, explained: “People in areas of longevity have a lower 
caloric intake and smaller physique than those in the rest of Japan.” The 
daily diet of school boys and girls in Okinawa was about 60 percent of 
recommended caloric intake. 





The idea that we are each allotted a fixed number of heartbeats is 
ancient. In modern times, Max Rubner at the University of Berlin, in 1908, 


proposed a variation on this idea: instead of a fixed number of heartbeats, 






Most mammals, Rubner calculated, use 
about 200 kilocalories per gram of body weight during their lifetime. For 
humans, assuming a lifespan of ninety years, the value is about 800. If an 
individual is able to delay the use of that amount of energy, his or her life 
will be correspondingly longer. Raymond Pearl, at The Johns Hopkins 
University, published a book along these lines in 1928 titled The Rate of 
Living. 

During 1916 and 1917 Jacques Loeb and John Northrop, at The 
Rockefeller Institute, experimented on fruit flies. Since flies are cold- 
blooded, their metabolism can be slowed merely by lowering the ambient 
temperature. The average duration of life, from egg to death, was 21 days at 
a temperature of 30? C; 39 days at 25? C; 54 days at 20? C; 124 days at 15? 
C; and 178 days at 10? C. The rule that low temperatures prolong life 
applies to all cold-blood animals. 

Another common way animals reduce their metabolism is by 
hibernating. Hibernating species of bats, for example, live on average six 
years longer than species that don't. And bats live far longer than other 
animals their size because, in effect, they hibernate on a daily basis. Bats 
are active, on the wing hunting for dinner, for only a few hours each night. 
They sleep the rest of the time, and sleeping bats are not warm-blooded. *It 
is sometimes possible in the laboratory to keep a rectal thermocouple in 
place while a bat settles down for a nap," wrote bat expert Donald Griffin, 
“and in one such case the body temperature fell in an hour from 40? when 
the bat was active to 1°, which was almost exactly the temperature of the air 
in which it was resting."!? This explains why bats weighing only a quarter 
of an ounce can live more than thirty years, while no laboratory mouse has 
ever lived more than five. 





Food-restricted animals always use less oxygen. A controversy 
arose among gerontologists because food-restricted animals also lose 


weight, and oxygen use per unit weight does not necessarily decline. But it 
declines where it counts. In humans, the internal organs, despite comprising 
less than 10 percent of our weight, are responsible for about 70 percent of 
our resting energy use. And it is our internal organs, not our fat or muscle 
tissues, that determine how long we will live. 


As researchers into the aging process have emphasized, the engine of our 
lives is the electron transport system in the mitochondria of our cells.!^ It is 
there that the oxygen we breathe and the food we eat combine, at a speed 
that determines our rate of living and our lifespan. That speed is in turn 
determined by our body temperature, and by the amount of food we digest. 

But there is a third way to slow our rate of living: by poisoning the 
electron transport chain. One way to do this is to expose it to an 
electromagnetic field. And since the 1840s, at a gradual but accelerating 
rate, we have immersed our world, and all biology, in a thickening fog of 
such fields, that exert forces on the electrons in our mitochondria and slow 
them down. Unlike calorie restriction, this does not promote health. It 
starves our cells not of calories, but of oxygen. Resting metabolic rate does 
not change, but maximum metabolism does. No cell—no brain cell, no 
heart cell, no muscle cell—can work to its capacity. Where calorie 
restriction prevents cancer, diabetes, and heart disease, electromagnetic 
fields promote cancer, diabetes, and heart disease. Where calorie restriction 
promotes well-being, oxygen deprivation promotes headaches, fatigue, 
heart palpitation, “brain fog,” and muscular aches and pains. But both will 
slow overall metabolism and prolong life. 

Industrial electricity in any of its forms always injures. If the injury is 
not too severe, it also prolongs life. 

In an experiment funded by the Atomic Energy Commission, exposure 
to simple electric shock for one hour each day throughout adulthood 
increase the average lifespan of mice by 62 days.!* 

Radio waves also increase lifespan. 

In the late 1960s, a proton accelerator was being built at Los Alamos 
National Laboratory that was going to use radio waves at a frequency of 
800 MHz. As a precaution, forty-eight mice were enrolled in an experiment 


to see if this radiation might be dangerous for workers in the facility. 
Twenty-four of the mice were irradiated at a power level of 43 milliwatts 
per square centimeter for two hours a day, five days a week, for three years. 
This is a huge exposure that is powerful enough to produce internal burns. 
And indeed four of the mice died from burn injuries. A fifth mouse became 
so obese that it could not be extracted from the exposure compartment and 
it died there. But the mice that weren't directly killed by the experiment 
lived a long time—on average, 19 days longer than the unexposed mice.” 

In the late 1950s, Charles Süsskind at the University of California, 
Berkeley received funding from the Air Force to determine the lethal dose 
of microwave radiation in mice, and to investigate its effects on growth and 
longevity. At that time, the Air Force thought that 100 milliwatts per square 
centimeter was a safe dose; Süsskind soon found out that it was not. It 
killed most mice within nine minutes. So after that, Süsskind only exposed 
mice for four and a half minutes at a time. He irradiated one hundred mice 
for 59 weeks, five days per week for four and a half minutes a day at a 
power density of 109 milliwatts per square centimeter. Some of the 
irradiated mice, which subsequently died, developed extraordinarily high 
white blood cell counts, and had enlarge lymphoid tissue and enormous 
liver abscesses. Testicular degeneration occurred in 40 percent of the 
irradiated mice, and 35 percent developed leukemia. However, the 
unirradiated mice, although they were much healthier, did not live as long. 
After 15 months, half the control mice were dead, and only 36 percent of 
the irradiated ones. 

From 1980 to 1982, Chung-Kwang Chou and Arthur William Guy led a 
famous experiment at the University of Washington. They had a contract 
with the United States Air Force to investigate the safety of the early 
warning radar stations recently installed at Beale Air Force Base in 
California, and on Cape Cod in Massachusetts. Known as PAVE PAWS, 
these were the most powerful radar stations in the world, emitting a peak 
effective radiated power of about three billion watts and irradiating millions 
of Americans. The University of Washington team approximated the PAVE 
PAWS signals at a “very low” level, irradiating one hundred rats 21.5 hours 
a day, 7 days a week, for 25 months. The Specific Absorption Rate— 


approximately that of the average cell phone today— was 0.4 watts per 
kilogram. During the two years of the experiment the exposed animals 
developed four times as many malignant tumors as the control animals. But 
they lived, on average, 25 days longer. 

Recently gerontologists at the University of Illinois exposed cell 
cultures of mouse fibroblasts to radio waves (50 MHz, 0.5 watts) for either 
0, 5, 15, or 30 minutes at a time, twice a week. The treatments lowered the 
mortality rate of the cells. The greater the exposure time, the lower the 
mortality, so that the 30-minute exposure reduced cell death by one-third 
after seven days, and increased their average lifespan from 118 days to 138 
days.!? 

Even ionizing radiation—X-rays and gamma rays—will prolong life if 
not too intense. Everything from Paramecia to coddling moths to rats and 
mice to human embryo cells have had their average and/or maximal life 
Spans increased by exposure to ionizing radiation. Even wild chipmunks 
have been captured, irradiated, and released—and had their average 
lifespans thereby extended.!9 Rajindar Sohal and Robert Allen, who 
irradiated house flies at Southern Methodist University, discovered that at 
moderate doses, an increase in lifespan occurred only if the flies were 
placed in compartments small enough so that they could not fly. 





Loren Carlson and Betty Jackson at the University of Washington 
School of Medicine reported that rats exposed daily to moderate doses of 
gamma rays for a year had their lives extended, on average, by 50 percent, 
but suffered a significant increase in tumors. Their oxygen consumption 
was reduced by one-third. 

Egon Lorenz, at the National Cancer Institute, exposed mice to gamma 
rays—one-tenth of a roentgen per eight-hour day—beginning at one month 
of age and for the rest of their lives. The irradiated females lived just as 
long, and the irradiated males one hundred days longer, than the 
unirradiated animals. But the irradiated mice developed many more 


lymphomas, leukemias, and lung, breast, ovarian, and other types of 
cancers. 

Even extremely low doses of radiation will both injure and extend 
lifespan. Mice exposed to only 7 centigrays per year of gamma radiation— 
only 20 times higher than background radiation—had their lives extended 
by an average of 125 days.? Human fibroblasts, exposed in cell culture 
once for only six hours to the same level of gamma rays that is received by 
astronauts in space, or during certain medical exams, lived longer than 
unexposed cells.? Human embryo cells exposed to very low dose X-rays 
for ten hours a day had their lifespans increased by 14 to 35 percent, 
although most of the cells also suffered several kinds of damage to their 
chromosomes.?? 

Modern medicine can take some but not all of the credit for the modern 
increase in the average human lifespan. For that increase began a century 
before the discovery of antibiotics, in a time when doctors still bled their 
patients and dosed them with medicines containing lead, mercury, and 
arsenic. But medicine can take none of the credit for the modern extension 
of the maximum human life span. For medicine still does not pretend to 
understand the aging process, and only a tiny minority of doctors are even 
beginning to try to do anything to reverse aging. Yet the maximum age at 
death, worldwide, has been steadily rising. 





Maximum age 





1860 1880 ^ 1900 1920 1940 1960 1980 2000 
Year of death 


Figure 1, Wilmoth et al. 2000 





In 1994, Väinö Kannisto, former United Nations advisor on 
demographic and social statistics, showed that the number of people living 
more than one hundred years was increasing spectacularly in the twenty- 
eight countries for which good data existed. The number of centenarians in 
Sweden had risen from 46 in 1950 to 579 in 1990. During the same period, 
the number of centenarians had risen from 17 to 325 in Denmark; from 4 to 
141 in Finland; from 265 to 4,042 in England and Wales; from 198 to 3,853 
in France; from 53 to 2,528 in West Germany; from 104 to 2,047 in Italy; 
from 126 to 3,126 in Japan; from 14 to 196 in New Zealand. The number of 
centenarians in all these countries, roughly doubling every ten years, had far 
outraced the increase in population. 

Even in Okinawa, long known for its longevity, there lived only a single 
person over one hundred years old as late as 1960. In Japan as a whole, 
noted Kagawa in 1978, the number of male centenarians had quadrupled in 
only 25 years, while the number of female centenarians had sextupled. And 
yet he observed, in middle-aged Japanese, almost a doubling in the rates of 
breast cancer and colon cancer, a tripling of lung cancer, a 40 percent rise in 


heart disease, and an 80 percent rise in diabetes: *extended life expectancy 
but increased diseases." 





15. You mean you can hear electricity? 


IN 1962, A LOCAL WOMAN contacted the University of California, Santa 
Barbara for help tracking down a mysterious noise. She had moved into a 
newly-built home in a quiet neighborhood and this noise, whose location 
she could not find, was accompanying her wherever she went like an 
unwanted ghost. It was impairing her health, keeping her awake, and 
forcing her, in desperation, to abandon her home for large periods of time 
just to get relief. In response to her plea for help, an engineer showed up at 
her house with a load of electronic equipment. 

Clarence Wieske, who was with the Laboratory for the Study of Sensory 
Systems in Tucson, a military contractor that was working on the interface 
between man and machine, happened to be involved with a project at the 
University at Santa Barbara when the woman's call came. His initial 
intention was to look for electric fields on her property that might be setting 
some metal object into vibration, creating the noise that was bothering her. 
He was startled by what he found. 





In a further experiment Wieske, without telling the woman, connected a 
low-power frequency generator to the water pipe about one hundred feet 
from her house. She remarked that there was peculiar noise “like a barking 
dog." When Wieske turned on the pickup equipment in her house and put 
on the headphones, he found that she was correct. He heard a sound like a 
barking dog! 





nd that the noise was 
not coming from her dental fillings. Wieske then set about to try to alleviate 
her problem. Electrically grounding her refrigerator, freezer case, door 
chimes, and other appliances reduced the noise level a bit but did not get rid 
of it. One day, during a power outage, she telephoned Wieske, ecstatic. The 
noise had stopped! But it returned as soon as the power came back on. 
Therefore Wieske contacted all the utility companies. With their 
cooperation, he put filters on her phone line, an isolation transformer on her 
electric line, and sections of non-conducting pipe into her water line and her 
gas line. These time-consuming, expensive measures prevented unwanted 
electric frequencies originating elsewhere in the neighborhood from being 
conducted over these paths. Finally, the noise was reduced to an endurable 
level and the woman could inhabit her home. 

After investigating a number of similar cases, Wieske predicted that 
with the continued electrification of society, complaints like hers would one 
day be common. His article about his experiences, published in Biomedical 
Sciences Instrumentation in 1963, concluded with a technical description of 
human hearing, including all of the places within the ear where 
electromagnetic fields might cause electric currents to flow. He speculated 
as to the reasons some people can hear them and not others: *If the nerve 
for some reason in some individuals is not as well insulated from these 
currents as in the normal individual, or 
from these currents in some individuals, perhaps this could make them 
sensitive to these electrical fields." 


Wieske's prediction has come to pass. Today companies serving the 
population that can feel and hear electromagnetic fields form a significant 
cottage industry in every part of the United States. One organization, the 
International Institute for Building Biology and Ecology, lists sixty 
consultants, scattered throughout the United States and Canada, that it has 
trained in the methods of detecting and mitigating residential 
electromagnetic pollution. 





he clues to what is happening were planted over two centuries 


ago. 

French electrotherapist Jean Baptiste Le Roy, in 1755, was apparently 
the first to elicit an auditory response to static electricity. He was treating a 
man blind from cataracts by winding wire around the man’s head and 
giving him twelve shocks from a Leyden jar. The man reported hearing the 
explosion of “twelve pieces of cannon.” 

Experimentation began in earnest when Alessandro Volta invented the 
electric battery in 1800. The metals he first used, silver and zinc, with salt 
water for an electrolyte, generated about a volt per pair—less when he 
stacked them up in his original “pile.” Applying a single pair of metals to 
his own tongue produced either a sour or sharp taste, depending on the 
direction of the current. Applying a piece of silver to his eye, and touching 
it with a piece of zinc held in his moistened hand, produced a flash of light 
—a flash, he said, that was “much more beautiful” if he placed the second 
piece of metal, or both pieces, inside his mouth. 

Stimulating the sense of hearing proved more difficult. Volta tried in 
vain to elicit a noise with only a single pair of metal plates. But with thirty 


pairs, roughly equivalent to a twenty-volt battery, he succeeded. “I 
introduced, a considerable way into both ears,” he wrote, “two probes or 
metallic rods with their ends rounded, and I made them to communicate 
immediately with both extremities of the apparatus. At the moment when 
the circle was thus completed I received a shock in the head, and some 
moments after (the communication continuing without any interruption) I 
began to hear a sound, or rather noise, in the ear, which I cannot well 
define: it was a kind of crackling with shocks, as if some paste or tenacious 
matter had been boiling.” Being afraid of permanent injury to his brain, 
Volta did not repeat the attempt. 

But hundreds of other people did. After this report by one of the most 
famous men in the world, everyone wanted to see if they could hear 
electricity. Carl Johann Grapengiesser, a physician, was careful to use only 
small currents on his patients, and he was a much more careful observer 
than Volta. His subjects varied widely in their sensitivity and in the sounds 
they heard. “The noises, in respect of their quality and strength, are very 
variable,” he wrote. “Most often, it seems to the patient that he hears the 
hissing of a boiling teakettle; another hears ringing and bell-pealing, a third 
thinks that outside a storm wind blows; to a fourth it seems that in each ear 
a nightingale sings most lustily.”! 





Physicist Johann Ritter was not afraid of currents much greater than 
those risked by Volta. Using batteries containing 100, 200, and more pairs 
of metals, he was able to hear a pure musical tone that was approximately g 
above middle c, and that persisted as long as the current flowed through his 
ears. 

Many were the doctors and scientists who, in the heady years following 
Volta’s gift to the world of its first reliable source of steady electricity, 
stimulated the acoustic nerve with greater or lesser quantities of current. 
The following list, limited to German scientists who published their 
research, was compiled by Rudolf Brenner in 1868: 


Carl Johann Christian Grapengiesser (Attempts to Use 
Galvanism in the Healing of Some Diseases, 1801) 


Johann Wilhelm Ritter (Contributions to the Recent 
Knowledge of Galvanism and the Results of 
Research, 1802) 

Friedrich Ludwig Augustin (Attempt at a Complete 
Systematic History of Galvanic Electricity and its 
Medical Use, 1801; On Galvanism and its Medical 
Use, 1801) 

Johann Friedrich Alexander Merzdorff (Treatment of 
Tinnitus with the Galvanic Current, 1801) 

Carl Eduard Flies (Experiments of Dr. Flies, 1801) 

Christoph Friedrich Hellwag (Experiments on the 
Healing Powers of Galvanism, and Observations on 
its Chemical and Physiological Effects, 1802) 

Christian August Struve (System of Medical Electricity 
with Attention to Galvanism, 1802) 

Christian Heinrich Wolke (Report on Deaf and Dumb 
Blessed by the Galvani-Voltaic Hearing-Giving Art 
at Jever and on Sprenger s Method of Treating Them 
with Voltaic Electricity, 1802) 

Johann Justus Anton Sprenger (Method of Using 
Galvani-Voltaic Metal-Electricity as a Remedy for 
Deafness and Hearing Loss, 1802) 

Franz Heinrich Martens (Complete Instructions on the 
Therapeutic Use of Galvanism; Together with a 
History of This Remedy, 1803) 


Ironically, the man who laid the foundation for such research— 
Alessandro Volta—was also the man whose mechanistic world view has so 
dominated scientific thinking for more than two centuries that it has not 
been possible to understand the results of these experiments. They have 
been regarded as little more than parlor tricks, when they have been 
remembered at all. 





By Brenner's time the work of all these early scientists had already been 
forgotten. A physician who specialized in diseases of the ear, he described 
this state of affairs in terms that could just as easily apply to today: 
"Nothing can be more instructive for the history of scientific development 
than the fate of the old experiments on galvanic stimulation of the acoustic 
nerve. Among contemporary researchers who deny the possibility of such 
stimulation are names of the very best repute. One must therefore ask: do 
these men really believe that Volta, Ritter, and the other old galvanists only 
imagined the tones and noises they heard?" Brenner's goal was to establish, 
once and for all, not only that electicity could be heard, but exactly how, 
why, and to what degree this occurs. "It is not established if, and it is 
unknown how the acoustic nerve reacts to the influence of electrical 
current," he wrote.? The results of his experiments filled a 264-page book. 
His apparatus contained 20 zinc-copper Daniell cells, each producing a 
maximum of about one volt, connected to a rheostat that could be adjusted 
to any of 120 positions. Any desired number of cells could be inserted into 
the circuit at the turn of a dial. He performed 47 different kinds of 
experiments on a large number of individuals. 

The average person, with 7 volts of direct current coursing through his 
or her ear canal, heard a clear metallic sound resembling a small dinner bell. 
The range of sensitivity of normal human beings, however, was enormous. 
Some heard nothing at all, even when all twenty Daniell cells were in the 
circuit. For others, who were deemed to have “acoustic nerve 
hyperaesthesia," the sound from only one cell was intense. Some heard 
nothing unless their ear canal was filled with salt water, which helped 
conduct the electricity. Others, their ear canals dry, heard the ringing bell 
when the knob-shaped electrode was simply placed on the cheek in front of 
the ear, or on the mastoid process, the bony protrusion behind the ear. 





This was elevated to “distant wagon roll,” 
then to “cannon roll,” “striking of a metal plate,” and finally the “ringing of 
a silver dinner bell,” as the current was gradually raised. The greater the 


current, the purer the tone, and the greater the resemblance to a bell. When 
Brenner asked his subjects to sing the tone they heard, some, agreeing with 
Ritter's report of 1802, heard a g above middle c. Others disagreed. But 
although the threshold of perception varied enormously, and the quality and 
exact pitch were different for everyone, each individual always heard the 
same thing. They always heard the identical sound and pitch, and had the 
same threshold, whenever they were tested, even at intervals years apart. 

After experimenting with different placements of the second, non-ear 
electrode on the skull, neck, torso, arms, and legs, Brenner became 
convinced that a sound was heard only when the inner ear was in the path of 
the current, and that direct stimulation of the acoustic nerve was the cause 
of the sensation of sound. 

American physician Sinclair Tousey, one of the last electrotherapists of 
the old school, wrote about electricity and the ear in the third edition of his 
textbook on Medical Electricity, published in 1921. Brenner's results with 
direct current, completely forgotten today, were still at that time taught, 
accepted, and verified by every electrical practitioner. 





The range of sensitivity was extraordinary. “Many individuals,” wrote 
Tousey, closely echoing Brenner’s words, “give no reactions whatever.” In 
others, the sound was so loud that the person was deemed to have “a 
distinct hyperesthesia of the auditory nerve."? 

With the disappearance of the electrotherapist's art and the dwindling of 
opportunities for the average physician to become familiar with the auditory 
response to electricity, the old knowledge was again almost forgotten. 





Nevertheless, the experiments of the radio engineers spawned a spate of 
genuine efforts by biologists to stimulate the inner ear with alternating 
current. This was typically done after the manner of Brenner—by inserting 
one electrode in the ear canal, which was first filled with salt water, and 
completing the circuit with a second electrode on the back of the forearm or 
hand. The subjects most often heard a tone that corresponded in pitch to the 
frequency of the applied current. The sensitivity of the subjects, as before, 
varied tremendously. In experiments done in Leningrad, the most sensitive 
individual, when tested with a current of 1,000 cycles per second, heard a 
sound as soon as the voltage exceeded a fifth of a volt; the least sensitive 
subject required six volts—a thirty-fold difference in sensitivity. There was 
nothing wrong with the hearing of any of these people. The variations in 
their ability to hear electricity bore no relation to the subjects’ ability to 
hear ordinary sound.° 

In 1936, Stanley Smith Stevens, an experimental psychologist at 
Harvard University, gave the hearing phenomenon a new name: 
"electrophonic hearing." Four years later, at his newly-created Psycho- 
Acoustics Laboratory, he proposed three different mechanisms of hearing 
by electrical stimulation. Most people with normal hearing, when 
stimulated by an electrode in their ear, heard a pitch that was exactly one 
octave higher than the frequency of the applied current. However, if a 
negative DC voltage was applied at the same time, they heard the 
fundamental frequency as well. His knowledge of physics led Stevens to 
conclude that the ear was responding like a condenser receiver, with the ear 
drum and the opposite wall of the middle ear being the vibrating “plates” of 
that condenser. 

People without ear drums, however, heard either the fundamental 
frequency or a *buzzing" noise, or both. None heard the higher octave. And 
as Brenner had also reported, eardrumless ears were much more sensitive to 
electricity than normal ears. One of Stevens' subjects heard a pure tone 
when stimulated with only one-twentieth of a volt. Stevens proposed that 
the hearing of the fundamental frequency was caused by direct stimulation 
of the hair cells of the inner ear. For those that heard a buzzing sound, he 
proposed that the auditory nerve was being stimulated directly. 





In 1960, biologist Allan Frey introduced yet another method of hearing 
electromagnetic energy, this time without placing electrodes on the body. A 
radar technician at Syracuse, New York swore to him that he could “hear” 
radar. Taking him at his word, Frey accompanied the man back to the 
Syracuse facility and found that he could hear it too. Frey was soon 
publishing papers about the effect, proving that even animals, and people 
with conduction deafness—but not nerve deafness—could hear brief pulses 
of microwave radiation at extremely low levels of average power. 

attracted a fair amount of 
publicity, but is probably not responsible for most of the sounds that 
torment so many people today. 

However, the 1960s would bring still more surprises. Renewed research 
into electrophonic hearing had both civilian and military goals. The medical 
community wanted to see if the deaf could be made to hear. The military 
community wanted to see if a new method of communication could be 
devised for soldiers or astronauts. 

In 1963, Gerhard Salomon and Arnold Starr, in Copenhagen, proved 
that 
They placed electrodes directly adjacent to the 
cochlea in two patients who had had surgical reconstruction of their middle 
ear. One patient heard “clicks” or “cracklings” when stimulated by only 
three microamperes (millionths of an ampere) of direct current. The second 
patient required 35 microamperes to hear the same sound. As the current 
was gradually increased, the clicks changed to “walking on dry snow” or 
the rush of “blowing air.” Alternating current elicited pure tones whose 





pitch matched the applied frequency, but this required about a thousand 
times more current. 

Then the Electromagnetic Warfare and Communication Laboratory at 
Wright-Patterson Air Force Base in Ohio published a report written by Alan 
Bredon of Spacelabs, Inc., investigating both electrophonic hearing and 
microwave hearing for their potential use in space. The goal was to develop 
“an efficient, dual-purpose transducer which can be worn with an absolute 
minimum of discomfort during long missions in the confines of pressure 
clothing and aerospace environments.” Bredon found that electrophonic 
devices were unsuitable because the sound they produced was too faint to 
be useful in the noisy environment of aircraft or space vehicles. And 
microwave hearing was judged useless because it appeared to depend on 
short pulses of energy and did not produce continuous sound. But Patrick 
Flanagan’s Neurophone, which had been recently publicized in Life 
magazine,’ caught Bredon’s interest. This device, which Flanagan claimed 
to have invented at the age of 15, was a radio wave device almost identical 
to the one Eichhorn had patented in 1927, and appeared to work by skin 
vibration. It differed, however, in one crucial respect: Flanagan used a 
carrier frequency in the ultrasonic range, specified as being between 20,000 
and 200,000 Hz. He had rediscovered the phenomenon that Stevens had 
briefly described back in 1937 and never followed up on. 

As a further result of the publicity surrounding Flanagan’s invention, 
Henry Puharich, a physician, and Joseph Lawrence, a dentist, under 
contract with the Air Force, investigated what they called “transdermal 
electrostimulation.” They delivered electromagnetic energy at ultrasonic 
frequencies via electrodes placed next to the ear. The audio signal, added to 
the ultrasonic carrier, was somehow demodulated by the body and heard 
like any other sound. Like Flanagan’s device, it appeared at first glance to 
work by skin vibration. However, several astonishing results were reported. 





Some even heard a true pitch as high as 25,000 


cycles per second— 5,000 cycles higher than most human beings are 
supposed to be able to hear. 

Second, the use of an ultrasonic carrier wave eliminated distortion. 
When the audio signal was fed directly into the electrodes without the 
carrier wave, speech could not be understood and music was 
unrecognizable. But when the speech or music was delivered only as a 
modulation to a high frequency carrier wave—in the same way that AM 
radio broadcasts deliver speech and music—the body, like a radio receiver, 
somehow decoded the signal and the person heard the speech or music 
perfectly without any distortion. The optimal carrier frequency, delivering 
the purest sound, was found to be between 30,000 and 40,000 Hz. 

Third, and most surprising, nine out of nine deaf people—even those 
with profound sensorineural deafness from birth—could hear sound in this 
way by transdermal stimulation. But the electrodes had to be pressed more 
firmly on the skin, and the deaf subject had to move the electrode around 
beneath or in front of the ear until he or she located the exact spot that 
stimulated hearing—as though the signal had to be focused on a target 
inside the head. The four subjects with residual hearing described the 
sensation as “sound,” not “vibration.” The two who were deaf from birth 
described it as something “new and intense.” The three who had acquired 
total deafness described it as hearing as they remembered it. 

When insulated electrodes were used, people with normal hearing 
responded to power levels as low as 100 microwatts (millionths of a watt). 
When bare metal electrodes were pressed directly against the skin, more 
current was required, but the deaf could hear as well or better, with this 
method, than hearing people. Once the proper skin pressure and location 
were found, the threshold electromagnetic stimulus was between one and 
ten milliwatts (thousandths of a watt) for both hearing and deaf people, 
while only the slightest increase in power brought the sound, as described 
by one of the deaf subjects, “from a comfortable level to one of great 
force.” 

Even more amazingly, ten out of ten profoundly deaf subjects, who had 
never heard speech before, were able to understand words, after very brief 
training, when delivered in this manner. And patients who had lesser 


sensorineural hearing loss, who could identify only 40 to 50 percent of 
words spoken through the air, scored 90 percent or better by transdermal 
stimulation, without training. 

For the first time in fifty years, there was evidence that an electrode 
carrying radio waves to the skin might be doing something more than just 
causing the skin to vibrate. These researchers speculated, based on 
measurements of cochlear microphonics (electrical signals generated by the 
inner ear), that transdermal stimulation produced a sound by a combination 
of acoustic and electrical effects—by both vibrating the skin and directly 
stimulating the hair cells in the inner ear. “However,” they wrote, “these 
two effects do not give a satisfactory explanation of word recognition 
response in those patients whose cochlea is non-functional.” 

The results of animal experiments were just as astonishing. Two dogs 
were rendered deaf—one through injections of streptomycin, which 
destroyed the cochlear hair cells, and one by surgical removal of the ear 
drums, middle ear bones, and cochleas. Both dogs had previously been 
conditioned to respond to transdermal stimulation by jumping over a 
divider in a box, and both had learned to respond correctly better than 90 
percent of the time. Incredibly, both dogs continued to respond correctly 90 
percent of the time to the high frequency stimulus when it was modulated 
with the audio signal, but only 1 percent of the time to the unmodulated 
high frequency signal alone. 

The implications of this research are profound. Since people and 
animals without any cochlear function at all, or even without any cochlea, 
can apparently hear this type of stimulation, either the brain is being 
stimulated directly—which is unlikely since the source of the sound always 
appears to the person to be coming from the direction of the electrode 
producing it—or there is another part of the inner ear besides the cochlea 
that responds to ultrasound, or to electromagnetic waves at ultrasonic 
frequencies. Since most hearing subjects were able to hear much higher 
frequencies than they could hear in the normal way, this is the most likely 
explanation. And we will see that there are good reasons to believe that 
most people who are bothered by electrical “tinnitus” are hearing 
electrically-delivered ultrasound. 


Puharich and Lawrence patented their device, and the Army acquired 
two prototype units for testing aboard Chinook helicopters and airboats 
used in Vietnam. The news editor for Electronic Design reported, after 
trying out one of the devices, that “the signals were almost, but not quite, 
like airborne sounds."? 

In 1968, Garland Frederick Skinner repeated some of Puharich and 
Lawrence's experiments at higher power, using a carrier frequency of 100 
kHz, for his master’s thesis at the Naval Postgraduate School. He did not 
test his “Trans-Derma-Phone” on any deaf people, but like Puharich and 
Lawrence, he concluded that “be it the ear, the nerves, or the brain, an AM 
detection mechanism exists.” 

In 1970, Michael S. Hoshiko, under a post-doctoral fellowship from the 
National Institutes of Health, tested the device of Puharich and Lawrence at 
the Neurocommunications Laboratory at The Johns Hopkins University’s 
School of Medicine. Subjects not only heard pure tones from 30 Hz up to 
the remarkable frequency of 20,000 Hz equally well at low sound levels, 
but scored 94 percent in speech discrimination. The twenty-nine college 
students who were tested performed equally well whether the words were 
delivered through the air as ordinary sounds, or whether they were 
delivered electronically as modulations to a radio wave in the ultrasonic 
range. 

Two more efforts to make people hear modulated radio waves were 
made by members of the military, but probably because they did not use 
ultrasonic frequencies they were unable to identify any cause of hearing 
besides the vibrating skin. One of the reports, a master’s thesis submitted by 
Lieutenants William Harvey and James Hamilton to the Air Force Institute 
of Technology at Wright-Patterson Air Force Base, specified a carrier 
frequency of 3.5 MHz. The other project was undertaken by M. 
Salmansohn, Command and Control Division at the Naval Air 
Development Center in Johnsville, Pennsylvania. He also did not use an 
ultrasonic carrier, in fact he later dispensed with the carrier wave altogether 
and used direct audio-frequency current. 

Finally, in 1971, Patrick Woodruff Johnson, for his master’s thesis at the 
Naval Postgraduate School, decided to revisit “ordinary” electrophonic 


hearing. He wanted to see how little electricity it took to make people hear a 
sound. Most previous researchers had exposed their subjects’ heads to up to 
one watt of power, resulting in large and potentially dangerous levels of AC 
current. Johnson found that by using a silver disc plated with silver chloride 
as one of the electrodes, and simultaneously applying a positive direct 
current, an alternating current of as little as 2 microamperes (millionths of 
an ampere), delivered with only 2 microwatts (millionths of a watt) of 
power, could be heard. Johnson proposed that “an extremely small low cost 
hearing aid” could be developed using this system. 

In June 1971, at M.I.T., Edwin Charles Moxon reviewed the entire field 
for his Ph.D. dissertation and added the results of his own experiments on 
cats. By recording the activity of the cats’ auditory nerves while their 
cochleas were electrically stimulated, he proved definitely that two distinct 
phenomena were occurring at the same time. The electrical signal was 
somehow being converted into ordinary sound, which was being processed 
by the cochlea in the normal way. And in addition, the current itself was 
stimulating the auditory nerve directly, producing a second, abnormal 
component of the discharge pattern of the nerve. 

At this point efforts at understanding how electricity affects the normal 
ear ceased, as practically all funding was diverted to the development of 
cochlear implants for the deaf. This was a natural outcome of the 
development of computers, which were beginning to transform our world. 
The brain was being modeled as a fantastically elaborate digital computer. 
Hearing researchers thought that if they separated sounds into their different 
frequency components, they could feed those components in digital pulses 
to the appropriate fibers of the auditory nerve for direct processing by the 
brain. And, considering they are stimulating thirty thousand nerve fibers 
with only eight to twenty electrodes, they have been remarkably successful. 





qn research into microwave hearing continued for another 


decade or so, and then ceased as well. The peak power levels that appear to 
be required for microwave hearing make it unlikely to be the source of 
sounds that bother most people today. The phenomenon discovered by 
Puharich and Lawrence is a much more likely candidate. To understand 
why requires an excursion into the anatomy of one of the most complex and 
least understood parts of the body. 


The Electromodel of the Ear 

In the normal ear, the ear drum receives sound and passes the vibrations on 
to three tiny bones in the middle ear. They are the malleus, incus, and stapes 
(hammer, anvil, and stirrup), named after the implements they resemble. 
The stapes, the last bone in the chain, although only half the size of a grain 
of rice, funnels the world of vibrational sound to the bony cochlea, a snail- 
shaped structure which itself is a marvel of miniaturization. 





o this day no one 
knows exactly how this is accomplished. And what little is known is 
probably wrong. 

“Tt is unfortunate,” wrote Augustus Pohlman, an anatomy professor and 
dean of the school of medicine at the University of South Dakota, “that no 
machinery is available for deleting from the literature those interpretations 
which have proven to be incorrect.” Pohlman stood, in 1933, looking back 
on seventy years of research that had failed to eradicate what he regarded as 
a fundamentally flawed assumption about the operation of the liquid-filled 
cochlea. Another eighty years have still failed to eradicate it. 

The tiny cochlear spiral is divided along its length into an upper and 
lower chamber by a partition called the basilar membrane. Upon this 
membrane sits the organ of Corti, containing thousands of hair cells with 
their attached nerve fibers. And in 1863, the great German physicist 
Hermann Helmholtz had proposed that the cochlea was a sort of an 
underwater piano, and suggested that the ear’s resonant “strings” were the 


different length fibers of the basilar membrane. The membrane increases in 
width as it winds round the cochlea. The longest fibers at the apex, he 
suggested, like the long bass strings of a piano, resonate with the deepest 
tones, while the shortest fibers at the base are set into vibration by the 
highest tones. 

Helmholtz assumed that the transmission of sound was a simple matter 
of mechanics and levers, and subsequent research, for one and a half 
centuries, has simply built upon his original theory with remarkably little 
change. According to this model, the motion of the stapes, like a tiny piston, 
pumps the fluid in the two compartments of the cochlea back and forth, 
causing the membrane separating them to flex up and down, thereby 
stimulating the hair cells on top of it to send nerve impulses to the brain. 
Only those parts of the membrane that are tuned to the incoming sounds 
flex, and only those hair cells sitting on those parts send signals to the brain. 

But this model does not explain the hearing of electricity. It also fails to 
explain some of the most obvious features of the inner ear. Why, for 
example, is the cochlea shaped like a snail shell? Why are the thousands of 
hair cells lined up in four perfectly spaced rows, one behind the other like 
the keyboards of a pipe organ? Why is the cochlea encased in the hardest 
bone of the human body, the otic capsule? Why is the cochlea the precise 
size that it is, fully formed in the womb at six months of gestation, never to 
grow any larger? Why is the cochlea only marginally bigger in a whale than 
in a mouse? How is it possible to fit a full set of resonators, vibrating over a 
greater musical range than the largest pipe organ, into a space no bigger 
than the tip of your little finger? 

Pohlman thought that the standard model of the ear was contradicted by 
modern physics, and a number of courageous scientists after him have 
agreed. By including electricity in their model of hearing, they have made 
progress in explaining the basic features of the ear. But they are up against a 
cultural barrier, which still does not permit electricity to play a fundamental 
role in biology. 

The ear is much too sensitive to work by a system of mechanics and 
levers, and Pohlman was the first to point out this obvious fact. The real 
resonators in the ear—the “piano strings”—had to be the thousands of hair 


cells, lined up in rows and graded in size from bottom to top of the cochlea, 
and not the fibers of the membrane they were sitting on. And the hair cells 
had to be pressure sensors, not motion detectors. The extreme sensitivity of 
the ear made that evident. This also explained why the cochlea is embedded 
in the densest bone in the human body. It is a soundproof chamber, and the 
function of the ear is to transmit sound, not motion, to the delicate hair 
cells. 

The next scientist to add pieces to the puzzle was an English physician 
and biochemist, Lionel Naftalin, who passed away in March 2011 at the age 
of 96 after working on the problem for half a century. He began by making 
precise calculations that proved conclusively that the ear is much too 
sensitive to work in the accepted fashion. It is a known fact that the quietest 
sound that a person can hear has an energy of less than 10-6 watts (one ten- 
thousandth of one trillionth of a watt) per square centimeter, which, 
calculated Naftalin, produces a pressure on the eardrum that is only slightly 
greater than the pressure exerted by randomly moving air molecules. 
Naftalin stated flatly that the accepted theory of hearing was impossible. 
Such tiny energies could not move the basilar membrane. They could not 
even move the bones of the middle ear by the assumed lever mechanism. 

The absurdity of the standard theory was obvious. At the threshold of 
hearing the eardrum is said to vibrate through a distance (0.1 ángstrom) that 
is only one-tenth the diameter of a hydrogen atom. And the motion of the 
basilar membrane is calculated to be as small as ten trillionths of a 
centimeter—only slightly larger than the diameter of an atomic nucleus, and 
much smaller than the random motions of the molecules that make up the 
membrane. This *movement" of subatomic dimensions supposedly causes 
the hairs on the hair cells to “bend,” triggering an electric depolarization of 
the hair cells and the firing of the attached nerve fibers. 

Recently some scientists, realizing the foolishness of such a notion, have 
introduced various ad hoc assumptions that increase the distance the basilar 
membrane must move from subatomic to only atomic dimensions—which 
still doesn't overcome the fundamental problem. Naftalin pointed out that 
the contents of the cochlea are not solid metal objects but liquids, gels, and 
flexible membranes, and that such infinitessimal distances could have no 


basis in physical reality. He then calculated that to move a resonant portion 
of the basilar membrane only one ángstrom—about the distance now 
claimed necessary to trigger a response from the hair cells?—would require 
over ten thousand times more energy than is contained in a threshold sound 
wave that hits the ear drum. 

During his fifty years of work on hearing, Naftalin thoroughly 
demolished the prevailing mechanical theory and created a model in which 
electrical forces are central. Instead of focusing on the basilar membrane, 
on which the hair cells sit, he drew his attention to a much more unusual 
membrane—the one that covers the tops of the hair cells. It has a jelly-like 
consistency and composition that occurs nowhere else in the human body. It 
also has unusual electrical properties, and a large voltage is always present 
across it. Elsewhere in the body, voltages of this magnitude—about 100 to 
120 millivolts—are usually found only across cell membranes. 

In 1965, Naftalin, thinking in terms of solid state physics, postulated 
that this membrane—called the tectorial membrane—is a semiconductor 
that is also piezoelectric. Piezoelectric substances, we recall, are those that 
convert mechanical pressure into electrical voltages, and vice versa. Quartz 
crystals are the most familiar example. Often used in radio receivers, they 
convert electrical vibrations into sound vibrations. Judging by its structure 
and chemical composition, Naftalin suggested that the tectorial membrane 
ought to have this property. He proposed that it is a piezoelectric liquid 
crystal that converts sound waves into electrical signals, which it 
communicates to the hair cell resonators embedded in it. He suggested that 
the large voltage across the membrane causes great amplification of these 
signals. 

Naftalin then built scale models of both the cochlea and the tectorial 
membrane, and began to find answers to some of the outstanding mysteries 
of the ear. He discovered that the snail-like shape of the cochlea is 
important to its function as a precision musical instrument. He also 
discovered that the makeup of the tectorial membrane has something to do 
with the instrument’s small size. While the speed of sound in air is 330 
meters per second, and in water is 1500 meters per second, in ten percent 
gelatin it is only 5 meters per second, and in the tectorial membrane it is 





George Offutt came to this problem as a marine biologist, and reached 
similar conclusions from an evolutionary perspective. His doctoral 
dissertation at the University of Rhode Island's School of Oceanography 
dealt with codfish hearing. His theory of human hearing, first published in 
1970, was later expanded into a book, The Electromodel of the Auditory 
System. I interviewed him in early 2013, shortly before his death. 





The mammalian cochlea, after all, evolved from a fish organ called the 
lagena, which has hair cells not too unlike ours, covered by a gelatinous 
membrane, also similar to ours. But the fish's membrane is in turn topped 
by structures called otoliths (*ear stones"), which are crystals of calcium 
carbonate and are known to be about one hundred times more piezoelectric 
than quartz. Offutt said that this is not accidental. The hair cells in the ears 
of fish, he said, are sensitive to the voltages generated by the otoliths in 
response to sound pressure.!? This, he said, explains why sharks can hear. 
Fish, being composed largely of water, are supposed to be transparent to 
water-borne sounds unless they have a swim bladder containing air. 
Therefore sharks, which have no swim bladder, ought to be deaf according 
to standard theories, but they aren't. In 1974, Offutt elegantly solved this 
contradiction by introducing electricity into his model for how fish hear. 
And by extension, he said, there is no reason why human hearing should not 
still work in the same basic fashion. If the cochlea evolved from the lagena, 
then the tectorial membrane evolved from the otolithic membrane and 
ought still to be piezoelectric. And the hair cells, which are substantially the 
same, should still function as electroreceptors. 





respond not only to water currents but also to low frequency sounds and to 
electric currents." These organs’ hair cells, too, are covered by a jellylike 
substance, called the cupula, and they, too, are supplied by a branch of the 
acoustic nerve. In fact, the lateral line and the inner ear are so closely 
related functionally, evolutionarily, and embryonically, that all such organs 
in all types of animals are referred to as the acoustico-lateralis system. 

Some fish have other organs, which evolved from this system, that are 
exquisitely and primarily sensitive to electrical currents. With these organs, 
sharks can detect the electric fields of other fish or animals, and can locate 
them in darkness, in murky water, or even when hidden in the sand or mud 
at the bottom. The hair cells of these electric organs lie beneath the surface 
of the body in sacs called ampullae of Lorenzini and are covered, again, 
with a gelatinous substance. 

All such fish organs, no matter their specialization, have proven to be 
sensitive to both pressure and electricity. Lateral line organs that primarily 
sense water currents also react to electrical stimuli, and ampullae of 
Lorenzini that primarily sense electric currents also react to mechanical 
pressure. Therefore marine biologists were once of the opinion that 
piezoelectricity was at play in both the lateral line and the ear.? Hans 
Lissman, once the world's foremost authority on electric fishes, thought that 
this was so. Later, anatomist Muriel Ross, who had a grant from NASA to 
study the effects of weightlessness on the ear, emphasized that the otoliths 
of fish, and the related otoconia (“hair sand”) of our own ears’ gravity 
sensors, are known to be piezoelectric. Mechanical and electrical energy, 
she said, are interchangeable, and feedback between hair cells and 
piezoelectric membranes will transform one form of energy into the other. 

In a related study in 1970, Dennis O’Leary exposed the gelatinous 
cupulas of frogs’ semicircular canals—the organs of balance in the inner ear 
—to infrared radiation. The response of the canals’ hair cells was consistent 
with the electrical and not the mechanical model of such organs. 

Recently the outer hair cells of the cochlea have themselves proven to 
be piezoelectric. They acquire a voltage in response to pressure, and they 
lengthen or shorten in response to an electric current. Their sensitivity is 
extreme: one picoamp (one trillionth of an amp) of current is enough to 


cause a measurable change in a hair cells length, Electric currents, 
traveling in complex paths, have also been found traversing the tectorial 
membrane and coursing through the organ of Corti.'^ And pulsating waves 
have been discovered, in the thin space between the tops of the hair cells 
and the bottom of the tectorial membrane, that reverberate between the 
outer hair cells, the tectorial membrane, and the inner hair cells.» Australian 
biologist Andrew Bell has calculated that in the human cochlea these fluid 
waves should have wavelengths roughly between 15 and 150 microns 
(millionths of a meter)—just the right size to put hair cells 20 to 80 microns 
in length into musical resonance. Bell has compared these waves to surface 
acoustic waves, and the organ of Corti to a surface acoustic wave resonator, 
a common electronic device that has replaced quartz crystals in a wide 
variety of industries. 

In the electromodel of hearing that these scientists have constructed, 
there are several places where electricity can act directly on the ear. The 
inner hair cells are electroreceptors. The outer hair cells are piezoelectric. 
The tectorial membrane is piezoelectric. And since both direct and 
alternating current can act on any of these structures, many of the early 
reports of the hearing of electricity, said Offutt, including reports that were 
dismissed as being due to “skin vibration,” should be reevaluated. 

The exquisite sensitivity of the organ of Corti to electricity explains the 
nineteenth century reports of the hearing of direct current and the twentieth 
century reports of the hearing of alternating current. And it forms a basis for 
understanding the torment suffered half a century ago by Clarence Wieske’s 
client in Santa Barbara, and the suffering of so many millions today. But a 
piece of the auditory puzzle is still missing. 

Direct or alternating current applied to the ear canal requires about one 
milliampere (one thousandth of an ampere) to stimulate hearing.'® If an 
electrode is placed directly in the cochlear fluid, about one microampere 
(millionth of an ampere) suffices." If current is applied directly to a hair 
cell, one picoampere (trillionth of an ampere) is all that is necessary to 
cause a mechanical reaction.!? Clearly, sticking electrodes in your outer ear 
is an inefficient way to stimulate the hair cells. Very little of the applied 
current ever reaches those cells. But in today's world, electrical energy is 


n e E hair cells are also bathed in electric 


and magnetic fields originating in the electric power grid and all the 
electronic appliances that are plugged into it. All those fields and radio 
waves penetrate the inner ear and induce electric currents to flow inside the 
cochlea itself. The question then becomes, why do we all not hear a 
constant cacophany of noise drowning out all conversation and music? Why 
is most electrical noise confined to either very low or very high 
frequencies? 


Hearing Ultrasound 

Human ultrasonic hearing has been rediscovered more than a dozen times 
since the 1940s, most recently by Professor Martin Lenhardt at Virginia 
Commonwealth University. *So outlandish is the concept that humans can 
have the hearing range of specialized mammals, such as bats and toothed 
whales," he writes, "that ultrasonic hearing has generally been relegated to 
the realm of parlor tricks rather than being considered the subject of 
scientific inquiry"? At the present time, apparently, ultrasonic hearing is 
being intensively investigated only by Lenhardt and by a small group of 
researchers in Japan. 





Bruce Deatherage, while doing shipboard research for the Department 
of Defense in the summer of 1952, rediscovered the ability to hear 
ultrasound by accident when he swam into a sonar beam broadcasting at 50 
kHz. Repeating the experiment with volunteers, he reported that each 
subject heard a very high-pitched sound that was the same as the highest 
pitch that person could ordinarily hear. Recently scientists at the Naval 


Submarine Base in New London, Connecticut verified the hearing of 
underwater ultrasound up to a frequency of 200 kHz.? 

What is known today is this: 

Virtually everyone with normal hearing can hear ultrasound. Elderly 
people who have lost their high frequency hearing can still hear ultrasound. 
Many profoundly deaf people with little or no functioning cochlea can hear 
ultrasound. The perceived pitch varies from person to person but is usually 
between 8 and 17 kHz. Pitch discrimination does occur, but requires a 
greater change in frequency in the ultrasonic range than in the normal 
auditory range. And, most surprisingly, when speech is transposed into the 
ultrasonic range and spread out over that range, it can be heard and 
understood. Somehow the brain recondenses the signal, and instead of high 
pitched "tinnitus," the person hears the speech as though it were normal 
sound. Speech can also be modulated onto an ultrasonic carrier, and it is 
demodulated by the brain and heard as normal sound. Lenhardt, who has 
built and patented bone conduction ultrasonic hearing aids based on these 
principles, reports that word comprehension is around 80 percent in normal 
hearing individuals, even in a noisy environment, and 50 percent in the 
profoundly deaf. 

Since even many deaf people can hear ultrasound, several investigators 
over the years, including Lenhardt and the Japanese group, have suggested 
that the ultrasound receptor lies not in the cochlea but in an older part of the 
ear, one which functions as a primary hearing organ in fish, amphibians and 
reptiles: the saccule. It still exists in humans, containing hair cells capped 
by a gelatinous membrane covered with piezoelectric calcium carbonate 
crystals. 

Although it is adjacent to the cochlea, and although its nerve fibers 
connect to both the vestibular and auditory cortex of the brain, the human 
saccule has usually been thought to be an exclusively vestibular, or balance 
organ, and to play no part in hearing. This dogma, however, has come under 
challenge periodically for the past eighty years. In 1932, Canadian 
physician John Tait presented a provocative paper, titled “Is all hearing 
cochlear?” at the 65th Annual Meeting of the American Otological Society 
in Atlantic City. He said that he and other investigators had failed to find 


any connection between the saccule and posture in fish, frogs, or rabbits, 
and proposed that even in humans the saccule is part of the hearing 
apparatus. Its construction, he said, indicates that the saccule is designed to 
detect vibrations of the head, including the vibrations that occur in 
speaking. The saccule in air-breathing animals, he proposed, “is a 
proprioceptor involved in the emission and regulation of voice. This would 
mean that we hear our own voice with the help of two kinds of receptors, 
while we hear the voice of our neighbors with only one.” In other words, 





Since that time, saccular hearing has been proven to exist in a variety of 
mammals and birds, including guinea pigs, pigeons, cats, and squirrel 
monkeys. Elephants may use their saccule to hear low frequency vibrations 
received through the earth by bone conduction. Even in human beings, 
audiologists have developed a hearing test involving the electrical response 
of neck muscles to sound—called “vestibular evoked myogenic potentials” 
(VEMP)—to evaluate the functioning of the saccule. This test is often 


normal in people with profound sensorineural hearing loss. 








2. Although airborne ultrasound is not audible, Puharich and Lawrence 
showed that electromagnetic energy at ultrasonic frequencies is audible, to 
both hearing and deaf people. 


3. The otoconia (calcium carbonate crystals) in the saccule, and the 
outer hair cells in the cochlea, are known to be piezoelectric, i.e. they will 
convert electric currents to sound. 


4. Electric and magnetic fields induce electric currents in the body 
whose strength is proportional to frequency. The higher the frequency, the 
greater the induced current. These principles of physics mean that the same 
field strength will produce 1,000 times more current at 50,000 Hz, in the 
ultrasonic range, than at 50 Hz, in the audible range. 


5. The measured threshold for hearing in the ultrasonic range is as low, 
or lower, than the threshold at 50 or 60 Hz. An exact comparison cannot be 


made because and extremely 
But superimposing 


typical air, bone, and ultrasonic hearing threshold curves gives an overall 
hearing curve that looks something like this:? 






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30 1,000 4.000 20,000 100,000 
Frequency (Hz) 


The inner ear looks to be about 5 to 10 times more sensitive to sound at 
50 kHz than at 50 Hz. Therefore the ear may be 5,000 to 10,000 times more 
sensitive to electric and magnetic fields at ultrasonic frequencies than at 
power lines frequencies. The ear's much greater sensitivity to sound in the 
middle of the hearing range is largely due to the resonant properties of the 
outer, middle and inner ear before they are transformed into electrical 
impulses.” This means that the ear is much more sensitive to electric 
currents at ultrasonic frequencies than to currents in either the middle or 


low parts of its range. The ear's insensitivity to electromagnetic fields at 50 
or 60 Hz explains why, thankfully, we do not hear a 60-cycle buzz from the 
power grid at all times. 

By consulting charts published by the World Health Organization,” it is 
possible to estimate the approximate minimum frequency at which we 
might expect to begin hearing an electromagnetic field. Since 1 picoampere 
of current is enough to stimulate one hair cell, and 50 picoamperes to 
trigger 50 hair cells—about the number required to stimulate hearing—one 
can look this amount of current up on the WHO'S charts. It turns out to be 
the amount of current per square centimeter that is induced in the ear at 20 
kHz by either a magnetic field of about one microgauss or an electric field 
of about ten millivolts per meter. These are about the magnitudes of some 
of the ultrasonic electric and magnetic fields that pollute our modern 
environment.” And one square centimeter is just about the area of the base 
of the human cochlea. 

In other words, given the dimensions of the cochlea, we can expect to 
hear electromagnetic fields in today's environment that are roughly above 
20 kHz and below 225 kHz, which is the upper limit of our ultrasonic 
hearing range. 

If the saccule is more sensitive to ultrasound than the cochlea, these 
estimates could be too conservative. As I was reminded some years ago by 
Canadian acoustic physicist Marek Roland-Mieszkowski, the ear is 
sensitive to sound energies of less than 1079 watts per square centimeter. 
Assuming, as he did, only a one percent efficiency in converting electrical 
energy into sound energy, the ear could be sensitive to magnetic fields of a 
hundredth of a microgauss, or to electric fields of 100 microvolts per meter. 
The ability of some people to hear the northern lights—said to resemble the 
sound of rustling silk?—indicates a potential sensitivity of about that 
level.28 


SOURCES OF ELECTRICAL SOUND 


Electronic consumer devices 
On April 2, 2000, Dave Stetzer, a former electronics technician for the Air 
Force, testified about “nonlinear loads” before the Michigan Public Service 


Commission. By this, he explained, he meant “computers, fax machines, 
copiers, and many other electronic devices, as well as various utility 
equipment including capacitors, solid state monitoring and switching 
devices, and transformers.” All these devices—in other words, virtually all 
modern electronic equipment—were putting tremendous amounts of high 
frequencies onto the power grid, and the grid, which was designed to 
transmit only 60 Hz, could no longer contain what was on it. The electrons 
in the wires, he explained, once they pass through a computerized device, 
vibrate not only at 60 Hz, but at frequencies extending throughout the 
ultrasonic range and well into the radio frequency spectrum. Since as much 
as seventy percent of all electric power flowing on the wires at any given 
time had passed through one or more computerized devices, the entire grid 
was being massively polluted. 

Stetzer first described some of the technical problems this was causing. 
The high frequencies increased the temperature of the wires, shortened their 
life span, degraded their performance, and forced substantial amounts of 
electric current to return to the power plant through the earth instead of 
through a return wire. And the high frequencies and “transients” (spikes of 
high current) emanating from everyone’s electronic equipment were 
causing interference and damage to everyone else’s electronic equipment. 
This was becoming expensive for homeowners, businesses, and utility 
companies. 

Even worse, all of the high frequency currents that were coursing 
through the earth, and the high frequency electromagnetic fields vibrating 
through the air, were making millions of people sick. Society was, and is, in 
denial about that, and that was not of great interest to the Michigan Public 
Service Commission. However, these fields and earth currents were also 
making dairy cows sick, all over Michigan, which was a threat to the state's 
economy. So the commissioners listened attentively while Stetzer spoke. 

“In my visits to the various farms,” he said, “I have observed over 6,000 
dairy cows and some horses. I have observed damaged cows with swollen 
joints, open sores, and other maladies, as well as aborted and deformed 
calves. I have even observed aborted twin calves, one of which was fully 
developed while its twin was grossly deformed. Ironically, the grossly 


deformed twin was the one directly in the current flow pathway between the 
cow's back legs." 

*[n addition," Stetzer told the stunned commissioners, *I have also 
observed stressed cows, cows reluctant to enter certain spaces, including 
barns and milking parlors, and even cows reluctant to drink water, such that 
they lap at the water instead of sucking it up as they normally do. I have 
seen numerous cows fall over dead for no apparent reason. I have observed 
cows whose entire sides and muscles spasm uncontrollably. The articles 
from the Wisconsin La Crosse Tribune accurately highlight and describe a 
few of the conditions that I have personally observed on farms in 
Wisconsin, Minnesota, and Michigan. These symptoms and impacts are not 
limited to Wisconsin; they appear everywhere I have found dirty power." 

My first experience of a health nature with modern electronics occurred 
back in the mid-1960s, when my family junked its old vacuum tube 
television set and acquired a transistorized model. As soon as it was 
plugged in, I heard an awful high-pitched sound—even though I was in the 
other end of the house with walls and doors in between—that apparently no 
one else could hear. Such was my introduction to the electronics age. I took 
care of myself by not watching television, which is one of the reasons why, 
from the day I moved out on my own to the present, I have never owned 
one. 

Auditory unpleasantness of that sort was not a widespread problem—at 
least not for me—until the 1990s. As long as I avoided televisions and 
computers, the world, in the places I chose to live, contained mostly natural 
sounds, and complete silence was easy to find. 

But at some point in the 1990s—the change was so gradual that I can’t 
pinpoint when—TI realized that I could not find silence any more. It 
happened after 1992, when I rented a cabin in northern Ontario—which was 
still silent—and before 1996, when I fled the new crop of digital cell towers 
in my native New York to save my life. Since at least 1996, I have found no 
escape, anywhere in North America, from the awful high-pitched sound that 
I first heard when I was about fifteen. In 1997, I sought silence in an 
underground cave in Clarksville, New York—and did not find it. The sound 
was greatly diminished underground but did not vanish. In 1998, I sought 


silence in Green Bank, West Virginia, the only place on earth that is legally 
protected from radio waves—and did not find it. The sound did not even 
diminish. I can make it louder by plugging in electronic devices, and softer 
again by unplugging them, but I cannot make it go away, not even by 
turning the power off in my house. I can hear appliances being turned on in 
a neighbor’s house. Without warning or explanation the sound sometimes 
becomes suddenly much louder all over my neighborhood. It becomes 
quieter when there is a power outage. But it never disappears. It matches 
17,000 Hz, which is the highest pitch that I can hear. 


Low frequency sounds 

The low frequency Hum is heard by between two and eleven percent of the 
population.” This is fewer than hear the high frequency sound, but the 
effects of the Hum can be far more disturbing. At its best it sounds like a 
diesel engine idling somewhere in the distance. At its worst it vibrates one's 
whole body, causes intense dizziness, nausea and vomiting, prevents sleep, 
and is completely incapacitating. It has driven people to suicide. 

The probable sources of the Hum are powerful ultrasonic radio 
broadcasts modulated at extremely low frequencies to communicate with 
submarines. To penetrate the oceans requires radio signals of immense 
power and long wavelengths, and the frequencies called VLF (very low 
frequency) and LF (low frequency)—corresponding to the ultrasonic range 
— fit the bill. The American military systems currently in use for this 
purpose include enormous antennas located in Maine, Washington, Hawaii, 
California, North Dakota, Puerto Rico, Iceland, Australia, Japan, and Italy, 
in addition to sixteen mobile antennas flown on aircraft whose locations at 
any given time are kept secret. Land stations of this type are also operated 
by Russia, China, India, England, France, Sweden, Japan, Turkey, Greece, 
Brazil, and Chile, and by NATO in Norway, Italy, France, the United 
Kingdom, and Germany. 








Since the wavelengths are so long, every VLF antenna is tremendous. 
The antenna array at Cutler, Maine, which has been operating since 1961, is 
in the form of two giant six-pointed stars, covering a peninsula of nearly 
five square miles and supported by 26 towers up to 1,000 feet tall. It 
broadcasts with a maximum power of 1.8 million watts. The facility at Jim 
Creek, Washington, built in 1953, has a 1.2-million-watt transmitter. Its 
broadcast antenna is strung between two mountaintops. 

The low frequencies that are required in order to penetrate the oceans 
limit the speed at which messages can be transmitted. The American 
stations send a binary code at 50 pulses per second, which is consistent with 
the frequency of the Hum that most people hear today. The enhanced 
system recently adopted by the Navy uses multiple channels to transmit 
more data, but each channel still pulses at 50 Hz. In addition, the binary 
code itself is created by two ultrasonic frequencies spaced 50 Hz apart. 
These signals are therefore doubly modulated at approximately the 
frequency that is tormenting people worldwide. 

Geology Professor David Deming at the University of Oklahoma, who 
was driven to investigate the Hum that he hears, has focused his attention 
on the mobile TACAMO (“Take Charge and Move Out") system. 
TACAMO planes, which trail long antennas behind them, have been flying 
out of Tinker Air Force Base in Oklahoma City since 1963, and the 
maximum power of each airborne transmitter is 200,000 watts. They use a 
variety of frequencies between 17.9 and 29.6 kHz, which are doubly 
modulated at 50 Hz like all other VLF stations that communicate with 


submarines. Navy TACAMO planes are always in the sky whenever there is 
a Hum in Oklahoma. The aircraft head out from Oklahoma to Travis Air 
Force Base in California and Naval Air Station Patuxent River in Maryland. 
From there the planes fly six to ten hour missions in predetermined orbits 
over the Atlantic and Pacific Oceans. 

One other ultrasonic, pulsed communication network deserves mention 
here—one which ceased broadcasting in North America in 2010, but which 
is still functioning in some parts of the world and may yet be fully 
resurrected here: the LORAN-C system. LORAN, which stands for LOng 
RAnge Navigation, is an old network of extremely powerful land-based 
navigation beacons whose function is now duplicated by Global Positioning 
Satellites. LORAN may have been responsible for the earliest reports of a 
Hum in England as well as the famous Hum in Taos, New Mexico that was 
the subject of a government investigation launched in 1992. 

LORAN-C operates at 100 kHz and is pulsed at multiples of 10 to 17 
Hz, depending on location. Placed under the control of the Coast Guard, the 
first LORAN-C stations were built along the east coast in 1957—in 
Martha’s Vineyard, Massachusetts; Jupiter, Florida; and Cape Fear, North 
Carolina. In the late 1950s, chains of LORAN-C stations were also built 
around the Mediterranean Sea and the Norwegian Sea, and by 1961 others 
were on the air in the Bering Sea, and in the Pacific Ocean centered on 
Hawaii. Although it was not the first long range navigation system, its 
predecessor, LORAN-A, operated at frequencies between 1850 and 1950 
kHz and was not in the ultrasonic range. 






California. Although Cornell University is quite near the 800,000-watt 
Seneca LORAN station that began operating in 1978, I had graduated from 
college there in 1971 and never heard a Hum. 





When, some years later, a Coast Guard official told me there was a 
LORAN antenna over in Middletown, I wondered if there was a connection 
to the annoying and puzzling Hum. The official had casually mentioned that 
the signal was so powerful that the people who worked at the facility could 
hear it. So I got in my car one morning and made the three-hour drive. As I 
approached within a half mile of the 63-story tower, my ears began to hurt. 





I obtained a copy of the LORAN-C User 
Handbook from the Coast Guard, and learned that the repetition rate for 
LORAN-C transmissions on the west coast was almost exactly 10 Hz. 
Apparently Further 
consultation with the Handbook provided an explanation. The West Coast 
Chain consisted of four stations—the one in Middletown, one in George, 
Washington, and two in Nevada—that transmitted once every tenth of a 
second in a precisely timed sequence. 

Fallon...George...Middletown...Searchlight.............. Fallon... 
George...Middletown...Searchlight.............. It took exactly one twentieth 
of a second to transmit the sequence of signals from the four beacons— 
corresponding to a repetition rate of 80 Hz, and reinforcing the eighth 
harmonic of the fundamental frequency. Taking the signals two at a time— 
Fallon-George and Middletown-Searchlight—gives a repetition rate of 40 
Hz, reinforcing the fourth harmonic. The predominance of the Middletown 
signal, when one was close enough to the Middletown tower, apparently 
made the fourth harmonic audible. 

By this time the Taos Hum was well known, and I wondered if it, too, 
was caused by LORAN. It had been investigated by a team of scientists 
from Los Alamos and Sandia National Laboratories, the Air Force’s Phillips 
Laboratory, and the University of New Mexico—who predictably didn’t 
find anything. But three items in their report stood out. First, 161 of the 
1,440 residents of the Taos area who responded to their survey heard the 
Hum. Second, the team heard back not only from Taos-area residents, but 
from people throughout the northern hemisphere who had heard about the 





investigation and contacted the team to report being tormented by the same 
sound. Third, 








he South Central LORAN Chain had a repetition rate of 10.4 
Hz, and the fourth harmonic was 41.6 Hz. The third harmonic was 31.2 Hz. 
Apparently many people were hearing the eighth harmonic as well. 

The evidence that LORAN-C caused the Taos Hum is abundant. The 
South Central Chain was the only LORAN chain that had six transmitting 
beacons, and Taos was near the geographic center of them. The South 
Central Chain was built from 1989 to 1991 and fully commissioned in April 
1991, precisely when residents of Taos began complaining. The combined 
electric field strength at Taos, from the six stations, was about 30 millivolts 
per meter, more than enough to trigger a hearing sensation.°° 

Some of the other Hums around the world seem also to have been 
caused by LORAN-C. The LORAN-C chain in the Norwegian Sea, with 
stations in Norway, Jan Mayen Island, Iceland, and the Faeroe Islands, 
provided coverage to England since 1959. The British Hum, which has been 
reported for about that long, suddenly decreased in loudness around 1994— 
the same year Iceland turned off the most powerful LORAN station in that 
chain. It increased in loudness again in 1996—at the same time that a new 
station in Værlandet in southern Norway was put into operation to again 
give better coverage to the British Isles. The new station also provided 
coverage for the first time to the area around Vanern Lake, Sweden—where 
the Hum was first reported in 1996. 





At this writing, an Enhanced LORAN-C, or eLORAN, network is being 
built in several areas of the world to ensure the operation of a backup 
navigation and timing system in case the GPS satellites fail or their 
broadcasts are jammed. eLORAN relies on the same immensely powerful 
long-wave radio transmissions as before, but the addition of a data channel 


provides much greater position accuracy. To achieve position accuracies to 
within 10 meters, networks of receiving stations, called differential- 
LORAN, or DLoran, are also being built. They monitor the powerful 
eLORAN signals and broadcast correction factors over the data channel, or 
over a cell tower network, to local mariners. South Korea is currently 
operating three eLORAN stations and plans to achieve full nationwide 
coverage in 2020. Iran has built an eLORAN system, and India, Russia, 
China, and Saudi Arabia are upgrading their existing LORAN-C stations to 
eLORAN. France, Norway, Denmark, and Germany ceased their LORAN- 
C transmissions at the end of 2015 and have dismantled their towers. The 
situation in the United States is less certain. The 625-foot LORAN-C tower 
at Wildwood, New Jersey went back on the air temporarily in 2015 under 
the aegis of the Department of Homeland Security. And in December 2018, 
President Trump signed into law the National Timing Resilience and 
Security Act, which mandates the establishment of a terrestrial backup 
system for the Global Positioning Satellites that will be able to penetrate 
underground and inside buildings throughout the United States. It 
authorizes the acquisition of the mothballed LORAN facilities for this 
purpose. 

To see if the shutoff of most of the European LORAN-C stations had 
any effect on the Hum in that part of the world, I consulted a worldwide 
database of Hum reports kept by Glen MacPherson, an instructor at the 
University of British Columbia. On January 1, 2016, the day after the 
planned LORAN-C shutoff, reports came in from Scotland and Northern 
Ireland saying that the Hum had suddenly stopped between 2:00 a.m. and 
3:00 a.m. that morning. 


OTHER SOURCES OF ULTRASONIC 
RADIATION 


Time broadcasts 

The National Institute of Standards and Technology broadcasts a time-of- 
day signal that synchronizes “atomic” clocks and watches throughout North 
America. Transmitting from Fort Collins, Colorado, the 60-kHz signal of 


station WWVB is even usable in parts of South America and Africa at 
night. Time stations using ultrasonic frequencies also broadcast from 
Anthorn, England; Mount Hagane and Mount Ootakadoya, Japan; 
Mainflingen, Germany; and Lintong, China. 


Energy efficient light bulbs 

In a contagious fit of insanity, countries are falling like dominoes for the 
myth that fluorescent lighting is good for the environment. Cuba, in 2007, 
was the first to ban outright all sales of ordinary incandescent bulbs—bulbs 
that have shed soft light into our dark evenings for a hundred and thirty-five 
years. Australia banned imports of incandescents in November 2008, and 
sales a year later. The European Union completed a three-year phase-out on 
September 1, 2012, and China banned 100-watt bulbs one month later, with 
total prohibition scheduled for 2016. Brazilians can no longer buy bulbs of 
60 watts or greater as of July 1, 2015. Canada and the United States, which 
had planned to ban 100-watt bulbs in 2012, temporarily relented in the face 
of strong public opposition. 

And the public are right. 





Not to mention the 
inconvenient fact that little, if any, energy is being saved if you live 
anywhere but the tropics. In summer, the heat given off by light bulbs is 
wasted and increases the demand for air conditioning. But in winter, we 
gain that cost back because the heat from light bulbs then warms our 
homes. When we lose that extra source of heat, we have to make up the 
difference by burning more oil and gas. In the United States, we have 
probably neither gained nor lost, environmentally. But in Canada, for 
example, which gets virtually all its electricity from hydro power, banning 


incandescent bulbs has been an unqualified mistake. It has done nothing but 
increase the consumption of fossil fuels, putting more carbon dioxide into 
the atmosphere and worsening global warming. 

And that mistake is being compounded. All manufacturers of 
fluorescent bulbs, under pressure from government regulators, are making a 
bad situation worse by attaching a miniature radio transmitter to each and 
every light bulb under the theory that this makes them even more energy 
efficient. The radio waves energize the mercury vapor without having to 
subject it to a high voltage. All compact fluorescent bulbs, and a large 
percentage of long fluorescent bulbs today are energized with these radio 
transmitters, which are called “electronic ballasts.” The frequencies used, 
between 20 and 60 kHz, are in the ultrasonic hearing range. The ubiquity of 
this type of lighting, and the growing difficulty of obtaining ordinary 
incandescents, even where they are still legal, means that these bulbs are a 
predominant source of ultrasonic radiation in homes and businesses, and on 
power lines throughout the world. Virtually all electricity that flows on the 
power grid and in the earth is contaminated to some extent with 20 to 60 
kHz, having passed through hundreds or thousands of these radio 
transmitters on its way to the next consumer, or back to the utility’s 
generating plant. And because the electronic ballasts put out so much 
electrical distortion, today’s fluorescent bulbs also emit measurable energy 
far into the microwave range. The FCC’s rules allow each and every energy 
efficient bulb to emit microwave radiation, at frequencies up to 1,000 MHz, 
at a field strength of up to 20 microvolts per meter, as measured at a 
distance of 100 feet from the bulb. 

LED bulbs, which are being offered as another substitute for 
incandescents, are no better. They too give off harsh light, and they contain 
a variety of toxic metals and require special electronic components that 
convert the alternating current in our homes to low-voltage direct current. 
Most often, these components are switch mode power supplies which 
operate at ultrasonic frequencies and are discussed below in connection 
with computers. 

Sadly, the North American reprieve was only temporary. Canada 
officially banished most incandescent bulbs as of January 1, 2015, and the 


U.S. effort to further postpone its death knell ended at the same time. The 
last examples of Edison's enduring invention vanished from the shelves of 
my local hardware stores a couple of months later. 

Only specialty bulbs and halogen 
lamps are left, and many countries are prohibiting those also. Incandescents 
are still completely legal, however, in most of Africa, most of the Middle 
East, much of southeast Asia, and all the island nations of the Pacific.?! 


Cell phones and cell towers 

Although cell phones and cell towers are best known as emitters of 
microwave radiation, that radiation is modulated at a bewildering array of 
much lower frequencies that the human body, as a radio receiver, perceives. 
For example, GSM (Global System for Mobile) is a telecommunications 
system long used by AT&T and T-Mobile in the United States, and by most 
companies in the rest of the world. The radiation from GSM cell phones 
and cell towers has components at 0.16, 4.25, 8, 217, 1733, 33,850 and 
270,833 Hz. In addition, the microwave carrier is divided into 124 
subcarriers, each 200 kHz wide, all of which can broadcast simultaneously, 
in order to accommodate up to about a thousand cell phone users at once in 
any given area. This generates many harmonics of 200,000 Hz. 

Although GSM is a *2G" technology, it has not gone away. Layered 
over it are “3G” and “4G” networks that smart phones of more recent 
vintage use. The 3G system, called Universal Mobile Telecommunications 
System, or UMTS, is completely different, containing modulation 
components at 100, 1500, 15,000, and 3,840,000 Hz. The 4G system, called 
Long-Term Evolution, or LTE, is modulated at yet another set of lower 
frequencies, including 100, 200, 1000, 2,000, and 15,000 Hz. In 4G, the 
carrier frequency is divided into hundreds of 15-kHz wide subcarriers, 
adding yet another set of harmonics. And since smart phones and flip 
phones of different vintages presently coexist, every cell tower has to emit 
all of the different modulation frequencies, old and new. Otherwise older 
phones would not continue to work. AT&T towers, for example, are 
therefore presently emitting modulation frequencies of 0.16, 4.25, 8.33, 
100, 200, 217, 1000, 1500, 1733, 2,000, 15,000, 33,850, 270,833 and 


3,840,000 Hz, plus harmonics of these frequencies and additional 
harmonics of 15,000 Hz and 200,000 Hz, not to mention the microwave 
carrier frequencies of 700 MHz, 850 MHz, 1700 MHz, 1900 MHz, and 
2100 MHz. Like the proverbial boiled frog, we are all immersed in a giant 
pot of radiation, whose intensity is increasing, and whose effect, though 
unperceived, is nevertheless certain.?? 

Cell phones spend a higher percentage of their energy on their low 
frequency components than do cell towers?— which may explain the high 
prevalence of "tinnitus" among cell phone users with otherwise normal 
hearing. In 2003, at a time when cell phone use was not as universal as it is 
today, it was still possible to do epidemiological studies of users and non- 
users. A team of scientists led by Michael Kundi at the Medical University 
of Vienna, comparing people with and without tinnitus at an ear, nose, and 
throat clinic, found a greater prevalence of tinnitus—often in both ears— 
among cell phone users than among non-users, and a clear trend of more 
tinnitus with increasing intensity of cell phone use.?^ The more minutes, the 
more tinnitus. 


Remote control devices 
Most remote control devices—the gadgets that open garages and car doors, 
and operate television sets—communicate using infrared radiation. But the 
infrared signals are pulsed between 30 and 60 thousand times per second, in 
the middle of the ultrasonic range. The most common frequency chosen by 
manufacturers is 36 kHz. 


The problem with computers 

In 1977, Apple gave the world a revolutionary new device. The personal 
computer, as it came to be known, was powered by a new type of gadget 
called a switch mode power supply. If you have a laptop, it’s the little 
transformer/charger that you plug into the wall. This gift from Apple was 
much lighter in weight, more efficient, and more versatile than previous 
methods of supplying low-voltage DC power to electrical equipment. It had 
only one glaring fault: instead of delivering only pure DC, it also polluted 
the electric power grid, the earth, the atmosphere, and even outer space with 
a broad range of frequencies. But its usefulness made it rapidly 


indispensible to the mushrooming electronics industry. Today computers, 
televisions, fax machines, cell phone chargers, and most other electronic 
equipment used in home and industry depend on it. 

Its method of operation makes it obvious why it causes such a huge 
amount of electrical pollution. Instead of regulating voltage in the 
traditional way with variable resistors, a switch mode power supply 
interrupts the current flow tens of thousands to hundreds of thousands of 
times per second. By chopping up the current into slightly more or fewer 
pieces, these little devices can regulate voltage very precisely. But they 
change 50- or 60-cycle current into something very different. The typical 
switch mode power supply operates at a frequency between 30 and 60 kHz. 

Computers, and all other electronic equipment that contains digital 
circuitry, also emit ultrasonic radiation from other components, as anyone 
can verify using an ordinary (non-digital) AM radio. Simply tune the radio 
to the beginning of the dial (about 530 kHz), bring it near a computer—or a 
cell phone, television, fax machine, or even a handheld calculator—and you 
will hear a variety of loud screaming noises coming from the radio. 

What you are hearing is called “radio frequency interference,” and much 
of that is harmonics of emissions that are in the ultrasonic range. A laptop 
computer produces such noise even when it is running off the battery. When 
it is plugged in, the switch mode power supply not only intensifies the 
noise, but communicates it to your house wiring. From your house wiring it 
travels onto the distribution line in your neighborhood and into everyone 
else’s homes, and down the ground wire attached to your electric meter into 
the earth. And the electric power grid, and the earth itself, contaminated 
with ultrasonic frequencies from billions of computers, becomes an antenna 
that radiates ultrasonic energy throughout the atmosphere and beyond. 


Dimmer switches 

Another device that chops up 50- or 60-cycle current is the ubiquitous 
dimmer switch. Here, too, the traditional variable resistor has been replaced 
with something else. The strategy is different than in your computer’s 
transformer—the modern dimmer switch interrupts the current only twice in 
each cycle—but the result is similar: the sudden starting and stopping of the 


current produces dirty power. Instead of a smooth flow of 50- or 60-cycle 
electricity, you get a tumultuous mixture of higher harmonics that flows 
through the light bulb, pollutes house wiring, and irritates the nervous 
system. A large portion of these unwanted frequencies are in the ultrasonic 
range. 


Power lines 

As early as the 1970s, Hiroshi Kikuchi, at Nihon University in Tokyo, 
reported that significant amounts of high frequency currents were occurring 
on the power grid due to transformers, motors, generators, and electronic 
equipment. And some of it was radiating into space. On the ground, 
radiation in a continuous spectrum from 50 Hz to as high as 100 MHz was 
being measured at distances as far as one kilometer from both low and high 
power lines. Frequencies up to about 10 kHz, originating from power lines, 
were being measured by satellites. 

In 1997, Maurizio Vignati and Livio Giuliani, at the National Institute 
for Occupational Health and Prevention in Rome, reported that they were 
detecting radio frequency emissions as far as 50 meters (165 feet) from 
power lines, at frequencies ranging from 112 to 370 kHz, that were 
amplitude modulated and seemed to be carrying data. These frequencies, 
they discovered, were deliberately put on the electric power grid by Italian 
utility companies. And the same technology is being used worldwide. It is 
called Power Line Communications. The technology is not new but its use 
has exploded. 

Electric companies have been sending radio signals over power lines 
since about 1922, using frequencies ranging from 15 to 500 kHz, for 
monitoring and control of their substations and distribution lines. The 
signals, as powerful as 1,000 watts or more, travel hundreds of miles. 

In 1978, small devices appeared in Radio Shack stores that transmitted 
at 120 kHz. Consumers could plug them in and use the wiring in their walls 
to carry signals that enabled them to control lamps and other appliances 
remotely from command consoles. Later the HomePlug Alliance developed 
devices that use home wiring to connect computers. HomePlug devices 


o 


work at 2 to 86 MHz, but have modulation components at 24.4 kHz and 
27.9 kHz, in the ultrasonic range. 


Smart Meters 
The use of the power grid to deliver Internet to homes and businesses— 
called Broadband over Power Lines—has not been commercially 
successful. But the use of the power grid to transmit data between homes, 
businesses and power plants is now being implemented for something 
called the Smart Grid, presently under construction all over the world. 
When the Smart Grid is fully implemented, electricity will be automatically 
sent where it is needed, when it is needed—even rerouted from one region 
to another to satisfy instantaneous demand. Utilities will continuously 
monitor every major appliance in every home and business, and will have 
the ability to automatically regulate thermostats and turn their customers’ 
air conditioners and washing machines on and off during times of greater or 
lesser demand for electricity. In order to accomplish this, radio transmitters 
are being installed on everyone’s electric meters and appliances, which 
communicate not only with each other, but with the utility company, either 
wirelessly, or via fiber optic cable, or by radio signals sent over the power 
lines. The FCC has allocated frequencies from 10 to 490 kHz for this latter 
purpose, but utility companies most often use frequencies below 90 kHz, in 
the ultrasonic range, for long-distance communication over the power lines. 
The wireless version of smart meters, especially the variety called a 
“mesh network,” has spread around the world like technological wildfire in 
the past few years, rapidly becoming the single most intrusive source of 
electronic noise in modern life. The meters in a mesh network communicate 
not only with the utility company but with each other, each meter chattering 
loudly to its neighbors as frequently as two hundred and forty thousand 
times a day. And the chattering is not silent. Shrill, high-pitched ringing and 
a variety of hissing and clicking noises are so consistently reported by 
utility customers following the installation of these smart meters that cause 
and effect can no longer be denied. The symbol transmission frequency of 
50 kHz for many of these systems, and the sheer power of the signal, 
outclassing other sources of radiation in the modern home, are likely 


responsible—that, and the pulsatile nature of the signal, like a woodpecker 
beating incessantly at all hours of the day and night. 


Tinnitus today 
Tinnitus rates have been rising for at least the last thirty years, and 
dramatically so for the last twenty. 

From 1982 to 1996, the National Health Interview Survey conducted by 
the United States Public Health Service included questions about both 
hearing impairment and tinnitus. Although the prevalence of hearing loss 
declined during those years, the rate of tinnitus climbed by one-third.? 
Later, the National Health and Nutrition Examination Surveys (NHANES), 
conducted by the Centers for Disease Control, found that the rate continued 
to climb. In 1982, about 17 percent of the adult population complained of 
tinnitus; in 1996, about 22 percent; between 1999 and 2004, about 25 
percent. The authors of the NHANES study estimated that by 2004, 50 
million adults suffered from tinnitus.°* 

In 2011, Sergei Kochkin, the Executive Director of the Better Hearing 
Institute in Washington, D.C., reported the very surprising result of a 
nationwide survey, conducted in 2010. What was so surprising was that 44 
percent of Americans who complained of ringing in their ears said they had 
normal hearing. Kochkin simply did not believe it. "It is widely 
acknowledged that people with tinnitus almost always have hearing loss," 
he said. He therefore assumed that millions of Americans who complain of 
ringing in their ears must have hearing loss but don't know it. But his 
assumption is no longer valid. 

Researchers who wish to study real tinnitus have to be careful. If you 
put the average human being in a soundproof room for several minutes, he 
or she will begin to hear sounds that are not there. Veterans Administration 
doctors Morris Heller and Moe Bergman demonstrated this in 1953, and a 
research team at the University of Milan repeated the experiment fifty years 
later with the same result: over 90 percent of their subjects heard sounds.? 
Therefore the results of tinnitus surveys may depend on the way the data are 
gathered as well as the way the questions are worded and even on the 
definition of "tinnitus." To really find out if tinnitus is increasing, we need 


virtually identical studies done a number of years apart by the same 
researchers in the same place on the same population. And we have just 
such a series of studies. 

During the years 1993 to 1995, 3,753 residents of Beaver Dam, 
Wisconsin, aged 48 to 92, were enrolled in a hearing study at the University 
of Wisconsin, Madison. Follow-up examinations were done on these 
subjects at five, ten, and fifteen year intervals. In addition, the children of 
the original subjects were enrolled in a similar study between 2005 and 
2008. As a result, data on the prevalence of tinnitus in this population are 
available almost continuously from 1993 to 2010. 

Since hearing disorders among older adults declined during this period, 
the researchers expected to see a corresponding decline in tinnitus. They 
found just the opposite: a steady increase in tinnitus in all age groups during 
the 1990s and 2000s. For example, the rate of tinnitus among people aged 
55 to 59 increased from 7.6 percent (at the beginning of the study) to 11.0 
percent, to 13.6 percent, to 17.5 percent (at the end of the study). Overall, 
the rate of tinnitus in this population increased by about 50 percent.*? 

We also have a series of studies, conducted during these same years, on 
young children, who have long been assumed to have almost no tinnitus. 

Kajsa-Mia Holgers is a professor of audiology at the University of 
Jonkoping in Sweden. She conducted her first study in 1997 on 964 seven- 
year-old school children in Góteborg who were undergoing routine 
audiometry testing—470 girls and 494 boys. Twelve percent of the children 
said they had experienced ringing in their ears, the vast majority of whom 
had perfect hearing. Nine years later Holgers, using the same study design 
and the same tinnitus questions, conducted an identical study on another 
large group of seven-year-old school children in Góteborg who were 
undergoing audiometry testing. This time an astonishing 42 percent of the 
children reported ringing in their ears. *We face a several fold increase in 
the problem in just a few years," an alarmed Holgers told the national daily 
newspaper, Dagens Nyheter. 

To further explore the problem, Holgers gave a detailed questionnaire to 
middle and high school students aged 13 to 16 during the 2003-2004 school 
year. More than half of these older students reported tinnitus in some form. 





And in 2004, Holgers studied another group of school children aged 9 to 
16, almost half of whom had spontaneous tinnitus. Even more alarming was 
the fact that 23 percent reported their tinnitus to be annoying, that 14 
percent heard it everyday, and that hundreds of children were showing up at 
Holgers' audiology clinic seeking help for their tinnitus. 

If what is occurring in Wisconsin and Sweden is also occurring in the 
rest of the world—and there is no reason to think otherwise—then in less 
than two decades, as computers, cell phones, fluorescent lights, and a 
crescendo of digital and wireless communication signals have penetrated 
every recess of our environment, at least a quarter of all adults and half of 
all children have entered a new world in which they must live, learn, and 
function while attempting to ignore an inescapable presence of intrusive 
electronic noise. 


16. Bees, Birds, Trees, and Humans 


ALFONSO BALMORI MARTÍNEZ is a wildlife biologist who lives in 
Valladolid, Spain. In his official capacity he works in wildlife management 
for the Environment Department of his region, Castilla y León. But for over 
a decade he has also labored for a cause that he considers at least as 
important. “It was in about the year 2000,” he says, “that I began to be 
aware of serious health problems that were being provoked by cell phone 
antennas in certain individuals who were my neighbors and acquaintances, 
including a serious situation in the school which my two oldest sons were 
attending at that time.” The problem at the school, the Colegio Garcia 
Quintana, was not easy to ignore, since he was confronted with it every 
time he dropped off his sons there. For looming over the playground, like a 
giant pincushion, a neighboring building’s rooftop harbored about sixty 
transmission antennas of all shapes and sizes. 





Alfonso Balmori Martinez 


The antenna farm sprouted its communication crop rapidly, and during 
the first year of its growth, between December 2000 and January 2002, five 
cases of leukemia and lymphoma were diagnosed in succession at the 
school—four in children aged four to nine, and the fifth in a seventeen- 
year-old young woman who did cleaning. Considering that only four cases 
of leukemia and lymphoma in children under twelve had been diagnosed 
during the previous year in all of the province of Valladolid, the community 
was frightened. The school was closed by the Health Department on 
January 10, 2002, and was reopened several weeks later after inspectors 
could find no dangerous conditions within. The antennas, however, were 
removed by court order of December 2001, and a new organization, 
AVAATE—Asociacion  Vallisoletana de  Afectadas por Antenas de 
TElefonía (Valladolid Association of People Affected by 
Telecommunication Antennas)—arose from their ashes, nurtured in part by 
a newly motivated Balmori, who was disturbed by what he was learning. 
People exposed to antennas were not just getting cancer, but in much 
greater numbers they were getting headaches, insomnia, memory loss, heart 
arrhythmias, and acute, even life-threatening neurological reactions. “After 
educating myself over a period of several months,” he recalls, “and 
discovering that something so evident was considered by the authorities to 
be groundless fear and little more than a ‘social psychosis’ without 
scientific basis, I decided to study the effects on fauna and flora. I thought 
that a ‘collective psychosis’ or ‘groundless fear’ could not be attributed to 
non-human organisms. And so I began to study storks, pigeons, trees, 
insects, tadpoles... and to publish the results that I was obtaining.” 

The effects Balmori found were dramatic and universal. Radiation from 
cell phone antennas affected every species he looked at. Storks, for 
example. White storks (Ciconia ciconia) are a common urban bird in many 
Spanish cities, inhabiting buildings and church steeples alongside sparrows 
and pigeons. Selecting 60 rooftop nests scattered throughout Valladolid—30 
that were within 200 meters of one or more cell sites, and 30 that were 
further than 300 meters (about 1,000 feet) from any cell sites—Balmori 
observed the storks with telescopes during the spring of 2003 to determine 
their breeding success. By measuring the electric field at each location, he 


verified that the radiation, on average, was four and a half times more 
intense at the closer locations. Between February 2003 and June 2004 he 
also paid several hundred visits to 20 nests that were within only 100 meters 
of a cell site in order to observe the birds during all phases of breeding. 

The results, for a wildlife biologist, were profoundly disturbing. The 
nests that were closer than 200 meters from the nearest cell tower fledged 
half the number of baby storks as the nests that were further away. Of the 
30 highly exposed nests, 12 fledged no chicks at all, while only one of the 
lesser exposed nests was barren. Of the 12 highly exposed nests where no 
young were flown, some had hatched out no chicks, and others had 
produced chicks that died soon after hatching. The behavior of the birds that 
nested within 100 meters of a tower was just as troubling. Stork couples 
fought over nest construction. Sticks fell to the ground while the couple 
tried to build the nest. 





In light of the plummeting numbers of house sparrows in Europe, 
Balmori also undertook to monitor the number of sparrows at thirty parks 
and park-like locations in Vallodolid between 2002 and 2006. He visited 
each of these points on Sunday mornings, once a month for four years, 
counting birds and measuring radiation. He found not only that sparrows 
were becoming generally much fewer over time, but that they were 
incredibly more numerous in less irradiated areas—42 sparrows per hectare 
where the electric field was 0.1 volts per meter, down to only one or two 
Sparrows per hectare where the electric field was over 3 volts per meter. It 
was clear to Balmori why the species was disappearing. The United 
Kingdom had even added the house sparrow to its Red List of threatened 
and endangered species after the bird’s population in British cities fell by 75 
percent between 1994 and 2002. “This coincides with the rollout of mobile 
telephony,” he wrote. If the declining trend that he observed in his home 
town continued, he said, the house sparrow would be extinct in Valladolid 
by 2020.! 





O 


Kestrel: “A general disappearance of the kestrels that had bred 
every year on nearby roofs, after antennas for mobile 
telecommunications were installed.” 


White Stork: “Although this species is quite opposed to abandon 
its nest, even under adverse conditions, the nests placed near 
phone masts’ radiation beams gradually disappeared.” 


Rock Dove (domestic): “Many dead specimens appeared near 
phone mast areas.” 


Magpie: “Anomalies were detected in a great number of 
specimens at points highly contaminated with microwave 
radiation; such as, plumage deterioration, especially in head and 
neck, locomotive problems (limps and difficulties in flying), 
partial albinism and melanism, especially in flanks, and a 
tendency to stay long in low parts of trees and on the ground.” 


Green woodpeckers, short toed treecreepers, and Bonnelli’s 
warblers, all previously common, disappeared sometime between 
1999 and 2001 and were not seen again. 


Half of the park’s 14 resident bird species had either seriously declined 
or vanished despite the fact, as Balmori points out, that air pollution 
improved. 





wrote Jenny De Laet and James Denis Summers- Smith. Their 
2007 study found spectacular declines of over 90 percent in house sparrow 
populations in London, Glasgow, Edinburgh, Dublin, Hamburg, Ghent, 
Antwerp, and Brussels. Scattered throughout Princes Street Gardens, a 50- 
acre park in central Edinburgh, at least 250 sparrows had resided as recently 
as 1984. In 1997, only 15 to 30 birds were left, in only a single location. 


central London, declined from 2,603 in 1925 to just four in 2002. This bird, 
which has associated with human beings for at least ten thousand years, is 
vanishing even where there are plenty of seeds and insects, where 
ornithologists can find no obvious cause for its decline. But there is a cause, 
and it is hidden in plain sight. Today, twenty-six antenna installations are 
lined up on the northern, western, and southern borders of Kensington 
Gardens, operated by Vodafone, T-Mobile, Orange, O2, 3, and Airwave. 
They are saturating this beautiful park with microwaves so that human 
visitors can use their cell phones and the police can use their radios. The 
situation in Edinburgh's Princes Street Gardens is even worse. Thirty-four 
cell sites surround this much smaller park, most of them less than five 
meters above the ground. The only location where sparrows still nested in 
1997—the Gatekeeper’s cottage—is nestled against the bottom of an 
artificial hill called The Mound, and is the only spot in the entire park that 
is not in the direct beam of multiple microwave antennas. The irradiation of 
these parks that began in 1992 parallels the catastrophic collapse of their 
house sparrow communities. 

The situation in Switzerland has become so alarming that the Swiss 
Association for the Protection of Birds declared the house sparrow “bird of 
the year” for 2015. A study conducted by zoologist Sainudeen Pattazhy in 
Kerala, India during 2008 and 2009 found that house sparrows were 
virtually extinct there. In Delhi, ornithologist Mohammed Dilawar 
reminisces that “till March 2001, they were in and out of our home. We left 
for a while to return to see, the commonest bird had flown the nest.”? 
Pattazhy’s conclusion is the same as Balmori’s: cell towers are leaving 
sparrows no place to live. “Continuous penetration of electromagnetic 
radiation through the body of birds affects their nervous system and their 
navigational skills. They become incapable of navigation and foraging. The 
birds which nest near towers are found to leave the nest within one week,” 
he says. “One to eight eggs can be present in a clutch. The incubation lasts 
for 10 to 14 days. But the eggs which are laid in nests near towers failed to 
hatch even after 30 days.” 

It may seem surprising that sparrows, of all birds, seem to be among the 
most sensitive to electricity. But we recall from chapter 7 that sparrows 


were noted 
following upon the return of sunspots to the sun, 


and the celestial aurora to polar skies. 

The impact of radio waves on bird reproduction is no longer a matter of 
conjecture. While Balmori was doing his field study on storks, scientists in 
Greece were proving the effects in their laboratory. Ioannis Magras and 
Thomas Xenos at Aristotle University of Thessaloniki first exposed 240 
newly laid quail eggs in an incubator to the type of radiation emitted by FM 
radio transmitters. The levels of radiation were about the same as if the 
birds had built nests one to three hundred yards away from a 50,000-watt 
tower. But these eggs were exposed for only three days, and for only one 
hour a day: thirty minutes in the morning and thirty minutes in the 
afternoon. Forty-five of the embryos died. None of 60 quail eggs, nearby in 
an unirradiated incubator, died. 

Then the same researchers exposed 60 more quail eggs to pulsed 
microwaves—the type of radiation emitted by cell towers—continuously 
for three days, this time at only 5 microwatts per square centimeter, a level 
of exposure commonly found in cities today. Under these conditions 65 
percent of the embryos were killed. 

In a third experiment 380 chicken eggs were exposed to microwave 
radiation at a power level of 8.8 microwatts per square centimeter. Instead 
of irradiating them as soon as they were laid, the researchers exposed the 
eggs between the third and tenth days of their development. Under these 
conditions most of the embryos lived but developed abnormally. Under 
continuous-wave radiation 86 percent of the eggs hatched, but 14 percent of 
the chicks died soon after birth. Almost half of the remaining chicks were 
developmentally retarded and 3 percent had severe birth defects. Pulsed 
radiation produced a similar number of deaths, about half the number of 
retarded chicks, and twice the number of birth defects. Of 116 unexposed 
eggs, only two failed to hatch, none had birth defects, and only two were 
retarded in development. 

Disastrous effects of radio waves on birds were first noticed during the 
1930s by those who were most intimately connected with them: homing 
pigeon racers, and divisions of the military that were still using carrier 


pigeons for communication. Charles Heitzman, a father of the pigeon- 
racing sport in the United States, and Major Otto Meyer, former head of the 
United States Army's Pigeon Corps, were both alarmed 





Apparently, after many pigeon generations, the birds learned to adjust to 
the new conditions and the problem was largely, though not entirely, 
forgotten. 

Then in the late 1960s a team of Canadian researchers shed some new 
light on the problem. They were J. Alan Tanner, at Control Systems 
Laboratory, National Research Council, Canada; César Romero-Sierra, 
professor of neuroanatomy at Queens University; and Jaime Bigu del 
Blanco, biophysicist and research associate in the Queens University 
Department of Anatomy. They began by exposing young chickens to 
microwave radiation at relatively high power levels, between 10 and 30 
milliwatts per square centimeter. The birds usually collapsed to the floor of 
their cage within 5 to 20 seconds. Even if only their tail feathers were 
exposed they would scream, defecate, and try to escape. Experiments using 
pigeons and seagulls gave similar results. But not if the birds were 
defeathered. Chickens that had been plucked showed no evident reaction to 
being irradiated until about the twelfth day when their regrowing feathers 
were about one centimeter long. 

The researchers then measured radiation patterns in the laboratory using 
both individual feathers and arrays of feathers spaced varying distances 
apart, and proved that bird feathers make fine receiving aerials for 
microwaves. If this takes place while the bird is flying, they said, “an 
increase in the microwave field strength should be 'sensed' by the bird."* 





In the 1990s and early 2000s, when cell phone towers proliferated, 
raising the ambient levels of microwave radiation tens to hundreds of times 


higher everywhere in the world, when white storks had trouble reproducing 
near antennas, and when house sparrows made it onto the endangered 
species list in the United Kingdom, membership in pigeon-racing clubs 
plummeted and pigeon fanciers were forced to pay renewed attention to a 
problem they had laid aside in the 1950s. The secretary of the New Ross 
and District Pigeon Club in Ireland, Jim Power, blamed the new problem of 
lost birds, which had begun in about 1995, on “satellite television and the 
mobile telecommunications network.” The story made the front page of the 
Irish Times.5 Both events—the explosion of cell towers and severe pigeon 
losses—came to America in 1997.7 

In early October 1998 the story made headlines all over the United 
States as, during a two-week period, pigeon races far and wide ended in 
disaster, with up to ninety percent of birds going missing. "They're turning 
up in barns. Under bird feeders. On window ledges. And sometimes just 
standing out in the rain,” read the first paragraph of an article in the 
Washington Post. Out of 1,800 birds competing in a race from New Market, 
Virginia to Allentown, Pennsylvania, about 1,500 vanished. In a race from 
western Pennsylvania to suburban Philadelphia, 700 out of 900 pigeons 
failed to return. In a 350-mile race from Pittsburgh to Brooklyn, 1,000 out 
of 1,200 birds never showed up. 





n September 23, 1998, Motorola’s 66 newly-launched 
Iridium satellites had begun providing the first-ever cell phone service from 
space, everywhere on earth, to its first 2,000 trial subscribers. 

Many members of the British Royal Pigeon Racing Association changed 
the route their birds flew so as to avoid cell towers and lose fewer pigeons.!? 
In 2004, the Association called for more research into the impact of 
microwave radiation on birds. And as old-time pigeon racers gradually left 
the sport in discouragement, they were replaced by young enthusiasts who 
do not remember what it was like when almost all released pigeons would 
fly directly back to their roosts. The kinds of extraordinary losses Larry 
Lucero of New Mexico complained about in 1997—an 80 percent loss of 


birds in eight weeks of racing—are no longer considered unusual. 





“The number of losses 
occurring each year,” says Kevin Murphy at Scotland’s Angus College, “is 
showing no signs of improvement and whenever you speak to pigeon 
fanciers it’s the same old story; high losses in young birds and very few 
fanciers that are able to build up an established team of 3, 4 and 5 year old 
experienced birds.” 


Radio-tagging animals 

In an exercise in scientific folly, Murphy is proposing to solve the problem 
by developing a GSM/GPS device that will be fitted onto pigeons’ legs to 
keep track of wayward birds. Initially this is a research project—designed, 
he says, to see if solar flares and magnetic storms affect the birds’ homing 
ability. But the devices will track birds by satellites and cell phone towers— 
the very things that are now responsible for far more pigeon losses than 
solar flares. Worse, the devices, being radio transmitters themselves, will 
expose the birds at point blank range to far more radiation than distant cell 
towers. 

Microchipping pigeons to keep track of them is not yet standard practice 
in this sport. But in recent years pigeon racers are already making a bad 
situation worse by attaching radio frequency identification (RFID) “chip 
rings” to each bird’s foot during every race, so that when the bird arrives 
home and crosses the finish line, an RFID scanner automatically records the 
time of arrival. These are passive devices containing no batteries and rely 
on external sources of energy to activate them. But sudden deaths of exotic 
birds immediately after being microchipped are not unusual.?? 





environment enough to affect the nervous systems even of organisms 


without any homing ability. 






Land-based wildlife tracking systems use 
frequencies between 148 and 220 MHz and emit 10 milliwatts of power, 
day and night. Satellite tracking systems, such as are used to track dolphins 
and whales, require the animal to wear a much stronger transmitter, 
radiating from 250 milliwatts up to 2 watts of power—equivalent to giving 
the animal a satellite phone to wear. These are also used to track turtles, 
sharks, polar bears, musk oxen, camels, wolves, elephants, and other 
animals that roam or swim very long distances. They are also used on long- 
migrating or elusive birds, such as albatrosses, bald eagles, penguins, and 
Swans. 


If a 
creature exists today that is large enough to fashion antennas for, you may 
be assured that resourceful wildlife biologists have devised ways to affix 
them onto members of its species, be it by means of collars, harnesses, or 
surgical implants. In a misguided effort to discover why honey bees are 
disappearing, Australia’s leading scientific research agency, the 
Commonwealth Scientific and Industrial Research Organization, is in 
process of attaching RFID tags with superglue to the backs of two and a 
half million bees and placing RFID readers inside one thousand hives. 





On February 6, 2002, the U.S. National Park Service issued a report 
warning wildlife biologists that radio tracking devices could radically alter 


the very behaviors they are using the devices to study, and that not only the 
physical dimensions of the devices, but the radio waves they emit could be 
detrimental to the animals’ health.? Effects of radio-tagging birds, 
according to this and other reports, have included increased preening, 
weight loss, abandonment of brood, reduced time spent in flight, increased 
metabolism, avoidance of water, decreased courtship activity, decreased 
feeding activity, decreased clutch survival, reduced wing growth, greater 
susceptibility to predation, lowered reproductive success, and increased 
mortality.'^ 

Radio collared mammals, including rabbits, voles, lemmings, badgers, 
foxes, deer, moose, armadillos, river otters, sea otters, and wild dogs in the 
Serengeti!’ have suffered increased mortality, impaired digging ability, 
weight loss, reduced activity levels, increased self-grooming, altered social 
interactions, reproductive failure, and profoundly altered sex ratios of 
offspring. In one study of moose, calves with plain ear tags and calves 
without any ear tags had equal mortality rates—about 10 percent 





16 [n another study, involving water voles at 

England's Bure Marshes National Nature Reserve, colonies that contained 

radio tagged females gave birth to more than four times as many males as 

females. The researchers concluded that likely none of the radio tagged 
female voles gave birth to any female offspring." 

In some cases radio tagging endangered species may drive them further 






toward extinction. 


The results of an extensive review of the literature, published in 2003, 
examining 836 scientific studies on radio tagged animals, found that 90 
percent of them ignored the effects of the radio tags on the animals, making 
a tacit assumption that they had no significant impact. But of those studies 
that asked the question, the majority found one or more detrimental effects 
of these devices on their bearers.!? 


Migratory Birds 

Professor Keeton's work has widespread importance for bird conservation. 
Even in captivity, when the migratory season is upon them, songbirds will 
face the direction in which they have an urge to fly. Therefore, scientists at 
the University of Oldenburg in Germany were shocked to find, beginning in 
2004, that the migratory songbirds they had been studying were no longer 
able to orient themselves toward the north in spring and toward the 
southwest in autumn. Suspecting that electromagnetic pollution might be 
responsible, they surrounded the aviaries in which they kept European 
robins with grounded aluminum sheeting beginning in the winter of 2006- 
2007. “The effect on the birds’ orientation capabilities was profound," 
wrote the authors of the study, which they published in 2014. Only when 
the aluminum sheeting was grounded did the birds orient normally in 
springtime. And since the enclosure, when not grounded, only admitted 
frequencies below 20 MHz, the birds were evidently being disoriented not 
by cell towers, but by radiation originating from AM radio towers, as well 
as from ordinary household electronic equipment. In a rural area outside 
Oldenburg, the robins were still able to orient themselves without the 
aluminum screening. But the scientists issued a warning: “If anthropogenic 
electromagnetic fields prevent migratory songbirds from using their 
magnetic compass, their chances of surviving the migratory journey might 
be significantly reduced, in particular during periods of overcast weather 
when sun and star compass information is unavailable. Night-migratory 
songbird populations are declining rapidly.””° 


Amphibians 

In 1996, when I was writing my first book, Microwaving Our Planet: The 
Environmental Impact of the Wireless Revolution, the decline of frogs, 
toads, salamanders, and other amphibians the world over caught my 
attention like an alarm bell. Why weren't people more concerned, I 
wondered? Like the debris of recently wrecked craft, this catastrophe 
should provide the ship of humanity with urgent cause to shift direction. 
“An Amphibian Horror Story,” screamed a headline from New York 
Newsday.” “Trouble in the Lily Pads,” announced Time Magazine.” “Space 


Aliens Stealing Our Frogs," read a supermarket tabloid.? It seemed that 
mutant frogs were turning up by the thousands in pristine lakes, streams, 
and forests all across the American midwest. Their deformed legs, extra 
legs, missing eyes, misplaced eyes, and other genetic mistakes were 
frightening school children out on field trips.^ Every species of frog and 
toad in Yosemite National Park, I learned, was disappearing. The boreal 
toad, which used to be so abundant near Boulder, Colorado that drivers 
would squish large numbers on mountain roads, had dwindled to about five 
percent of its former population. When I dug deeper I learned that frogs 
were falling silent in other countries too, and had been doing so for over a 
decade. In the Monteverde Cloud Forest Preserve of Costa Rica, the famous 
and highly protected golden toad, named for its brightly colored skin, had 
gone extinct. Eight of thirteen frog species in a Brazilian rainforest preserve 
had vanished. The gastric-brooding frog of Australia, I read, named for its 
habit of incubating its young in its stomach, “broods no longer.” Seventy- 
five species of the colorful harlequin frogs that once lived near streams in 
the tropics of the Western Hemisphere had not been seen since the 1980s.?’ 

What so puzzled scientists was not just that an entire very ancient class 
of animals—the Amphibia—were disappearing, but that they were 
vanishing in so many pristine, remote environments that were thought to be 
unpolluted. Which is one of the aspects of the story that so grabbed my 
attention. Environmentalists, for the most part, like the rest of modern 
humanity, have one terrific blind spot: they don’t acknowledge 
electromagnetic radiation as an environmental factor, and they are 
comfortable with placing power lines, telephone relay towers, cell towers, 
and radar stations in the middle of the most remote, pristine mountainous 
locations, never realizing that they are intensely polluting those 
environments. I was only speculating, at that time, that the discovery of 
grossly deformed frogs in the midwest was related to the increasingly 
frequent reports from farmers in the midwest of cows and horses born with 
webbed necks and legs on backwards after cell towers were built on or next 
to their farms.” It seemed more than coincidental that the reports of 
misshapen amphibia were coming from popular lake vacation districts, 
which were almost certain to have had cell towers built during 1996. 


Balmori's curiosity paralleled mine, and in 2009, he put his speculations 
to the test. During a two-month period he took care of two almost identical 
tanks of tadpoles of the common frog that he set out on the fifth floor 
terrace of an apartment in Valladolid. One hundred forty meters (450 feet) 
away, on the roof of an eight-story building, stood four cellular phone base 
stations, which were irradiating the neighborhood. The only difference 
between the two tanks of tadpoles was that a layer of thin fabric was draped 
over one. The fabric, woven with metallic fibers, admitted air and light but 
kept out radio waves. The results were a shocking confirmation of what was 
occurring out in the rest of the world: in a period of two months, the 
mortality rate was 90 percent in the exposed tank, and only 4 percent in the 
shielded tank. Almost all of the exposed tadpoles—exposed only to what 
the residents of the apartment building were also exposed to—swam in an 
uncoordinated fashion, showed little interest in food, and died after six 
weeks. Balmori titled his 2010 article, “Mobile Phone Mast Effects on 
Common Frog (Rana temporaria) Tadpoles: The City Turned Into a 
Laboratory.” 

In the late 1990s, researchers in Moscow had put these kinds of effects 
to the test in another urban laboratory, using another device that we all take 
for granted. They exposed developing frog embryos and tadpoles to an 
ordinary personal computer. The resulting frogs had severe malformations 
that included anencephaly (absence of a brain), absence of a heart, absence 
of limbs, tail necrosis, and other deformities that were “incompatible with 
survival.”?9 


Insects 

The insect world is as susceptible to electromagnetic pollution as the 
amphibian world. In fact, as Alexander Chan discovered in 2004, it is so 
easy to demonstrate the effects of computers and cell phones on diminutive 
creatures that even a sophomore in high school can do it for a science fair 
project. Then fifteen years old and a student at Benjamin Cardozo High 
School in Queens, New York, Chan exposed fruit fly larvae daily to a 
loudspeaker, a computer monitor, and a cell phone and observed their 
development. The flies that were exposed to the cell phone failed to develop 


wings. “Radiation and electromagnetic emissions are really more harmful 
than anyone realizes," the stunned teenager concluded.°° 





Photo by Alan Raia, New York Newsday 


At the University of Athens, Dimitris Panagopoulous has been doing 
similar work with fruit flies for a decade and a half, and producing results 
that are just as alarming. Like Chan—and unlike most other scientists doing 
research on electromagnetic radiation—he and his colleagues in the 
Department of Cell Biology and Biophysics decided to expose their flies 
not to specialized equipment, but to an ordinary cell phone in use. In their 
first experiments, in 2000, they found that a few minutes’ exposure was 
enough to radically interfere with fly reproduction. Exposing adult flies to 
the antenna of a working cell phone for just six minutes a day for five 
consecutive days reduced the number of eggs they laid by 50 to 60 percent. 
When the insects were exposed for only two days, i.e. a total of twelve 
minutes of radiation, the number of eggs was reduced by an average of 42 
percent. Even flies that were exposed for only one minute a day for five 
days produced 36 percent fewer offspring than their unexposed cousins. 
Regardless of whether just male flies, just female flies, or both were 
exposed, the number of offspring was greatly reduced. Their experiments 


cried out for an explanation, because such rapid sterilization was an effect 
scientists were used to seeing from X-rays, not from an ordinary cell 
phone.*! So in follow-up experiments, after zapping the flies with a cell 
phone for five days—again for six minutes a day—the researchers killed the 
flies and used a standard technique—the TUNEL assay—to look for 
fragmented DNA in the ovaries and egg chambers of the female flies. Using 
this technique they proved that the brief exposure to a cell phone was 
causing the death and degeneration of 50 to 60 percent of both eggs and 
their supporting cells at all stages of development.? 
In later experiments these scientists 
a not uncommon finding in electromagnetic research. 





Using a 900 MHz phone, Panagopoulos' flies produced 
even fewer offspring when the antenna was held a foot away—reducing the 
exposure level by a factor of almost 40—than when the antenna was 
actually touching the vial of flies. With an 1800 MHz phone, maximum 
mortality occurred at a distance of eight inches. In a large series of further 
experiments, exposure to a cordless phone base station, a cordless phone 
handset, a WiFi router, a baby monitor, a microwave oven, and several 
different kinds of bluetooth devices each lowered the numbers of offspring 
of two different species of fruit flies by up to 30 percent. Exposure time 
varied from 6 minutes, just once, up to thirty minutes a day for nine days. 
Every experiment, regardless of exposure time, produced cell death in the 
developing eggs and at least a ten percent reduction in the number of 
offspring.*4 





the phone—even though it was still turned off—the ants' helter-skelter 
movements became radically disturbed. The little creatures darted back and 
forth with increased vigor, as if trying to escape an enemy they could not 
see. The rate at which they changed directions—their angular speed— 
increased by 80 percent. When the phone was then put into standby mode, 
they changed directions even more. Finally, Cammaerts turned the phone 
on. Within two to three seconds, the insects visibly slowed down. 

Cammaerts next exposed a fresh ant colony to a smartphone and then a 
“DECT” cordless phone. In each case the creatures’ angular speed doubled 
or tripled, while their actual walking speed drastically slowed. This 
happend within one to three seconds. When the DECT phone was on, the 
ants were “nearly paralyzed.” After being thus exposed for three minutes to 
each of the two pieces of equipment, they required two to four hours before 
they appeared normal again. Cammaerts then repeated the experiment with 
a fresh colony, this time placing a flip phone in standby mode under the 
ants’ nest instead of under its foraging area. Immediately all the ants left 
their nest, taking their eggs, larvae, and nymphs with them. “It looked 
spectacular,” she said. “They relocated their nest far from the place under 
which the mobile phone was located. After the experimentation, when the 
mobile phone has been removed, the ants returned to their initial nest, 
transporting back their brood into the nest. This relocation lasted about one 
hour.” 

Finally, Cammaerts tested a WiFi router, placed between two colonies of 
ants, about one foot away from each colony. While the router was still 
switched off, nothing unusual happened. But “after a few seconds of 
exposure, the ants clearly presented signs of bad health and, consequently, a 
disturbed behavior.” After being exposed to the router for thirty minutes, 
the ants had to recover for six to eight hours before foraging as usual again. 
“Unfortunately,” wrote Cammaerts, “several ants never recovered and were 
found dead a few days later.” 

For his part, Panagopoulous, in a chapter of a 2012 book about 
Drosophila melanogaster, has issued a severe and unusual warning to the 
world: “The experimental results of ours as well as of other experimenters 
show that microwave exposure even for a few minutes per day and for only 


a few days, at exposure levels encountered in our everyday environment, is 
maybe the most intense modern environmental stress factor compared to 
other environmental stress factors tested so far, like starvation, heat, 
chemicals, electric or magnetic fields." He warned that DNA damage to the 
developing egg may "result in inherited mutations transferred to subsequent 
generations. For this reason the biological changes due to microwave 
radiation may be far more dangerous as they may not be restricted only to 
changes in reproductive capacity." 


Colony Collapse Disorder 

In recent years an apocryphal story has circulated about Albert Einstein. “If 
the bee disappears from the surface of the earth," he is supposed to have 
said, “man would have no more than four years to live." 





Perishing honey bees do constitute a warning to the world, but the real 
story is not circulating because it is not yet acceptable to remove the 
cultural blinders regarding electricity. Beekeepers the world over are still 
poisoning their bees against parasites that are not killing them, instead of 
paying attention to the influence that is. 

“I observed a pronounced restlessness in my bee colonies," wrote 
Ferdinand Ruzicka to the Austrian beekeeping community in 2002, “and a 
greatly increased urge to swarm.” Ruzicka, a medical physicst retired from 
the University of Vienna, is also an amateur beekeeper. He observed the 
strange behavior after telecommunications antennas appeared in a field near 
his hives. “I am a frame-hive beekeeper,” he wrote. “The bees now built 
their honeycombs not in the manner prescribed by the frames, but in a 
helter skelter fashion. In the summer, the colonies collapsed without any 


obvious cause. In the winter, despite snow and below zero temperatures, the 
bees would fly out and freeze to death next to the hive. Colonies that 
exhibited this behavior collapsed, even though they were strong, healthy 
colonies with active queens before the winter. They were provided with 
adequate additional food and the fall pollen supply had been more than 
sufficient." 





As we saw in chapter 9, bee colonies have been disappearing near 
communication towers for over a century. On the small island lying off 
England's southern coast where Marconi sent the world's first long-distance 
radio transmission in 1901, the bees began to vanish. By 1906, the island, 
then host to the greatest density of radio transmissions in the world, was 
almost empty of bees. Thousands, unable to fly, were found crawling and 
dying on the ground outside their hives. Healthy bees imported from the 
mainland began dying within a week of arrival. 

During the next few decades “Isle of Wight disease” was reported 
throughout Great Britain and in Italy, France, Switzerland, Germany, Brazil, 
Australia, Canada, South Africa, and the United States.” Almost everyone 
assumed it was infectious, and in 1912, when Graham Smith at Cambridge 
University found a parasite called Nosema apis in the stomachs of some 
diseased bees, most people thought the mystery had been solved. However, 
this theory was soon disproven by John Anderson and John Rennie in 
Scotland; 





So the search went on for a different parasite, and in 1919 Rennie 
presented Acarapis woodi, which inhabited bees’ breathing passages. His 
article in the Transactions of the Royal Society of Edinburgh had such wide 


influence that the tracheal mite is today regarded as one of the two major 
parasitic infections of bees that are responsible for colony collapse disorder. 
It supposedly kills bees by sucking their blood and clogging their breathing 
tubes. In fact, this is so widely accepted that it is standard practice for 
commercial beekeepers to treat all their bees with miticides to kill both 
tracheal mites and a second kind of mite, the Varroa mite. However, in the 
late 1950s the tracheal mite theory was disproven, too, by the eminent 
British bee pathologist, Leslie Bailey. Not only did he show that mite- 
infested bees did not die at greater rates than non-infested bees, but he 
deliberately infected healthy bees with the parasite and proved that it did 
not cause disease. The only effect of infestations, wrote Bailey in 1991, is to 
"shorten very slightly the life of bees, but usually causing no obvious 
sickness in spite of the abnormal appearance of infested tracheae." 

Bailey also warned against attaching too much importance to the Varroa 
mite, which, he said, had achieved its notoriety partly because of its size: it 
is the only common parasite of honey bees that can be seen with the naked 
eye and identified with a hand lens. Varroa mites, after all, while not 
harmless, have coexisted with wild populations of honey bees for a century 
in Japan? and Russia, and more recently in Serbia,“ Tunisia, Sweden,” 
Brazil,^ Uruguay,^ and even parts of California^ and New York.^ Other 
environmental factors, said Bailey, determine the amount of damage done 
by this parasite. 

The problem of Isle of Wight disease smoldered for decades, not often 
making the news. But the number of managed honey bee colonies in the 
United States has been quietly declining since the 1940s.*? During the 1960s 
and 1970s unexplained large losses acquired a new name— “disappearing 
disease"—and was reported in Montana, Nebraska, Louisiana, California, 
Texas, Europe, Mexico, Argentina, and Australia. Beekeepers would open 
their hives in autumn or winter to find ample supplies of stored pollen and 
honey but no bees. Where some dead or living bees remained, they were not 
malnourished and had no mites or other parasites, bacteria, viruses, or 
poisons. Attempts to transmit the condition by introducing bees from 
“diseased” hives into healthy ones failed. When a survey was conducted by 
the United States Department of Agriculture in 1975, the problem turned up 


in 33 states, with beekeepers often volunteering that it had been prevalent in 
their colonies for ten or fifteen years, and that it was getting worse with 
each passing year.^ 

Then, during the last half of the 1990s, when the telecommunications 
industry was beginning to weave its web of antennas over cities, farmland, 
and wildland, American farmers reawoke to a crisis. The smoldering, half- 
forgotten problem about disappearing bees was erupting in flames. 
"Farmers Stung By Bee Shortages," warned a headline in the June 15, 1996 
edition of the Washington Post. During the previous winter, beekeepers had 
lost 45 percent of their hives in Kentucky, 60 percent in Michigan, 80 
percent in Maine.°° Farmers were also waking up to the fact that wild bees 
weren't going to be there to take over the job of pollinating their crops, 
because 90 percent of all feral honey bee colonies nationwide had already 
disappeared.*! All this havoc—at least in the United States—was thought to 
have been caused by two bee parasites, the tracheal mite and the even more 
voracious Varroa mite, assumed to have hitchhiked into the United States in 
shipments of infected bees from Europe and Asia during the 1980s. 

But the alarm spread to Europe during the winter of 2002-2003. 
Officially there was no panic: colony losses were “only” 20 percent in 
Sweden and 29 percent in Germany. Swedish beekeeper Bórje Svensson, 
who published an article titled *Silent Spring in northern Europe?", begged 
to differ. When he opened up his hives that winter, 50 out of 70 colonies 
were devoid of life. A neighbor had lost 95 of 120 colonies, and another 
neighbor lost 24 of 25. Fellow beekeepers in Austria, Germany, Belgium, 
Denmark, and Finland were reporting similar huge losses, although many 
could find no Varroa mites, and no sign of foulbrood, sacbrood, chalkbrood, 
Nosema, or other bee diseases. 

Finally, during the winter of 2006-2007, what was once known as Isle of 
Wight disease became a worldwide panzootic, frightening farmers and the 
public everywhere, and was given yet another name: colony collapse 
disorder.? The United States lost one-third of its honey bees in just a few 
months, with many beekeepers experiencing a total loss of their bees.” First 
thought to be confined to Europe, North America and Brazil,^ colony 
collapse disorder soon spread to China, India, Japan, and Africa.» Farmers 


in many countries are pollinating growing acreages of crops with half as 
many bees, and replenishing their losses with greater difficulty and expense 
with each succeeding year. 

And the culprit, according to a study conducted by a joint team of 
American and Belgian researchers, does not seem to be tracheal mites, 
Varroa mites, Nosema, or any other particular infectious disease vector. 
During the disastrous winter of 2006-2007, this team, headed by Jeffery 
Pettis of the United States Department of Agriculture's Bee Research 
Laboratory, examined thirteen large apiaries owned by eleven different 
commercial beekeepers in Florida and California, and to their amazement 
were unable to find any specific nutritional, toxic, or infectious factor that 
differentiated bees or colonies with and without colony collapse disorder. 
Tracheal mites were actually more than three times as prevalent in the 
healthy colonies as in the decimated colonies. Even the supposedly 
devastating Varroa mite was not more prevalent in collapsed or collapsing 
colonies. The only helpful conclusion that these scientists were able to 
come to was that “some other factor” must be responsible for the bees’ 
weakened state, and that the “other factor” seemed to be location-specific: 
colonies with this disorder tended to cluster together. 

The picture of this disease that has beekeepers so thoroughly baffled 
resembles nothing so much as the scene of an apparent mass murder where 
there is not even any real evidence of a crime. A million colonies a year in 
the United States disappear overnight without leaving a trace. The queen 
bee and mother of the hive is simply abandoned by the workers and left to 
starve and die. What has scientists even more stumped is that the dead 
colonies tend to be left alone even by the parasites that normally infest dead 
honey bee colonies. It is as though there were a large “KEEP OUT” sign at 
the entrance to these hives that is respected by friend and foe alike. 

The international beekeeping community is extremely resistant to giving 
up its long-standing belief in the infectious nature of bee losses, and so, in 
the absence of evidence, most beekeepers are falling back on the only thing 
they know: more toxic pesticides to kill mites.% 

But the decimation of so many other insect species that are not subject 
to the same parasites is a strong hint that a non-infectious agent is at work. 


The Franklin bumble bee, once prevalent in southwestern Oregon, has not 
been seen in a decade. Until the mid-1990s, the western bumblebee was 
abundant in forests, fields, and urban backyards throughout western North 
America, from New Mexico to Saskatchewan to Alaska. It has vanished 
except for small pockets in the Colorado Rockies. The rusty-patched 
bumble bee, a familiar visitor to flowers on the Cornell University campus 
when I was a student there, has not been seen in New York State since 
2004. Once common in 26 states and two Canadian provinces, this insect 
has disappeared from the eastern United States and Canada and has 
drastically declined in the American midwest. The Xerces Society for 
Invertebrate Conservation lists 57 species of bees and 49 species of 
butterflies and moths native to North America and Hawaii as vulnerable, 
imperiled, or extinct in their entire range. The Massachusetts Division of 
Fisheries and Wildlife lists 46 species of butterflies and moths that are 
threatened and endangered in Massachusetts. 

Exquisite sensitivity to electromagnetic fields has been demonstrated in 
a variety of insects. Termites, for example, will avoid building their 
galleries near other groups of termites, so as not to compete for food. In 
1977, Günther Becker proved that the signal that enables groups of termites 
to avoid competing with each other passes through walls and can be 
blocked by aluminum, but not by thick polystyrene and not by solid glass. 
The signal blocked by the aluminum had to be alternating electric fields 
emitted by the insects. 

It must not be forgotten, warns German biologist Ulrich Warnke, that 
every insect is equipped with a pair of antennas, which are demonstrably 
electromagnetic sensors.” In fact, the signals communicated between honey 
bees when they meet and touch antennas can be recorded by an oscilloscope 
and appear to be frequency modulated between 180 Hz and 250 Hz.*»? 

And the famous waggle dance, Warnke reminds us, by means of which 
honey bees tell each other the precise direction of food sources with respect 
to the sun, depends on their knowing the exact position of the sun, even on 
cloudy days, and within the darkness of the hive. Bees accomplish this feat 
by sensing minute variations in the earth's magnetic field—a sense, he says, 


o 


that can be rendered useless under the assault of wireless transmissions with 
their constantly changing magnetic fields.9? 

The quickest way to destroy a bee hive, investigators have found, is to 
place a wireless telephone inside it. The results of such experiments, 
considering the complete denial by our society that wireless technology has 
any environmental effects at all, have been almost unbelievable. 

In 2009, environmental scientist Ved Parkash Sharma and zoologist 
Neelima Kumar, at Panjab University in India, placed two cell phones each 
—one in talk mode and one in listening mode in order to maintain the 
connection—in two of four hives. They turned them on at 11:00 in the 
morning for 15 minutes, and at 3:00 in the afternoon for another 15 
minutes. They did this twice a week between February and April. As soon 
as the phones were turned on the bees would become quiet and still *as if 
unable to decide what to do." During the course of three months fewer and 
fewer bees flew in and out of those two hives. The number of eggs laid by 
the queen declined from 546 to 145 per day. The area under brood declined 
from 2,866 to 760 square centimeters. Honey stores declined from 3,200 to 
400 square centimeters. “At the end of the experiment there was neither 
honey, nor pollen nor brood nor bees in the colony resulting in complete 
loss of the colony,” wrote the authors. 

The following year Kumar performed a landmark experiment, described 
in more detail in chapter 11, that showed dramatically and simply how 
electromagnetic fields interfere with cellular metabolism. She repeated the 
exposure of the previous year and then analyzed the bees’ blood, or 
hemolymph, as it is called. After the cell phones had been on for only ten 
minutes, the concentration of glucose, cholesterol, total carbohydrates, total 
lipids, and total protein rose tremendously. In other words, after just ten 
minutes of exposure to cell phones, the bees practically could not 
metabolize sugars, proteins, or fats. As in humans (see chapters 11, 12, 13, 
and 14), their cells were becoming oxygen starved. But it happens much 
faster in bees. When the phones were left on longer than 20 minutes, the 
bees, at first quiet, became aggressive and started beating their wings in 
agitation. 


Daniel Favre, at the Apiary School of the City of Lausanne, 
Switzerland, repeated the experiment and took it yet another step farther: he 
made a detailed analysis of the sounds made by the suddenly aggressive 
bees. He confirmed that bees exposed to a cell phone would become quiet 
and still when first exposed to a cell phone, and that within 30 minutes they 
would start to produce loud, high frequency sounds. When the phones had 
been on for 20 hours, the bees were still buzzing like mad 12 hours later. 
When Favre analyzed the sounds, he determined that they were the so- 
called *worker piping," which is usually produced by bees only when they 
are preparing to swarm, shortly before takeoff. 

Favre's bees did not actually leave their hive after a single 20-hour 
exposure, but Sainudeen Pattazhy's bees did, after a much shorter total 
exposure. A professor at Sree Narayana College, Pattazhy basically 
repeated Kumar's initial experiment, except that instead of exposing his 
bees only twice a week he exposed them briefly everyday. He placed one 
cell phone inside each of six bee hives and turned the phone on for just ten 
minutes, once a day for ten days. While the phone was on, the bees became 
still. An average of 18 bees left the hive per minute while the phone was on, 
compared to 38 per minute at other times. The egg-laying rate of the queen 
declined from 355 to 100 per day. And after ten days no bees were left in 
any of the hives.5! 





owned until recently by the United States Air 
Force and operated jointly with the Navy and the University of Alaska, 





Capable of 
emitting a peak effective radiated power of four billion watts, its purpose is 
to set the biosphere to ringing. HAARP, whose 180 antenna towers sit on 


the northwest tip of Alaska's Wrangell-St. Elias National Park, has turned 
the ionosphere itself—the life-giving layer of sky to which every creature is 
tuned (see chapter 9)—into a gigantic radio transmitter useful for military 
communications, including communication with submarines. By aiming a 
narrow beam of pulsating energy upwards, there near the North Pole where 
the aurora meets the earth, Project HAARP can force rivers of sky to 
broadcast radio transmissions at the frequency of the pulsations, and to send 
those signals to almost everywhere on earth. In 1988, when planning for 
HAARP was still in its early stages, physicist Richard Williams, a 
consultant to Princeton University's David Sarnoff Laboratory, called the 
project *an irresponsible act of global vandalism." *Look at the power 
levels that will be used!” he wrote in Physics and Society, the newsletter of 
the American Physical Society. “This is equivalent to the output of ten to 
100 large power-generating stations.” In 1994, when HAARP’s first 18 
antennas were about to be put into service, Williams was interviewed by 
Earth Island Journal. “A ten-billion-watt generator,” he said, “running 
continuously for one hour, would deliver a quantity of energy equal to that 
of a Hiroshima-sized atomic bomb.” 

In March 1999, HAARP expanded to 48 antennas and an effective 
radiated power of almost one billion watts. The rest of its complement of 
180 antennas were delivered between 2004 and 2006, enabling the facility 
to reach its full intended power during the winter of 2006-2007. Although 
the Air Force shut HAARP down in 2014 and proposed to dismantle the 
facility, it instead was acquired by the University of Alaska Fairbanks, 
which reopened the facility in February 2017 and has made it available to 
the scientific community for research. The university is operating the 
facility at a loss, and it announced in 2019 that if it does not get sufficient 
funding, it will shut down HAARP permanently. 

The frequencies of HAARP, says Warnke, superimpose unnatural 
magnetic fields on the natural resonant frequencies of the sky, whose daily 
variations have not changed since life appeared on earth. This is disastrous 
for bees. They “lose an orientation,” he says, “that served them for millions 
of years as a reliable indicator of the time of day.” 


The Path Into the Dying Forest 
Around 1980 the world awoke to a new, seemingly random environmental 
problem: forest die-off. Large swaths of trees would grow up stunted, age 
prematurely, drop their leaves, and perish without visible cause. Other 
stands, tall and vigorous, would suddenly lose all their upper leaves and die 
from the top down. In the Great Smoky Mountains of Tennessee, in 
Canada's Bay of Fundy, and in Central Europe such tragedies were blamed 
on acid rain, contaminated by the sulphuric effluent of industrial 
civilization. But on remote mountain ridges, forests breathing unpolluted air 
were suffering from a similar infirmity. Wolfgang Volkrodt, retired physicist 
and electrical engineer, thought he knew why. 

Volkrodt, who formerly worked for Siemens, the multinational 
technology giant, had become interested in trees because of the strange 
behavior of the forests in the wooded development at Bad Neustadt, 
Germany, where he lived. On the north side of his home the fir trees had 
been sickly for years, while on the south side all the trees were strong and 
robust. 

This astute observation led him to investigate not only the trees but the soil. 
“It seems clear that soil acidification in Central Europe has increased 
significantly during the past decades,” he wrote later. “Paradoxically this is 
true even in clean air regions that receive only traces of ‘acid rain.’ 






The existence of a military installation twelve miles to the north of his 
home made an impression on Volkrodt as an electrical engineer, and when 
he took measurements on his property he found that the dying trees north of 
his house were not only being exposed to distant military radar, 








The electrons migrate as ionic bonds 
from the leaves, the trunk and then through the roots into the soil. In the soil 
a kind of electrolytic deposition happens, making aluminum, among other 
things, soluble and generally making the soil acidic similar to the effect of 
acid rain." Of course, no formal studies had been done on the magnitude of 
induced currents in trees caused by radar stations, but his theory generated 
interest among the forest biologists at the conference and elsewhere. He 
soon was receiving reports from observers in Canada confirming his 
prediction that the line of early warning radar stations lining the Canadian 
far north from Atlantic to Pacific were killing the trees in front of them. 


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Forest damage in West Germany during the Cold War. 
From Forest Decline, Jülich, Germany, 1988, published by Jülich Nuclear Research Center for the 
U.S. Environmental Protection Agency and German Ministry of Research and Technology. 


Following up on experiments by forest biologist Aloys Hüttermann, 
who had measured microwave-induced current flow in tree needles and 
leaves, Volkrodt did some elementary calculations. He assumed that a tiny 
amount of energy—a tenth of a watt—was being absorbed by a section of 
forest standing before a directional radio antenna transmitting long distance 
telephone service at a few watts of power from one point to another. He 
further assumed that the stand contained 100 trees, each having 100 square 


meters of leaf surface, 
the total of only a tenth of a 


watt of microwave radiation, spread out over an acre of soil, seemed 
insignificant, but when Volkrodt took into consideration the factor of time, 
he came to an astonishing conclusion. *Within 10 years of exposure to the 
directional energy,” he wrote, “the seemingly minute 0.1 watts received by 
the group of trees adds up to 8.8 kilowatt hours.” 8.8 kilowatt hours of 
electricity, he calculated, is sufficient to create 2,000 liters of hydrogen gas 
within the soil by the electrolytic splitting of water. This would acidify the 
soil, even without a trace of acid rain. And when Volkrodt considered that 
radar installations sometimes broadcast not a few watts but a few million 
watts, he realized that such an installation could acidify a phenomenal 
amount of soil. 

Partial confirmation of Volkrodt’s theory came from unpublished field 
experiments in Switzerland. Young fir trees were irradiated with 
microwaves at a power density below 10 milliwatts per square centimeter. 
After four months the trees had lost nearly all their needles, and the soil in 
which they were growing was dead and acid. 

Meanwhile, foresters in Central Europe were observing a very rapid 
deterioration in forest health. In West Germany, where the alarm was first 
sounded, white fir trees began mysteriously to decline around 1970. Spruce 
caught the affliction in about 1979, Scots pine in about 1980, and European 
beech in about 1981. Before long, symptoms of ill health and abnormal 
growth afflicted almost every species of forest tree and several herbs and 
shrubs. The area of forest affected rose from about 8 percent in 1982, to 
about 34 percent in 1983, to about half the forests in 1984.9 Die-off was 
most severe at high elevations. To Volkrodt, a simple explanation was at 
hand: a large number of powerful radar stations, built or upgraded during 
the 1970s and 1980s, were irradiating the mountain ranges on both sides of 
the border between East and West Germany. 

When Germany was reunited, and the radars protecting its former parts 
were scrapped, Volkrodt made another prediction: “The forest, with parts of 
it having been irradiated by these installations for two to three decades, now 
has a chance to regenerate.” And this prediction also came true. In 2002, the 
United Nations Economic Commission for Europe, in cooperation with the 
European Commission, surveyed the conditions of all of the forests of 





During those years of the 1990s, famous experiments were done in 
Switzerland, Poland, and Latvia, sponsored by the governments of those 
countries, proving the effects of radio transmissions on people, farm 
animals, wildlife, and forests—experiments that it would shortly not be 
possible to do any more. 


The small town of Skrunda, 150 kilometers from Latvia's capital, Riga, was 
once just a few kilometers away from a Russian early warning radar station 
that scanned the northwestern sky. Its two units went into operation in 1967 
and 1971. From the very beginning these radars, situated in a green valley 
surrounded by farms, were the subject of vigorous complaints from local 
residents—complaints that the radiation was destroying their health, their 
crops, their animals, and their forests. Finally, in 1989, 

the government put out a call for 
scientists to submit proposals for studies that would put these claims to the 
test. Physicians, epidemiologists, cell biologists, botanists, ornithologists, 
and physicists from throughout Latvia converged on the region to do field 
studies. And to the surprise of the organizers the researchers, almost 
without exception, found evidence of biological damage. The findings were 
presented at a conference held June 17 to 21, 1994, called The Effect of 
Radio Frequency Electromagnetic Radiation on Organisms. 

School children in the area—even children who lived twenty kilometers 
away from the radar—had impaired motor function, memory, and attention. 
When asked to press two keys with their right and left hands as fast as they 
could for thirty seconds, children from Skrunda could not do it as fast as 
children from Preili, an agricultural community similar in every respect 
except that no radar station stood nearby. Asked to press a button when they 
heard a tone or saw a flash of light, they could not react as fast. The Preili 
children could remember longer and more complex numbers than the 
Skrunda children. And within Skrunda, children who lived on the western 
slope of the valley, directly exposed to the radar, had worse memories than 


children who lived further away. Standard psychological tests evaluated 
their ability to focus attention on a task, and to switch attention between 
tasks. Again the Preili children did better than the lesser exposed Skrunda 
children, who did better than the children living on the western slope. 

The directly exposed children also had lower lung capacity and higher 
white blood cell counts than other children. In fact, the entire population of 
Skrunda had higher white cell counts and suffered from more headaches 
and sleep disturbances than a more distant community.“ The radiation even 
appeared to have impacted human reproduction, affecting the sex ratio of 
the community. Fewer boys than girls had been born during the early years 
of the radar. There were 16 percent fewer grade 9 boys in Skrunda as a 
whole, and 25 percent fewer in the directly exposed area.® 

The effects on farm animals and wildlife were just as obvious. Blood 
samples were drawn from sixty-seven Latvian Brown cows that grazed on 
land in front of the radar station. Chromosome damage was found in more 
than half. 

Six hundred nest-boxes were provided for birds, placed at distances of 
up to nineteen kilometers from the radar station. Only 14 percent of the 
nest-boxes were occupied by pied flycatchers, an extremely low number for 
Latvia. The numbers of great and blue tits that took up residence in the nest- 
boxes increased steadily with distance from the radars.9 

The effects on the area’s forests were equally profound. Stands of Scots 
pines were sampled at twenty-nine locations at various distances in front of 
the radars. The trees in all of the stands, without exception, had laid down 
much thinner growth rings, beginning precisely in 1971 and continuing 
throughout the period of operation of the radars. The average growth rings 
were half as wide as before the radars were constructed. 

Pine cones were collected from the tops of fifty- or sixty-year-old trees. 
All of the seeds from trees that were less exposed to the radars germinated, 
while only a quarter to a half of the seeds from highly exposed locations 
did. Abundant secretion of resin from pine needles indicated that the 
exposed trees were aging prematurely.” 

In yet another experiment, newly germinated duckweed plants were 
exposed to the radars from two kilometers away for just 88 hours and then 


moved to a distant location. Duckweed is a tiny floating plant that lives on 
the surfaces of ponds and reproduces by budding. For the first twenty days 
after exposure, the plants reproduced at nearly double the normal rate. 
Reproduction then dropped precipitously. Ten days later, many of the plants 
began to grow abnormally. They became misshapen, sprouted roots that 
grew upwards, budded from the wrong side, and produced deformed 
daughter plants. Exposure of additional plants to the radar for just 120 hours 
reduced their average lifespan from 86 days to 67 days, and lowered their 
reproductive capacity by 20 percent.” 

The Skrunda Radio Location Station was shut down permanently on 
August 31, 1998. 





In 1991, a government study proved them right. The research, overseen 
by Dr. Wieslaw Flakiewicz, who worked in the Radiation Protection 
Department in the County of Plock, was simple and inexpensive: it 
consisted of analyzing blood samples drawn from 99 randomly selected 
residents of two communities, Sanniki and Gabin, each six kilometers from 
the tower. The first results indicated that something was indeed affecting the 
residents' health. For 68 percent of the people in Gabin had abnormally 
high levels of cortisol, a stress hormone. Forty-two percent had 
hypoglycemia, 30 percent had elevated thyroid hormones, 32 percent had 
high cholesterol, and 32 percent had abnormally high red blood cell counts. 
Fifty-eight percent had disturbed electrolytes: they tended to have high 
calcium, sodium, and potassium levels, and low phosphorus. The pattern in 
Sanniki was similar, except that thyroid and electrolyte disturbances were 


even more common and serious, and 41 percent of the population also had 
elevated platelets, indicating overstimulation of their bone marrow. 

Then, on August 8, 1991, a serendipitous event took place: the tallest 
structure in the world fell down. Flakiewicz took full advantage of the 
opportunity, and in October he recalled the 50 subjects from Gabin into his 
laboratory to draw a fresh set of blood samples. The new results were 
startling. A handful of the youngest subjects, who had been the most 
severely affected by the radiation, still had abnormal glucose levels and red 
blood cell counts, and the older subjects still had elevated cholesterol. But 
all of the electrolyte levels, all of the thyroid levels, and all of the cortisol 
levels, without exception, were now completely normal. 

Experiments on plants exposed to the radio station produced equally 
stunning results. Dr. Antonina Cebulska-Wasilewska, who worked at the 
Institute of Nuclear Physics in Kraków, directed this phase of the research. 
As subjects she selected spiderwort (Tradescantia) plants, with which she 
was very familiar in her work on nuclear radiation, and which are used as 
standard assays for ionizing radiation throughout the world. When exposed 
to X-rays or gamma rays, the stamen hairs of spiderwort flowers mutate, 
changing from blue to pink. The more ionizing radiation they are exposed 
to, the greater the number of pink hair cells. 

Here, too, there was a before and after study. Potted plants containing at 
least 30 spiderwort blossoms were placed at each of four locations in Gabin 
and Sanniki from June 10-20, 1991, while the radio station was still 
operating, and then taken to a laboratory in Kraków where, between 11 and 
25 days after the exposure, their stamen hairs were examined. The flowers 
that had been at three of the sites had approximately double the number of 
pink mutations as flowers that had never been near the radio station. 
Flowers that had been at the fourth site, which was inside a schoolroom 
near a telephone stand— whose wires acted as an antenna that amplified the 
radiation—had nearly nine times as many pink mutations. The plants near 
the telephone stand also had 100 times as many lethal mutations, and only 
three of their thirty blossoms ever opened. 

After the tower fell down the experiment was repeated, with a ten-day 
exposure period from August 14-23, 1991. This time there was no increase 


in mutations at the first three locations. The plants near the telephone stand 
still had double the normal number of pink mutations, but all of their 
blossoms opened this time. Dr. Cebulska-Wasilewska, who usually used 
these plants to assess levels of ionizing radiation, stated that exposing the 
plants to the radio tower for only eleven days, at a distance of six 
kilometers, had been the equivalent to exposing them to a 3 centigray dose 
of X-rays or gamma rays. That is roughly 1,000 times more radiation than a 
chest X-ray, 10 times more than a CT-scan, and about as much radiation as 
the average survivor of the atomic bomb received in Hiroshima. 

In January 1995, the Polish parliament passed, and the President signed, 
an act authorizing the reconstruction of the long wave radio station at 
Konstantynow. Fierce local protests followed. The Society for the 
Protection of People Living near the Highest Mast in Europe formed in the 
village of Topólno. Fifteen people participated in a month-long hunger 
strike. 

The tower was not rebuilt. 





Almost four 
decades later the Federal Department of Transport and Energy finally 
launched an investigation. The Swiss Federal Office of Environment, 
Forests and Landscape was involved, and Professor Theodor Abelin, Head 
of the Department of Social and Preventive Medicine at the University of 
Berne, was placed in charge. 


Measurements of the magnetic field strength were taken at numerous 
outdoor locations, and in the bedrooms of participants. Residents were 
given diaries in which to record symptoms and complaints at one-hour 
intervals during four ten-day periods, spread out over two summers. Blood 
pressure was monitored, school records examined, and urine samples 
collected to measure melatonin levels. Saliva, collected from area cows, 
measured their melatonin levels as well. During the second summer, at an 
unannounced time, the transmitter was turned off for three days. 

The results confirmed the long-standing complaints. Of the people who 
lived within 900 meters (about half a mile) from the antennas, one-third 
complained of difficulty sleeping—three and a half times as frequently as 
people who lived four kilometers away. They complained of limb and joint 
pains four times as often, and of weakness and tiredness three and a half 
times as often. They woke up at night three times as often. They were more 
constipated, had more trouble concentrating, and had more stomach pains, 
heart palpitations, shortness of breath, headaches, vertigo, and *cough and 
sputum." One-third had abnormal blood pressure. Forty-two percent spent 
their leisure time away from home, compared with only six percent of the 
people who lived four kilometers away. 

The second year's diaries showed the dramatic effect of turning off the 
transmitter. Even the people who lived four kilometers away woke up only 
about half as often during the nights when the transmitter was off. 
Melatonin levels did not change significantly in humans, but cows' 
melatonin levels rose two- to seven-fold during the three days the 
transmitter was off, and were suppressed again when the transmitter was 
turned back on. 

School records from two schools showed that between 1954 and 1993, 
children at the school nearer to the antennas had a significantly smaller 
chance of being promoted from primary to secondary school. 





the trees had tried "to get out of the path of a threat to their lives." His 1991 
article in Raum & Zeit, published two months before Volkrodt's article, is 
strewn with photographs of forests in the Schwarzenburg area that were 
sick and dying. 

On May 29, 1996, Phillippe Roch, the Director of the Federal Bureau 
for Environment, Forests, and Landscapes, stated that “a connection 
between the established sleep disturbances and the transmitting operation is 
proven.” The Federal Bureau of Health agreed. On March 28, 1998, the 
short wave transmitter station of Schwarzenburg was shut down forever. 

Hans-Ulrich Jakob, a long time resident, wrote: “The most surprising 
thing for me is the fact that the people have got back their joyfulness, their 
frankness, which I never saw before. And I have been living here for more 
than 40 years, in this region. The depressive, sometimes also aggressive 
behavior of many of my acquaintances has completely disappeared. A 
farmer, about 50 years old, told me that two weeks after the transmitter was 
switched off, he slept through the whole night for the first time in his life.” 

And Jakob had a story to tell about the trees. “It is wonderful to see,” he 
remarked, “how quickly the forests, which were treated with radiation, are 
recovering now. The rate of growth, I think, is twice the growth of years 
past. The young trees are also growing up straight as a dart and don’t try to 
flee in a direction away from the transmitter.” 

Dr. Abelin’s team took advantage of the planned termination to conduct 
a before-and-after sleep study on 54 of their original subjects. It lasted from 
March 23 until April 3, 1998. Not only did sleep quality improve after the 
shutdown on March 28, but melatonin levels rebounded just as they had in 
the cows. During the week after the shutdown, melatonin levels in the 
people who lived closest to the antennas rose between one-and-a-half- and 
six-fold. 


The recovery of Europe’s forests at the end of the Cold War lasted only a 
decade. In 2002, almost one-quarter of the trees visited by a United Nations 
team again showed signs of damage, with one out of every five trees in 
Europe suffering from defoliation. Acid rain, meanwhile, had been 
transferred along with heavy industry to China and India. Many foresters 


Cedar trees, some of which are three thousand years old, having 
outlasted the Medieval Warm Period, the Little Ice Age, and innumerable 
droughts and floods, are disappearing from the face of the earth. 

The venerable Cedars of Lebanon, whose twelve remaining stands cover 
about 5,000 acres, are in visible decay. 

The cedars of Algeria's Atlas Mountains began to decline about 1982, 
and the cedars of Morocco have been dying rapidly since 2000.” 





Approximately 70 percent of 
the mature trees are dead, with some areas now completely devoid of 
cedars. Foresters are left thunderstruck by massive mortality on wet soils 
where yellow cedars have always thrived, and where no disease organisms 
can be isolated, on which to pin the blame. 

In 1990, Paul Hennon, a United States Forest Service scientist stationed 
in Juneau, made a startling discovery: old aerial photographs showed that 
some of the stands of yellow cedars that are damaged today were already 
damaged in 1927, 1948, 1965, and 1976. And to his further amazement, the 
areas of decline in 1990 were only slightly larger than they had been in 
1927. He then scoured the old forestry literature. Reports from expeditions 
throughout the 1800s had all included observations of yellow cedar near 
Sitka and elsewhere in southeast Alaska, and none had mentioned dying 
trees. Charles Sheldon, the first to report dead yellow cedar anywhere in 
Alaska, had seen them on Admiralty Island near Pybus Bay in the Sitka 
region in 1909, stating that “vast areas are rolling swamp, with yellow 
cedar, mostly dead.” Harold E. Anderson, in 1916, also saw dying cedars 
near Sitka.” 

Hennon concluded that no human factor could have caused cedar 
decline in the Alaska panhandle so long ago, but he was wrong. 





Army radio stations were installed at Petersburg 
and Wrangell in 1908. Private radio stations were also operating. A 1913 
list of the radio stations of the United States includes five operated by the 


Marconi Company in southeast Alaska, including one at Kake, on 
Kupreanof Island, directly across Frederick Sound from Pybus Bay.” 

That trees are dying without obvious cause throughout the Amazon 
rainforest was first noticed in 2005 and is being blamed, again, on global 
warming, which caused an unusual drought in that year.^ Researchers 
connected with the worldwide RAINFOR network went back to the plots of 
forest, scattered through Brazil and seven neighboring countries, that they 
had been monitoring every three to five years, in some cases since the 
1970s. To their surprise the intensity of the drought in individual locations 
was only weakly related to the health of the forest. Some areas had tree 
mortality but no drought, and some had drought but no mortality. Pockets of 
high mortality were surrounded by trees with little or no decline in growth. 
But overall, only half the plots gained biomass during 2005, an 
unprecedented circumstance. The Amazon, they feared, was changing from 
a net carbon sink to a net carbon source, with grave implications for our 
atmosphere. They blamed the change on global warming since they could 
find no other reason for a shift. But like Hennon and his team in Alaska, 
they were wrong. 

On July 27, 2002, the environment everywhere in the Amazon was 
suddenly, drastically altered. For on that day, an American-financed, 
Raytheon-built, 1.4-billion-dollar system of radars and sensors called 
SIVAM (System for Vigilance of the Amazon) began its monitoring 
activities in a two-million-square-mile area of remote and inaccessible 
wilderness. The primary purpose of the new system was to deprive drug 
traffickers and guerrillas of the protection that the trackless jungle had 
always offered. But this required pretending that blasting the rainforest with 
radiation at levels that were unprecedented in the history of the world was 
of no consequence to the forest's precious inhabitants, human or otherwise. 
Since 2002, the system's 25 enormously powerful surveillance radars, 10 
Doppler weather radars, 200 floating water-monitoring stations, 900 radio- 
equipped “listening posts," 32 radio stations, 8 airborne state-of-the-art 
surveillance jets equipped with  fog-penetrating radar, and 99 
"attack/trainer" support aircraft have enabled Brazil to track images as 
small as human beings anywhere. The system is so pervasive that Brazilian 


officials boast that they can hear a twig snap anywhere in the Amazon.” 
But it comes at the expense of the greatest diversity of animals and plants 
on earth, of the people who depend on them, and of our atmosphere. 

In a small backyard laboratory in the foothills of Colorado’s Rocky 
Mountains, Katie Haggerty performed the simplest, most elegant 
experiment of all: she hung aluminum window screening around nine 
potted trembling aspen seedlings to keep out the radio waves, and watched 
them grow. The screens didn’t keep out much light, but to make sure the 
experiment was well controlled, she bought twenty-seven aspen trees and 
grew them side by side. Nine grew without any enclosure, nine were 
surrounded by aluminum screening, and nine were surrounded by fiberglass 
screening, which kept out just as much light but let in all the radio waves. 
She began the experiment on June 6, 2007. After just two months, the new 
shoots of the radio-shielded aspens were 74 percent longer, and their leaves 
60 percent larger in area, than those of either the mock-shielded or the 
unshielded aspens. 

On October 5-6, she evaluated the conditions of the three groups of 
plants. The mock-shielded and unshielded plants looked just like what most 
aspens in Colorado now look like every fall, their leaves and leaf veins 
yellow to green, their leafstalks light red to pink, and all their leaves 
covered to some degree with gray and brown areas of decay. 

The shielded aspens looked like what aspens used to look like not long 
ago. Their leaves were much bigger, largely free of spots and decay, and 
displayed a wide palette of brilliant fall colors: bright orange, yellow, green, 
dark red, and black. Their leaf veins were dark to bright red, and their 
leafstalks were bright red as well. 

The suddenness and simultaneity of aspen decline throughout Colorado, 
which began precisely in 2004, has been a source of wonder and despair to 
all who love and miss the vivid fall colors of these striking trees. In just 
three years, from 2003 to 2006, the area of aspen damage increased from 
twelve thousand acres to one hundred and forty thousand acres. Aspen 
mortality in the national forests rose three- to sevenfold, with some stands 
losing 60 percent of these trees." There is a reason. 


o 


The State of Colorado operates a sophisticated public safety 
communications network, called the Digital Trunked Radio System, 
consisting of 203 tall radio towers whose transmissions cover every square 
inch of the state. They are heavily used by police, firefighters, park rangers, 
emergency medical service providers, schools, hospitals, and a wide variety 
of other municipal, state, federal, and tribal officials. Between 1998 and 
2000 the pilot phase of the system, covering the Denver metropolitan area, 
was built and tested. In 2001 and 2002, radio towers were built throughout 
northeastern and southeastern Colorado and the eastern plains. And in 2003, 
2004, and 2005, the system invaded the western, mountainous part of the 
state: aspen territory. 

“At times,” says Alfonso Balmori, “I compare what is occurring to a 
collective ritual of suicide in slow motion.” But he does not think it can 
continue indefinitely. “I don’t know when,” he continues, “but there will 
come a day of realization, when society will awaken to the serious problem 
of electromagnetic contamination and its dangerous effects on sparrows, 
frogs, bees, trees, and all other living beings, including ourselves.” 


Photographs 





Unshielded seedling October 6, 2007. Photo by Katie Haggerty 2008 





a a 


Mock-shielded seedling October 6, 2007. Photo by Katie Haggerty 2008 





Shielded seedlings. October 6, 2007. Photo by Katie Haggerty 2008 





Effect of radar on city landscaping plant in Valladolid, Spain (24 GHz speed detector). Photo by 
Alfonso Balmori. 


17. In the Land of the Blind 


WHAT IF, ON ANOTHER PLANET, in a distant universe, the sun was 
dark. God never said, *Let there be light," and there was none. But people 
invented it anyway and lit up the world, lit it with light so bright that it 
burned all it touched. What if you were the only person who could see it. 
What if there were a thousand, a million, ten million others? How many 
aware people would it take to make the destruction stop? 





Gro Harlem Brundtland, M.D., M.P.H 


A tremendous number of people get headaches from their cell phone. 
Almost one-quarter of Norwegians who would now be considered moderate 
cell phone users (more than one hour per day) admitted it to the scientists 
who asked the question in 1996.! Almost two-thirds of Ukrainian university 
students who were heavy cell phone users (more than three hours per day) 
admitted it to the scientists who asked the question in 2010.2 Perhaps there 


are some who really don't get headaches, but few people are asking the 
question, and to publicly admit to the true answer is not socially acceptable. 

Gro Harlem Brundtland got headaches from cell phones. And since she 
was the Director-General of the World Health Organization and the former 
Prime Minister of Norway, she did not feel the need to apologize for it, and 
simply ordered that no one was to enter her office in Geneva carrying a cell 
phone on their person. She even gave an interview about it in 2002 to a 
Norwegian national newspaper? The following year she was no longer 
Director-General of the World Health Organization. No other public 
officials have repeated her mistake. 

Even for those who really don't get headaches, their cell phones affect 
their sleep and their memory. Folk singer Pete Seeger wrote to me twenty 
years ago. “At age 81,” he said, “it’s normal for me to start losing my 
memory. But everybody I tell this to, says, ‘Well, I seem to be losing my 
memory, too.’” 

Those of us whose injuries are so severe, so devastating that we can no 
longer ignore them, and who are lucky enough to figure out what has 
happened to us and why, have here and there formed tiny, isolated groups, 
and for lack of a more acceptable term we call our injury “electrical 
sensitivity,” or worse, “electromagnetic hypersensitivity” (EHS), a travesty 
of a name for a disease that affects the whole world and everyone in it, a 
name as absurd as “cyanide sensitivity” would be if anyone were foolish 
enough to apply such a name to those poisoned. The problem is that we are 
all being electrocuted to a greater or lesser extent, and because society has 
been in denial about that for more than two hundred years, we invent terms 
that hide the truth instead of speaking in plain language and admitting what 
is happening. 

After pulsed microwave radiation came to my hometown for the first 
time, all over the city at once, on November 14, 1996, I was so sure it had 
killed masses of people that I telephoned epidemiologist John Goldsmith to 
ask for advice on how to prove it. Formerly with the California Department 
of Health Services, Goldsmith was then at Ben Gurion University of the 
Negev in Israel. He directed me to the weekly mortality statistics published 
online by the Centers for Disease Control for 122 cities, and advised me to 


find out exactly when, for each city, digital cell phone service had begun. 
Here, for nine large cities in different parts of the country, whose digital 


service began at different times, are the results: 


Weekly mortality, Los Angeles 
Onset of service (Pacific Beil): 


+708 July 3, 1997 
ava. 
I 
I 
I 
$05 
EEEERSESTEEETEREKEREEERIEEE 
nu«uczüouzd*4dgmzuuumuocdgszgoomaus 
w P m 
e o a 
Weekly mortality, New York City 
Onset of service (Omripoint): 
("43$ Nov, 14, 1996 
eva 
-213% 
di» 2nL5b»UmDGOMMLumÉgumosuenmnalM 
FEEESIEERITEDEETERTTES: 
wo t a 
p 2 ? 


Weekly mortality, San Diego 
Onset of service (Pacific Bell): 


Nov. 1, 1996 
4805 
ave 
I 
I 
-235% ! 
222533:230B22205 52521 
SAG SBA SSR eH Ra EZRS LE 
E Lx ac 
o o 
Weekly mortality, Boston 
Onset of service (Sprint): 
+41% Nov. 12, 1997 
avy 
1 
I 
I 
l 
-24% 
ADMe+e FOR DHH eR oe Hoe Pog oe 
seconda m3 2suo0oucdsosrsx 
han COagninee BRVAMOSCAANHE 
“ i e 
e m e 


Weekly Mortality, Portland Weekly Mortality, Tulsa 
Onset of service (Sprint): Orset (Western Wireless}: 
Dec. 22, 1996 












Weekly mortality, Jacksonville Weekly mortality, Chicago 
Onset of service (Powertel): Onset of service iPrimeco): 


Oct. 15, 1996 Nov. 12, 1996 





Weekly mortality, Sacramento 
Onset of Service (Pacific Bell): 
Mar. 12, 1997 





I had been sure, because the sudden irradiation of my city had almost 
killed me, and because I knew people who had died from it. 





became so weak I couldn't lift a book. My skin became so sensitive I 
couldn't bear to be touched. My head was roaring like a freight train. After 
November 20 I did not sleep, and could not eat. During the night of 
November 22, my larynx went into spasm and I couldn't draw a breath in or 
out. In the morning I grabbed my sleeping bag, got on the Long Island 
Railroad, and left town. 

My relief was unbelievable. 

I learned that on November 14, while I was in Vermont, Omnipoint 
Communications, New York's first digital cell phone company, had begun 
selling its service to the public. Thousands of rooftop antennas at six 
hundred locations were operational: New Yorkers were now living inside a 
computer. 

I compared notes with a few friends. Together we compiled a list of 
symptoms and placed the following classified ad in a local newspaper: *If 
you have been ill since 11/15/96 with any of the following: eye pain, 
insomnia, dry lips, swollen throat, pressure or pain in the chest, headaches, 
dizziness, nausea, shakiness, other aches and pains, or flu that won't go 
away, you may be a victim of a new microwave system blanketing the city. 
We need to hear from you.” 

And we did hear from them, by the hundreds—men and women, whites, 
blacks, Hispanics, and Asians, office workers, computer operators, 
stockbrokers, teachers, doctors, nurses, and lawyers, all of whom had 
woken up suddenly sometime between mid-November and Thanksgiving, 
their hearts racing, their heads pounding, thinking they were having a heart 
attack, a stroke, or a nervous breakdown—now relieved to find out they 
were not alone. The very first person to answer the ad was a forty-one-year- 
old airline employee who lived in the Bronx. Joe Sanchez’s head suddenly 
began to hurt on about November 15, so badly that he was afraid he was 
having a stroke. Five and a half months later, on May 8, 1997, he died—of 
a hemorrhagic stroke. 

For the next two years, without letup, Janet Ostrowski, a nurse who 
worked in a family practice office in Manhattan, and then on Long Island, 
saw a constant stream of patients with “viral syndrome,” typically with 
excruciating headache, ear pain, swollen gland deep in the neck, nasal 


congestion they could not get rid of, facial pain, sore throat, fatigue, and 
sometimes profound dehydration. *No flu lasts an entire year," Ostrowski 
told us. She also noticed that the majority of her patients were suddenly not 
responding to medication. *I have done triage in various emergency rooms 
throughout the Tri-State area over the course of twenty-five years of 
nursing,” she said. “Whatever used to be stabilized on routine medication, 
be it hypertension, diabetes, whatever, now seems to become unstabilized 
easily and not responding to current meds.” She also saw a tremendous 
increase in the number of people complaining of stress and anxiety, many of 
whom, in their thirties and forties, were found, on routine EKG, to have 
cardiac changes. 


Say 
To Countryside Goodbye, When Even Healthy People Die,* wrote Olle 
Johansson, the guru of electrical sensitivity in Sweden and one of the 
world’s foremost authorities on electrical illness and injury. The old 
wisdom, that if you wish to escape civilization you can do so if you go far 
enough away, is no longer true, because secondhand radiation no longer 
comes only from cell phones, WiFi, and other personal devices. The 
invisible tentacles of civilization, in the form of cell towers, radar 
installations, and two-way satellite dishes, have made radiation ubiqui- 
tous, impossible to escape no matter how far away you go and how much 
land you buy. And even if you find one of the last hidden sanctuaries, it can 
be destroyed in an instant, invisibly and without warming. There is no 
protection. Quite the opposite—laws have been passed preventing citizens 
from protecting themselves, or elected officials from doing anything about 
the radiation. But no one is immune. 

“Recently I celebrated my forty-first birthday,” said Dafna Tachover in 
2013, “and I am not sure that the word celebration is appropriate.” An 
attractive young attorney with an MBA, Tachover was licensed in New 
York and Israel, and just a few years previously had been working for an 



investment company in Manhattan as advisor to the chairman. She had been 
married to a doctor who was also a research scientist at Princeton 
University. They had decided to have a baby, and she had decided to open 
up a private law practice. All of life, seemingly, was hers for the taking. 

When I interviewed her in 2013, she was divorced, unemployed, still 
childless, and struggling just to survive in a remote farmhouse in upstate 
New York. *My life is pretty much impossible," she said, *as I am a 
prisoner in my own house. I cannot go anywhere, I cannot even walk on the 
street and drive into town. I cannot work and be in the presence of other 
people. I cannot fly, travel, go to a restaurant, or sleep in a hotel. I cannot 
access a doctor, a hospital, or even go to court to enforce my rights which 
are being crushed. When I needed to move, I could not look for a house by 
myself, as driving on roads saturated with antennas and cars with wireless 
systems has become impossible. My father had to come from Israel to help 
me and after two months of searching, and five hundred houses, I found just 
one house which I could tolerate. The closest neighbor is 300 yards away 
(such distance is required in order to not be affected by a neighbor’s WiFi, 
cordless phones, and other gadgets), there is only spotty cell phone 
reception, and radiation from only one radio station. I live in an isolated 
cabin in the woods and my only ‘outing’ to civilization is a once-a-month 
trip to buy groceries. Many times I am not well enough to even do that and I 
depend on friends to buy me food. As I cannot work and my money is 
almost exhausted, I don’t know how I will survive financially, and with the 
spread of ‘smart’ meters, soon there will not be even one house I would be 
able to live in. It is very frustrating knowing that without this radiation I can 
live a normal and full life, but because of it I am forced into an absurd 
existence.” 

Tachover was a confirmed cell phone user who had no landline and 
spent hours on her cell phone and in front of her wireless computer. “My 
laptop was my best friend,” she says. “I was one of the first to purchase a 
cellular wireless Internet connection to my laptop, to ensure that I had 
Internet access wherever I went.” Finally, like so many other people, she 
was injured—injured by a new laptop computer she had bought for the law 
practice she was starting. “Every time I used the computer I felt pressure in 


my chest, the rapid pounding of my heart, difficulty breathing, dizziness, 
pressure in my head, my face would become red and hot, and I was 
nauseous. I had weird cognitive problems—I could not find words and 
when my husband spoke to me, five minutes later I would not remember 
that he did. I suddenly was unable to touch my cell phone and if I put it near 
my head it felt as if someone were drilling into my brain." 

The first action she took was to go home to Israel to recover her health. 
“Tt was an unfortunate choice," she said. “On my first day there my body 
collapsed. While I was driving I felt excruciating pain. I looked up and saw 
‘white stripes’ on the roof of the mall, and when I asked my mother what 
they were, she told me that they were cell phone antennas. Until that 
moment I did not know I felt antennas. I had tears in my eyes and all I 
could say was ‘For God’s sake, there are children growing up here!’ From 
that moment on my condition quickly went downhill and my life became a 
nightmare. I could not sleep any more and the pain was unbearable.” 

Back in New York, Tachover spent months living in her car. “I could not 
be in my apartment, could not find a house, and I spent my days desperately 
trying to find a place without radiation in which to park my car. At nights I 
parked my car in parking lots and would cover the windows with dark 
cloths and sheets so people would not see me.” 

Unfortunately Tachover’s experience is very common, and becoming 
more so. Although she is now focusing her efforts as a lawyer to try to win 
“basic human and civil rights” for those who are called electrically 
sensitive, Tachover knows that the real problem is much bigger. “Humans 
are electric beings,” she says, “and there is no mechanism in the human 
body that protects it from the radiation. Therefore, to claim that this 
radiation is not affecting us is ignorant and absurd. EHS is not a disease, it 
is an environmentally induced condition to which no one is immune. I want 
to believe that the day in which the extent of this disaster will be exposed is 
not far. Ignoring the facts and reality do not change them and ignoring a 
problem is guaranteed to worsen its scale." 

Olle Johansson, who for decades was on the faculty of the world- 
famous Karolinska Institute—the institute that awards the Nobel Prize in 
Medicine every year—first became interested in the effects of microwave 


radiation in 1977 when he heard a presentation about leakage of the blood- 


brain barrier at a conference in Finland. He began to study the problem of 
skin rashes in computer operators in the early 1980s after hearing a radio 
program by Kajsa Vedin. Vedin, who later wrote “In the Shadow of a 
Microchip,” an analysis of the occupational risks of computer work, asked 
for expertise in neurology. “As a neuroscientist,” says Johansson, “I thought 
I was close enough, and I strongly believed that the issues she wanted to 
highlight, using the conventional repertoire of scientific ‘tools,’ ought to be 
easily investigated. I did not realize at all that there were other forces not 
wanting to see such studies initiated, but very soon I understood that these 
very clear-cut and simple and obvious investigations proposed by Kajsa 
Vedin would be very, very hard to start. 





Olle Johansson, Ph.D. 


“For me,” he recalls, “it was immediately clear that persons claiming 
skin reactions after having been exposed to computer screens very well 
could be reacting in a highly specific way and with a completely correct 
avoidance reaction, especially if the provocative agent was radiation and/or 
chemical emissions—just as you would do if you had been exposed to, for 
example, sun rays, X-rays, radioactivity, or chemical odors. Very soon, 
however, from different clinical colleagues a large number of other 
‘explanations’ became fashionable—that the persons claiming screen 
dermatitis were only imagining this, or they were suffering from post- 


menopausal psychological aberrations, or they were old, or had a short 
school education, or were the victims of classical Pavlovian conditioning. 
Strangely enough, most of the, often self-made, ‘experts’ who proposed 
these explanations had themselves never met anyone with screen dermatitis 
and had never done any investigations of their proposed explanatory 
models.” 

When he first contacted Vedin, Johansson did not personally know 
anyone with screen dermatitis either, but he quickly learned that they were 
hidden all around him in plain view. 





“After all these years,” he says, “today I now 
regularly communicate with many thousands of such people, spread all 
around the world, and coming from all aspects of life. Nothing protects you 
from this functional impairment, not political stance, not your income, not 
sex, skin color, age, where you live or what you do for a living. Anyone can 
be affected. These people suffer radiation damage from gadgets that have 
been very rapidly introduced without ever having been formally tested for 
potential toxic environmental exposures or any other types of health 
hazards.” 





He went riding on his motorcycle with 
his wife one day, and while still going slow, he suddenly lost control of the 
vehicle. Twenty-seven spokes of the rear wheel had been cleanly sawed 
through, so professionally that it had been impossible to see. 


hat disturbed me a 
lot. The EHS had become a model of the democratic world, or rather a 
model of how democracies fail to protect their citizens. It was, and is, not 





hard to imagine yourself in such a situation. Today the EHS person, but 
what about tomorrow? Who will then be an outsider? Myself even? You? 
Who? The EHS became a kind of medical outcast, facing difficulties not 
shared by the rest of society. A very scary panorama. Anyone, as a fellow 
human being, would have been equally affected by what I witnessed over 
and over again. 





“What keeps me going? One must stick to the task; to give in and move 
to another field would leave these persons very much without hope. As a 
government scientist I am supposed to work for people in need, not for my 
own personal career. When I grew up in the 1950s and 1960s, in Sweden, 
my family were very poor. I learned then the value of a hand stretched out, 
willing to support and help you. Such a lesson you never forget." 

Dr. Erica Mallery-Blythe is an engaging physician, born in England, 
who has dual British and American citizenship, and who has also dedicated 
her life to this problem, having experienced it firsthand. After graduating 
from medical school in 1998, she worked at hospitals all over England, 
becoming an instructor in trauma medicine. In 2007, she moved to the 
United States with her husband, who was an F-16 pilot with the British 
Royal Air Force, working as an exchange officer with NATO. She became 
injured while she was pregnant. Like so many other young professionals, 
Mallery-Blythe had become dependent on technology. In fact, she was one 
of the earliest cell phone users, her father having bought her one when she 
was ten years old, in the mid-1980s. She had always noticed that she got a 
headache if she used her cell phone too long, but like most people, she had 
not paid too much attention. 

Now, however, the pain became intense after every phone call, and the 
right side of her face would become bright red as if she were sunburned. 
She had also just acquired her first WiFi-enabled laptop computer, which 


she used a great deal for medical research, and which she rested on her legs 
—but not for long, because every time she did that she would get severe, 
deep aching pain inside her legs. “It felt like my legs were cooking from the 
inside,” she recalls. Soon she could no longer use her computer at all, even 
at a distance. “As a doctor,” she says, “I knew that when there’s pain there’s 
something wrong.” Eventually she had to give up using both the computer 
and the telephone. By this time she was not sleeping, and had acquired a 
heart arrhythmia and severe tremors, in addition to the dizziness and 
headaches that were tormenting her. But everything she read on the Internet 
reassured her that she was not going to get cancer from her cell phone, and 
she could not put her experience into any medical context that she had ever 
been taught. She finally heard the term “electromagnetic hypersensitivity” 
after her daughter was born, but still did not grasp the seriousness of it. 
“How could there be a condition that was so profound that I’d never heard 
of it?” she wondered. It was not until she underwent an MRI to rule out a 
brain tumor that she finally realized that her life had been permanently, 
utterly altered. For when the high frequency pulse of the MRI was turned 
on she saw “a million grains of golden sand exploding outwards,” and had 
“a feeling of impending doom.” The final piece of the puzzle fell into place 
when she and her husband visited an isolated campground on the edge of 
Death Valley where there was no WiFi and no cell phone reception. “The 
relief was unbelievable,” she says. For the first time in a long time, she felt 
completely well and completely normal. 

But, like Tachover, and like so many other people throughout the world, 
life was now impossible. Mallery-Blythe and her husband moved out of 
their home and began camping in tents or sleeping in the back of their car. 
She describes it as “living like war refugees.” She could not enter a market 
or a gas station without becoming crippled. “You can’t do the basic things 
you need to live. You almost feel like you’re going to wake up, like it’s 
some kind of bizarre dream.” Almost worse than the physical hardship was 
the fact that they had to hide the truth of what was happening from 
everybody they knew and met. They lived like that for more than half a 
year, until they found a log cabin by a lake in South Carolina, where they 
were forced to live without electricity so that she could recover her health. 


She was living there when I first met her. Eventually she moved back to 
England, but before she did she had met many other people who were 
injured by electricity, especially by wireless technology, and had attended a 
medical conference on the subject in Dallas. And she decided that she had 
no choice but to devote the rest of her life to the needs of this population, 
including the most urgent need for a sanctuary where people can save their 
lives, recover their health, and become productive individuals again. “The 
first and foremost need,” says Mallery-Blythe, “is a safe refuge for those 
who need urgent care, with supportive medical staff. What makes me sad is 
to see all the people who can’t escape and get to a pure environment, 
because if you can’t get to a pure environment, it will destroy you.” 





has been working on radiation since 1949. After 
graduating from the Military Medical Academy he was assigned to research 
the biological effects of atomic weapons at the Institute of Biophysics at the 
U.S.S.R. Ministry of Health. Since 1977 he has been the head of research 
on non-ionizing radiation (i.e., radio waves) at the same institute, since 
renamed the A. I. Burnazyan Federal Medical and Biophysical Center. He is 
also the Honorary Chairman of the Russian National Committee on Non- 
Ionizing Radiation Protection. His most recent book, Mobile 
Communication and Children’s Health, was published in 2014, a year 
before his ninetieth birthday. His greatest fear is for the children. 








Yury Grigorievich Grigoriev, M.D. 


“In the early period,” says Grigoriev, “the government deliberately 
underestimated the risk of nuclear radiation, before the accident at 
Chernobyl. This accident caused fear among the population, and as a result 
the Russian government agreed to provide full information to the public 
about the dangers of ionizing radiation. Now we are dealing with similar 
issues surrounding mobile communications. I believe that the time has 
arrived, here too, to provide full information to the general public.” 

Scarcely a day goes by when I don’t receive terrifying new information 
that is being tragically ignored. 

“Children’s Cell Phone Use May Increase Their Risk of ADHD,” reads 
a recent news headline about a Korean study. The more calls made by a 
child, the more time spent on the phone, and the more time playing games 
on the phone, the greater the risk of ADHD.°® 

“Computer Screens Can Make You Blind,” screams another headline. 
This research, out of Japan, found that spending more than four hours per 
day on a computer for ten years more than doubles one’s risk of glaucoma.’ 

“Are Mobiles Bad for Your Skin?” Also out of Japan, this research 
found that mobile phones worsen eczema.® 

“Mobiles Can Make You Blind.” This study in China found that 
microwave radiation at levels emitted by cell phones caused cataracts to 
form on the eyes of rabbits.? 


"Could Microwaves Be Associated with Children's Asthma?" This 
investigation was done at Kaiser Permanente in Oakland, California. 
Women who were exposed to higher magnetic fields while pregnant gave 
birth to children who were at greater risk for asthma.!? 

“Talking on the Phone Makes You Deaf.” I have received a number of 
studies saying this. Teams of researchers at Dicle University in Turkey," at 
a hospital in Chandigarh, India,!? and at the University of Malaysia in Kuala 
Lumpur? found that heavy cell phone use is associated with permanent 
hearing loss. Scientists at King Edward Memorial Hospital in Mumbai, 
India found that chronic use of a cell phone for ten minutes a day causes 
hearing loss.'* Research at the University of Southampton, England showed 
that even a single short exposure to a cell phone causes temporary hearing 
loss. 

*Cell Phones Now Tied to Alzheimer's." A team of Swedish scientists, 
led by neurosurgeon Leif Salford, proved in the late 1990s that a cell phone 
disrupts the blood-brain barrier of laboratory rats within two minutes of 
exposure. When they reduced the power of the phone a thousandfold—the 
equivalent of a person keeping a phone several feet away from his or her 
head—the damage increased. In 2003, they proved that a single two-hour 
exposure causes permanent brain damage. They exposed 12- to 26-week- 
old rats to an ordinary cell phone, just once for two hours, and waited eight 
weeks before sacrificing them and examining their brains. Like human 
teenagers, these rats had brains that were still developing. In those animals 
that had been exposed once to a cell phone, up to two percent of the 
neurons in all areas of the brain were shrunken and degenerated.'* Salford 
called the potential implications “terrifying.” In 2007, they exposed rats 
chronically, for two hours once a week for 55 weeks, beginning in their 
“teenage years.” At the end of the experiment, the exposed rats, by now in 
middle age, had memory deficits." To mimic cell phone use by very young 
children, scientists in Turkey experimented on 8-week-old rats. In their 
study, published in 2015, they exposed the animals to cell phone-like 
radiation for one hour a day for a month, and then examined a particular 
area of the brain called the hippocampus, which is involved in learning and 
memory. The exposed rats had 10 percent fewer brain cells in the 


hippocampus than the unexposed rats. And a large number of brain cells in 
the exposed rats were abnormal, dark, and shrunken, just like the brain cells 
in Salford’s rats.'® In another large set of experiments, the Turkish team 
exposed pregnant female rats to cell phone-like radiation at low power for 
one hour a day for nine days. The exposed rats’ offspring had degenerative 
changes in their brains, spinal cords, hearts, kidneys, livers, spleens, 
thymuses, and testes.? In yet a further experiment, the same scientists 
exposed young rats to cell phone-like radiation for one hour a day during 
their early and mid-adolescence, which for a rat is from 21 to 46 days of 
age. The exposed rats’ spinal cords were atrophied and had significant 
losses of myelin, similar to what occurs in multiple sclerosis.”° 





On April 24, 2019, the American health 
insurance company Blue Cross Blue Shield released a report titled “The 
Health of Millennials.” It showed not only that the health of this generation 
takes a sharp decline beginning at age 27, but also that the prevalence of 
many medical conditions had risen precipitously among millennials in just 
three years. 

The prevalence of eight of the top ten conditions among all millennials 
showed a double-digit increase in 2017 as compared with 2014. Major 
depression increased 31 percent. Hyperactivity increased 29 percent. Type 2 
diabetes increased 22 percent. Hypertension increased 16 _ percent. 
Psychoses increased 15 percent. High cholesterol increased 12 percent. 
Crohn’s disease and ulcerative colitis increased 10 percent. Substance use 
disorder increased 10 percent. 

The decline in millennials’ health from 2014 to 2017 was not due to 
their being three years older. The report also compared the health of 
millennials who were 34 to 36 years old in 2017 to the health of Gen Xers 
who were 34 to 36 years old in 2014. At the same age, millenials in 2017 
had 37 percent more hyperactivity, 19 percent more diabetes, 18 percent 
more major depression, 15 percent more Crohn’s disease and ulcerative 


colitis, 12 percent more substance use disorder, 10 percent more 
hypertension, and 7 percent more high cholesterol than Gen Xers had in 
2014. 

When the researchers looked at all health conditions, they found that 34- 
to 36-year-olds in 2017 had a 21 percent increase in cardiovascular 
conditions, a 15 percent increase in endocrine conditions, and an 8 percent 
increase in other physical conditions compared to 34- to 36-year-olds in 
2014. 





People who were 34 to 36 years old in 2017 were 17 to 19 
years old in 2000. People who were 34 to 36 years old in 2014 were 20 to 
22 years old in 2000. No other environmental factor changed so radically in 
just three years. Microwave radiation is responsible for the tragic state of 
the millennial generation's health compared to the health of every other 
generation that preceded them.?! 

The incidence of stroke overall is steady or declining but it is rising in 
adults younger than 50, and shockingly so in very young adults, who are the 
heaviest users of cell phones. Studies out of France,?? Sweden,”? and 
Finland^ all say the same thing. A Danish study published in 2016 
examined the rate of strokes in people aged 15 to 30—a population that 
never used to have strokes at all. The annual number of strokes in that age 
group in Denmark rose 50 percent between 1994 and 2012, and the annual 
number of transient ischemic attacks (mini-strokes) in that age group 
tripled.? Cell phones were marketed in Europe three years earlier than in 
America. 

Women in their twenties and thirties who keep their cell phones in their 
bras are getting a distinctive type of breast cancer directly underneath where 
they keep their phones.?5 










Between 2000 and 2010 the 


number of annual hip replacements in the United States more than doubled, 
and the rate of hip replacements among people aged 45 to 54 more than 
tripled.? Rates of colon cancer among Americans aged 20 to 54, which had 
been declining for decades, began to rise suddenly in 1997. The rise has 
been steepest and began earliest in people aged 20 to 29; the rate of colon 
cancer in young men and women aged 20 to 29 doubled between 1995 and 
2013.78 Rates of prostate cancer—the prostate is also in the same part of the 
body—have been rising worldwide since 1997.?? The number of cases of 
prostate cancer among Swedish men aged 50 to 59 was stable for decades 
until 1996 and rose nine-fold between 1997 and 2004.°° The incidence of 
metastatic prostate cancer among American men under 55 increased 62 
percent between 2004 and 2013, and nearly doubled for men aged 55 to 69 
during the same period.?! An American study conducted from 2003 to 2013 
found that young men had lower sperm counts than their elders for the first 
time in human history, and that men born between 1990 and 1995 had on 
average 40 percent lower sperm counts than men born earlier.*? 

And the kind of brain damage that occurred in a Swedish laboratory in 
teenaged rats, and in a Turkish laboratory in preteen rats, is now being 
found in preschool children in America. Not only did the scientists at 
Cincinnati Children’s Hospital Medical Center find that children who spent 
more time per day on a wireless device have poorer language and literacy 
skills, but MRIs of the children showed structural damage to the white 
matter of their brains.? 





At about the same time that Broomhall presented his report, 





In 2017, scientists reported a 75 to 80 percent 
decline in total flying insects in 63 nature protection areas in Germany.? In 
2018, another group of scientists reported a 97 to 98 percent decline in total 
insects caught in sticky traps in a Puerto Rican rainforest. In 2019, 
scientists from Australia, Vietnam, and China reviewed 73 reports of insect 
declines from across the globe, and concluded that 40 percent of all insect 
species on earth are threatened with extinction.?? 





And yet it is impossible to continue on the 
present path any longer. Decisions are being made to intensify the global 
microwave rain, before 2020, from a steady drizzle to a downpour. 

Instead of cell towers every few miles, there are going to be cell towers 
every few houses. This is already being implemented throughout China and 
South Korea and is spreading like wildfire to every city in the world. 
Although the new antennas are small—little boxes on top of telephone 
poles—they expose the population to tens or hundreds of times more 
radiation than the tall structures they are replacing. 

Dense rows of similar antennas are being sown like so much rice along 
the sides of highways and beneath the pavement, and the electric fields that 
sprout from their seeds to cover the adjacent countrysides will guide cars 
and trucks that are outfitted with their own antennas and driven by robots 
instead of human beings. 

These are the structures that are replacing men and women with 
machines within cities and along highways. It is called “SG” because it is 
the 5th generation of wireless technology. 5G will enable the creation of the 
“Internet of Things”: not only cars, trucks, and home appliances, but 
virtually everything we buy is being outfitted with antennas and microchips 


in order to be connected to the wireless cloud that will take over the 
business of the world from human beings. Cars will drive themselves, milk 
cartons will instruct refrigerators to order milk, and your baby's diaper will 
tell your phone when it needs to be changed. By some estimates, as many as 
one trillion antennas will soon be talking to one another, outnumbering 
people on the earth by a hundred to one. 

Not just people, but all of nature is being replaced by electrical 
pulsations, and not just in cities and suburbs. Radio waves are replacing 
eagles and hawks in national parks and wilderness areas, fish and whales in 
the earth's oceans, and penguins and auks in Antarctica and Greenland, 
where ice is melting into electric fog. 

Four billion people, you see, still have little or no access to the Internet. 
And the remedy for that deficiency is now at hand, via balloons, drones, or 
satellites from space. Humankind is now willing and able to finally fulfill 
the original promise of the telegraph, put into words for the first time a 
century and a half ago. Space and time are poised to be thoroughly 
annihilated. That promise, however, 





In 1998, the launch of the 66-satellite constellation called Iridium 
brought cell phone service for the first time to the vast unserved regions of 
the earth, previously owned by penguins and whales. As we saw in the last 
chapter, however, it also unleashed a new kind of rain that emptied the skies 
of birds for a couple of weeks. 


The fact that wild birds were also not flying received only brief mention. 
The human toll was not mentioned at all. 

On about October 1, 1998, I contacted fifty-seven electrically sen- sitive 
people in six countries. I also surveyed two support groups, and interviewed 
two nurses and one physician who served this population. My survey?? 
found that eighty-six percent of the electrically sensitive people 
interviewed, and a majority of patients and support group members, had 


become ill on Wednesday, September 23 exactly, with typical symptoms of 
electrical illness such as headaches, dizziness, nausea, insomnia, 
nosebleeds, heart palpitations, asthma attacks, ringing in the ears, and so 
forth. One person said it felt like a knife went through the back of her head 
early Wednesday morning. Another had stabbing pains in his chest. 






Follow-ups revealed that some of these people were acutely 
ill for up to three weeks. I suddenly lost my sense of smell on September 
23, 1998, and it still today has not returned to normal. 
Mortality statistics obtained from the Centers for Disease Control reveal 
the following numbers for 1998: 


Week Deaths 
Sept. 6 11,351 
Sept. 13 11,601 
Sept. 20 11,223 
Sept. 27 11,939 
Oct. 4 11,921 
Oct. 11 11,497 
Oct. 18 11,387 


As recommended by the CDC, the above numbers are based on an 
average three-week delay between the time of death and the filing of a 
death certificate, and have been adjusted to account for missing data for 
some cities. A four to five percent rise in the national death rate occurred 
during those two weeks in which electrically sensitive people were the 
sickest and birds were not flying in the sky. 

The commencement of service by the second satellite cell phone 
company, Globalstar, was again accompanied by widespread sudden illness. 
Globalstar announced the beginning of full commercial service in the 
United States and Canada from its 48 satellites on Monday, February 28, 
2000. Widespread reports of nausea, headaches, leg pain, respiratory 
problems, depression, and lack of energy began on Friday, February 25, the 
previous business day, and came from people both with and without EHS.*9 


Iridium, which had gone bankrupt in the summer of 1999, was 
resurrected on December 5, 2000, when it signed a contract to provide 
satellite phones to the United States Armed Forces. On March 30, 2001, 
commercial service was resumed, and on June 5, Iridium added mobile 
satellite data services, including the ability to connect to the Internet. 
Nausea, flu-like symptoms, and feelings of oppression accompanied both 
events. Hoarseness was a prominent complaint of many who contacted me 
in early June. But the reports that grabbed headlines had nothing to do with 
human beings. 

The March 30 event was unusual in several respects. First, it was the 
night of a rare red aurora that was visible in the northern hemisphere as far 
south as Mexico, as well as in the southern hemisphere. It was a time of 
intense solar activity, so I was tempted to attribute this to pure coincidence, 
except that I was reminded of the reddish sky that some reported the night 
of September 23, 1998, when Iridium was turned on the first time. No one 
understands all the interactions of these satellite operations with the earth's 
magnetic field and atmosphere. 

But the second item that attracted notice was a catastrophic loss of 
Kentucky race horse foals in late April and early May.^ Since mares, 
according to the Merck Veterinary Manual, abort several weeks to a month 
after, for example, a viral infection, this would put the triggering event at 
the end of March. Except that no such virus was ever found. In the United 
States, unusual foaling problems were reported simultaneously not only 
from Kentucky and nearby states like Ohio, Tennesee, Pennsylvania, and 
Illinois, but also from Maryland, Texas, and northern Michigan. Lenn 
Harrison, director of the University of Kentucky's Livestock Disease 
Diagnostic Center, said he had received similar reports from as far away as 
Peru.^! 

Between 2001 and now, our skies have not essentially changed. The 
number of satellites in low orbit has gradually increased, but Iridium and 
Globalstar are still the only providers of satellite phones, and the amount of 
data raining on us all from space is still dominated by those two fleets. 
That, however, is poised to change in a grand way. In 2017, we had a total 
of some 1,100 functioning artificial satellites of all types circling the earth. 


By the end of 2019, the number had already doubled. In 2020, several 
companies are competing to launch new fleets of 500 to 42,000 satellites 
each, for the sole purpose of bringing high-speed wireless Internet to the 
furthest reaches of the earth, and recruiting billions of untapped consumers 
into the ranks of social media. These plans call for the satellites to fly in 
orbits as low as 210 miles in altitude, and to aim highly focused beams at 
the earth with an effective radiated power per beam of up to twenty million 
watts. The names of some of these companies are familiar to everyone: 
Google, Facebook, and Amazon. Others, as yet, are less well known. 
SpaceX is the space transport company created by billionaire Elon Musk, 
the man who wants to put a colony on Mars—and to provide high speed 
Internet to both planets. OneWeb, based in the United Kingdom, has 
attracted major investments by Qualcomm and Virgin Galactic, and has 
signed up Honeywell International as its first large customer. Google, in 
addition to investing one billion dollars in Musk’s satellite project, has a 
contract to supply Internet from high-flying balloons to remote parts of the 
Amazon rainforest in Peru. 

As this book goes to press, SpaceX has submitted applications for 
42,000 satellites to the U.S. Federal Communications Commission and the 
International Telecommunication Union and is already is in process of 
launching them, 60 at a time. SpaceX has announced that as soon as 420 
satellites are in place, which could be as early as February 2020, it will turn 
them on and begin providing service to some areas of the earth. OneWeb 
has submitted applications for 5,260 satellites, plans to begin launching 30 
at a time in January 2020, and has projected the beginning of service to the 
Arctic and Antarctic in late 2020 and full global service from 650 satellites 
in 2021. Telesat, based in Canada, expects to begin launching a fleet of up 
to 512 satellites in 2021 and to provide global service in 2022. Amazon 
projects that its 3,236 satellites will serve the entire world except the Arctic 
and Antarctic. Facebook, thus far, has an experimental satellite license from 
the FCC under which it is not required to disclose its plans to the public. A 
new company called Lynk also has an experimental license; it plans to 
deploy “several thousand” satellites by 2023 and boasts that “we’re going to 
turn all mobile phones into satellites phones.” 


These plans must not happen. The roots of our life-support system are 
firmly anchored in the pillars of the earth's magnetic field, far above our 
heads, where the pulsations of the universe, nourished and watered by the 
sun, are absorbed, animating all living things below. The engineers, who 
believe that all these satellites will be too far away to affect life, miss the 
mark. Even the first small fleet of 28 military satellites, launched into orbit 
in 1968, ushered in a worldwide pandemic of influenza. The direct radiation 
is only part of the problem. Satellites have a profound effect, as we learned 
in chapter 9, because they are already in the earth's magnetosphere. Unlike 
radiation from earthly towers, which is greatly attenuated by the time it 
reaches outer space, radiation from satellites works its full force on the 
magnetosphere, and is demodulated and amplified there by mechanisms 
that are poorly understood. 

Not only will all these satellites be located in the magnetosphere, but 
most will be located in the ionosphere, which is the lower part of the 
magnetosphere. The ionosphere, as we learned in chapter 9, is charged to an 
average of 300,000 volts and provides the power for the global electrical 
circuit. The global electrical circuit provides the energy for all living things: 
it is why we are alive, and it is the source of all health and healing. All 
doctors of oriental medicine know this, except they call that energy *qi" or 
"chi." It flows from the sky to the earth, and it circulates through our 
meridians and gives us life. It is electricity. You cannot contaminate the 
global electrical circuit with millions of pulsed, modulated electronic 
signals without destroying all of life. 

The reason the engineering perspective fails is fundamental: it 
perpetuates the error that our ancestors made in 1800, the terrible decision 
to treat electricity as a foreign element, a strange beast that operates outside 
the laws of nature. We acknowledge the existence of electricity only to the 
extent that it does work for us; otherwise we pretend it is not there. We 
ignore the warning, issued in 1748 by Jean Morin, that harnessing 
electricity is tampering with life. We pretend, contrary to all scientific 
evidence, that there is a safe level of exposure, and that if the authorities 
only set the safety standards low enough, we can have our radar stations 
and computer screens and cell phones and not suffer the consequences. We 


forget the admonitions of Ross  Adey, the grandfather of 
bioelectromagnetics, and of atmospheric physicist Neil Cherry, that we are 
electrically tuned to the world around us and that the safe level of exposure 
to radio waves is zero. 

The satellite projects have made the growing efforts to educate the 
world much more urgent. In 2009, an international coalition formed whose 
mission is to bring the matters addressed in this book to global awareness. 
At this writing, the International EMF Alliance (IEMFA) collaborates with 
one hundred and twenty-one organizations from twenty- four countries. The 
Global Union Against Radiation Deployment from Space (GUARDS) 
formed in 2015; its mission is to prevent the planned rain of wireless 
Internet from satellites, drones, and balloons. And in 2019, an International 
Appeal to Stop 5G on Earth and in Space has gathered the signatures of 
thousands of organizations and hundreds of thousands of individuals from 
two hundred and two countries and territories. Scientists, doctors, 
engineers, nurses, psychologists, architects, builders, veterinarians, 
beekeepers, and other individuals from almost every nation have signed this 
appeal, and preparations are underway to deliver it to all of the world’s 
governments. 

In 2014, Japanese physician Tetsuharu Shinjyo published a before-and- 
after study that is a harbinger of the direction in which the world needs to 
go. He evaluated the health of the residents of an apartment building in 
Okinawa, upon whose roof cell phone antennas had been operating for a 
number of years. One hundred and twenty-two individuals, representing 39 
of the 47 apartments, were interviewed and examined. Prior to the removal 
of the antennas, 21 people suffered from chronic fatigue; 14 from dizziness, 
vertigo, or Méniére’s disease; 14 from headaches; 17 from eye pain, dry 
eyes, or repeated eye infections; 14 from insomnia; 10 from chronic 
nosebleeds. Five months after the antennas were removed, no one in the 
building had chronic fatigue. No one had nosebleeds any more. No one had 
eye problems. Only two people still had insomnia. One still had dizziness. 
One still had headaches. Cases of gastritis and glaucoma resolved. Like the 
residents of that building before the study, the majority of the people in the 
world today do not know that their acute and chronic illnesses are in large 





As awareness spreads, it will become acceptable to turn to your 
neighbor and ask them to turn off their cell phone, or unplug their WiFi. 
And that will be the beginning of recognition that we have a problem, one 
that is more than two centuries old. It is a problem that pits the apparent 
ease of living, the limitless power at our fingertips brought to us by 
electrical technology, against the unavoidable, irreversible effects of that 
same technology on the natural world of which we are part. The unfolding 
human rights emergency, already affecting perhaps one hundred million 
people worldwide, and the environmental emergency threatening so many 
plant and animal species with extinction, must be faced with open eyes. 


Notes 


Chapter 1. Captured in a Bottle 


1. Musschenbroek 1746. 

2. Letter from Allamand to Jean Antoine Nollet, partially quoted in Nollet 1746b, pp. 3-4; 
summarized in Trembley 1746. 

3. Priestley 1767, pp. 82-84. 

4. Mangin 1874, p. 50. 

5. Ibid. 

6. Franklin 1774, pp. 176-77. 

7. Wesley 1760, pp. 42-43. 

8. Graham 17789, p. 185. 

9. Lowndes 1787, pp. 39-40. See discussion in Schiffer 2003, pp. 155-56. 


10. 


Heilbron 1979, pp. 490-91. 


Chapter 2. The Deaf to Hear, and the Lame to Walk 


. La Beaume 1820, p. 25. 

. Duchenne (de Boulogne) 1861, pp. 988-1030. 
. Humboldt 1799, pp. 304-5, 313-16. 

. Volta 1800, p. 308. 


. Kratzenstein 1745, p. 11. 

. Gerhard 1779, p. 148. 

. Steiglehner 1784, pp. 118-19. 
. Jallabert 1749, p. 83. 


10. 
11. 
12. 
13. 
14. 
15. 
16. 
17. 
18. 
19. 
20. 
. Humboldt 1799, p. 310. 
22. 
23. 


21 


1 
2 
3 
4 
5. Humboldt 1799, pp. 333, 342-46. 
6 
7 
8 
9 


Sauvages de la Croix 1749, pp. 372-73. 
Mauduyt de la Varenne 1779, p. 511. 
Bonnefoy 1782, p. 90. 

Sigaud de la Fond 1781, pp. 591-92. 
Sguario 1756, pp. 384-85. 

Veratti 1750, pp. 112, 118-19. 

van Barneveld 1787, pp. 46-55. 
Sguario 1756, p. 384. 

Humboldt 1799, p. 318. 

Gerhard 1779, p. 147. 
Thillaye-Platel 1803, p. 75. 


Donovan 1847, p. 107. 
Nollet 1753, pp. 390-99. 


24. Steiglehner 1784, p. 123. 


Chapter 3. Electrical Sensitivity 


1. Wilson 1752, p. 207. 

2. Reported in Gralath 1756, p. 544, and in Nouvelle Bibliothéque Germanique 1746, p. 439. 

3. Letter of March 5, 1756 to Elizabeth Hubbart; letters of March 30, 1756, January 14, 1758, 
September 21, 1758, February 21, 1760, February 27, 1760, March 18, 1760, December 27, 1764, 
and August 5, 1767 to Deborah Franklin; letter of January 22, 1770 to Mary Stevenson; letter of 
March 23, 1774 to Jane Mecom. 

4. Morin 1748, pp. 171-73. 

5. Bertholon 1780, pp. 53-54. 

6. Sigaud de la Fond 1781, pp. 572-3. 

7. Mauduyt 1777, p. 511. 

8. Nollet 1746a, p. 134; 1753, pp. 39-40. 

9. Stukeley 1749, p. 534. 

10. Humboldt 1799, p. 154. 

11. Brydone 1773, vol. 1, pp. 219-20. 

12. Humboldt 1799, pp. 151-52. 

13. Martin 1746, p. 20. 

14. Musschenbroek 1769, vol. 1, p. 343. 

15. Bertholon 1786, vol. 1, p. 303. 

16. Louis 1747, p. 32. 

17. Sguario 1756, p. 288. 

18. Morin 1748, p. 192. 

19. Wilson 1752, p. 208. 

20. Morin 1748, pp. 170-71, 192-97. 

21. Nollet 1748, p. 197. 

22. Morin 1748, pp. 183-86. 

23. Nollet 1753, pp. 90-91. 

24. Heilbron 1979, p. 288. 

25. Beard and Rockwell 1883, pp. 248-56. 

26. Sulman 1980. 

27. Michael Persinger, personal communication. 

28. Sulman, pp. 11-12. 

29. ICB 2008. Proceedings of the 18th International Congress of Biometeorology, 22-26 Sept. 
2008, Tokyo, p. 128. 

30. Michael Persinger, personal communication. 

31. Mauduyt 1777, p. 509. 

32. Bertholon 1786, vol. 1, p. 61. 

33. Priestley 1775, pp. 429-30. 

34. Yellow Emperor s Classic of Internal Medicine, chap. 5. Translation by Zhang Wenzhi, Center 
for Zhouyi and Ancient Chinese Philosophy, Shanding University, Jinan, China. 

35. Faust 1978, p. 326; Mygge 1919. 


Chapter 4. The Road Not Taken 


1. Newton 1713, p. 547. 
2. Nollet 1746, p. 33. 


. Marcelin Du Carla-Bonifas, Cosmogonie, quoted in Bertholon 1786, vol. 1, p. 86. 
. Voltaire 1772, pp. 90-91. 

. Marat 1782, p. 362. 

. Wesley 1760, p. 1. 


nuk WwW 


Chapter 5. Chronic Electrical Illness 


. Charles Dickens, “House-Top Telegraphs,” All the Year Round, Nov. 26, 1859. 
. Highton 1851, pp. 151-52. 

. Dana 1923, p. 429. 

. Beard 1875. 

. Prescott 1860, pp. 84, 270, 274. 

. Morse 1870, p. 613. 

7. London District Telegraph Company used a single-needle apparatus and an alphabet code that 
required an average 2.9 needle positions per letter. 

8. Gosling 1987; Lutz 1991; Shorter 1992; Winter 2004. 

9. Flint 1866, pp. 640-41. 

10. Tourette 1889, p. 61. 

11. Cleaves 1910, pp. 9, 80, 96, 168-69. 

12. Anonymous 1905. 

13. Letter to W. Wilkie Collins, Jan. 17, 1858. 

14. Gellé 1889; Castex 1897 a, b; Politzer 1901; Tommasi 1904; Blegvad 1907; Department of 
Labour, Canada 1907; Heijermans 1908; Julliard 1910; Thébault 1910; Butler 1911; Capart 1911; 
Fontégne 1918; Picaud 1949; Le Guillant 1956; Yassi 1989. 

15. Desrosiers 1879, citing Jaccoud. 

16. Arndt 1885, pp. 102-4. 

17. Kleinman 1988, p. 103; World Psychiatric Association 2002, p. 9. Flaskerud 2007, p. 658 
reports that neurasthenia is the second most common psychiatric diagnosis in China. 

18. World Psychiatric Association 2002, p. 10. 

19. Tsung-Yi Lin 1989b, p. 112. 

20. Goering 2003, p. 35. 


No BWN 


Chapter 6. The Behavior of Plants 


. Nollet 1753, pp. 356-61. 

. Jallabert 1749, pp. 91-92. 

. Bose 1747, p. 20. 

. Bertholon 1783, p. 154. 

. Marat 1782, pp. 359-60. 

. Quotation in Hull 1898, pp. 4-5. 

. Stone 1911, p. 30. 

. Paulin 1890; Crépeaux 1892; Hull 1898, pp. 9-10. 

. Bose 1907, pp. 578-86, “Inadequacy of Pflüger's Law." 
10. Bose 1915. 

11. Bose 1919, pp. 416-24, “Response of Plants to Wireless Stimulation.” 
12. Bose 1923, pp. 106-7. 

13. Bose 1927, p. 94. 


WOANAUNMBRWNHH 


Chapter 7. Acute Electrical Illness 


1. Scientific American 1889d. 

2. Stuart-Harris 1965, fig. 54, p. 87. 

3. Hope-Simpson 1992, p. 59. 

4. Mygge 1930, p. 10. 

5. Mygge 1919, p. 1255. 

6. Hogan 1995, p. 122. 

7. Here is a sampling of opinion as to the time span of this pandemic: 1727-34 (Gordon 1884); 
1729-38 (Taubenberger 2009); 1729-33 (Vaughan 1921; van Tam and Sellwood 2010). Some authors 
divide it into two separate pandemic periods: 1725-30 and 1732-33 (Harries 1892); 1727-29 and 
1732-33 (Creighton 1894); 1728-30 and 1732-33 (Arbuthnot 1751 and Thompson 1852); 1729-30 
and 1731-35 (Schweich 1836); 1729-30 and 1732-37 (Bosser 1894, Leledy 1894, and Ozanam 1835); 
1729-30 and 1732-33 (Webster 1799; Hirsch 1883; Beveridge 1978; Patterson 1986). 

8. Thompson 1852, pp. 28-38. 

9. Ibid., p. 43. 

10. Marian and Miháescu 2009. 

11. Parsons 1891, pp. 9, 14. 

12. Lee 1891, p. 367. 

13. Parsons 1891, p. 43. 

14. Journal of the American Medical Association 1890a. 

15. Parsons 1891, p. 33. 

16. Brakenridge 1890, pp. 997, 1007. 

17. Parsons 1891, p. 11 note. 

18. Clemow 1903, p. 198. 

19. Parsons 1891, p. 20. 

20. Ibid., p. 16. 

21. Ibid., p. 24. 

22. Clemow 1903, p. 200. 

23. Parsons 1891, p. 15. 

24. Ibid., p. 24. 

25. Ibid., p. 22. 

26. Ibid., p. 22. 

27. Ibid., p. 19. 

28. Bowie 1891, p. 66. 

29. Lee 1891, p. 367. 

30. Creighton 1894, p. 430. See also Webster 1799, vol. 1, p. 289; Hirsch 1883, pp. 19-21; 
Beveridge 1978, p. 47. 

31. Beveridge 1978, p. 35. 

32. Ricketson 1808, p. 4. 

33. Jones 1827, p. 5. 

34. Thompson 1852, p. ix. 

35. Mackenzie 1891, p. 884. 

36. Birkeland 1949, pp. 231-32. 

37. Bordley and Harvey 1976, p. 214. 

38. McGrew 1985, p. 151. 

39. Beveridge 1978, 15-16. 

40. Parsons 1891, pp. 54, 60. 

41. Lee 1891, p. 367. 

42. Mackenzie 1891, pp. 299-300. 


43. Beveridge 1978, p. 11. 

44. Schnurrer 1823, p. 182. 

45. Webster 1799, vol. 1, p. 98; Jones 1827, p. 3; Journal of the Statistical Society of London 
1848, p. 173; Thompson 1852, pp. 42, 57, 213-15, 285-86, 291-92, 366, 374-75; Gordon 1884, p. 
363-64; Creighton 1894, p. 343; Beveridge 1978, pp. 54-67; Taubenberger 2009, p. 6. 

46. Beveridge 1978, p. 56. 

47. E.g., Lancet 1919; Beveridge 1978, p. 57. 

48. Hope-Simpson 1979, p. 18. 

49. Kilbourne 1975, p. 1; Beveridge 1978, p. 38. 

50. Jefferson 2006, 2009. See also Glezen and Simonsen 2006; Cannell 2008. 


Chapter 8. Mystery on the Isle of Wight 


1. d'Arsonval 1892a. 

2. d’Arsonval 1893a. 

3. Ibid. 

4. Underwood and van Engelsdorp 2007. 

5. Carr 1918. 

6. Baker 1971, p. 160. 

7. Nimitz 1963, p. 239. 

8. Annual Report of the Surgeon General 1919, p. 367. 

9. Berman 1918. 

10. Annual Report of the Surgeon General 1919, pp. 411-12. 

11. Nuzum 1918. 

12. Journal of the American Medical Association 1918e, p. 1576. 

13. Pflomm 1931; Schliephake 1935, p. 120; Kyuntsel’ and Karmilov 1947; Richardson 1959; 
Schliephake 1960, p. 88; Rusyaev and Kuksinskiy 1973; Kuksinskiy 1978. See also Person 1997; 
Firstenberg 2001. 

14, Jordan 1918. 

15. Berman 1918, p. 1935. 

16. Bircher 1918. 

17. Journal of the American Medical Association 1918g. 

18. Armstrong 1919, p. 65; Sierra 1921. 

19. Journal of the American Medical Association 1919b. 

20. Firstenberg 1997, p. 29. 

21. Annual Report of the Surgeon General 1919, p. 408. 

22. Ibid., pp. 409-10. 

23. Menninger 1919a. 

24. Annual Report of the Surgeon General 1919, pp. 426-35. 

25. Erlendsson 1919. 

26. Soper 1918, p. 1901. 

27. Rosenau 1919. See also Leake 1919; Public Health Reports 1919. 


Chapter 9. Earth's Electric Envelope 


1. The Immense Journey. NY: Random House, 1957, p. 14. 

2. Burbank 1905, p. 27. 

3. Rheinberger and Jasper 1937, p. 190; Ruckebusch 1963; Klemm 1969; Pellegrino 2004, pp. 
481-82. 


4. Kónig 1974b; Kónig 1975, pp. 77-81. 

5. Helliwell 1965, p. 1. 

6. Reiter 1954, p. 481. 

7. Lyman and O'Brien 1977, pp. 1-27. 

8. Brewitt 1996; Larsen 2004. 

9. Xiang et al. 1984; Hu et al. 1993; Huang et al. 1993; Wu et al. 1993; Zhang et al. 1999; 
Starwynn 2002. 


10. 
IL. 
12. 


Wei et al. 2012. 
de Vernejoul et al. 1985. 
Jiang et al. 2002; Baik, Park, et al. 2004; Baik, Sung, et al. 2004; Cho et al. 2004; Johng et al. 


2004; Kim et al. 2004; Lee 2004; Park et al. 2004; Shin et al. 2005; Johng et al. 2006; Lee et al. 
2008; Lee et al. 2010; Soh et al. 2012; Avijgan and Avijgan 2013; Park et al. 2013; Soh et al. 2013. 


13. 
14. 
l8. 
16. 
17. 
18. 
19. 
20. 


21 


Lee et al. 2009. 

Fujiwara and Yu 2012. 

Lim et al. 2015. 

Helliwell 1977. 

Davis 1974; Fraser-Smith et al. 1977. 

Park and Chang 1978. 

Bullough 1995. 

Fraser-Smith 1979, 1981; Villante et al. 2004; Guglielmi and Zotov 2007. 


. Fraser-Smith 1979. 
22. 
25. 
24. 
25. 
26. 
Zr. 
28. 


Guglielmi and Zotov 2007. 

Bullough et al. 1976; Tatnall et al. 1983; Bullough 1995. 

Boerner et al. 1983. 

Bullough 1985. 

Cannon and Rycroft 1982. 

Bullough et al. 1976; Luette et al. 1977, 1979; Park et al. 1983; Imhof et al. 1986. 
Kornilov 2000. 


Chapter 10. Porphyrins and the Basis of Life 


1. Randolph 1987, chap. 4. 

2. Leech 1888; Matthes 1888; Hay 1889; Ireland 1889; Marandon de Montyel 1889; Revue des 
Sciences Médicales 1889; Rexford 1889; Bresslauer 1891; Fehr 1891; Geill 1891; Hammond 1891; 
Lepine 1893; With 1980. 

3. Morton 2000. 

4. Morton 1995, 1998, 2000, 2001, personal communication. 

5. Morton 1995, p. 6. 

6. Hoffer and Osmond 1963; Huszák et al. 1972; Irvine and Wetterberg 1972; Pfeiffer 1975; 
McCabe 1983; Durkó et al. 1984; McGinnis et al. 2008a, 2008b; Mikirova 2015. 

7. Moore et al. 1987, pp. 42-43. 

8. Gibney et al. 1972; Petrova and Kuznetsova 1972; Holtmann and Xenakis 1978, 1978; Pierach 
1979; Hengstman et al. 2009;. 

9. Quoted in Mason et al. 1933. 


10. 


Athenstaedt 1974; Fukuda 1974. 


11. Adler 1975. 


12. 
La. 


Kim et al. 2001; Zhou 2009; Hagemann et al. 2013. 
Aramaki et al. 2005. 


14. Szent-Gyórgyi 1957, p. 19. 

15. Becker and Selden 1985, p. 30. 

16. Burr 1945b, 1950, 1956. 

17. Ravitz 1953. 

18. Becker 1960; Becker and Marino 1982, p. 37; Becker and Selden 1985, p. 116. 

19. Gilyarovskiy et al. 1958. 

20. Becker 1985, pp. 238-39. 

21. Rose 1970, pp. 172-73, 214-15; Lund 1947 (comprehensive review and bibliography). 

22. Becker and Selden 1985, p. 237. 

23. Becker 1961a; Becker and Marino 1982, pp. 35-36. 

24. Klüver 1944a, 1944b; Harvey and Figge 1958; Peters et al. 1974; Becker and Wolfgram 1978; 
Chung et al. 1997; Kulvietis et al. 2007; Felitsyn et al. 2008. 

25. Peters 1993. 

26. Felitsyn et al. 2008. 

27. Soldán and Pirko 2012. 

28. Hargittai and Lieberman 1991; Ravera et al. 2009; Morelli et al. 2011; Morelli et al. 2012; 
Ravera, Bartolucci, et al. 2013; Rivera, Nobbio, et al. 2013; Ravera et al. 2015; Ravera and Panfoli 
2015. 

29. Peters 1961. 

30. Peters et al. 1957; Peters et al. 1958; Peters 1961; see also Painter and Morrow 1959; Donald 
et al. 1965. 

31. Lagerwerff and Specht 1970; Wong 1996; Wong and Mak 1997; Apeagyei et al. 2011; 
Tamrakar and Shakya 2011; Darus et al. 2012; Elbagermi et al. 2013; Li et al. 2014; Nazzal et al. 
2014. 

32. Flinn et al. 2005. 

33. Hamadani et al. 2002. 

34. Hamadani et al. 2001. 

35. Buh et al. 1994. 

36. McLachlan et al. 1991; Cuajungco et al. 2000; Regland et al. 2001; Ritchie et al. 2003; 
Frederickson et al. 2004; Religa et al. 2006; Bush and Tanzi 2008. 

37. Religa et al. 2006. 

38. Hashim et al. 1996. 

39. Cuajungco et al. 2000; Que et al. 2008; Baum et al. 2010; Cristóvão et al. 2016. 

40. Voyatzoglou et al. 1982; Xu et al. 2013. 

41. Milne et al. 1983; Taylor et al. 1991; Johnson et al. 1993; King et al. 2000. 

42. Johnson et al. 1993; King et al. 2000. 

43. Andant et al. 1998. See also Kauppinen and Mustajoki 1988. 

44. Linet et al. 1999. 

45. Halpern and Copsey 1946; Markovitz 1954; Saint et al. 1954; Goldberg 1959; Eilenberg and 
Scobie 1960; Ridley 1969; Stein and Tschudy 1970; Beattie et al. 1973; Menawat et al. 1979; 
Leonhardt 1981; Laiwah et al. 1983; Laiwah et al. 1985; Kordač et al. 1989. 

46. Ridley 1975. 

47. I. P. Bakšiš, A. I. Lubosevičute, and P. A. Lopateve, “Acute Intermittent Porphyria and 
Necrotic Myocardial Changes,” Terapevticheskii arkhiv 8: 145-46 (1984), cited in Kordaé et al. 1989. 

48. Sterling et al. 1949; Rook and Champion 1960; Waxman et al. 1967; Stein and Tschudy 1970; 
Herrick et al. 1990. 

49. Berman and Bielicky 1956. 


50. Labbé 1967; Laiwah et al. 1983; Laiwah et al. 1985; Herrick et al. 1990; Kordaé et al. 1989; 
Moore et al. 1987; Moore 1990. 


Chapter 11. Irritable Heart 


1. Maron et al. 2009. 

2. Milham 2010a, p. 345. 

3. White 1938, pp. 171-72, 586; White 1971; Flint 1866, p. 303. 

4. Chadha et al. 1997. 

5. Milham 2010b. 

6. Dawber et al. 1957; Doyle et al. 1957; Kannel 1974; Hatano and Matsuzaki 1977; Rhoads et al. 
1978; Feinleib et al. 1979; Okumiya et al. 1985; Solberg et al. 1985; Stamler et al. 1986; Reed et al. 
1989; Tuomilehto and Kuulasmaa 1989; Neaton et al. 1992; Verschuren et al. 1995; Njølstad et al. 
1996; Wilson et al. 1998; Stamler et al. 2000; Navas-Nacher et al. 2001; Sharrett et al. 2001; Zhang 
et al. 2003. 

7. Phillips et al. 1978; Burr and Sweetnam 1982; Frentzel-Beyme et al. 1988; Snowdon 1988; 
Thorogood et al. 1994; Appleby et al. 1999; Key et al. 1999; Fraser 1999, 2009. 

8. Phillips et al. 1978; Snowden 1988; Fraser 1999; Key et al. 1999. 

9. Sijbrands et al. 2001. 

10. Dawber et al. 1957. 

11. Doyle et al. 1957. 

12. Fox 1923, p. 71. 

13. Ratcliffe et al. 1960, p. 737. 

14. Rigg et al. 1960. 

15. Vastesaeger and Delcourt 1962. 

16. Daily 1943; Barron et al. 1955; McLaughlin 1962. 

17. Barron et al. 1955; Brodeur 1977, pp. 29-30. 

18. Sadchikova 1960, 1974; Klimková-Deutschová 1974. 

19. See Pervushin 1957; Drogichina 1960; Letavet and Gordon 1960; Orlova 1960; Gordon 1966; 
Dodge 1970 (review); Healer 1970 (review); Marha 1970; Gembitskiy 1970; Subbota 1970; Marha et 
al. 1971; Tyagin 1971; Barański and Czerski 1976; Bachurin 1979; Jerabek 1979; Silverman 1979 
(review); McRee 1979, 1980 (reviews); Sadchikova et al. 1980; McRee et al. 1988 (review); 
Afrikanova and Grigoriev 1996. For bibliographies, see Kholodov 1966; Novitskiy et al. 1970; 
Presman 1970; Petrov 1970a; Glaser 1971-1976, 1977; Moore 1984; Grigoriev and Grigoriev 2013. 

20. Personal communication, Oleg Grigoriev and Yury Grigoriev, Russian National Committee on 
Non-Ionizing Radiation Protection. Russian textbooks include Izmerov and Denizov 2001; Suvorov 
and Izmerov 2003; Krutikov et al. 2003; Krutikov et al. 2004; Izmerov 2005, 2011a, 2011b; Izmerov 
and Kirillova 2008; Kudryashov et al. 2008. 

21. Tyagin 1971, p. 101. 

22. Frey 1988, p. 787. 

23. Brodeur 1977, p. 51. 

24. Presman and Levitina 1962a, 1962b; Levitina 1966. 

25. Frey and Seifert 1968; Frey and Eichert 1986. 

26. Cohen, Johnson, Chapman, et al. 1946. 

27. Cohen 2003. 

28. Haldane 1922, p. 56; Jones and Mellersh 1946; Jones and Scarisbrick 1946; Jones 1948. 

29. Cohen, Johnson, Chapman, et al. 1946, p. 121. 


30. See also Jones and Scarisbrick 1943; Jones 1948; Gorman et al. 1988; Holt and Andrews 
1989; Hibbert and Pilsbury 1989; Spinhoven et al. 1992; Garssen et al. 1996; Barlow 2002, p. 162. 

31. Cohen and White 1951, p. 355; Wheeler et al. 1950, pp. 887-88. 

32. Craig and White 1934; Graybiel and White 1935; Dry 1938. See also Master 1943; Logue et 
al. 1944; Wendkos 1944; Friedman 1947, p. 23; Blom 1951; Holmgren et al. 1959; Lary and 
Goldschlager 1974. 

33. Orlova 1960; Bachurin 1979. 

34. Dumanskiy and Shandala 1973; Dumanskiy and Rudichenko 1976; Zalyubovskaya et al. 1977; 
Zalyubovskaia and Kiselev 1978; Dumanskiy and Tomashevskaya 1978; Shutenko et al. 1981; 
Dumanskiy and Tomashevskaya 1982; Tomashevskaya and Soleny 1986; Tomashevskaya and 
Dumanskiy 1989; Tomashevskaya and Dumanskiy 1988. 

35. Chernysheva and Kolodub 1976; Kolodub and Chernysheva 1980. 

36. Da Costa 1871, p. 19. 

37. Plum 1882. 

38. Johnston 1880, pp. 76-77. 

39. Plum 1882, vol. 1, pp. 26-27. 

40. Oglesby 1887; MacLeod 1898. 

41. Smart 1888, p. 834. 

42. Howell 1985, p. 45; International Labour Office 1921, Appendix V, p. 50. 

43. Lewis 1918b, p. 1; Cohn 1919, p. 457. 

44. Munro 1919, p. 895. 

45. Aschenheim 1915; Brasch 1915; Braun 1915; Devoto 1915; Ehret 1915; Merkel 1915; Schott 
1915; Treupel 1915; von Dziembowski 1915; von Romberg 1915; Aubertin 1916; Galli 1916; 
Korach 1916; Lian 1916; Cohn 1919. 

46. Conner 1919, p. 777. 

47. Scriven 1915; Corcoran 1917. 

48. Howell 1985, p. 37. 

49. Corcoran 1917. 

50. Worts 1915. 

51. Scriven 1915; Popular Science Monthly 1918. 

52. Lewis 1940; Master 1943; Stephenson and Cameron 1943; Jones and Mellersh 1946; Jones 
1948. 

53. Mäntysaari et al. 1988; Fava et al. 1994; Sonimo et al. 1998. 

54. Freud 1895, pp. 97, 107; Cohen and White 1972. 

55. Reyes et al. 2003, Reeves et al. 2007. 

56. Caruthers and van de Sande 2011. 

57. Cholesterol in anxiety disorder: Lazarev et al. 1989; Bajwa et al. 1992; Freedman et al. 1995; 
Peter et al. 1999. Heart disease in anxiety disorder: Coryell et al. 1982; Coryell et al. 1986; Coryell 
1988; Hayward et al. 1989; Weissman et al. 1990; Eaker et al. 1992; Nutzinger 1992; Kawachi et al. 
1994; Rozanski et al. 1999; Bowen et al. 2000; Paterniti et al. 2001; Huffman et al. 2002; Grace et al. 
2004; Katerndahl 2004; Eaker et al. 2005; Csaba 2006; Rothenbacher et al. 2007; Shibeshi et al. 
2007; Vural and Başar 2007; Frasure-Smith et al. 2008; Phillips et al. 2009; Scherrer et al. 2010; 
Martens et al. 2010; Seldenrijk et al. 2010; Vogelzangs et al. 2010; Olafiranye et al. 2011; Soares- 
Filho et al. 2014. Cholesterol in chronic fatigue syndrome: van Rensburg et al. 2001; Peckerman et 
al. 2003; Jason et al. 2006. Heart disease in chronic fatigue syndrome: Lerner et al. 1993; Bates et al. 
1995; Miwa and Fujita 2009. Heart disease in myalgic encephalomyelitis: Caruthers and van de 
Sande 2011. Cholesterol in radio wave sickness: Klimkova-Deutschova 1974; Sadchikova 1981. 


58. Heart disease in porphyria: Saint et al. 1954; Goldberg 1959; Eilenberg and Scobie 1960; 
Ridley 1969, 1975; Stein and Tschudy 1970; Beattie et al. 1973; Bonkowsky et al. 1975; Menawat et 
al. 1979; Leonhardt 1981; Kordaé et al. 1989; Crimlisk 1997. Cholesterol in porphyria: Taddeini et 
al. 1964; Lees et al. 1970; Stein and Tschudy 1970; York 1972, pp. 61-62; Whitelaw 1974; Kaplan 
and Lewis 1986; Shiue et al. 1989; Fernández-Miranda et al. 2000; Blom 2011; Park et al. 2011. 

59. Chin et al. 1999; Newman et al. 2001; Coughlin et al. 2004; Robinson et al. 2004; Li et al. 
2005; McArdle et al. 2006; Li et al. 2007; Savransky et al. 2007; Steiropoulous et al. 2007; Gozal et 
al. 2008; Dorkova et al. 2008; Lefebvre et al. 2008; Cuhadaroglu et al. 2009; Drager et al. 2010; 
Nadeem et al. 2014. 

60. Behan et al. 1991; Wong et al. 1992; McCully et al. 1996; Myhill et al. 2009. 

61. Marazziti et al. 2001; Gardner et al. 2003; Fattal et al. 2007; Gardner and Boles 2008, 2011; 
Hroudová and Fišar 2011. 

62. See note 34. Also Ammari et al. 2008. 

63. Goldberg et al. 1985; Kordač et al. 1989; Herrick et al. 1990; Moore 1990; Thunell 2000. 

64. Sanders et al. 1984. 

65. Haldane 1922, pp. 56-57; Haldane and Priestley 1935, pp. 139-41. 

66. Numbers of residential electric customers for 1930-1931 were obtained from National Electric 
Light Association, Statistical Bulletin nos. 7 and 8, and for 1939-1940 from Edison Electric Institute, 
Statistical Bulletin nos. 7 and 8. For states east of the 100th meridian, “Farm Service” customers 
(1930-1931) or “Rural Rate” customers (1939-1940) were added to “Residential or Domestic” 
customers to get the true residential count, as recommended in the Statistical Bulletins. “Farm” and 
“Rural Rate” service in the west referred mainly to commercial customers, usually large irrigation 
systems. The same terms, east of the 100th meridian, were used for residential service on distinct 
rural rates. A discrepancy in the number of farm households in Utah was resolved by consulting 
Rural Electrification in Utah, published in 1940 by the Rural Electrification Administration. 

67. Johnson 1868. 

68. Koller 1962. 

69. Parikh et al. 2009. 

70. McGovern et al. 2001. 

71. Roger et al. 2004. 

72. Ghali et al. 1990. 

73. Fang et al. 2008. 

74. McCullough et al. 2002. 

75. Cutler et al. 1997; Martin et al. 2009. 

76. Zheng et al. 2005. 

77. National Center for Health Statistics 1999, 2006. 

78. Arora et al. 2019. 


Chapter 12. The Transformation of Diabetes 


1. The Sun 1891; Howe 1931; Joslin Diabetes Clinic 1990. 

2. Gray 2006, pp. 46, 261, 414. 

3. Hirsch 1885, p. 645. 

4. Harris 1924; Brun et al. 2000. 

5. Joslin 1917, p. 59. 

6. Annual consumption of sugar and other sweeteners from 1822 to 2014 was obtained from tables 
published in Annual Report of the Commissioner of Agriculture for the Year 1878; American 
Almanac and Treasury of Facts (New York: American News Company, 1888); Proceedings of the 


Interstate Sugar Cane Growers First Annual Convention (Macon, GA: Smith and Watson, 1903); A. 
Bouchereau, Statement of the Sugar Crop Made in Louisiana in 1905-’06 (New Orleans, 1909); 
Statistical Abstracts of the United States for 1904-1910; Ninth Census of the United States, vol. 3, 
The Statistics of Wealth and Industry of the United States (1872); Twelfth Census of the United States, 
vol. 5, Agriculture (1902); Thirteenth Census of the United States, vol. 5, Agriculture (1914); United 
States Census of Agriculture, vol. 2 (1950); Statistical Bulletin No. 3646 (U.S. Dept. of Agriculture, 
1965); Supplement to Agricultural Economic Report No. 138 (U.S. Dept. of Agriculture, 1975); and 
Sugar and Sweeteners Outlook, Table 50 — U.S. per capita caloric sweeteners estimated deliveries for 
domestic food and beverage use, by calendar year (U.S. Dept. of Agriculture, 2003). Honey was 
estimated to contain 81 percent sugar; molasses, 52 percent sugar; cane syrup, 56.3 percent sugar; 
maple syrup, 66.5 percent sugar; and sorghum syrup, 68 percent sugar. 

7. Gohdes 1995. 

8. Black Eagle, personal communication. 

9. Levy et al. 2012; Welsh et al. 2010. 

10. Pelden 2009. 

11. Giri et al. 2013. 

12. Joslin 1917, 1924, 1927, 1943, 1950; Woodyatt 1921; Allen 1914, 1915, 1916, 1922; Mazur 
2011. 

13. Fothergill 1884. 

14. Joslin 1917, pp. 100, 102, 106, 107. 

15. Simoneau et al. 1995; Gerbiz et al. 1996; Kelley et al. 1999; Simoneau and Kelley 1997; 
Kelley and Mandarino 2000; Kelley et al. 2002; Bruce et al. 2003; Morino et al. 2006; Toledo et al. 
2008; Ritov et al. 2010; Patti and Corvera 2010; DeLany et al. 2014; Antoun et al. 2015. 

16. DeLany et al. 2014. 

17. Ritov et al. 2010. 

18. Gel’fon and Sadchikova 1960. 

19. Gel'fon and Sadchikova 1960; Syngayevskaya 1962; Bartonícek and Klimková-Deutschová 
1964; Petrov 1970a, p. 164; Sadchikova 1974; Klimková-Deutschová 1974; Dumanskiy and 
Rudichenko 1976; Dumanskiy and Shandala 1974; Dumanskiy and Tomashevskaya 1978; Gabovich 
et al. 1979; Kolodub and Chemysheva 1980; Belokrinitskiy 1981; Shutenko et al. 1981; Dumanskiy 
et al. 1982; Dumanskiy and Tomashevskaya 1982; Tomashevskaya and Soleny 1986; Tomashevskaya 
and Dumanskiy 1988; Navakatikian and Tomashevskaya 1994. 

20. Kwon et al. 2011. 

21. Li et al. 2012. 

22. 1917 figure from Joslin 1917, p. 25. 

23. Kuczmarski et al. 1994. See also Prentice and Jebb 1995. 

24. Flegal et al. 1998, 2002, 2010; Ogden et al. 2012. 

25. Kim et al. 2006. 

26. Flegal 1998, p. 45. 

27. 'Thatcher et al. 2009. 

28. Klimentidis et al. 2011. 


Chapter 13. Cancer and the Starvation of Life 


1. Warburg 1925, p. 148. 

2. Warburg 1908. 

3. Warburg et al. 1924; Warburg 1925. 
4. Warburg 1925, p. 162. 


5. Warburg 1930, p. x. 

6. Warburg 1956. 

7. Warburg 1966b. 

8. Krebs 1981, pp. 23-24, 74. 

9. Harris 2002; Ferreira and Campos 2009. 

10. Ristow and Cuezva 2006; van Waveren et al. 2006; Srivastava 2009; Sánchez-Aragó et al. 
2010. 

11. Kondoh 2009, p. 101; Sánchez-Aragó et al. 2010. 

12. Apte and Sarangarajan 2009a. 

13. Ferreira and Campos 2009, p. 81. 

14. Vaupel et al. 1998; Gatenby and Gillis 2004; McFate et al. 2008; Gonzáles-Cuyar et al. 2009, 
pp. 134-36; Semenza 2009; Werner 2009, pp. 171-72; Sánchez-Aragó et al. 2010. 

15. Vigneri et al. 2009. 

16. Giovannuca et al. 2010. 

17. Lombard et al. 1959. 

18. From Williams 1908, p. 53. 

19. Guinchard 1914. 

20. Hoffman 1915, p. 151. 

21. Ibid., pp. 185-186. 

22. Stein et al. 2011. 

23. From volumes of Vital Statistics of the United States (United States Bureau of the Census) and 
National Vital Statistics Reports (Centers for Disease Control and Prevention). 

24. Moffat 1988. 

25. Data on smoking rates from National Center for Health Statistics. Data on lung cancer from 
Vital Statistics of the United States (1970, 1980, 1990) and National Vital Statistics Reports (2000, 
2010, 2015). 

26. National Cancer Institute 2009. 

27. Schüz et al. 2006. 

28. Barlow et al. 2009. 

29. Teppo et al. 1994. 

30. Jacob Easaw, Southern Alberta Cancer Research Institute, personal communication. 

31. Hardell and Carlberg 2009; Hardell et al. 2011a. 

32. Anderson and Henderson 1986. 


Chapter 14. Suspended Animation 


1. Beard 1980, pp. 2-3; Beard 1881a, pp. viii, ix, 105. 
2. Weindruch and Walford 1988. 

3. Walford 1982. 

4. Riemers 1979. 

5. Austad 1988. 

6. Dunham 1938. 

7. Johnson et al. 1984. 

8. Fischer-Piette 1989. 

9. Hansson et al. 1953. 

10. Colman et al. 2013. 

11. Ross and Bras 1965; for other studies of tumors in rats, see Weindruch and Walford, pp. 76-84. 
12. Colman et al. 2009; Mattison et al. 2003. 


l3. 
14. 
15. 
16. 
17. 
18. 
19. 
20. 
21. 
22. 


Griffin 1958, p. 35. 

Ramsey et al. 2000; Lynn and Wallwork 1992. 
Ramsey et al. 2000. 

Ordy et al. 1967. 

Spalding et al. 1971. 

Perez et al. 2008. 

Tryon and Snyder 1971. 

Caratero et al. 1998. 

Okada et al. 2007. 

Suzuki et al. 1998. 


Chapter 15. You mean you can hear electricity? 


. Grapengiesser 1801, p. 133. Quoted in Brenner 1868, p. 38. 

. Brenner 1868, pp. 41, 45. 

. Tousey 1921, p. 469. 

. Meyer 1931. 

. Gersuni and Volokhov 1936. 

. Stevens and Hunt 1937, unpublished, described in Stevens and Davis 1938, pp. 354-55. 
. Moeser, W. “Whiz Kid, Hands Down,” Life, September 14, 1962. 

. Einhorn 1967. 

. Russell et al. 1986. 


. See also Degens et al. 1969. 


11. Lissman, p. 184; Offutt 1984, pp. 19-20. 

12. de Vries 1948a, 1948b. 

13. Honrubia 1976; Mountain 1986; Ashmore 1987. 

14. Zwislocki 1992; Gordon, Smith and Chamberlain 1982, cited in Zwislocki. 

15. Nowotny and Gummer 2006. 

16. Brenner 1868. 

17. Mountain 1986. 

18. Mountain et al. 1986; Ashmore 1987; Honrubia and Sitko 1976. 

19. Lenhardt 2003. 

20. Combridge and Ackroyd 1945, Item No. 7, p. 49. 

21. Gavrilov et al. 1980. 

22. Qin et al. 2011. 

23. Stevens 1938, p. 50, fig. 17; Corso 1963; Moller and Pederson 2004, figs. 1-3; Stanley and 
Walker 2005. 

24. Stevens 1937. 

25. Environmental Health Criteria 137, 1993 edition, pp. 160 and 161, figs. 23 and 24. 

26. Duane Dahlberg, Ph.D., personal communication. 

27. Petrie 1963, pp. 89-92. 

28. Maggs 1976. 

29. Reported by the Low Frequency Noise Sufferer’s Association of England, Jean Skinner, 


personal communication; by Sara Allen of Taos, New Mexico, personal communication; and by 


Mulli 
30 


ns and Kelley 1995. 
. Calculation based on Jansky and Bailey 1962, fig. 35, Ground Wave Field Intensity; and 


Garufi 1989, fig. 6, U.S. Coast Guard Conductivity Map. 


31. In Africa, only Egypt, Tunisia, Ghana, Senegal, Ethiopia, Zambia, Zimbabwe, and South 
Africa currently have bans in place or in progress. In the Middle East, only Israel, Lebanon, Kuwait, 
Bahrain, Qatar, and the United Arab Emirates currently have bans. Other countries where prohibition 
is neither in place nor in progress include Haiti, Jamaica, St. Kitts and Nevis, Granada, Antigua and 
Barbuda, St. Vincent and the Grenadines, St. Lucia, Trinidad and Tobago, Dominica, Venezuela, 
Bolivia, Paraguay, Uruguay, Suriname, Albania, Moldova, Belarus, Uzbekistan, Kyrgyzstan, 
Turkmenistan, Mongolia, Turkey, Afghanistan, Pakistan, Nepal, Bhutan, India, Bangladesh, 
Myanmar, Singapore, Cambodia, Laos, Indonesia, East Timor, Papua New Guinea, New Zealand, 
Bosnia and Herzegovinia, Kosovo, and North Macedonia. 

32. Signal structure for GSM: superframe (6.12 sec), control multiframe (235.4 msec), traffic 
multiframe (120 msec), frame (4.615 msec), time slot (0.577 msec), symbol (270,833 per second per 
channel, 33,850 per second per user). Signal structure for UMTS: frame (10 msec), time slot (0.667 
msec), symbol (66.7 psec), chip (0.26 psec). Signal structure for LTE: frame (10 msec), half-frame (5 
msec), subframe (1 msec), slot (0.5 msec), symbol (0.667 msec). 

33. Mild and Wilén 2009. 

34. Hutter et al. 2010. 

35. National Center for Health Statistics 1982-1996. 

36. Shargorodsky et al. 2010. 

37. Del Bo et al. 2008. 

38. Nondahl et al. 2012. 


Chapter 16. Bees, Birds, Trees, and Humans 


1. Balmori and Hallberg 2007. 
2. Sen 2012. 
3. Deccan Herald 2012. 
4. Personal communication from New Mexico pigeon racer Larry Lucero, 1999. 
5. Bigu del Blanco et al. 1973. 
6. Haughey 1997. 
7. Larry Lucero, personal communication. 
8. Robert Costagliola, of Fogelsville, Pennsylvania, personal communi- cation. 
9. Gary Moore, the "liberator" for the western Pennsylvania-to-Philadelphia race, personal 
communication. 
10. Elston 2004. 
11. Indian Express 2010. 
12. Roberts 2000. 
13. Mech and Barber 2002, p. 29. 
14. Withey et al. 2001, pp. 47-49; Mech and Barber 2002, p. 30. 
15. Burrows et al. 1994, 1995 on wild dogs; Mech and Barber 2002, pp. 50-51. 
16. Swenson et al. 1999. 
17. Moorhouse and Macdonald 2005. 
18. Reader s Digest 1998. 
19. Godfrey and Bryant 2003. 
20. Engels et al. 2014. 
21. Souder 1996. 
22. Hallowell 1996. 
23. Stern 1990. 
24. Hallowell 1996; Souder 1996. 


20: 
26. 
27. 
28. 


29 


Watson 1998. 
Ibid. 

Revkin 2006. 
Hawk 1996. 


. Hoperskaya et al., p. 254. 
30. 
31. 
32. 
33. 


Serant 2004. 

Panagopoulos et al. 2004. 

Panagopoulous, Chavdoula, Nezis, and Margaritis 2007; Panagopoulos 2012a. 
Panagopoulos and Margaritis 2008, 2010; Panagopoulos, Chavdoula, and Margaritis 2010; 


Panagopoulos 2011. 


34. 
35. 
36. 
37. 
38. 
39. 
40. 
41. 
42. 
3. 
44. 
45. 
46. 
47. 
48. 
49. 
50. 
Di. 
5d. 
53. 
54. 
55: 
56. 
57: 
58. 
59. 
60. 
. Pattazhy 2011a, 2011b, 2012, and personal communication. 
62. 
63. 
64. 
65. 
66. 
67. 
68. 
69. 
70. 
E 


61 


Margaritis et al. 2014. 

Bienenvater, issue no. 9, 2003. 

Ruzicka 2006. 

Phillips 1925; Bailey 1964; Underwood and vanEngelsdorp 2007. 
Bailey 1991, pp. 97-101. 

Ibid., p. 101. 

Rinderer et al. 2001. 

Sanford 2004. 

Boecking and Ritter 1993. 

Fries et al. 2006. 

Page 1998; Rinderer et al. 2001. 

Rinderer et al. 2001. 

Kraus and Page 1995. 

Seeley 2007. 

National Research Council 2007; Kluser and Peduzzi 2007; vanEngelsdorp 2009. 
Wilson and Menapace 1979; Underwood and vanEngelsdorp 2007; McCarthy 2011. 
Also Finley et al. 1996. 

O'Hanlon 1997. 

Hamzelou 2007. 

Kluser and Peduzzi 2007. 

Borenstein 2007. 

McCarthy 2011; Pattazhy 2012. 

Le Conte et al. 2010. 

Evans et al. 2008. 

Warnke 1976; Becker 1977. 

Warnke 1989. 

Lindauer and Martin 1972; Warnke 2009. 


Warnke 2009. 

Schütt and Cowling 1985. 
Microwave News 1994. 
Kolodynski and Kolodynska 1996. 
Balode 1996. 

Liepa and Balodis 1994. 

Balodis et al. 1996. 

Selga and Selga 1996. 

Magone 1996. 

Lorenz et al. 2003. 


72. Bentouati and Bariteau 2006. 

73. Hennon et al. 1990; Hennon and Shaw 1994; Hennon et al. 2012. 

74. Navy Department, Bureau of Equipment 1907, 1908; United States Department of Commerce, 
Bureau of Navigation 1913. 

75. Phillips et al. 2009. 

76. Rohter 2002. 

77. Worrall et al. 2008. 


Chapter 17. In the Land of the Blind 


. Mild et al. 1998. 

. Yakymenko et al. 2011. 

. Dalsegg 2002. 

. Johansson 2004. 

. Hallberg and Oberfeld 2006. 
. Byun et al. 2013. 

. Tatemichi et al. 2004. 

. Kimata 2002. 

. Ye et al. 2001. 

10. Li et al. 2011. 

11. Oktay and Dasdag 2006. 

12. Panda et al. 2011. 

13. Velayutham et al. 2014. 

14. Mishra 2011. 

15. Mishra 2010, p. 51. 

16. Salford et al. 2003. 

17. Nittby et al. 2008. 

18. Sahin et al. 2015. 

19. Bas et al. 2013; Hanci et al. 2013; İkinci et al. 2013; Odacı et al. 2013; Hancı et al. 2015; 
Odacı, Hancı, İkinci et al. 2015; Odacı and Özyılmaz 2015; Odacı, Ünal, et al. 2015; Topal et al. 
2015; Türedi et al. 2015; Odacı, Hancı, Yuluğ et al. 2016. 

20. İkinci et al. 2015. 

21. Blue Cross Blue Shield 2019. 

22. Bejot et al. 2014. 

23. Rosengren et al. 2013. 

24. Putaala et al. 2009. 

25. Tibæk et al. 2016. 

26. West et al. 2013. 

27. Wolford et al. 2015. 

28. Siegel et al. 2017. 

29. Wong et al. 2016 

30. Hallberg and Johansson 2009. 

31. Weiner et al. 2016. 

32. Centola et al. 2016. 

33. Hutton et al. 2019. 

34. Broomhall 2017. 

35. Hallman et al. 2017 

36. Lister and Garcia 2018. 


WOANAUNBRWNH 


37. Sánchez-Bayo and Wyckhuys 2019. 

38. "Satellites Begin Worldwide Service," No Place To Hide 2(1): 3 (1999). 

39. “Satellites: An Urgent Situation," No Place To Hide 2(3): 18 (2000). 

40. “Update on Satellites," No Place To Hide 3(2): 15 (2001). 

41. Janet Patton, *Foal deaths remain a mystery," Lexington Herald-Leader, May 9, 2001; Lenn 
Harrison, personal communication. 

42. The actual power in each beam will be 100 watts or less, but since all of that power will be 
focused in a laser-like beam, the effective radiated power (EIRP) is reported to the FCC. The EIRP is 
the amount of power the satellite would have to emit in order to have the same strength in all 
directions as it has in the focused beam. 


Bibliography 


Note: JPRS - Joint Publications Research Service. 


Chapters 1-4 

Adams, George. 1787, 1799. An Essay on Electricity, 3rd ed. London: R. Hindmarsh; 5th ed. 
London: J. Dillon. 

Aldini, Jean. 1804. Essai Théorique et Expérimental sur le Galvanisme. Paris: Fournier Fils. 

Baker, Henry. 1748. “A Letter from Mr. Henry Baker, F.R.S. to the President, concerning several 
Medical Experiments of Electricity.” Philosophical Transactions 45: 370-75. 

Beard, George Miller and Alphonso David Rockwell. 1883. A Practical Treatise on the Medical and 
Surgical Uses of Electricity, 4th ed. New York: William Wood. 

Beaudreau, Sherry Ann and Stanley Finger. 2006. “Medical Electricity and Madness in the 18th 
Century: The Legacies of Benjamin Franklin and Jan Ingenhousz.” Perspectives in Biology and 
Medicine 49(3): 330-45. 

Beccaria, Giambatista. 1753. Dell’Elettricismo Artificiale e Naturale. Torino: Filippo Antonio 
Campana. 

Becket, John Brice. 1773. An Essay on Electricity. Bristol. 

Bell, Whitfield Jenks, Jr. 1962. “Benjamin Franklin and the Practice of Medicine.” Bulletin of the 
Cleveland Medical Library 9: 51-62. 

Berdoe, Marmaduke. 1771. An Enquiry Into the Influence of the Electric Fluid in the Structure and 
Formation of Animated Beings. Bath: S. Hazard. 

Bertholon, Pierre Nicholas. 1780. De l'Électricité du Corps Humain dans l'État de Santé et de 
Maladie. Lyon: Bernusset. 

. 1783. De l'Électricité des Végétaux. Paris: P. F. Didot Jeune. 

. 1786. De l'Électricité du Corps Humain dans l’État de Santé et de Maladie, 2 vols. Paris: 
Didot le jeune. 

Bertucci, Paola. 2007. *Sparks in the Dark: the Attraction of Electricity in the Eighteenth Century." 
Endeavor 31(3): 88-93. 

Bonnefoy, Jean-Baptiste. 1782. De l'Application de l'Éléctricité a l'Art de Guérir. Lyon: Aimé de la 
Roche. 

Bose, Georg Matthias. 1744a. Tentamina electrica in Academiis Regiis Londinensi et Parisina. 
Wittenberg: Johann Joachim Ahlfeld. 

. 1744b. Die Electricitát nach ihrer Entdeckung und Fortgang, mit poetischer Feder 
entworffen. Wittenberg: Johann Joachim Ahlfeld. 

Bresadola, Marco. 1998. “Medicine and Science in the Life of Luigi Galvani.” Brain Research 
Bulletin 46(5): 367-80. 

Bryant, William. 1786. “Account of an Electric Eel, or the Torpedo of Surinam.” Transactions of the 
American Philosophical Society 2: 166-69. 











Brydone, Patrick. 1773. A Tour Through Sicily and Malta, 2 vols. London: W. Strahan and T. Cadell. 

Cavallo, Tiberius. 1786. Complete Treatise on Electricity in Theory and Practice. London: C. Dilly. 

Chaplin, Joyce E. 2006. The First Scientific American: Benjamin Franklin and the Pursuit of Genius. 
New York: Basic Books. 

Delbourgo, James. 2006. A Most Amazing Scene of Wonders: Electricity and Enlightenment in Early 
America. Cambridge, MA: Harvard University Press. 

Donndorf, Johann August. 1784. Die Lehre von der Elektricitüt theoretisch und praktisch aus 
einander gesetzt, 2 vols. Erfurt: Georg Adam Kayser. 

Donovan, Michael. 1846, 1847. *On the Efficiency of Electricity, Galvanism, Electro-Magnetism, 
and Magneto-Electricity, in the Cure of Disease; and on the Best Methods of Application." Dublin 
Quarterly Journal of Medical Science 2: 388-414, 3: 102-28. 

Dorsman, C. and C. A. Crommelin. 1951. The Invention of the Leyden Jar. Leyden: National 
Museum of the History of Science. Communication no. 97. 

Duchenne (de Boulogne), Guillaume Benjamin Amand. 1861. De l'Électrisation Localisée, 2nd ed. 
Paris: J.-B. Bailliére et Fils. 

Duhamel du Monceau, Henri Louis. 1758. La Physique des Arbres. Paris: H. L. Guérin & L. F. 
Delatour. 

Elliott, Paul. 2008. *More Subtle than the Electric Aura: Georgian Medical Electricity, the Spirit of 
Animation and the Development of Erasmus Darwin's Psychophysiology." Medical History 52(2): 
195-220. 

Flagg, Henry Collins. 1786. *Observations on the Numb Fish, or Torporific Eel." Transactions of the 
American Philosophical Society 2: 170-73. 

Franklin, Benjamin. 1758. *An Account of the Effects of Electricity in Paralytic Cases. In a Letter to 
John Pringle, M.D. F.R.S." Philosophical Transactions 50: 481-83. 

. 1774. Experiments and Observations on Electricity, 5th ed. London: F. Newbery. 

. Benjamin Franklin Papers, <http://franklinpapers.org>. 

Gale, T. 1802. Electricity, or Ethereal Fire. Troy: Moffitt & Lyon. 

Galvani, Luigi. 1791. De viribus electricitatis in motu musculari. Commentarius. Bologna: Istituto 
delle Scienze. Translation by Robert Montraville Green, Commentary on the Effect of Electricity 
on Muscular Motion (Cambridge: Elizabeth Licht), 1953. 

Gerhard, Carl Abraham. 1779. “De l'Action de Électricité Sur le Corps humain, et de son usage 
dans les Paralysies." Observations Sur la Physique, Sur l'Histoire Naturelle, et Sur les Arts 14: 
145-53. 

Graham, James. 1779. The General State of Medical and Chirurgical Practice, Exhibited; Showing 
Them to be Inadequate, Ineffectual, Absurd, and Ridiculous. London. 

Gralath, Daniel. 1747, 1754, 1756. *Geschichte der Electricitát." Versuche und Abhandlungen der 
Naturforschenden Gesellschaft in Danzig 1: 175-304, 2: 355-460, 3: 492-556. 

Haller, Albrecht von. 1745. *An historical account of the wonderful discoveries, made in Germany, 
etc. concerning Electricity." The Gentleman's Magazine 15: 193-97. 

Hart, Cheney. 1754. “Part of a Letter from Cheney Hart, M.D. to William Watson, F.R.S. giving 
some Account of the Effects of Electricity in the County Hospital at Shrewsbury.” Philosophical 
Transactions 48: 786-88. 

Heilbron, John L. 1979. Electricity in the 17th and 18th Centuries: A Study of Early Modern Physics. 
University of California Press: Berkeley. 

Histoire de l'Academie Royale des Sciences. 1746. “Sur |’ Électricité," pp. 1-17. 

. 1747. *Sur l Électricité," pp. 1-32. 

. 1748. *Des Effets de lÉlectricité sur les Corps Organisés," pp. 1-13. 














Houston, Edwin J. 1905. Electricity in Every-Day Life, 3 vols. New York: P. F. Collier & Son. 

Humboldt, Friedrich Wilhelm Heinrich Alexander von. 1799. Expériences sur le Galvanisme. Paris: 
Didot Jeune. 

Jallabert, Jean. 1749. Expériences sur l'Électricité. Paris: Durand & Pissot. 

Janin, Jean. 1772. Mémoires et Observations Anatomiques, Physiologiques, et Physiques sur l'GEil. 
Lyon: Perisse. 

Kratzenstein, Christian Gottlieb. 1745. Abhandlung von dem Nutzen der Electricitüt in der 
Arzneywissenschaft. Halle: Carl Hermann Hemmerde. 

La Beaume, Michael. 1820. Remarks on the History and Philosophy, But Particularly on the Medical 
Efficacy of Electricity in the Cure of Nervous and Chronic Disorders. London: F. Warr. 

. 1842. On Galvanism. London: Highley. 

Ladame, Paul-Louis. 1885. *Notice historique sur l'Électrothérapie a son origine." Revue Médicale 
de la Suisse Romande 5: 553-72, 625-56, 697-717. 

Laennec, René. 1819. Traité de l'Auscultation Médiate, 2 vols. Paris: Brosson & Chaudé. 

Lindhult, Johann. 1755. *Kurzer Auszug aus des Doctors der Arztneykunst, Johann Lindhults, 
táglichem Verzeichnisse wegen der Krankheiten, die durch die Electricitát sind gelindert oder 
glücklich geheilet worden. In Stockholm im November und December 1752 gehalten." 
Abhandlungen aus der Naturlehre 14: 312-15. 

Louis, Antoine. 1747. Observations sur l'Électricité. Paris: Osmont & Delaguette. 

Lovett, Richard. 1756. The Subtil Medium Prov'd. London: Hinton, Sandby and Lovett. 

Lowndes, Frances. 1787. Observations on Medical Electricity. London: D. Stuart. 

Mangin, Arthur. 1874. Le Feu du Ciel: Histoire de | "Électricité, 6th ed. Tours: Alfred Mame et Fils. 

Marat, Jean-Paul. 1782. Recherches Physiques sur l'Électricité. Paris: Clousier. 

. 1784. Mémoire sur l'électricité médicale. Paris: L. Jorry. 

Martin, Benjamin. 1746. An Essay on Electricity: being an Enquiry into the Nature, Cause and 
Properties thereof, on the Principles of Sir Isaac Newton's Theory of Vibrating Motion, Light and 
Fire. Bath. 

Mauduyt de la Varenne, Pierre-Jean-Claude. 1777. “Premier Mémoire sur l'électricité, considérée 
relativement à l'économie animale et à l'utilité dont elle peut étre en Médecine." Mémoires de la 
Société Royale de Médecine, Année 1776, pp. 461-513. 

. 1778. “Lettre sur les précautions nécessaires relativement aux malades qu'on traite par 

l'électricité." Journal de Médecine, Chirurgie, Pharmacie, &c. 49: 323-32. 

. 1780. *Mémoire sur le traitement électrique, administré à quatre-vingt-deux malades." 

Mémoires de la Société Royale de Médecine, Années 1777 et 1778, pp. 199-455. 

. 1782. “Nouvelles observations sur |’Electricité médicale.” Histoire de la Société Royale de 

Médecine, Année 1779, pp. 187-201. 

. 1785. *Mémoire sur les différentes maniéres d'administrer l'Électricité." Mémoires de la 
Société Royale de Médecine, Année 1783, pp. 264-413. 

Mazéas, Guillaume, Abbé. 1753-54. *Observations Upon the Electricity of the Air, made at the 
Chateau de Maintenon, during the Months of June, July, and October, 1753." Philosophical 
Transactions 48(1): 377-84. 

Morel, Auguste Désiré Cornil. 1892. Étude historique, critique et expérimentale de l'action des 
courants continus sur le nerf acoustique à l'état sain et à l'état pathologique. Bordeaux: E. 
Dupuch. 

Morin, Jean. 1748. Nouvelle Dissertation sur l'Électricité des Corps. Chartres: J. Roux. 

Musschenbroek, Pieter van. 1746. Letter to René de Réaumur. Procés-verbaux de l'Académie Royale 
des Sciences 65: 6. 























. 1748. Institutiones Physice. Leyden: Samuel Luchtman and Son. 

. 1769. Cours de Physique Expérimentale et Mathématique, 3 vols. Paris: Bailly. 

Mygge, Johannes. 1919. *Om Saakaldte Barometermennesker: Bidrag til Belysning af Vejrneurosens 
Patogenese.” Ugeskrift for Leger 81(31): 1239-59. 

Nairne, Edward. 1784. Déscription de la machine électrique. Paris: P. Fr. Didot le jeune. 

Newton, Isaac. 1713. Philosophie Naturalis Principia Mathematica, 2nd ed. Cambridge. English 
translation by Andrew Motte, Newton’s Principia. The Mathematical Principles of Natural 
Philosophy (New York: Daniel Adee), 1846. 

Nollet, Jean Antoine (Abbé). 1746a. Essai sur I’Electricité des Corps. Paris: Guérin. 

. 1746b. “Observations sur quelques nouveaux phénoménes d’Electricité.” Mémoires de 

l'Académie Royale des Sciences 1746: 1-23. 

1747. “Eclaircissemens sur plusieurs faits concernant |’Electricité.” Mémoires de 

l'Académie Royale des Sciences 1747: 102-131. 

. 1748. *Éclaircissemens sur plusieurs faits concernant Électricité. Quatrième Mémoire. Des 

effets de la vertu électrique sur les corps organisés." Mémoires de l'Académie Royale des Sciences 

1748: 164-99. 

. 1753. Recherches sur les Causes Particuliéres des Phénoménes Électriques. Paris: Guérin. 

Nouvelle Bibliothéque Germanique. 1746. *Nouvelles Littéraires, Allemagne, de Greifswald." 2 (part 
1): 438-40. 

Paulian, Aimé-Henri. 1790. La Physique à la Portée de Tout le Monde. Nisme: J. Gaude. 

Pera, Marcello. 1992. The Ambiguous Frog: The Galvani-Volta Controversy on Animal Electricity. 
Princeton University Press. Translation of La rana ambigua (Torino: Giulio Einaudi), 1986. 

Plique, A. F. 1894. “L’électricité en otologie,” Annales des Maladies de l'Oreille, du Larynx, du Nez 
et du Pharynx 20: 894-910. 

Priestley, Joseph. 1767. The History and Present State of Electricity. London: J. Dodsley, J. Johnson, 
B. Davenport, and T. Cadell. 

. 1775. The History and Present State of Electricity, 3rd ed. London: C. Bathurst and T. 
Lowndes. 

Recueil sur l'Électricité Médicale. 1761. Second ed., 2 vols. Paris: P. G. Le Mercier. 

Rowbottom, Margaret and Charles Susskind. 1984. Electricity and Medicine: History of Their 
Interaction. San Francisco Press. 

Sauvages de la Croix, François Boissier de. 1749. “Lettre de M. de Sauvages.” In: Jean Jallabert, 
Expériences sur l'Électricité (Paris: Durand & Pissot), pp. 363-79. 

Schiffer, Michael Brian. 2003. Draw the Lightning Down: Benjamin Franklin and Electrical 
Technology in the Age of Enlightenment. Berkeley: University of California Press. 

Sguario, Eusebio. 1746. Dell'elettricismo. Venezia: Giovanni Battista Recurti. 

Sigaud de la Fond, Joseph. 1771. Lettre sur l'Électricité Médicale. Amsterdam. 

. 1781. Précis Historique et Expérimental des Phénoménes Électriques. Paris: Rue et Hótel 

Serpente. 

. 1803. De l'Électricité Médicale. Paris: Delaplace et Goujon. 

Sparks, Jared. 1836-40. The Works of Benjamin Franklin, 10 vols. Boston: Hilliard, Gray. 

Sprenger, Johann Justus Anton. 1802. “Anwendungsart der Galvani-Voltaischen Metall-Electricitat 
zur Abhelfung der Taubheit und Harthórigkeit." Annalen der Physik 11(7): 354-66. 

Steiglehner, Celestin. 1784. *Réponse à la Question sur l'Analogie de l'Électricité et du 
Magnétisme." In: Jan Hendrik van Swinden, Recueil de Mémoires sur l'Analogie de l'Électricité 
et du Magnétisme (The Hague: Libraires Associés), vol. 2, pp. 1-214. 


























Stukeley, William. 1749. *On the Causes of Earthquakes." Philosophical Transactions Abridged 10: 
526-41. 

Sue, Pierre, ainé. 1802-1805. Histoire du Galvanisme, 4 vols. Paris: Bernard. 

Symmer, Robert. 1759. “New Experiments and Observations concerning Electricity.” Philosophical 
Transctions 51: 340-93. 

Thillaye-Platel, Antoine. 1803. Essai sur l'Emploi Médical de l'Électricité et du Galvanisme. Paris: 
André Sartiaux. 

Torlais, Jean. 1954. L'Abbé Nollet. Paris: Sipuco. 

Trembley, Abraham. 1746. “Part of a Letter concerning the Light caused by Quicksilver shaken in a 
Glass Tube, proceeding from Electricity.” Philosophical Transactions 44: 58-60. 

van Barneveld, Willem. 1787. Medizinische Elektricitát. Leipzig: Schwickert. 

van Swinden, Jan Hendrik. 1784. Recueil de Mémoires sur l'Analogie de l'Électricité et du 
Magnétisme, 3 vols. The Hague: Libraires Associés. 

Veratti, Giovan Giuseppi. 1750. Observations Physico-Médicales sur l'Électricité. Geneva: Henri- 
Albert Gosse. 

Volta, Alessandro. 1800. *On the Electricity excited by the mere Contact of conducting Substances of 
different Kinds." The Philosophical Magazine 7 (September): 289-311. 

. 1802. "Lettera del Professore Alessandro Volta al Professore Luigi Brugnatelli sopra 
l'applicazione dell'elettricità ai sordomuti dalla nascita." Annali di Chimica e Storia Naturale 21: 
100-5. 

Voltaire (Frangois-Marie Arouet). 1772. Des Singularités de la Nature. London. 

Wesley, John. 1760. The Desideratum: Or, Electricity Made Plain and Useful. London: W. Flexney. 

Whytt, Robert. 1768. The Works of Robert Whytt, M.D. Edinburgh: Balfour, Auld, and Smellie. 
Reprinted by The Classics of Neurology and Neurosurgery Library, Birmingham, AL, 1984. 

Wilkinson, Charles Hunnings. 1799. The Fffects of Electricity. London: M. Allen. 

Wilson, Benjamin. 1752. A Treatise on Electricity. London: C. Davis and R. Dodsley. 

Winkler, John Henry. 1746. “An Extract of a Letter from Mr. John Henry Winkler, Grac. & Lat. Litt. 
Prof. publ. Ordin. at Leipsick, to a Friend in London; concerning the Effects of Electricity upon 
Himself and his Wife.” Philosophical Transactions 44: 211-12. 

Wosk, Julie. 2003. Women and the Machine. Baltimore: Johns Hopkins University Press. 

Zetzell, Pierre. 1761. *Théses sur la médecine électrique.” In: Recueil sur l'Électricité Médicale, 2nd 
ed. (Paris: P. G. Le Mercier), vol. 1, pp. 283-300. 





Weather Sensitivity 

Buzorini, Ludwig. 1841. Luftelectricitét, Erdmagnetismus und Krankheitsconstitution. Constanz: 
Belle-Vue. 

Craig, William. 1859. On the Influence of Variations of Electric Tension as the Remote Cause of 
Epidemic and Other Diseases. London: John Churchill. 

Faust, Volker. 1978. Biometeorologie: Der Einfluss von Wetter und Klima auf Gesunde und Kranke. 
Stuttgart: Hippokrates. 

Hippocrates. The Genuine Works of Hippocrates. Translation by Francis Adams (Baltimore: Wilkins 
& Williams), 1939. 

Hoppe, Peter. 1997. “Aspects of Human Biometeorology in Past, Present and Future.” International 
Journal of Biometeorology 40(1): 19-23. 

International Journal of Biometeorology. 1973. “Symposium on Biological Effects of Natural 
Electric, Magnetic and Electromagnetic Fields. Held During the 6th International 
Biometeorological Congress at Noordwijk, The Netherlands, 3-9 September 1972.” 17(3): 205- 
309. 





. 1985. Issue on air ions and atmospheric electricity. 29(3). 

Kevan, Simon M. 1993. “Quests for Cures: a History of Tourism for Climate and Health.” 
International Journal of Biometeorology 37(3): 113-24. 

Konig, Herbert L. 1975. Unsichtbare Umwelt: Der Mensch im Spielfeld Elektromagnetischer Krdfte. 
Miinchen: Heinz Moos Verlag. 

Peterson, William F. 1935-1937. The Patient and the Weather, 4 vols. Ann Arbor, MI: Edwards 
Brothers. 

. 1947. Man, Weather and Sun. Chicago: Thomas. 

Sulman, Felix Gad. 1976. Health, Weather and Climate. Basel: Karger. 

. 1980. The Effect of Air Ionization, Electric Fields, Atmospherics and Other Electric 

Phenomena on Man and Animal. Charles C. Thomas: Springfield, IL. 

. 1982. Short- and Long-Term Changes in Climate, 2 vols. Boca Raton, FL: CRC Press. 

Sulman, Felix Gad, D. Levy, Y. Pfeifer, E. Superstine, and E. Tal. 1975. “Effects of the Sharav and 
Bora on Urinary Neurohormone Excretion in 500 Weather-Sensitive Females.” International 
Journal of Biometeorology 19(3): 202-209. 

Tromp, Solco W. 1983. Medical Biometeorology: Weather, Climate and the Living Organism. 
Amsterdam: Elsevier. 











Chapter 5 

American Psychiatric Association. 2013. DSM-V, Diagnostic and Statistical Manual for Mental 
Disorders. Washington, DC. 

Anonymous. 1905. *Die Nervositát der Beamten." Zeitschrift fiir Eisenbahn- Telegraphen-Beamte 
23: 179-81. 

Aronowitz, Jesse N., Shoshana V. Aronowitz, and Roger F. Robison. 2007. “Classics in 
Brachytherapy: Margaret Cleaves Introduces Gynecologic Brachytherapy.” Brachytherapy 6: 293- 
97. 

Arndt, Rudolf. 1885. Die Neurasthenie (Nervenschwdche). Wien: Urban & Schwarzenberg. 

Bartholow, Roberts. 1884. “What is Meant by Nervous Prostration?” Boston Medical and Surgical 
Journal 110(3): 53-56, 63-64. 

Beard, George Miller. 1869. “Neurasthenia, or Nervous Exhaustion.” Boston Medical and Surgical 
Journal, new ser., 3(13): 217-21. 

. 1874. “Cases of Hysteria, Neurasthenia, Spinal Irritation and Allied Affections, with 

Remarks.” Chicago Journal of Nervous and Mental Disease 1: 438-51. 

. 1875. “The Newly-Discovered Force.” Archives of Electrology and Neurology 2(2): 256-82. 

. 1876. Hay-Fever; Or, Summer Catarrh: Its Nature and Treatment. New York: Harper. 

. 1877. “The Nature and Treatment of Neurasthenia (Nervous Exhaustion), Hysteria, Spinal 

Irritation, and Allied Neuroses.” The Medical Record 12: 579-85, 658-62. 

. 1878. “Certain Symptoms of Nervous Exhaustion.” Virginia Medical Monthly 5(3): 161-85. 

. 1879a. “The Nature and Diagnosis of Neurasthenia (Nervous Exhaustion).” New York 

Medical Journal 29(3): 225-51. 

. 1879b. “The Differential Diagnosis of Neurasthenia — Nervous Exhaustion.” Medical 

Record 15(8): 184-85. 

. 1880. A Practical Treatise on Nervous Exhaustion (Neurasthenia). New York: William 

Wood. 

. 1881a. American Nervousness: Its Causes and Consequences. New York: G. P. Putnam’s 

Sons. 
































. 1881b. A Practical Treatise on Sea-Sickness: Its Symptoms, Nature and Treatment. New 
York: Treat. 

Berger, Molly W. 1995. “The Old High-Tech Hotel.” Invention and Technology Magazine 11(2): 46- 
52. 

Bernhardt, P. 1906. Die Betriebsunfälle der Telephonistinnen. Berlin: Hirschwald. 

Beyer, Ernst. 1911. “Prognose und Therapie bei den Unfallneurosen der Telephonistinnen.” 
Medizinische Klinik, no. 51, pp. 1975-78. 

Blegvad, Niels Reinhold. 1907. “Über die Einwirkung des berufsmässigen Telephonierens auf den 
Organismus mit besonderer Rücksicht auf das Gehörorgan.” Archiv für Ohrenheilkunde 71: 111- 
16, 205-36; 72: 30-49. Original in Swedish in Nordiskt Medicinskt Arkiv (Kirurgi) 39(3): 1-109. 

Böhmig, H. 1905. “Hysterische Unfallerkrankungen bei Telephonistinnen.” Münchener medizinische 
Wochenschrift 52(16): 760-62. 

Bouchut, Eugéne. 1860. De l’État Nerveux Aigu et Chronique, ou Nervosisme. Paris: J. B. Baillière et 
Fils. 

Bracket, Cyrus F., Franklin Leonard Pope, Joseph Wetzler, Henry Morton, Charles L. Buckingham, 
Herbert Laws Webb, W. S. Hughes, John Millis, A. E. Kennelly, and M. Allen Starr. 1890. 
Electricity in Daily Life. New York: Charles Scribner’s Sons. 

Butler, Elizabeth Beardsley. 1909. “Telephone and Telegraph Operators.” In: Butler, Women and the 
Trades, Pittsburgh, NY, 1907-1908 (New York: Charities Publication Committee), pp. 282-94. 

Calvert, J. B. 2000. District Telegraphs. University of Denver. 

Campbell, Hugh. 1874. A Treatise on Nervous Exhaustion. London: Longmans, Green, Reader, and 
Dyer. 

Capart, fils (de Bruxelles). 1911. “Maladies et accidents professionnels des téléphonistes.” Archives 
Internationales de Laryngologie, d'Otologie et de Rhinologie 31: 748-64. 

Castex, André. 1897a. *La médecine légale dans les affections de l'oreille, du nez, du larynx et des 
organes connexes: L'oreille dans le service des téléphones." Bulletins et Mémoires de la Société 
Francaise d'Otologie, de Laryngologie et de Rhinologie 13 (part 1): 86-87. 

. 1897b. La médecine légale dans les affections de l'oreille, du nez, du larynx et des organes 
connexes. Bordeaux: Férét et Fils. 

Cerise, Laurent. 1842. Des fonctions et des maladies nerveuses dans leur rapports avec l'éducation 
sociale et privée, morale et physique. Paris: Germer-Bailliére. 

Chatel, John C. and Roger Peele. 1970. *A Centennial Review of Neurasthenia." American Journal 
of Psychiatry 126(10): 1404-13. 

Cherry, Neil. 2002. *Schumann Resonances, a Plausible Biophysical Mechanism for the Human 
Health Effects of Solar/Geomagnetic Activity." Natural Hazards Journal 26(3): 279-331. 

Cheyne, George. 1733. The English Malady: Or, a Treatise of Nervous Diseases of all Kinds. 
London: G. Strahan. 

Cleaves, Margaret Abigail. 1899. Report of the New York Electro-therapeutic Clinic and Laboratory. 
For the Period Ending June 1, 1899. 

. 1904. Light Energy: Its Physics, Physiological Action and Therapeutic Applications. New 

York: Rebman. 

. 1910. Autobiography of a Neurasthene. Boston: Richard G. Badger. 

Cronbach, E. 1903. *Die Bescháftigungsneurose der Telegraphisten." Archiv für Psychiatrie und 
Nervenkrankheiten 37: 243-93. 

Dana, Charles Loomis. 1921. Text-book of Nervous Diseases, 9th ed. Bristol: John Wright and Sons. 
Chapter 24, *Neurasthenia," pp. 536-56. 














. 1923. “Dr. George M. Beard: A Sketch of His Life and Character, with Some Personal 
Reminiscences.” Archives of Neurology and Psychiatry 10: 427-35. 

Department of Labour, Canada. 1907. Report of the Royal Commission on a Dispute Respecting 
Hours of Employment between The Bell Telephone Company of Canada, Ltd. and Operators at 
Toronto, Ont. Ottawa: Government Printing Bureau. 

Desrosiers, H. E. 1879. “De la neurasthénie.” L’Union Médicale du Canada 8: 145-54, 201-11. 

D’Hercourt, Gillebert. 1855. “De l'hydrothérapie dans le traitement de la surexcitabilité nerveuse." 
Bulletin de l'Académie Impériale de Médecine 21: 172-76. 

. 1867. Plan d'études simultanées de Nosologie et de Météorologie, ayant pour but de 
rechercher le róle des agents cosmiques dans la production des maladies, chez l'homme et chez 
les animaux. Montpellier: Boehm et fils. 

Dickens, Charles. 1859. *House-Top Telegraphs." All the Year Round, November 26. Reproduced in 
George B. Prescott, History, Theory, and Practice of the Electric Telegraph (Boston: Ticknor and 
Fields), 1860, pp. 355-62. 

Dubrov, Aleksandr P. 1978. The Geomagnetic Field and Life. New York: Plenum. 

Durham, John. 1959. Telegraphs in Victorian London. Cambridge: Golden Head Press. 

Engel, Hermann. 1913. Die Beurteilung von Unfallfolgen nach Reichsversicherungsordnung: Ein 
Lehrbuch für Arzte. Berlin: Urban & Schwarzenberg. 

Eulenburg, A. 1905. “Uber Nerven- und Geisteskrankheiten nach elektrischen Unfállen." Berliner 
Klinishe Wochenschrift 42: 30-33, 68-70. 

Fisher, T. W. 1872. *Neurasthenia." Boston Medical and Surgical Journal 9(5): 65-72. 

Flaskerud, Jacquelyn H. 2007. *Neurasthenia: Here and There, Now and Then." Issues in Mental 
Health Nursing 28(6): 657-59. 

Flint, Austin. 1866. A Treatise on the Principles and Practice of Medicine. Philadelphia: Henry C. 
Lea. 

Fontégne, J. and E. Solari. 1918. *Le travail de la téléphoniste." Archives de Psychologie 17(66): 81- 
136. 

Freedley, Edwin T. 1858. Philadelphia and its Manufactures. Philadelphia: Edward Young. 

Freud, Sigmund. 1895. "Über die Berechtigung von der Neurasthenie einen bestimmten 
Symptomencomplex als ‘Angstneurose’ abzutrennen.” Neurologisches Centralblatt 14: 50-66. 
Published in English as “On the Grounds for Detaching a Particular Syndrome from Neurasthenia 
under the Description ‘Anxiety Neurosis,” in The Standard Edition of the Complete 
Psychological Works of Sigmund Freud (London: The Hogarth Press), 1962, vol. 3, pp. 87-139. 

Fulton, Thomas Wemyss. 1884. “Telegraphists’ Cramp.” The Edinburgh Clinical and Pathological 
Journal 1(17): 369-75. 

Gellé, Marie-Ernest. 1889. “Effets nuisibles de |’audition par le téléphone.” Annales des maladies de 
l'oreille, du larynx, du nez et du pharynx 1889: 380-81. 

Goering, Laura. 2003. “‘Russian Nervousness’: Neurasthenia and National Identity in Nineteenth- 
Century Russia.” Medical History 47: 23-46. 

Gosling, Francis George. 1987. Before Freud: Neurasthenia and the American Medical Community 
1870-1910. Urbana: University of Illinois Press. 

Graham, Douglas. 1888. “Local Massage for Local Neurasthenia.” Journal of the American Medical 
Association 10(1): 11-15. 

Gully, James Manby. 1837. An Exposition of the Symptoms, Essential Nature, and Treatment of 
Neuropathy, or Nervousness. London: John Churchill. 

Harlow, Alvin F. 1936. Old Wires and New Waves: The History of the Telegraph, Telephone, and 
Wireless. New York: D. Appleton-Century. 





Heijermans, Louis. 1908. Handleiding tot de kennis der beroepziekten. Rotterdam: Brusse. 

He-Quin, Yan. 1989. *The Necessity of Retaining the Diagnostic Concept of Neurasthenia." Culture, 
Medicine, and Psychiatry 13(2): 139-45. 

Highton, Edward. 1851. The Electric Telegraph: Its History and Progress. London: John Weale. 

Hoffmann, Georg, Siegfried Vogl, Hans Baumer, Oliver Kempski, and Gerhard Ruhenstroth-Bauer. 
1991. “Significant Correlations between Certain Spectra of Atmospherics and Different Biological 
and Pathological Parameters." International Journal of Biometeorology 34(4): 247-50. 

Hubbard, Geoffrey. 1965. *Cooke and Wheatstone and the Invention of the Electric Telegraph." 
London: Routledge & Kegan Paul. 

Jenness, Herbert T. 1909. Bucket Brigade to Flying Squadron: Fire Fighting Past and Present. 
Boston: George H. Ellis. 

Jewell, James S. 1879. *Nervous Exhaustion or Neurasthenia in its Bodily and Mental Relations." 
Journal of Nervous and Mental Disease 6: 45-55, 449-60. 

. 1880. *The Varieties and Causes of Neurasthenia." Journal of Nervous and Mental Disease 
7: 1-16. 

Jones, Alexander. 1852. Historical Sketch of the Electric Telegraph. New York: George P. Putnam. 

Journal of the American Medical Association. 1885. “Functional Troubles Dependent on 
Neuasthenia.” 5(14): 381-82. 

Julliard, Charles. 1910. “Les accidents par l'électricité." Revue Suisse des Accidents du Travail. 
Summarized in Revue de Médecine Légale 17(1): 343-45. 

Killen, Andreas. 2003. *From Shock to Schreck: Psychiatrists, Telephone Operators and Traumatic 
Neurosis in Germany, 1900-26." Journal of Contemporary History 38(2): 201-20. 

Kleinman, Arthur. 1988. “Weakness and Exhaustion in the United States and China.” In: Kleinman, 
The Illness Narrative (New York: Basic Books), pp. 100-20. 

Konig, Herbert L. 1971. “Biological Effects of Extremely Low Frequency Electrical Phenomena in 
the Atmosphere.” Journal of Interdisciplinary Research 2(3): 317-23. 

. 1974a. “ELF and VLF Signal Properties: Physical Characteristics.” In: Michael A. 

Persinger, ed., ELF and VLF Electromagnetic Field Effects (New York: Plenum), pp. 9-34. 

. 1974b. “Behavioral Changes in Human Subjects Associated with ELF Electric Fields.” In: 
Michael A. Persinger, ed., ELF and VLF Electromagnetic Field Effects (New York: Plenum), pp. 
81-99. 

Kowalewsky, P. J. 1890. “Zur Lehre vom Neurasthenia.” Zentralblatt fiir Nervenheilkunde und 
Psychiatrie 13: 241-44, 294-304. 

The Lancet. 1862. “The Influence of Railway Travelling on Public Health. Report of the 
Commission.” 1: 15-19, 48-53, 79-84, 107-10, 130-32, 155-58, 231-35, 258, 261. 

Le Guillant, Louis, R. Roelens, J. Begoin, P. Béquart, J. Hansen, and M. Lebreton. 1956. “La névrose 
des téléphonistes.” Presse médicale 64(13): 274-77. 

Levillain, Fernand. 1891. La Neurasthénie, Maladie de Beard. Paris: A. Maloine. 

Lin, Tsung-yi, Guest Editor. 1989a. “Neurasthenia in Asian Cultures.” Culture, Medicine and 
Psychiatry 13(2), June issue. 

. 1989b. *Neurasthenia Revisited: Its Place in Modern Psychiatry." Culture, Medicine, and 
Psychiatry 13(2): 105-29. 

Ludwig, H. Wolfgang. 1968. “A Hypothesis Concerning the Absorption Mechanism of Atmospherics 
in the Nervous System.” International Journal of Biometeorology 12(2): 93-98. 

Lutz, Tom. 1991. American Nervousness, 1903: An Anecdotal History. Ithaca, NY: Cornell 
University Press. 














Ming-Yuan, Zhang. 1989. “The Diagnosis and Phenomenology of Neurasthenia: A Shanghai Study." 
Culture, Medicine, and Psychiatry 13(2): 147-61. 

Morse, Samuel Finley Breese. 1870. “Telegraphic Batteries and Conductors.” Van Nostrand’s 
Eclectic Engineering Magazine 2: 602-13. 

Miiller, Franz Carl. 1893. Handbuch der Neurasthenie. Leipzig: F. C. W. Vogel. 

Nair, Indira, M. Granger Morgan, and H. Keith Florig. 1989. Biological Effects of Power Frequency 
Electric and Magnetic Fields. Washington, DC: Office of Technology Assessment. 

Nature. 1875. “The Progress of the Telegraph.” Vol. 11, pp. 390-92, 450-52, 470-72, 510-12; Vol. 12, 
pp. 30-32, 69-72, 110-13, 149-51, 254-56. 

Onimus, Ernest. 1875. “Crampe des Employés au Télégraphe.” Comptes Rendus des Séances et 
Mémoires de la Société de Biologie, pp. 120-21. 

. 1878. Le Mal Télégraphique ou Crampe Télégraphique. Paris: de Cusset. 

. 1880. *Le Mal Télégraphique ou Crampe Télégraphique." Comptes Rendus des Séances et 
Mémoires de la Société de Biologie, pp. 92-96. 

Pacaud, Suzanne. 1949. “Recherches sur le travail des téléphonistes: Etude psychologique d'un 
métier." Le travail humain 1-2: 46-65. 

Persinger, Michael A., ed. 1974. ELF and VLF Electromagnetic Field Effects. New York: Plenum. 

Persinger, Michael A., H. Wolfgang Ludwig, and  Klaus-Peter  Ossenkopp. 1973. 
“Psychophysiological Effects of Extremely Low Frequency Electromagnetic Fields: A Review.” 
Perceptual and Motor Skills 36: 1131-59. 

Politzer, Adam. 1901. Lehrbuch der Ohrenheilkunde, 4th ed. Stuttgart: Enke. Pp. 649-50 on 
telephone operators’ illnesses. 

Pomme, Pierre. 1763. Traité des Affections Vaporeuses des Deux Sexes, ou Maladies Nerveuses, 
Lyon: Benoit Duplain. 

Preece, William Henry. 1876. “Railway Travelling and Electricity.” Popular Science Review 15: 138- 
48. 

Prescott, George B. 1860. History, Theory, and Practice of the Electric Telegraph. Boston: Ticknor 
and Fields. 

. 1881. Electricity and the Electric Telegraph, Ath ed. New York: D. Appleton. 

Reid, James D. 1886. The Telegraph in America. New York: John Polhemus. 

Robinson, Edmund. 1882. “Cases of Telegraphists’ Cramp.” British Medical Journal 2: 880. 

Sandras, Claude Marie Stanislas. 1851. Traité Pratique des Maladies Nerveuses. Paris: Germer- 
Bailliére. 

Savage, Thomas, ed. 1889. Manual of Industrial and Commercial Intercourse between the United 
States and Spanish America. San Francisco: Bancroft. Pages 113-23 on the extent of telegraphs in 
Central and South America. 

Scherf, J. Thomas. 1881. History of Baltimore City and County. Philadelphia: Louis H. Everts. 

Schilling, Karl. 1915. *Die nervósen Stórungen nach Telephonunfillen." Zeitschrift für die gesamte 
Neurologie und Psychiatrie 29(1): 216-51. 

Schlegel, Kristian and Martin Füllekrug. 2002. “Weltweite Ortung von Blitzen: 50 Jahre Schumann- 
Resonanzen.” Physik in unserer Zeit 33(6): 256-61. 

Sheppard, Asher R. and Merril Eisenbud. 1977. Biological Effects of Electric and Magnetic Fields of 
Extremely Low Frequency. New York: NYU Press. 

Shixie, Liu. 1989. “Neurasthenia in China: Modern and Traditional Criteria for its Diagnosis.” 
Culture, Medicine, and Psychiatry 13(2): 163-86. 

Shorter, Edward. 1992. From Paralysis to Fatigue: A History of Psychosomatic Illness in the Modern 
Era. New York: The Free Press. 











Sterne, Albert E. 1896. “Toxicity in Hysteria, Epilepsy and Neurasthenia — Relations and Treatment." 
Journal of the American Medical Association, 26(4): 172-74. 

Strahan, J. 1885. “Puzzling Conditions of the Heart and Other Organs Dependent on Neurasthenia.” 
British Medical Journal 2: 435-37. 

Suzuki, Tomonori. 1989. “The Concept of Neurasthenia and Its Treatment in Japan.” Culture, 
Medicine, and Psychiatry 13(2): 187-202. 

Thébault, M. V. 1910. “La névrose des téléphonistes.” Presse médicale 18: 630-31. 

Thompson, H. Theodore and J. Sinclair. 1912. “Telegraphists’ Cramp.” Lancet 1: 888-90, 941-44. 

Tommasi, Jacopo. 1904. “Le lesioni professionali e traumatiche nell’orecchio. Otopathie nei 
telefonisti.” Atti del settimo congresso della societa italiana di Laringologia, d’Otologia e di 
Rinologia, Rome, October 29-31, 1903, pp. 97-100. Napoli: E. Pietrocola. 

Tourette, Georges Gilles de la. 1889. *Deuxiéme lecon: Les états neurasthéniques et leur traitement." 
In: Gilles de la Tourette, Lecons de clinique thérapeutique sur les maladies du systéme nerveux 
(Paris: E. Plon, Nourrit), pp. 58-127. 

Trotter, Thomas. 1807. A View of the Nervous Temperament. London: Longman, Hurst, Rees, and 
Orme. 

Trowbridge, John. 1880. “The Earth as a Conductor of Electricity." American Journal of Science, 
120: 138-41. 

Turnbull, Laurence. 1853. The Electro-Magnetic Telegraph. Philadelphia: A. Hart. 

Wallbaum, G. W. 1905. "Ueber funktionelle nervóse Stórungen bei Telephonistinnen nach 
elektrischen Unfällen.” Deutsche medizinische Wochenschrift 31(18): 709-11. 

Webber, Samuel Gilbert. 1888. “A Study of Arterial Tension in Neurasthenia.” Boston Medical and 
Surgical Journal 118(18): 441-45. 

Whytt, Robert. 1768. Observations on the Nature, Causes, and Cure of those Disorders which are 
commonly called Nervous, Hypochondriac or Hysteric. In: The Works of Robert Whytt, M.D. 
(Edinburgh: Balfour, Auld, and Smellie), pp. 487-713. 

Winter, Thomas. 2004. “Neurasthenia.” In: Michael S. Kimmel and Amy Aronson, eds., Men and 
Masculinities: A Social, Cultural, and Historical Encyclopedia (Santa Barbara: ABC-CLIO), pp. 
567-69. 

World Psychiatric Association. 2002. Neurasthenia — A Technical Report from the World Psychiatric 
Association Group of Experts, Beijing, April 1999, printed in Melbourne, Australia in June 2002. 

Yassi, Annalee, John L. Weeks, Kathleen Samson, and Monte B. Raber. 1989. “Epidemic of ‘Shocks’ 
in Telephone Operators: Lessons for the Medical Community.” Canadian Medical Association 
Journal 140: 816-20. 

Young, Derson. 1989. “Neurasthenia and Related Problems.” Culture, Medicine, and Psychiatry 
13(2): 131-38. 


Chapter 6 

Beccaria, Giambatista. 1775. Della Elettricita Terrestre Atmosferica a Cielo Sereno. Torino. 

Bertholon, Pierre Nicholas. 1783. De l'Électricité des Végétaux. Paris: P. F. Didot Jeune. 

Blackman, Vernon H. 1924. “Field Experiments in Electro-Culture.” Journal of Agricultural Science 
14(2): 240-67. 

Blackman, Vernon H., A. T. Legg, and F. G. Gregory. 1923. “The Effect of a Direct Electric Current 
of Very Low Intensity on the Rate of Growth of the Coleoptile of Barley.” Proceedings of the 
Royal Society of London B 95: 214-28. 

Bose, Georg Mathias. 1747. Tentamina electrica tandem aliquando hydraulicae chymiae et 
vegetabilibus utilia. Wittenberg: Johann Joachim Ahlfeld. 


Bose, Jagadis Chunder. 1897. *On the Determination of the Wavelength of Electric Radiation by a 
Diffraction Grating." Proceedings of the Royal Society of London 60: 167-78. 

. 1899. “On a Self-Recovering Coherer and the Study of the Cohering Action of Different 

Metals.” Proceedings of the Royal Society of London 65: 166-73. 

. 1900. “On Electric Touch and the Molecular Changes Produced in Matter by Electric 

Waves.” Proceedings of the Royal Society of London 66: 452-74. 

. 1902. “On the Continuity of Effect of Light and Electric Radiation on Matter." Proceedings 

of the Royal Society of London 70: 154-74. 

. 1902. “On Electromotive Wave Accompanying Mechanical Disturbance in Metals in 
Contact with Electrolyte.” Proceedings of the Royal Society of London 70: 273-94. 

—— ———. 1906. Plant Response. London: Longmans, Green. 

———. 1907. Comparative Electro-Physiology. London: Longmans, Green. 

——. 1910. Response in the Livng and Non-Living. London: Longmans, Green. 

—. 1913. Researches on Irritability of Plants. London: Longmans, Green. 

1915. “The Influence of Homodromous and Heterodromous Electric Currents on 

Transmission of Excitation in Plant and Animal.” Proceedings of the Royal Society of London B 

88: 483-507. 

. 1919. Life Movements in Plants. Transactions of the Bose Research Institute, Calcutta, vol. 
2. Calcutta: Bengal Government Press. 

—. 1923. The Physiology of the Ascent of Sap. London: Longmans, Green. 

———.. 1926. The Nervous Mechanism of Plants. London: Longmans, Green. 

—— —— .. 1927a. Collected Physical Papers. London: Longmans, Green. 

. 1927b. Plant Autographs and Their Revelations. London: Longmans, Green. 

Bose, Jagadis Chunder and Guru Prasanna Das. 1925. *Physiological and Anatomical Investigations 
on Mimosa pudica." Proceedings of the Royal Society of London B 98: 290-312. 

Browning, John. 1746. “Part of a Letter concerning the Effect of Electricity on Vegetables.” 
Philosophical Transactions 44: 373-75. 

Crépeaux, Constant. 1892. “L’électroculture.” Revue Scientifique 51: 524-32. 

Emerson, Darrel T. 1997. “The Work of Jagadis Chandra Bose: 100 Years of Millimeter-wave 
Research" IEEE Transactions on Microwave Theory and Techniques 45(12): 2267-73. 

Gardini, Giuseppe Francesco. 1784. De influxu electricitatis atmosphericae in vegetantia. Torino: 
Giammichele Briolo. 

Geddes, Patrick. 1920. The Life and Work of Sir Jagadis C. Bose. London: Longmans, Green. 

Goldsworthy, Andrew. 1983. “The Evolution of Plant Action Potentials.” Journal of Theoretical 
Biology 103: 645-48. 

. 2006. “Effects of Electrical and Electromagnetic Fields on Plants and Related Topics." In: 
Alexander Volkov, ed., Plant Electrophysiology (Heidelberg: Springer), pp. 247-67. 

Gorgolewski, Stanislaw. 1996. “The Importance of Restoration of the Atmospheric Electrical 
Environment in Closed Bioregenerative Life Supporting Systems.” Advances in Space Research 
18(4-5): 283-85. 

Gorgolewski, Stanislaw and B. Rozej. 2001. “Evidence for Electrotropism in Some Plant Species.” 
Advances in Space Research 28(4): 633-38. 

Hicks, W. Wesley. 1957. “A Series of Experiments on Trees and Plants in Electrostatic Fields.” 
Journal of the Franklin Institute 264(1): 1-5. 

Hull, George S. 1898. Electro-Horticulture. New York: Knickerbocker. 

Ingen-Housz, Jean. 1789. “Effet de l'Électricité sur le Plantes.” In: Ingen-Housz, Nouvelles 
Expériences et Observations Sur Divers Objets de Physique (Paris: Théophile Barrois le jeune), 


























vol. 2, pp. 181-226. 

Ishikawa, Hideo and Michael L. Evans. 1990. *Electrotropism of Maize Roots." Plant Physiology 94: 
913-18. 

Jallabert, Jean. 1749. Expériences sur l'Électricité. Paris: Durand et Pissot. 

Krueger, Albert Paul, A. E. Strubbe, Michael G. Yost, and E. J. Reed. 1978. *Electric Fields, Small 
Air Ions and Biological Effects." International Journal of Biometeorology 22(3): 202-12. 

Kunkel, A. J. 1881. *Electrische Untersuchungen an pflanzlichen und thierischen Gebilden." Archiv 
für die gesamte Physiologie des Menschen und der Tiere 25(1): 342-79. 

Lemstróm, Selim. 1904. Electricity in Agriculture and Horticulture. London: “The Electrician.” 

Marat, Jean-Paul. 1782. Recherches Physiques sur I’Electricité. Paris: Clousier. 

Marconi, Giuglielmo. 1902. “Note on a Magnetic Detector of Electric Waves, Which Can Be 
Employed as a Receiver for Space Telegraphy.” Proceedings of the Royal Society of London 70: 
341-44. 

Molisch, Hans. 1929. *Nervous Impulse in Mimosa pudica." Nature 123: 562-63. 

Murr, Lawrence E. 1966. “The Biophysics of Plant Growth in a Reversed Electrostatic Field: A 
Comparison with Conventional Electrostatic and Electrokinetic Field Growth Responses.” 
International Journal of Biometeorology 10(2): 135-46. 

Nakamura, N., A. Fukushima, H. Iwayama, and H. Suzuki. 1991. “Electrotropism of Pollen Tubes of 
Camellia and Other Plants.” Sexual Plant Reproduction 4: 138-43. 

Nollet, Jean Antoine (Abbé). 1753. Recherches sur les Causes Particuliéres des Phénoménes 
Électriques. Paris: Guérin. 

Nozue, Kazunari and Masamitsu Wada. 1993. “Electrotropism of Nicotiana Pollen Tubes." Plant and 
Cell Physiology 34(8): 1291-96. 

Paulin, le Frére. 1890. De l'influence de l'électricité sur la végétation. Montbrison: E. Brassart. 

Pohl, Herbert A. 1977. “Electroculture.” Journal of Biological Physics 5(1): 3-23. 

Pozdnyakov, Anatoly and Larisa Pozdnyakova. 2006. “Electro-tropism in ‘Soil-Plant System.’” 18th 
World Congress of Soil Science, July 9-15, Philadelphia, poster 116-29. 

Rathore, Keerti S. and Andrew Goldsworthy. 1985a. “Electrical Control of Growth in Plant Tissue 
Cultures.” Nature Biotechnology 3: 253-54. 

. 1985b. “Electrical Control of Shoot Regeneration in Plant Tissue Cultures." Nature 
Biotechnology 3: 1107-9. 

Sibaoka, Takao. 1962. *Physiology of Rapid Movements in Higher Plants." Annual Review of Plant 
Physiology 20: 165-84. 

. 1966. *Action Potentials in Plant Organs." Symposia of the Society for Experimental 
Biology 20: 49-73. 

Sidaway, G. Hugh. 1975. *Some Early Experiments in Electro-culture." Journal of Electrostatics 1: 
389-93. 

Smith, Edwin. 1870. "Electricity in Plants." Journal of the Franklin Institute 89: 69-71. 

Stahlberg, Rainer. 2006. “Historical Introduction to Plant Electrophysiology." In: Alexander G. 
Volkov, ed., Plant Electrophysiology (Heidelberg: Springer), pp. 3-14. 

Stenz, Hans-Gerhard and Manfred H. Weisenseel. 1993. “Electrotropism of Maize (Zea mays L.) 
Roots.” Plant Physiology 101: 1107-11. 

Stone, George E. 1911. “Effect of Electricity on Plants.” In: L. H. Bailey, ed., Cyclopedia of 
American Agriculture, 3rd ed. (London: Macmillan), vol. 2. pp. 30-35. 








Chapter 7 


Althaus, Julius. 1891. *On the Pathology of Influenza, with Special Reference to its Neurotic 
Character." Lancet 2: 1091-93, 1156-57. 

. 1893. *On Psychoses after Influenza." Journal of Mental Science 39: 163-76. 

Andrewes, Christopher H. 1951. *Epidemiology of Influenza in the Light of the 1951 Outbreak." 
Proceedings of the Royal Society of Medicine 44(9): 803-4. 

Appleyard, Rollo. 1939. The History of the Institution of Electrical Engineers (1871-1931). London: 
Institution of Electrical Engineers. 

Arbuthnot, John. 1751. An Essay Concerning the Effects of Air on Human Bodies. London: J. and R. 
Tonson. 

Bell, J. A., J. E. Craighead, R. G. James, and D. Wong. 1961. “Epidemiologic Observations on Two 
Outbreaks of Asian Influenza in a Children's Institution." American Journal of Hygiene 73: 84-89. 

Beveridge, William Ian. 1978. Influenza: The Last Great Plague. New York: Prodist. 

Birkeland, Jorgen. 1949. Microbiology and Man. New York: Appleton-Century-Crofts. 

Blumenfeld, Herbert L., Edwin D. Kilbourne, Donald B. Louria, and David E. Rogers. 1959. 
*Studies on Influenza in the Pandemic of 1957-1958. I. An Epidemiologic, Clinical and Serologic 
Investigation of an Intrahospital Epidemic, with a Note on Vaccination Efficacy." Journal of 
Clinical Investigation 38: 199-212. 

Boone, Stephanie A. and Charles P. Gerba. 2005. “The Occurrence of Influenza A on Household and 
Day Care Center Fomites." Journal of Infection 51: 103-09. 

Borchardt, Georg. 1890. *Nervóse Nachkrankheiten der Influenza." Berlin: Gustav Schade. 

Bordley, James III and A. McGehee Harvey. 1976. Two Centuries of American Medicine, 1776-1976. 
Philadelphia: W. B. Saunders. 

Bossers, Adriaan Jan. 1894. Die Geschichte der Influenza und ihre nervósen und psychischen 
Nachkrankheiten. Leiden: Eduard Ijdo. 

Bowie, John. 1891. “Influenza and Ear Disease in Central Africa.” Lancet 2: 66-68. 

Brakenridge, David J. 1890. “The Present Epidemic of So-called Influenza.” Edinburgh Medical 
Journal, 35 (part 2): 996-1005. 

Brankston, Gabrielle, Leah Gitterman, Zahir Hirji, Camille Lemieux, and Michael Gardam. 2007. 
“Transmission of Influenza A in Human Beings.” Lancet Infectious Diseases 7(4): 257-65. 

Bright, Arthur A., Jr. 1949. The Electric-Lamp Industry: Technological Change and Economic 
Development from 1800 to 1947. New York: Macmillan. 

Bryson, Louise Fiske 1890. “The Present Epidemic of Influenza.” Journal of the American Medical 
Association 14: 426-28. 

. 1890. “The Present Epidemic of Influenza.” New York Medical Journal 51: 120-24. 

Buzorini, Ludwig. 1841. Luftelectricitét, Erdmagnetismus und Krankheitsconstitution. Constanz: 
Belle-Vue. 

Cannell, John Jacob, Michael Zasloff, Cedric F. Garland, Robert Scragg, and Edward Giovannucci. 
2008. “On the Epidemiology of Influenza.” Virology Journal 5: 29. 

Cantarano, G. 1890. *Sui rapporti tra l'influenza e le malattie nervose e mentali.” La Psichiatria 8: 
158-68. 

Casson, Herbert N. 1910. The History of the Telephone. Chigago: A. C. McClurg. 

Chizhevskiy, Aleksandr Leonidovich. 1934. “L'action de l'activité périodique solaire sur les 
épidémies.” In: Marius Piéry, Traité de Climatologie Biologique et Médicale (Paris: Masson) vol. 
2, pp. 1034-41. 

. 1936. *Sur la connexion entre l'activité solaire, l'électricité atmosphérique et les épidémies 

de la grippe." Gazette des Hópitaux 109(74): 1285-86. 














. 1937. “L’activité corpusculaire, électromagnétique et périodique du soleil et l'électricité 
atmosphérique, comme régulateurs de la distribution, dans la suite des temps, des maladies 
épidémiques et de la mortalité générale." Acta Medica Scandinavica 91(6): 491-522. 

. 1938. Les Épidémies et Les Perturbations Électromagnétiques Du Milieu Extérieur. Paris: 

Dépôt Général: Le François. 

. 1973. Zemnoe ekho solnechnykh bur’ (“The Terrestrial Echo of Solar Storms”). Moscow: 

Mysl’ (in Russian). 

. 1995. Kosmicheskiy pul's zhizni: Zemlia v obiatiyakh Solntsa. Geliotaraksiya (“Cosmic 
Pulse of Life: The Earth in the Embrace of the Sun”). Moscow: Mysl’ (in Russian). Written in 
1931, published in abridged form in 1973 as “The Terrestrial Echo of Solar Storms.” 

Clemow, Frank Gerard. 1903. The Geography of Disease, 3 vols. Cambridge: University Press. 

Clouston, Thomas Smith. 1892. Clinical Lectures on Mental Diseases. London: J. & A. Churchill. 
Page 647 on influenza. 

. 1893. “Eightieth Annual Report of the Royal Edinburgh Asylum for the Insane, 1892.” 
Journal of Nervous and Mental Disease, new ser., 18(12): 831-32. 

Creighton, Charles. 1894. “Influenza and Epidemic Agues.” In: Creighton, A History of Epidemics in 
Britain (Cambridge: Cambridge University Press), vol. 2, pp. 300-433. 

Crosby, Oscar T. and Louis Bell. 1892. The Electric Railway in Theory and Practice. New York: W. 
J. Johnston. 

Dana, Charles Loomis. 1889. “Electrical Injuries.” Medical Record 36(18): 477-78. 

. 1890. “The Present Epidemic of Influenza.” Journal of the American Medical Association 
14(12): 426-27. 

Davenport, Fred M. 1961. “Pathogenesis of Influenza.” Bacteriological Reviews 25(3): 294-300. 

D’Hercourt, Gillebert. 1867. Plan d’études simultanées de Nosologie et de Météorologie, ayant pour 
but de rechercher le rôle des agents cosmiques dans le production des maladies, chez l'homme et 
chez les animaux. Montpellier: Boehm et fils. 

Dimmock, Nigel J. and Sandy B. Primrose. 1994. Introduction to Modern Virology, 4th ed. Oxford: 
Blackwell Science. 

Dixey, Frederick Augustus. 1892. Epidemic Influenza. Oxford: Clarendon Press. 

Dominion Bureau of Statistics. 1958. Influenza in Canada: Some Statistics on its Characteristics and 
Trends. Ottawa: Queen’s Printer. 

DuBoff, Richard B. 1979. Electric Power in American Manufacturing, 1889-1958. New York: Arno 
Press. 

Dunsheath, Percy. 1962. A History of Electrical Power Engineering. Cambridge, MA: MIT Press. 

Eddy, John A. 1976. “The Maunder Minimum.” Science 192: 1189-1202. 

. 1983. “The Maunder Minimum: A Reappraisal.” Solar Physics 89: 195-207. 

Edison, Thomas Alva. 1891. “Vital Energy and Electricity.” Scientific American 65(23): 356. 

Edström, Gunnar O. 1935. “Studies in National and Artificial Atmospheric Electric Ions.” Acta 
Medica Scandinavica. Supplementum 61: 1-83. 

Electrical Review. 1889. “Proceedings of the Ninth Convention of the National Electric Light 
Association.” March 2, pp. 1-2. 

. 1890a. “Manufacturing and Central Station Companies.” August 30, p. 1. 

. 1890b. “The Cape May Convention.” August 30, pp. 1-2. 

Electrical Review and Western Electrician. 1913. “Public Street Lighting in Chicago.” 63: 453-59. 

Erlenmeyer, Albrecht. 1890. “Jackson’sche Epilepsie nach Influenza.” Berliner klinische 
Wochenschrift 27(13): 295-97. 

Field, C. S. 1891. “Electric Railroad Construction and Operation.” Scientific American, 65(12): 176. 


























Firstenberg, Arthur. 1998. *Is Influenza an Electrical Disease?" No Place To Hide 1(4): 2-6. 

Fisher-Hinnen, Jacques. 1899. Continuous-Current Dynamos in Theory and Practice. London: Biggs. 

Fleming, D. M., M. Zambon, and A. I. M. Bartelds. 2000. *Population Estimates of Persons 
Presenting to General Practitioners with Influenza-like Illness, 1987-96: A Study of the 
Demography of Influenza-like IlIness in Sentinel Practice Networks in England and Wales, and in 
the Netherlands." Epidemiology & Infection 124: 245-63. 

Friedlander, Amy. 1996. Power and Light: Electricity in the U.S. Energy Infrastructure, 1870-1940. 
Reston, VA: Corp. for National Research Initiatives. 

Gill, Clifford Allchin. 1928. The Genesis of Epidemics and the Natural History of Disease. New 
York: William Wood. 

Glezen, W. Paul and Lone Simonsen. 2006. *Commentary: Benefits of Influenza Vaccine in U.S. 
Elderly — New Studies Raise Questions." International Journal of Epidemiology 35: 352-53. 

Gordon, Charles Alexander. 1884. An Epitome of the Reports of the Medical Officers To the Chinese 
Imperial Maritime Customs Service, from 1871 to 1882. London: Bailliére, Tindall, and Cox. 

Halley, Edmund. 1716. *An Account of the late surprizing Appearance of the Lights seen in the Air, 
on the sixth of March last; With an Attempt to explain the Principal Phaenomena thereof." 
Philosophical Transactions 29: 406-28. 

Hamer, William H. 1936. *Atmospheric Ionization and Influenza." British Medical Journal 1: 493- 
94. 

Harlow, Alvin F. 1936. Old Wires and New Waves: The History of the Telegraph, Telephone, and 
Wireless. New York: Appleton-Century. 

Harries, H. 1892. “The Origin of Influenza Epidemics.” Quarterly Journal of the Royal 
Meteorological Society 18(82): 132-42. 

Harrington, Arthur H. 1890. *Epidemic Influenza and Insanity." Boston Medical and Surgical 
Journal 123: 126-29. 

Hedges, Killingworth. 1892. Continental Electric Light Central Stations. London: E. & F. N. Spon. 

Heinz, F., B. Tümová, and H. Scharfenoorth. 1990. “Do Influenza Epidemics Spread to Neighboring 
Countries?" Journal of Hygiene, Epidmiology, Microbiology, and Immunology 34(3): 283-88. 

Hellpach, Willy Hugo. 1911, 1923. Die geopsychischen Erscheinungen: Wetter, Klima und 
Landschaft in ihrem Einfluss auf das Seelenleben. Leipzig: Wilhelm Engelmann. 

Hering, Carl. 1892. Recent Progress in Electric Railways. New York: W. J. Johnston. 

Hewetson, W. M. 1936. *Atmospheric Ionization and Influenza." British Medical Journal 1: 667. 

Higgins, Thomas James. 1945. "Evolution of the Three-phase 60-cycle Alternating System." 
American Journal of Physics 13(1): 32-36. 

Hirsch, August. 1883. "Influenza." In: Hirsch, Handbook of Geographical and Historical Pathology 
(London: New Sydenham Society), vol. 1, pp. 7-54. 

Hogan, Linda. 1995. Solar Storms. New York: Simon & Schuster. 

Hope-Simpson, Robert Edgar. 1978. *Sunspots and Flu: A Correlation." Nature 275: 86. 

. 1979. *Epidemic Mechanisms of Type A Influenza." Journal of Hygiene (Cambridge) 

83(1): 11-25. 

. 1981. *The Role of Season in the Epidemiology of Influenza." Journal of Hygiene (London) 

86(1): 35-47. 

. 1984. *Age and Secular Distributions of Virus-Proven Influenza Patients in Successive 

Epidemics 1961-1976 in Cirencester: Epidemiological Significance Discussed.” Journal of 

Hygiene, (Cambridge) 92: 303-36. 

. 1992. The Transmission of Epidemic Influenza. New York: Plenum. 

Hoyle, Fred and N. Chandra Wickramasinghe. 1990. “Sunspots and Influenza.” Nature 43: 3-4. 














Hughes, C. H. 1892. *The Epidemic Inflammatory Neurosis, or, Neurotic Influenza." Journal of the 
American Medical Association 18(9): 245-49. 

Hughes, Thomas P. 1983. Networks of Power: Electrification in Western Society, 1880-1930. 
Baltimore: Johns Hopkins University Press. 

Hutchings, Richard H. 1896. *An Analysis of Forty Cases of Post Influenzal Insanity." State 
Hospitals Bulletin 1(1): 111-19. 

Jefferson, Tom. 2006. “Influenza Vaccination: Policy Versus Evidence.” British Medical Journal 333: 
912-15. 

Jefferson, Tom, C. D. Pietrantonj, M. G. Debalini, A. Rivetti, and V. Demicheli. 2009. “Relation of 
Study Quality, Concordance, Take Home Message, Funding, and Impact in Studies of Influenza 
Vaccines: Systematic Review.” British Medical Journal 338: 354-58. 

Jones, Alexander. 1826. “Observations on the Influenza or Epidemic Catarrh, as it Prevailed in 
Georgia during the Winter and Spring of 1826.” Philadelphia Journal of the Medical and Physical 
Sciences, new ser., 4(7): 1-30. 

Jordan, Edwin O. 1927. Epidemic Influenza: A Survey. Chicago: American Medical Association. 

Jordan, William S., Jr. 1961. “The Mechanism of Spread of Asian Influenza.” American Review of 
Respiratory Disease 83(2): 29-40. 

Jordan, William S., Jr., Floyd W. Denny, Jr., George F. Badger, Constance Curtis, John H. Dingle, 
Robert Oseasohn, and David A. Stevens. 1958. “A Study of Illness in a Group of Cleveland 
Families. XVII. The Occurrence of Asian Influenza.” American Journal of Hygiene 68: 190-212. 

Journal of the American Medical Association. 1890a. “The Influenza Epidemic of 1889.” 14(1): 24- 
25. 





. 1890b. “Influenza and Cholera.” 14(7): 243-44. 

Journal of the Statistical Society of London. 1848. “Previous Epidemics of Influenza in England.” 11: 
173-79. 

Kilbourne, Edwin D. 1975. The Influenza Viruses and Influenza. New York: Academic. 

. 1977. “Influenza Pandemics in Perspective.” JAMA 237(12): 1225-28. 

Kirn, Ludwig. 1891. “Die nervösen und psychischen Störungen der Influenza.” Sammlung Klinischer 
Vorträge, new ser., no. 23 (Innere Medicin, no. 9), pp. 213-44. 

Kraepelin, Emil. 1890b. “Über Psychosen nach Influenza.” Deutsche medicinische Wochenschrift 
16(11): 209-12. 

Ladame, Paul-Louis. 1890. “Des psychoses après l'influenza.” Annales médico-psychologiques, 7th 
ser., 12: 20-44. 

Lancet. 1919. “Medical Influenza Victims in South Africa.” 1: 78. 

Langmuir, Alexander D. 1964. “The Epidemiological Basis for the Control of Influenza.” American 
Journal of Public Health 54(4): 563-71. 

Lee, Benjamin. 1891. “An Analysis of the Statistics of Forty-One Thousand Five Hundred Cases of 
Epidemic Influenza.” Journal of the American Medical Association 16(11): 366-68. 

Leledy, Albert. 1891. La Grippe et l'Alienation Mentale. Paris: J.-B. Bailliére et Fils. 

Local Government Board. 1893. Further Report and Papers on Epidemic Influenza, 1889-1892. 
London. 

Mackenzie, Morell. 1891. “Influenza.” Fortnightly Review 55: 877-86. 

Macphail, S. Rutherford. 1896. “Post-Influenzal Insanity.” British Medical Journal 2: 810-11. 

Mann, P. G., M. S. Pereira, J. W. G. Smith, R. J. C. Hart, and W. O. Williams. 1981. *A Five-Year 
Study of Influenza in Families." Journal of Hygiene (Cambridge) 87(2): 191-200. 

Marian, Christine and Grigore Mihdescu. 2009. “Diversification of Influenza Viruses.” 
Bacteriologia, Virusologia, Parazitologia, Epidemiologia 54: 117-23 (in Romanian). 





Mathers, George. 1917. “Etiology of the Epidemic Acute Respiratory Infections Commonly Called 
Influenza.” Journal of the American Medical Association 68(9): 678-80. 

McGrew, Roderick E. 1985. Encyclopedia of Medical History. New York: McGraw-Hill. 

Meyer, Edward Bernard. 1916. Underground Transmission and Distribution for Electric Light and 
Power. New York: McGraw-Hill. 

Mispelbaum, Franz. 1890. “Ueber Psychosen nach Influenza.” Allgemeine Zeitschrift ftir Psychiatrie 
47(1): 127-53. 

Mitchell, Weir. 1893. Paper read at the National Academy of Sciences, Washington. Cited in 
Johannes Mygge, “Om Saakaldte Barometermennesker: Bidrag til Blysning af Vejrneurosens 
Patogenese,” Ugeskrift for Leger 81(31): 1239-59, at p. 1251. 

Morrell, C. Conyers. 1936. “Atmospheric Ionization and Influenza.” British Medical Journal 1: 554- 
55. 

Munter, D. 1890. “Psychosen nach Influenza.” Allgemeine Zeitschrift für Psychiatrie 47: 156-65. 

Mygge, Johannes. 1919. “Om Saakaldte Barometermennesker: Bidrag til Belysning af Vejrneurosens 
Patogenese.” Ugeskrift for Leger 81(31): 1239-59. 

. 1930. *Étude sur l'éclosion épidémique de l'influenza." Acta Medica Scandinavica. 
Supplementum 32: 1-145. 

National Institutes of Health. 1973. *Epidemiology of Influenza — Summary of Influenza Workshop 
IV." Journal of Infectious Diseases 128(3): 361-99. 

Ozanam, Jean-Antoine-Frangois. 1835. Histore medicale générale et particulière des maladies 
épidémiques, contagieuses et épizootiques, 2 vols. Lyon: J. M. Boursy. 

Parsons, Franklin. 1891. Report on the Influenza Epidemic of 1889-1890. London: Local 
Government Board. 

Patterson, K. David. 1986. Pandemic influenza 1700-1900. Totowa, NJ: Rowman & Littlefield. 

Peckham, W. C. 1892. “Electric Light for Magic Lantern.” Scientific American 66(12): 183. 

Perfect, William. 1787. Select Cases in the Different Species of Insanity. Rochester: Gilman. Pages 
126-31 on insanity from influenza. 

Preece, William Henry and Julius Maier. 1889. The Telephone. London: Whittaker. 

Reckenzaun, A. 1887. “On Electric Street Cars, with Special Reference to Methods of Gearing.” 
Proceedings of the American Institute of Electrical Engineers 5(1): 2-32. 

Revilliod, L. 1890. “Des formes nerveuses de la grippe.” Revue Médicale de la Suisse Romande 
10(3): 145-53. 

Ribes, J. C. and E. Nesme-Ribes. 1993. “The Solar Sunspot Cycle in the Maunder Minimum AD 
1645 to AD 1715.” Astronomy and Astrophysics 276: 549-63. 

Richter, C. M. 1921. “Influenza Pandemics Depend on Certain Anticyclonic Weather Conditions for 
their Development.” Archives of Internal Medicine 27(3): 361-86. 

Ricketson, Shadrach. 1808. A Brief History of the Influenza. New York. 

Rorie, George A. 1901. “Post-Influenzal Insanity in the Cumberland and Westmoreland Asylum, 
with Statistics of Sixty-Eight Cases.” Journal of Mental Science 47: 317-26. 

Schmitz, Anton. 1891-92. “Ueber Geistesstérung nach Influenza.” Allgemeine Zeitschrift für 
Psychiatrie 47: 238-56; 48: 179-83. 

Schnurrer, Friedrich. 1823. Die Krankheiten des Menschen-Geschlechts. Tübingen: Christian 
Friedrich Osiander. 

Schónlein, Johann Lucas. 1840. Allgemeine und specielle Pathologie und Therapie, 5th ed., 4 vols. 
St. Gallen: Litteratur-Comptoir. Vol. 2, pp. 100-3 on influenza. 

Schrock, William M. 1892. “The Progress of Electrical Science." Scientific American 66(7) :100. 





Schweich, Heinrich. 1836. Die Influenza: Ein historischer und Gtiologischer Versuch. Berlin: 
Theodor Christian Friedrich Enslin. 


Science. 
. 1888b. *The Westinghouse Company's Extentions.” 12: 247. 





1888a. “Electric Street Railways.” 12: 246-47. 


1888c. “Electric-Lighting.” 12: 270. 


. 1888d. “The Edison Electric-Lighting System in Berlin.” 12: 270. 


1888e. “Trial of an Electric Locomotive at Birmingham, England.” 12: 270. 


. 1888f. “An Electric Surface Road in New York.” 12: 270-71. 
. 1888g. “Electric Propulsion.” 12: 281-82. 

. 1888h. “Electric Power-Distributrion.” 12: 282-84. 

. 1888i. “The Sprague Electric Road at Boston.” 12: 324-25. 

. 1888). “The Advances in Electricity in 1888.” 12: 328-29. 


1889. “Westinghouse Alternating-Current Dynamo.” 13: 451-52. 


. 1890a. “A Big Road Goes in for Electricity.” 15: 153. 
. 1890b. “The Electric Light in Japan.” 15: 153. 


Scientific American. 1889a. “The Danger of Electric Distribution.” 60(2): 16. 





. 1889b. “Edison Electric Light Consolidation.” 60(3): 34. 

. 1889c. “The Advances of Electricity in 1888” 60(6): 88. 

. 1889d. “Progress of Electric Illumination.” 60(12): 176-77. 

. 1889e. “Progress of Electric Installations in London.” 60(13): 196. 

. 1889f. “Electricity in the United States." 61(12): 150. 

. 1889¢. “The National Electric Light Association Meeting." 61(14): 184. 

. 1889h. “The Westinghouse Electric Company.” 61(20): 311. 

. 1890a. “Progress of Electric Lighting in London.” 62(3): 40-41. 

. 1890b. “The Westinghouse Alternating Current System of Electrical Distribution.” 62(8): 


117, 120-21. 











. 1890c. “The National Electric Lighting Association.” 62(8): p. 118. 

. 1890d. “The Growth of the Alternating System.” 62(17): 57. 

. 1890e. “Electricity in the Home." 62(20): 311. 

. 1890f. “Electrical Notes." 63(7): 97. 

. 1890g. “Long Distance Electrical Power." 63(8): 120. 

. 1890h. “Local Interests Improved by Electricity." 63(12): 182. 

. 1890i. *History of Electric Lighting." 63(14): 215. 

. 1891a. “Meeting of the National Electric Light Association.” 64(9): 128. 
. 1891b. “The Electric Transmission of Power." 64(14): 209. 

. 1891c. “Electricity in Foreign Countries.” 64(15): 229. 

. 1891d. “Electricity for Domestic Purposes.” 64(20): 310. 

. 1891e. “The Edison Electric Illuminating Co.’s Central Station in Brooklyn, N.Y.” 64(24): 


. 1891f. “Long Distance Electrical Power.” 65(19): 293. 

. 1892a. “Electric Lights for Rome, Italy." 66(2): 25. 

. 1892b. “What is Electricity?” 66(6): 89. 

. 1892c. “The Electrical Transmission of Power between Lauffen on the Neckar and Frankfort 


on the Main.” 66(7): 102. 
Shope, Richard E. 1958. “Influenza: History, Epidemiology, and Speculation” Public Health Reports 
73(2): 165-78. 


Solbrig, Dr. 1890. *Neurosen und Psychosen nach Influenza." Neurologisches Centralblatt 9(11): 
322-25. 

Soper, George A. 1919. “Influenza in Horses and in Man." New York Medical Journal 109(17): 720- 
24. 

Stuart-Harris, Sir Charles H., Geoffrey C. Schild, and John S. Oxford. 1985. Influenza: The Viruses 
and the Disease, 2nd ed. Edward Arnold: London. 

Tapping, Ken F., R. G. Mathias, and D. L. Surkan. 2001. *Influenza Pandemics and Solar Activity." 
Canadian Journal of Infectious Diseases 12(1): 61-62. 

Taubenberger, J. K. and D. M. Morens. 2009. “Pandemic Influenza — Including a Risk Assessment of 
H5N1.” Revue scientifique et tecnnique 28(1): 187-202. 

Thompson, Theophilus. 1852. Annals of Influenza or Epidemic Catarrhal Fever in Great Britain 
From 1510 to 1837. London: Sydenham Society. 

Trevert, Edward. 1892. Electric Railway Engineering. Lynn, MA: Bubier. 

. 1895. How to Build Dynamo-Electric Machinery. Lynn, MA: Bubier. 

Tuke, Daniel Hack. 1892. “Mental Disorder Following Influenza.” In: Tuke, A Dictionary of 
Psychological Medicine (London: J. & A. Churchill), vol. 2, pp. 688-91. 

United States Department of Commerce and Labor, Bureau of the Census. 1905. Central Electric 
Light and Power Stations 1902. Washington, DC: Government Printing Office. 

van Tam, Jonathan and Chloe Sellwood. 2010. Introduction to Pandemic Influenza. Wallingford, UK: 
CAB International. 

Vaughan, Warren T. 1921. Influenza: An Epidemiologic Study. Baltimore: American Journal of 
Hygiene. 

von Niemeyer, Felix. 1874. A Text-book of Practical Medicine. New York: D. Appleton. Pages 61-62 
on influenza. 

Watson, Thomas. 1857. Lectures on the Principles and Practice of Physic, 4th ed. London: John W. 
Parker. Vol. 2, pp. 41-52 on influenza. 

Webster, J. H. Douglas. 1940. “The Periodicity of Sun-spots, Influenza and Cancer.” British Medical 
Journal 2: 339. 

Webster, Noah. 1799. A Brief History of Epidemic and Pestilential Diseases, 2 vols. New York: Burt 
Franklin. 

Whipple, Fred H. 1889. The Electric Railway. Detroit: Orange Empire Railway Museum. 

Widelock, Daniel, Sarah Klein, Olga Simonovic, and Lenore R. Peizer. 1959. “A Laboratory 
Analysis of the 1957-1958 Influenza Outbreak in New York City.” American Journal of Public 
Health 49(7): 847-56. 

Yeung, John W. K. 2006. “A Hypothesis: Sunspot Cycles May Detect Pandemic Influenza A in 1700- 
2000 A.D.” Medical Hypotheses 67: 1016-22. 

Zinsser, Hans. 1922. “The Etiology and Epidemiology of Influenza.” Medicine 1(2): 213-309. 





Chapter 8 

Alexanderson, Ernst F. W. 1919. “Transatlantic Radio Communication.” Proceedings of the 
American Institute of Electrical Engineers 38(6): 1077-93. 

All Hands. 1961. “Flying the Atlantic Barrier.” April, pp. 2-5. 

Anderson, John. 1930. “‘Isle of Wight Disease’ in Bees.” Bee World 11(4): 37-42. 

Annual Report of the Surgeon General, U.S. Navy. 1919. Washington, DC: Government Printing 
Office. “Report on Influenza,” pp. 358-449. 

Archer, Gleason L. 1938. History of Radio. New York: American Historical Society. 


Armstrong, D. B. 1919. "Influenza: Is it a Hazard to be Healthy? Certain Tentative Considerations." 
Boston Medical and Surgical Journal 180(3): 65-67. 

Ayres, Samuel, Jr. 1919. “Post-Influenzal Alopecia.” Boston Medical and Surgical Journal 180(17): 
464-68. 

Baker, William John. 1971. A History of the Marconi Company. New York: St. Martins. 

Bailey, Leslie 1964. “The ‘Isle of Wight Disease’: The Origin and Significnce of the Myth.” Bee 
World 45(1): 32-37, 18. 

Beauchamp, Ken. 2001. History of Telegraphy. Hertfordshire, UK: Institution of Electrical 
Engineers. 

Beaussart, P. *Orchi-Epididymitis with Meningitis and Influenza." 1918. Journal of the American 
Medical Association 70(26): 2057. 

Berman, Harry. 1918. *Epidemic Influenza in Private Practice." Journal of the American Medical 
Association 71(23): 1934-35. 

Beveridge, William Ian. 1978. Influenza: The Last Great Plague. New York: Prodist. 

Bircher, E. *Influenza Epidemic." 1918. Journal of the American Medical Association 71(23): 1946. 

Blaine, Robert Gordon. 1903. Aetheric or Wireless Telegraphy. London: Biggs and Sons. 

Bouchard, Joseph F. 1999. *Guarding the Cold War Ramparts." Naval War College Review 52(3): 
111-35. 

Bradfield, W. W. 1910. “Wireless Telegraphy for Marine Inter-Communication." The Electrician — 
Marine Issue. June 10, pp. 135 ff. 

Brittain, James E. 1902. Alexanderson: Pioneer in American Electrical Engineering. Baltimore: 
Johns Hopkins University Press. 

Bucher, Elmer Eustice. 1917. Practical Wireless Telegraphy. New York: Wireless Press. 

Carr, Elmer G. 1918. *An Unusual Disease of Honey Bees." Journal of Economic Entomology 11(4): 
347-51. 

Carter, Charles Frederick. 1914. *Getting the Wireless on Board Train." Technical World Magazine 
20(6): 914-18. 

Chauvois, Louis. 1937. D'Arsonval: Soixante-cinq ans à travers la Science. Paris: J. Oliven. 

Conner, Lewis A. 1919. *The Symptomatology and Complications of Influenza." Journal of the 
American Medical Association 73(5): 321-25. 

Coutant, A. Francis. 1918. “An Epidemic of Influenza at Manila, P.I.” Journal of the American 
Medical Association 71(19): 1566-67. 

Cowie, David Murray and Paul Webley Beaven. 1919. “On the Clinical Evidence of Involvement of 
the Suprarenal Glands in Influenza and Influenzal Pneumonia.” Archives of Internal Medicine 
24(1): 78-88. 

Craft. E. B. and E. H. Colpitts. 1919. “Radio Telephony.” Proceedings of the American Institute of 
Electrical Engineers 38(1): 337-75. 

Crawley, Charles G. 1996. How Did the Evolution of Communications Affect Command and Control 
of Airpower: 1900-1945? Maxwell Air Force Base, AL. 

Crosby, Alfred W., Jr. 1976. Epidemic and Peace, 1918. Westport, CT: Greenwood. 

d’Arsonval, Jacques Arséne. 1892a. “Recherches d’électrothérapie. La voltaisation sinusoidale." 
Archives de physiologie normale et pathologique 24: 69-80. 

. 1892b. "Sur les effets physiologiques comparés des divers procédés d’électrisation.” 

Bulletin de l'Académie de Médecine 56: 424-33. 

. 1893a. *Action physiologique des courants alternatifs a grande fréquence." Archives de 

physiologie normale et pathologique 25: 401-8. 











. 1983b. “Effets physiologiques de la voltaisation sinusoidale." Archives de physiologie 

normale et pathologique 25: 387-91. 

. 1893c. “Expériences faites au laboratoire de médecine du Collège de France.” Archives de 

physiologie normale et pathologique 25: 789-90. 

. 1893d. “Influence de la fréquence sur les effets physiologiques des courants alternatifs.” 

Comptes rendus hebdomadaires des séances de l'Académie des Sciences 116: 630-33. 

. 1896a. *À propos de l'atténuation des toxines par la haute fréquence." Comptes rendus 

hebdomadaires des séances et mémoires de la Société de Biologie 48: 764-66. 

1896b. "Effets thérapeutiques des courants à haute fréquence." Comptes rendus 
hebdomadaires des séances de l'Académie des Sciences 123: 23-29. 

d'Arsonval, Jacques Arséne and Albert Charrin. 1893a. “Influence de l'électricité sur la cellule 
microbienne." Archives de physiologie normale et pathologique, 5th ser., 5: 664-69. 

. 1893b. “Électricité et Microbes.” Comptes rendus hebdomadaires des séances et mémoires 

de la Société de Biologie 45: 467-69, 764-65. 

. 1896a. "Action des diverses modalités électriques sur les toxines bactériennes.” Comptes 

rendus hebdomadaires des séances et mémoires de la Société de Biologie 48: 96-99. 

1896b. “Action de l'électricité sur les toxines bactériennes." Comptes rendus 

hebdomadaires des séances et mémoires de la Société de Biologie 48: 121-23. 

. 1896b. "Action de l'électricité sur les toxines et les virus." Comptes rendus hebdomadaires 
des séances et mémoires de la Société de Biologie 48: 153-54. 

del Pont, Antonino Marcó. 1918. "Historia de las Epidemias de Influenza." La Semana Médica 
25(27): 1-10. 

Eccles, William Henry. 1933a. Wireless Telegraphy and Telephony, 2nd ed. London: Benn Brothers. 

. 1933b. Wireless. London: Thornton Butterworth. 

Ehrenberg, L. 1919. “Transmission of Influenza.” Journal of the American Medical Association 
72(25): 1880. 

Elwell, Cyril Frank. 1910. “The Poulsen System of Wireless Telephony and Telegraphy.” Journal of 
Electricity, Power and Gas 24(14): 293-97. 

. 1920. “The Poulsen System of Radiotelegraphy. History of Development of Arc Methods.” 
The Electrician 84: 596-600. 

Erlendsson, V. 1919. “Influenza in Iceland.” Journal of the American Medical Association 72(25): 
1880. 

Erskine, Arthur Wright and B. L. Knight. 1918. “A Preliminary Report of a Study of the 
Coagulability of Influenzal Blood.” Journal of the American Medical Association 71(22): 1847. 
Erskine-Murray, J. 1920. “The Transmission of Electromagnetic Waves About the Earth.” Radio 

Review 1: 237-39. 

Fantus, Bernard. 1918. “Clinical Observations on Influenza.” Journal of the American Medical 
Association 71(21): 1736-39. 

Firstenberg, Arthur. 1997. Microwaving Our Planet. New York: Cellular Phone Taskforce. 

. 2001. “Radio Waves, the Blood-Brain Barier, and Cerebral Hemorrhage.” No Place To Hide 
3(2): 23-24. 

Friedlander, Alfred, Carey P. McCord, Frank J. Sladen, and George W. Wheeler. 1918. “The 
Epidemic of Influenza at Camp Sherman, Ohio.” Journal of the American Medical Association 
71(20): 1652-56. 

Frost, W. H. 1919. “The Epidemiology of Influenza.” Journal of the American Medical Association 
73(5): 313-18. 



































Goldoni, J. 1990. *Hematological Changes in Peripheral Blood of Workers Occupationally Exposed 
to Microwave Radiation." Health Physics 58(2): 205-7. 

Grant, John. 1907. *Experiments and Results in Wireless Telephony." American Telephone Journal 
15(4): 49-51. 

Harris, Wilfred. 1919. *The Nervous System in Influenza." The Practitioner 102: 89-100. 

Harrison, Forrest Martin. 1919. “Influenza Aboard a Man-of-War: A Clinical Summary.” Medical 
Record 95(17): 680-85. 

Headrick, Daniel R. 1988. The Tentacles of Progress: Technology Transfer in the Age of Imperialism, 
1850-1940. New York: Oxford University Press. 

. 1991. The Invisible Weapon: Telecommunications and International Politics, 1851-1945. 
New York: Oxford University Press. 

Hewlett, A. W. and W. M. Alberty. 1918. “Influenza at Navy Base Hospital in France.” Journal of the 
American Medical Association 71(13): 1056-58. 

Hirsch, Edwin F. 1918. “Epidemic of Bronchopneumonia at Camp Grant, Ill.” Journal of the 
American Medical Association 71(21): 1735-36. 

Hong, Sungook. 2001. Wireless: From Marconi’s Black-Box to the Audion. Cambridge, MA: MIT 
Press. 

Hopkins, Albert A. and A. Russell Bond, eds. 1905. “Wireless Telegraphy.” Scientific American 
Reference Book (New York: Munn & Co.), pp. 199-205. 

Howe, George William Osborn. 1920a. “The Upper Atmosphere and Radio Telegraphy.” Radio 
Review 1: 381-83. 

. 1920b. “The Efficiency of Aerials.” Radio Review 1: 540-43. 

. 1920c. “The Power Required for Long Distance Transmission.” Radio Review 1:598-608. 

Howeth, Linwood S. 1963. History of Communications — Electronics in the United States Navy. 
Washington, DC: Bureau of Ships and Office of Naval History. 

Huurdeman, Anton A. 2003. The Worldwide History of Telecommunications. Hoboken, NJ: Wiley. 

Imms, Augustus Daniel. 1907. “Report on a Disease of Bees in the Isle of Wight.” Journal of the 
Board of Agriculture 14(3): 129-40. 

Jordan, Edwin O. 1918. Discussion in: “The Etiology of Influenza,” Proceedings of the American 
Public Health Association, Forty-Sixth Annual Meeting, Chicago, December 8-11, 1918. Journal 
of the American Medical Association 71(25): 2097. 

. 1922. *Interepidemic Influenza." American Journal of Hygiene 2(4): 325-45. 

. 1927. Epidemic Influenza: A Survey. Chicago: American Medical Association. 

Journal of the American Medical Association. 1918a. “Spanish Influenza.” 71(8): 660. 

—. 1918b. “The Epidemic of Influenza.” 71(13): 1063-64. 

——.. 1918c. “Epidemic Influenza.” 71(14): 1136-37. 

——. 1918d. “The Present Epidemic of Influenza.” 71(15): 1223. 

———. 1918e. “Abstracts on Influenza.” 71(19): 1573-80. 

— — —. 1918f. “Influenza in Mexico.” 71(20): 1675. 

— — ——. 1918g. “Paris Letter. The Influenza Epidemic.” 71(20): 1676. 

———.. 1918h. “The Influenza Epidemic.” 71(24): 2009-10. 

———.. 1918i. “Influenza.” 71(25): 2088. 

— — ——. 1918j. “Mexico Letter.” 71(25): 2089. 

——. 1918k. “Febrile Epidemic [in Peru].” 71(25): 2090. 

———. 1918l. “The Etiology of Influenza.” 71(25): 2097-2100, 2173-75. 

—. 1919a. “Unsuccessful Attempts to Transmit Influenza Experimentally.” 72(4): 281. 

———. 1919b. “Heart Block and Bradycardia Following Influenza." 73(11): 868. 

















—.. 1920a. “The 1920 Influenza." 74(9): 607. 

———.. 1920b. “Influenza in Alaska.” 74(12): 796. 

—.. 1920c. “Influenza in the Navy Personnel.” 74(12): 813. 

—.. 1920d. “After Effects of Influenza.” 75(1): 61. 

—.. 1920e. “The Influenza Pandemic in India.” 75(9): 619-20. 

. 1920f. “Eye Disease Following Influenza Epidemic.” 75(10): 709. 

Keegan, J. J. 1918. “The Prevailing Epidemic of Influenza.” Journal of the American Medical 
Association 71(13): 1051-55. 

Keeton, Robert W. and A. Beulah Cushman. 1918. “The Influenza Epidemic in Chicago.” Journal of 
the American Medical Association 71(24): 1962-67. 

Kilbourne, Edwin D. 1975. The Influenza Viruses and Influenza. New York: Academic. 

Klessens, J. J. H. M. 1920. “Nervous Manifestations Complicating Influenza.” Journal of the 
American Medical Association 74(3): 216. 

Kuksinskiy, V. E. 1978. “Coagulation Properties of the Blood and Tissues of the Cardiovascular 
System Exposed to an Electromagnetic Field.” Kardiologiya 18(3): 107-11 (in Russian). 

Kyuntsel’, A. A. and V. I. Karmilov. 1947. “The Effect of an Electromagnetic Field on the Blood 
Coagulation Rate.” Klinicheskaya Meditsina 25(3): 78 (in Russian). 

La Fay, Howard. 1958. “DEW Line: Sentry of the Far North.” National Geographic 114(1): 128-46. 

Leake, J. P. 1919. “The Transmission of Influenza.” Boston Medical and Surgicial Journal 181(24): 
675-79. 

Logwood, C. V. 1916. “High Speed Radio Telegraphy.” The Electrical Experimenter, June, p. 99. 

Loosli, Clayton G., Dorothy Hamre, and O. Warner. 1958. “Epidemic Asian A Influenza in Naval 
Recruits.” Proceedings of the Society for Experimental Biology and Medicine 98(3): 589-92. 

Lyle, Eugene P., Jr. 1905. “The Advance of ‘Wireless.’” World’s Work, February, pp. 5843-48. 

MacNeal, Ward J. 1919. “The Influenza Epidemic of 1918 in the American Expeditionary Forces in 
France and England.” Archives of Internal Medicine 23(6): 657-88. 

Maestrini, D. 1919. “The Blood in Influenza.” Journal of the American Medical Association 72(11): 
834. 

Marconi, Degna. 2001. My Father, Marconi, 2nd ed. Toronto: Guernica. 

Marconi, Maria Cristina. 1999. Marconi My Beloved. Boston: Dante University of America Press. 

Marshall, C. J. 1957. “North America’s Distant Early Warning Line.” Geographical Magazine 
29(12): 616-28. 

Martin, Donald H. 1991. Communication Satellites 1958-1992. El Segundo, CA: The Aerospace 
Corporation. 

Menninger, Karl A. 1919a. *Psychoses Associated with Influenza." Journal of the American Medical 
Association 72(4): 235-41. 

. 1919b. “Influenza and Epileptiform Attacks." Journal of the American Medical Association 
73(25): 1896. 

Ministry of Health. 1920. Report on the Pandemic of Influenza, 1918-19. Reports on Public Health 
and Medical Subjects, no. 4. London. 

Morenus, Richard. 1957. DEW Line. New York: Rand McNally. 

Navy Department, Bureau of Equipment. 1906. List of Wireless-Telegraph Stations of the World. 
Washingon: Government Printing Office. 

Nicoll, M., Jr. 1918. “Organization of Forces against Influenza.” American Public Health 
Association, Forty-Sixth Annual Meeting, Chicago, Dec. 8-11, 1918, Journal of the American 
Medical Association 71(26): 2173. 








Nuzum, John W., Isadore Pilot, F. H. Stangl, and B. E. Bonar. 1918. “Pandemic Influenza and 
Pneumonia in a Large Civil Hospital.” Journal of the American Medical Association 71(19): 
1562-65. 

Oliver, Wade W. 1919. “Influenza — the Sphinx of Diseases.” Scientific American 120(9): 200, 212- 
13. 

Persson, Bertil R. R., Leif G. Salford, and Arne Brun. 1997. *Blood-brain Barrier Permeability in 
Rats Exposed to Electromagnetic Fields Used in Wireless Communication." Wireless Networks 3: 
455-61. 

Pettigrew, Eileen. 1983. The Silent Enemy: Canada and the Deadly Flu of 1918. Saskatoon: Western 
Producer Prairie Books. 

Pflomm, Erich. 1931. *Experimentelle und klinische Untersuchungen über die Wirkung ultrakurzer 
elektrischer Wellen auf die Entzündung." Archiv für klinische Chirurgie 166: 251-305. 

Phillips, Ernest F. 1925. *The Status of Isle of Wight Disease in Various Countries." Journal of 
Economic Entomology 18: 391-95. 

Prince, C. E. 1920. *Wireless Telephony on Aeroplanes." Radio Review 1: 281-83, 341. 

Public Health Reports. 1919. “Some Interesting Though Unsuccessful Attempts to Transmit 
Influenza Experimentally.” 34(2): 33-39. 

. 1919. “Influenza Among American Indians." 34: 1008-9. 

Radio Review. 1919. “The Transmission of Electromagnetic Waves Around the Earth.” 1: 78-80. 

. 1920. “The Generation of Large Powers at Radio Frequencies.” 1: 490-91. 

Reid, Ann H., Thomas G. Fanning, Johan V. Hultin, and Jeffery K. Taubenberger. 1999. “Origin and 
Evolution of the 1918 ‘Spanish’ Influenza Virus Hemagglutinin Gene.” Proceedings of the 
National Academy of Sciences 96(4): 1651-56. 

Richardson, Alfred W. 1959. “Blood Coagulation Changes Due to Electromagnetic Microwave 
Irradiations.” Blood 14: 1237-43. 

Robertson, H. E. 1918. “Influenzal Sinus Disease and its Relation to Epidemic Influenza.” Journal of 
the American Medical Association 70(21): 1533-35. 

Rosenau, Milton J. 1919. “Experiments to Determine Mode of Spread of Influenza.” Journal of the 
American Medical Association 73(5): 311-13. 

Rusyaev, V. P. and V. E. Kuksinskiy. 1973. “Study of Electromagnetic Field Effect on Coagulative 
and Fibrinolytic Properties of Blood.” Biofizika 11(1): 160-63 (in Russian with English abstract). 

Saleeby, C. W. 1920. “Mapping the Influenza.” Literary Digest, May 29, p. 32. 

Schaffel, Kenneth. 1991. The Emerging Shield: The Air Force and the Evolution of Continental Air 
Defense 1945-1960. Washington, DC: United States Air Force. 

Scheips, Paul J., ed. 1980. Military Signal Communications, 2 vols. New York: Arno Press. 

Schliephake, Erwin. 1935. Short Wave Therapy: The Medical Uses of Electrical High Frequencies. 
London: Actinic Press. 

. 1960. Kurzwellentherapie, 6th ed. Stuttgart: Gustav Fischer. 

Scriven, George P. 1914. “Report of the Chief Signal Officer, U.S. Army, 1914.” Annual Reports of 
the War Department, pp. 505-56. Reproduced in Scheips 1980, vol. 1. 

Sierra, Álvarez. 1921. “Particularidades clínicas de la última epidemia gripal.” El Siglo Médico 68: 
765-66. 

Simici, D. 1920. “The Heart in Influenza.” Journal of the American Medical Association 75(10): 703. 

Sofre, G. 1918. “Influenza.” Journal of the American Medical Association 71(21): 1782. 

Soper, George A. 1918. “The Pandemic in the Army Camps.” Journal of the American Medical 
Association 71(23): 1899-1909. 











Staehelin, R. 1918. *The Influenza Epidemic." Journal of the American Medical Association 71(14): 
1176. 

Stuart-Harris, Charles H. 1965. Influenza and Other Virus Infections of the Respiratory Tract, 2nd ed. 
Baltimore: Williams & Wilkins. 

Symmers, Douglas. 1918. “Pathologic Similarity between Pneumonia of Bubonic Plague and of 
Pandemic Influenza.” Journal of the American Medical Association 71(18): 1482-85. 

Synnott, Martin J. and Elbert Clark. 1918. “The Influenza Epidemic at Camp Dix, N.J.” Journal of 
the American Medical Association 71(22): 1816-21. 

Taubenberger, Jeffery K., Ann H. Reid, Amy E. Krafft, Karen E. Bijwaard, and Thomas G. Fanning. 
1997. “Initial Genetic Characterization of the 1918 ‘Spanish’ Influenza Virus.” Science 275: 1793- 
96. 

Thompson, George Raynor. 1965. “Radio Comes of Age in World War I.” In: Max L. Marshall, ed., 
The Story of the U.S. Army Signal Corps (New York: Watts), pp. 157-66. Reproduced in Scheips 
1980, vol. 1. 

Turner, Laurence Beddome. 1921. Wireless Telegraphy and Telephony. Cambridge: University Press. 

. 1931. Wireless: A Treatise on the Theory and Practice of High-Frequency Electric 
Signalling. Cambridge: Cambridge University Press. 

Underwood, Robyn M. and Dennis vanEngelsdorp. 2007. *Colony Collapse Disorder: Have We Seen 
This Before?" Bee Culture 35: 13-18. 

United States Signal Corps. 1917. Radiotelegraphy. Washington, DC: Government Printing Office. 

Vandiver, Ronald Wayne. 1995. Reflections on the Signal Corps: The Power of Paradigms in Ages of 
Uncertainty. Maxwell Air Force Base, AL. 

van Hartesveldt, Fred R. 1992. *The 1918-1919 Pandemic of Influenza." Lewiston, NY: Edwin 
Mellen. 

Vaughan, Warren T. 1921. Influenza: An Epidemiologic Study. Baltimore: American Journal of 
Hygiene. 

Watkins-Pitchford, Herbert. 1917. *An Enquiry into the Horse Disease Known as Septic or 
Contagious Pneumonia." Veterinary Journal 73: 345-62. 

Weightman, Gavin. 2003. Signor Marconi’s Magic Box. Cambridge, MA: Da Capo Press. 

Wiedbrauk, Danny L. 1997. “The 1996-1997 Influenza Season — A View From the Benches.” Pan 
American Society for Clinical Virology Newsletter 23(1). 

Zinsser, Hans. 1922. “The Etiology and Epidemiology of Influenza.” Medicine 1(2): 213-309. 





Chapter 9 

Adams, A. J. S. 1886. “Earth Conduction.” Van Nostrand’s Engineering Magazine 35: 249-52. 

Alfvén, Hannes Olof Gésta. 1950. “Discussion of the Origin of the Terrestrial and Solar Magnetic 
Fields.” Tellus 2(2): 74-82. 

. 1955. “Electricity in Space.” In: The New Astronomy (New York: Scientific American 

Books), pp. 74-79. 

. 1969. Atom, Man, and Universe: The Long Chain of Complications. San Francisco: W. H. 

Freeman. 

. 1981. Cosmic Plasma. Dordrecht: D. Reidel. 

. 1984. *Cosmology: Myth or Science?" Journal of Astrophysics and Astronomy 5: 79-98. 

. 1986a. “Double Layers and Circuits in Astrophysics.” IEEE Transactions on Plasma 

Science PS-14(6): 779-93. 

. 1986b. “Model of the Plasma Universe.” IEEE Transactions on Plasma Science PS-14(6): 

629-38. 




















—. 1986c. “The Plasma Universe.” Physics Today, September, pp. 22-27. 

— — — 1987. “Plasma Universe.” Physica Scripta T18: 20-28. 

—— ——-. 1988. "Memoirs of a Dissident Scientist." American Scientist 76: 249-51. 

1990. “Cosmology in the Plasma Universe: An Introductory Exposition.” IEEE 
Transactions on Plasma Science PS-18(1): 5-10. 

Alfvén, Hannes and Gustaf Arrhenius. 1976. Evolution of the Solar System. Washington, DC: 
National Aeronautics and Space Administration. 

Alfvén, Hannes and Carl-Gunne Falthammar. 1963. Cosmical Electrodynamics, 2nd ed. Oxford: 
Clarendon Press. 

Ando, Yoshiaki and Masashi Hayakawa. 2002. “Theoretical Analysis on the Penetration of Power 
Line Harmonic Radiation into the Ionosphere.” Radio Science 37(6): 5-1 to 5-12. 

Arnoldy, Roger L. and Paul M. Kintner. 1989. “Rocket Observations of the Precipitation of Electrons 
by Ground VLF Transmitters.” Journal of Geophysical Research 94(A6): 6825-32. 

Arrhenius, Svante. 1897. “Die Einwirkung kosmischer Einflüsse auf physiologische Verhältnisse.” 
Skandinavisches Archiv für Physiologie 8(1): 367-416. 

. 1905. “On the Electric Charge of the Sun.” Terrestrial Magnetism and Atmospheric 
Electricity 10(1): 1-8. 

Avijgan, Majid and Mahtab Avijgan. 2013. “Can the Primo Vascular System (Bong Han Duct 
System) Be a Basic Concept for Qi Production?” International Journal of Integrative Medicine 
1(20): 1-10. 

Baik, Ku-Youn, Eun Sung Park, Byung-Cheon Lee, Hak-Soo Shin, Chunho Choi, Seung-Ho Yi, 
Hyun-Min Johng, Tae Jeong Nam, Kyung-Soon Soh, Yong-Sam Nahm, Yeo Sung Yoon, In-Se 
Lee, Se-Young Ahn, and Kwang-Sup Soh. 2004. “Histological Aspect of Threadlike Structure 
Inside Blood Vessel.” Journal of International Society of Life Information Science 22(2): 473-76. 

Baik, Ku-Youn, Baeckkyoung Sung, Byung-Cheon Lee, Hyeon-Min Johng, Vyacheslava Ogay, Tae 
Jung Nam, Hak-Soo Shin, and Kwang-Sup Soh. 2004. “Bonghan Ducts and Corpuscles with 
DNA-contained Granules on the Internal Surfaces of Rabbits.” Journal of International Society of 
Life Information Science 22(2): 598-601. 

Bailey, V. A. and David Forbes Martyn. 1934. “Interaction of Radio Waves.” Nature 133: 218. 

Balser, Martin and Charles A. Wagner. 1960. “Observations of Earth-Ionosphere Cavity 
Resonances.” Nature 188: 638-41. 

Barr, Richard. 1979. “ELF Radiation from the New Zealand Power System.” Planetary and Space 
Science 27: 537-40. 

Barr, Richard, D. Llanwyn Jones, and Craig J. Rodger. 2000. “ELF and VLF Radio Waves.” Journal 
of Atmospheric and Solar-Terrestrial Physics 62(17-18): 1689-1718. 

Bauer, Louis A. 1921. “Measures of the Electric and Magnetic Activity of the Sun and the Earth, and 
Interrelations.” Terrestrial Magnetism and Atmospheric Electricity 26(1-2): 33-68. 

Beard, George Miller. 1874. “Atmospheric Electricity and Ozone: Their Relation to Health and 
Disease.” Popular Science Monthly 4: 456-69. 

Becker, Robert Otto. 1963. “The Biological Effects of Magnetic Fields — A Survey." Medical 
Electronics and Biological Engineering 1(3): 293-303. 

Becker, Robert O., Maria Reichmanis, Andrew A. Marino, and Joseph A. Spadaro. 1976. 
“Electrophysiological Correlates of Acupuncture Points and Meridians.” Psychoenergetic Systems 
1: 105-12. 

Becquerel, Antoine César. 1851. “On the Causes of the Disengagement of Electricity in Plants, and 
upon Vegeto-terrestrial Currents.” American Journal of Science and Arts, 2nd ser., 12: 83-97. 








Translation from: “Sur les causes qui dégagent de l'électricité dans les végétaux, et sur les 
courants végétaux-terrestres," Annales de Chimie et de Physique, 3rd ser., 31: 40-67. 

Bell, Timothy F. 1976. *ULF Wave Generation through Particle Precipitation Induced by VLF 
Transmitters." Journal of Geophysical Research 81(19): 3316-26. 

Belyaev, G. G., V. M. Chmyrev, and N. G. Kleimenova. 2003. *Hazardous ULF Electromagnetic 
Environment of Moscow City." Physics of Auroral Phenomena. Proceedings of the 26th Annual 
Seminar, Apatity, pp. 249-52. 

Bering, Edgar A., III, Arthur A. Few, and James R. Benbrook. 1998. “The Global Electric Circuit.” 
Physics Today, October, pp. 24-30. 

Boerner, Wolfgang M., James B. Cole, William R. Goddard, Michael Z. Tarnawecky, Lotfallah 
Shafai, and Donald H. Hall. 1983. “Impacts of Solar and Auroral Storms on Power Line Systems.” 
Space Science Reviews 35: 195-205. 

Bowen, Melissa M., Antony C. Fraser-Smith, and Paul R. McGill. 1992. Long-Term Averages of 
Globally-Measured ELF/VLF Radio Noise. Space, Telecommunication, and RadioScience 
Laboratory, Stanford University. Technical Report E450-2. 

Bradley, Philip B. and Joel Elkes. 1957. “The Effects of Some Drugs on the Electrical Activity of the 
Brain.” Brain 80: 77-117. 

Brazier, Mary A. B. 1977. The Electrical Activity of the Nervous System, 4th ed. Baltimore: Williams 
& Wilkins. 

Brewitt, Barbara. 1996. “Quantitative Analysis of Electrical Skin Conductance in Diagnosis: 
Historical and Current Views of Bioelectric Medicine.” Journal of Naturopathic Medicine 6(1): 
66-75. 

Bullough, Ken. 1983. “Satellite Observations of Power Line Harmonic Radiation.” Space Science 
Reviews 35: 175-83. 

. 1995. “Power Line Harmonic Radiation: Sources and Environmental Effects.” In: Hans 
Volland, ed., Handbook of Atmospheric Electrodynamics, (CRC Press: Boca Raton, FL), vol. 2, 
pp. 291-332. 

Bullough, Ken, Thomas Reeve Kaiser, and Hal J. Strangeways. 1985. “Unintentional Man-made 
Modification Effects in the Magnetosphere.” Journal of Atmopheric and Terrestrial Physics 
47(12): 1211-23. 

Bullough, Ken , Adrian R. L. Tatnall, and M. Denby. 1976. “Man-made E.L.F./V.L.F. Emissions and 
the radiation belts.” Nature 260: 401-3. 

Burbank, J. E. 1905. “Earth-Currents: And a Proposed Method for Their Investigation.” Terrestrial 
Magnetism and Atmospheric Electricity 10: 23-49. 

Cannon, P. S. and Michael J. Rycroft. 1982. “Schumann Resonance Frequency Variations during 
Sudden Ionospheric Disturbances.” Journal of Atmospheric and Terrestrial Physics 44(2): 201-6. 

Cherry, Neil. 2002. “Schumann Resonances, a Plausible Biophysical Mechanism for the Human 
Health Effects of Solar/Geomagnetic Activity.” Natural Hazards 26(3): 279-331. 

Chevalier, Gaetan. 2007. The Earth’s Electrical Surface Potential: A Summary of Present 
Understanding. Encinitas, CA: California Institute for Human Science. 

Cho, Sung-Jin, Byeong-Soo Kim, and Young-Seok Park. 2004. “Thread-like Structures in the Aorta 
and Coronary Artery of Swine.” Journal of International Society of Life Information Science 
22(2): 609-11. 

Cresson, John C. 1836. “History of Experiments on Atmospheric Electricity.” Journal of the Franklin 
Institute 22: 166-72. 

Davis, John R. 1974. “A Quest for a Controllable ULF Wave Source.” IEEE Transactions on 
Communications COM-22(4): 578-86. 





de Vernejoul, Pierre, Pierre Albaréde, and Jean-Claude Darras. 1985. *Étude des méridiens 
d'acupuncture par les traceurs radioactifs." Bulletin de l'Académie Nationale de Médecine 169(7): 
1071-75. 

Dolezalek, Hans. 1972. *Discussion of the Fundamental Problem of Atmospheric Electricity." Pure 
and Applied Geophysics 100(1): 8-43. 

Dowden, R. L. and B. J. Fraser. 1984. *Waves in Space Plasmas: Highlights of a Conference Held in 
Hawaii, 7-11 February 1983." Space Science Reviews 39: 227-53. 

Fálthammar,  Carl-Gunne. 1986.  *Magnetosphere-Ionosphere Interactions — Near-Earth 
Manifestations of the Plasma Universe." IEEE Transactions on Plasma Science PS-14(6): 616-28. 

Faust, Volker. 1978. Biometeorologie: Der Einfluss von Wetter und Klima auf Gesunde und Kranke. 
Stuttgart: Hippokrates. 

Fraser-Smith, Antony C. 1979. “A Weekend Increase in Geomagnetic Activity.” Journal of 
Geophysical Research 84(A5): 2089-96. 

. 1981. “Effects of Man on Geomagnetic Activity and Pulsations." Advances in Space 
Research 1: 455-66. 

Fraser-Smith, Antony C. and Peter R. Bannister. 1998. “Reception of ELF Signals at Antipodal 
Distances.” Radio Science 33(1): 83-88. 

Fraser-Smith, Antony C. and Melissa M. Bowen. 1992. “The Natural Background Levels of 50/60 
Hz Radio Noise.” IEEE Transactions on Electromagnetic Compatibility 34(3): 330-37. 

Fraser-Smith, Antony C., D. M. Bubenick, and Oswald G. Villard, Jr. 1977. Air/ Undersea 
Communication at Ultra-Low-Frequencies Using Airborne Loop Antennas. Technical Report 
4207-6, Radio Science Laboratory, Stanford Electronics Laboratories, Department of Electrical 
Engineering, June 1977, SEL-77-013. 

Fraser-Smith, Antony C. and D. B. Coates. 1978. “Large-amplitude ULF fields from BART.” Radio 
Science 13(4): 661-68. 

Fraser-Smith, Antony C., Paul R. McGill, A. Bernardi, Robert A. Helliwell, and M. E. Ladd. 1992. 
Global Measurements of Low-Frequency Radio Noise. Space, Telecommunications and 
Radioscience Laboratory, Stanford University. Final Technical Report E450-1. 

Frélich, O. 1895. “Kompensationsvorrichtung zum Schutze physikalischer Institute gegen die 
Einwirkung elektrischer Bahnen.” Elektrotechnische Zeitschrift no. 47, pp. 745-48. 

. 1896. “Demonstration der Kompensationsvorrichtung zum Schutz physikalischer Institute 
gegen elektrische Bahnen.” Elektrotechnische Zeitschrift, no. 3, pp. 40-44. 

Fujiwara, Satoru and Sun-Bong Yu. 2012. “A Follow-up Study on the Morphological Characteristics 
in Bong-Han Theory: An Interim Report.” In: Kwang-Sup Soh, Kyung A. Kang, and David K. 
Harrison, eds., The Primo Vascular System (New York: Springer), pp. 19-21. 

Fiillekrug, Martin. 1995. “Schumann Resonances in Magnetic Field Components.” Journal of 
Atmorpheric and Terrestrial Physics 57(5): 479-84. 

Gerland, E. 1886. “On the Origin of Atmospheric Electricity.” Van Nostrand’s Engineering Magazine 
34: 158-60. 

Guglielmi, A. and O. Zotov. 2007. “The Human Impact on the Pcl Wave Activity.” Journal of 
Atmospheric and Solar-Terrestrial Physics 69: 1753-58. 

Hamer, James R. 1965. Biological Entrainment of the Human Brain by Low Frequency Radiation. 
NSL 65-199, Northrop Space Labs. 

Harrison, R. Giles. 2004. “The Global Atmospheric Electrical Circuit and Climate.” Surveys in 
Geophysics 25(5-6): 441-84. 

. 2013. “The Carnegie Curve.” Surveys in Geophysics 34: 209-32. 











Hayashi, K., T. Oguti, T. Watanabe, K. Tsuruda, S. Kokubun, and R. E. Horita. 1978. “Power 
Harmonic Radiation Enhancement during the Sudden Commencement of a Magnetic Storm." 
Nature 275: 627-29. 

Helliwell, Robert A. 1965. Whistlers and Related Ionospheric Phenomena. Stanford, CA: Stanford 
University Press. 

. 1977. *Active Very Low Frequency Experiments on the Magnetosphere from Siple Station, 
Antarctica." Philosophical Transactions of the Royal Society B 279: 213-24. 

Helliwell, Robert A. and John P. Katsufrakis. 1974. *VLF Wave Injection into the Magnetosphere 
from Siple Station, Antarctica." Journal of Geophysical Research 79(16): 2511-18. 

Helliwell, Robert A., John P. Katsufrakis, Timothy F. Bell, and Rajagopalan Raghuram. 1975. *VLF 
Line Radiation in the Earth's Magnetosphere and Its Association with Power System Radiation." 
Journal of Geophysical Research 80(31): 4249-58. 

Hess, Victor F. 1928. The Electrical Conductivity of the Atmosphere and its Causes. London: 
Constable. 

Ho, A. M.-H., Antony C. Fraser-Smith, and Oswald G. Villard, Jr. 1979. *Large-Amplitude ULF 
Magnetic Fields Produced by a Rapid Transit System: Close-Range Measurements." Radio 
Science 14(6): 1011-15. 

Hu, X., X. Huang, J. Xu, and B. Wu. 1993. “Distribution of Low Skin Impedance Points Along 
Meridians over the Medial Side of Forearm.” Zhen Ci Yan Jiu (“Acupuncture Research”) 18(2): 
94-97 (in Chinese). 

Hu, X., B. Wu, J. Xu, X. Huang, and J. Hau. 1993. “Studies on the Low Skin Impedance Points and 
the Feature of its Distribution Along the Channels by Microcomputer. II. Distribution of LSIPs 
Along the Channels.” Zhen Ci Yan Jiu (“Acupuncture Research”) 18(2): 163-67 (in Chinese). 

Huang, X., J. Xu, B. Wu, and X. Hu. 1993. “Observation on the Distribution of LSIPs Along Three 
Yang Meridians as Well as Ren and Du Meridians.” Zhen Ci Yan Jiu (“Acupuncture Research”) 
18(2): 98-103 (in Chinese). 

Imhof, W. L., H. D. Voss, M. Walt, E. E. Gaines, J. Mobilia, D. W. Datlowe, and J. B. Reagan. 1986. 
“Slot Region Electron Precipitation by Lightning, VLF Chorus, and Plasmaspheric Hiss.” Journal 
of Geophysical Research 91(A8): 8883-94. 

Itoh, Shinji, Keisuke Tsujioka, and Hiroo Saito. 1959. “Blood Clotting Time under Metal Cover 
(Biological P-Test).” International Journal of Bioclimatology and Biometeorology 3(1): 269-70. 
Jenssen, Matz. 1950. “On Radiation From Overhead Transmission Lines.” Proceedings of the IEE, 

part III, 97(47): 166-78. 

Jiang, Xiaowen, Byung-Cheon Lee, Chunho Choi, Ku-Youn Baik, Kwang-Sup Soh, Hee-Kyeong 
Kim, Hak-Soo Shin, Kyung-Soon Soh, and Byeung-Soo Cheun. 2002. “Threadlike Bundle of 
Tubules Running Inside Blood Vessels: New Anatomical Structure.” arXiv: physics/0211085. 

Johng, Hyeon-Min, Hak-Soo Shin, Jung Sun Yoo, Byung-Cheon Lee, Ku-Youn Baik, and Kwang- 
Sup Soh. 2004. “Bonghan Ducts on the Surface of Rat Liver.” Journal of International Society of 
Life Information Science 22(2): 469-72. 

Johng, Hyeon-Min, Jung-Sun Yoo, Tae-Jong Yoon, Hak-Soo Shin, Byung-Cheon Lee, Changhoon 
Lee, Jin-Kyu Lee, and Kwang-Sup Soh. 2006. “Use of Magnetic Nanoparticles to Visualize 
Threadlike Structures Inside Lymphatic Vessels of Rats.” Evidence-Based Complementary and 
Alternative Medicine 4: 77-82. 

Karinen, A., K. Mursula, Th. Ulich, and J. Manninen. 2002. “Does the Magnetosphere Behave 
Differently on Weekends?” Annales Geophysicae 20: 1137-42. 

Kikuchi, Hiroshi. 1983a. “Overview of Power-Line Radiation and its Coupling to the Ionosphere and 
Magnetosphere.” Space Science Reviews 35: 33-41. 








. 1983b. *Power Line Transmission and Radiation." Space Science Reviews 35: 59-80. 

Kim, Bong Han. 1963. “On the Kyungrak System.” Journal of the Academy of Medical Sciences of 
the Democratic People’s Republic of Korea, vol. 1963, no. 5. 

. 1964. On the Kyungrak System. Pyongyang, Democratic People’s Republic of Korea: 
Foreign Languages Publishing House. 

Kim, Soyean, Kyu Jae Lee, Tae Eul Jung, Dan Jin, Dong Hui Kim, and Hyun-Won Kim. 2004. 
“Histology of Unique Tubular Structures Believed to Be Meridian Line.” Journal of International 
Society of Life Information Science 22(2): 595-97. 

Klemm, William R. 1969. Animal Electroencephalography. New York: Academic. 

Kolesnik, A. G. 1998. “Electromagnetic Background and Its Role in Environmental Protection and 
Human Ecology.” Russian Physics Journal 41(8): 839-50. 

Konig, Herbert L. 1971. “Biological Effects of Extremely Low Frequency Electrical Phenomena in 
the Atmosphere.” Journal of Interdisciplinary Cycle Research 2(3): 317-23. 

. 1974a. “ELF and VLF Signal Properties: Physical Characteristics.” In: Michael A. 

Persinger, ed., ELF and VLF Electromagnetic Field Effects (New York: Plenum), pp. 9-34. 

. 1974b. “Behavioral Changes in Human Subjects Associated with ELF Electric Fields.” In: 

Michael A. Persinger, ed., ELF and VLF Electromagnetic Field Effects (New York: Plenum), pp. 

81-99. 

. 1975. Unsichtbare Umwelt: Der Mensch im Spielfeld elektromagnetischer Kráfte. München: 
Heinz Moos. 

Kornilov, I. A. 2000. *VLF Emissions and Electron Precipitations Stimulated by Emissions of Power 
Transmission Line Harmonics." Geomagnetism and Aeronomy 40(3): 388-92. 

Lanzerotti, Louis J. and Giovanni P. Gregori. 1986. *Telluric Currents: The Natural Environment and 
Interactions with Man-made Systems." In: Geophysics Study Committee, National Research 
Council, The Earth's Electrical Environment (Washington, DC: National Academy Press), pp. 
232-57. 

Larkina, V. I., O. A. Maltseva and O. A. Molchanov. 1983. “Satellite Observations of Signals from a 
Soviet Mid-latitude VLF Transmitter in the Magnetic-Conjugate Region." Journal of Atmospheric 
and Terrestrial Physics 45(2/3): 115-19. 

Larsen, Adrian P. 2004. Ryodoraku Acupuncture Measurement and Treatment. Doctoral thesis, Logan 
College of Chiropractic, Chesterfield, MO. 

Lee, Byung-Cheon, Jung Sun Yoo, Ku Youn Baik, Baeckkyoung Sung, Jawoong Lee, and Kwang- 
Sup Soh. 2008. *Development of a Fluorescence Stereomicroscope and Observation of Bong-Han 
Corpuscles Inside Blood Vessels." Indian Journal of Experimental Biology 46: 330-35. 

Lee, Byung-Cheon, Ki-Hoon Uhm, Kyoung-Hee Bae, Dae-In Kang, and Kwang-Sup Soh. 2009. 
*Visualization of Potential Acupuncture Points in Rat and Nude Mouse and Dil Tracing Method." 
Journal of Pharmacopuncture 12(3): 25-30. 

Lee, Jong-Su. 2004. *Bonghan System and Hypothesis on Oncogenesis." Journal of International 
Society of Life Information Science 22(2): 606-8. 

Lee, Sanghun, Yeonhee Ryu, Yungju Yun, Sungwon Lee, Ohsang Kwon, Jaehyo Kim, Inchul Sohn, 
and Seonghun Ahn. 2010. “Anatomical Discrimination of the Differences between Torn 
Mesentery Tissues and Internal Organ-surface Primo- vessels.” Journal of Acupunture and 
Meridian Studies 3(1): 10-15. 

Lerner, Eric J. 1991. The Big Bang Never Happened. New York: Times Books. 

Lim, Chae Jeong, So Yeong Lee, and Pan Dong Ryu. 2015. "Identification of Primo-Vascular System 
in Abdominal Subcutaneous Tissue Layer of Rats." Evidence-Based Complementary and 
Alternative Medicine, article ID 751937. 














Lin, Hsiao-Tsung. 2008. “Physics Model of Internal Chi System.” Journal of Accord Integrative 
Medicine 4(1): 78-83. 

Lovering, Joseph. 1854. “Atmospheric Electricity.” American Almanac, 1854, pp. 70-82. 

Lowes, Frank J. 1982. “On Magnetic Observations of Electric Trains.” The Observatory 102: 44. 

Ludwig, Wolfgang and Reinhard Mecke. 1968. “Wirkung künstlicher Atmospherics auf Sàuger." 
Archiv für Meteorologie, Geophysik und Bioklimatologie, ser. B, 16: 251-61. 

Luette, James Paul, Chung G. Park, and Robert A. Helliwell. 1977. *Longitudinal Variations of Very- 
Low-Frequency Chorus Activity in the Magnetosphere: Evidence of Excitation By Electrical 
Power Transmission Lines." Geophysical Research Letters 4(7): 275-78. 

. 1979. “The Control of the Magnetosphere by Power Line Radiation.” Journal of 
Geophysical Research 84: 2657-60. 

Lyman, Charles P. and Regina C. O’Brien. 1977. “A Laboratory Study of the Turkish Hamster 
Mesocricetus brandti.” Breviora 442: 1-27. 

Makarova, L. N. and A. V. Shirochkov. 2000. “Magnetopause Position as an Important Index of the 
Space Weather.” Physics and Chemistry of the Earth C 25(5-6): 495-98. 

. 2005. “Atmospheric Electrodynamics Modulated by the Solar Wind.” Advances in Space 
Research 35(8): 1480-83. 

Markson, Ralph and Michael Muir. 1980. “Solar Wind Control of the Earth’s Electric Field.” Science 
208: 979-90. 

Mathias, Emile, Jean Bosler, Pierre Loisel, Raphaél Dongier, Charles Maurain, G. Girousse, and 
René Mesny. 1924. Traité d'Électricité Atmosphérique et Tellurique. Paris: Presses Universitaires 
de France. 

Matteucci, Carlo. 1869. On the Electrical Currents of the Earth. Washington, DC: Smithsonian 
Institution. 

Matthews, J. P. and Keith H. Yearby. 1981. *Magnetospheric VLF Line Radiation Observed at 
Halley, Antarctica." Planetary and Space Science 29(1): 95-112. 

Maurain, Charles. 1905. “Influence perturbatrice des lignes de tramway électriques sur les appareils 
de mésures électriques et magnétiques: moyens de défense." Revue Électrique 4(45): 257-63. 

Molchanov, Oleg and Michel Parrot. 1995. *PLHR Emissions Observed on Satellites." Journal of 
Atmospheric and Terrestrial Physics 57(5): 493-505. 

Molchanov, Oleg, Michel Parrot, Mikhail M. Mogilevsky, and François Lefeuvre. 1991. “A Theory 
of PLHR Emissions to Explain the Weekly Variation of ELF Data Observed by a Low-Altitude 
Satellite." Annales Geophysicae 9: 669-80. 

Moore-Ede, Martin C., Scott S. Campbell, and Russel J. Reiter, eds. 1992. Electromagnetic Fields 
and Circadian Rhythmicity. Boston: Birkháuser. 

National Research Council, Geophysics Study Comittee. 1986. The Earth's Electrical Environment. 
Washington, DC: National Academy Press. 

Němec, František, Ondfej Santolík, Michel Parrot, and Jean-Jacques Berthelier. 2007. “On the Origin 
of Magnetospheric Line Radiation." WDS '07 Proceedings of Contributed Papers, part 2, pp. 64- 
70. 











2007. “Power Line Harmonic Radiation: A Systematic Study Using DEMETER 
Spacecraft.” Advances in Space Research 40: 398-403. 

Nunn, D., J. Manninen, T. Turunen, V. Trakhtengerts, and N. Erokhin. 1999. “On the Nonlinear 
Triggering of VLF Emissions by Power Line Harmonic Radiation.” Annales Geophysicae 17: 79- 
94. 

Ogawa, Toshio, Yoshikazu Tanaka, Teruo Miura, and Michihiro Yasuhara. 1966. *Observations of 
Natural ELF and VLF Electromagnetic Noises by Using Ball Antennas." Journal of 


Geomagnetism and Geoelectricity 18(4): 443-54. 

Ortega, Pascal, Anirban Guha, Earle Williams, and Gabriella Satori. 2014. *Schumann Resonance 
Observations from the Central Pacific Ocean." Paper presented at XV International Conference on 
Atmospheric Electricity, 15-20 June 2014, Norman, OK. 

Palmer, C. W. 1935. “The ‘Luxembourg Effect’ in Radio.” Radio-Craft, February, pp. 467, 499. 

Park, Chung. G. and D. C. D. Chang. 1978. “Transmitter Simulation of Power Line Radiation Effects 
in the Magnetosphere.” Geophysical Research Letters 5(10): 861-64. 

Park, Chung G. and Robert A. Helliwell. 1978. “Magnetospheric Effects of Power Line Radiation.” 
Science 200: 727-30. 

Park, Chung G., Robert A. Helliwell, and Francois Lefeuvre. 1983. “Ground Observations of Power 
Line Radiation Coupled to the Ionosphere and Magnetosphere.” Space Science Reviews 35: 131- 
37. 

Park, Eun-sung, Hee Young Kim, and Dong-ho Youn. 2013. “The Primo Vascular Structures 
Alongside Nervous System: Its Discovery and Functional Limitation.” Evidence-Based 
Complementary and Alternative Medicine, article ID 538350. 

Park, Joong Wha, In Soo Hong, Jin Ha Yoon, and Hyun-Won Kim. 2004. “Migration of Lipiodol 
Along the Meridian Line.” Journal of International Society of Life Information Science 22(2): 
592-94. 

Parrot, Michel, Oleg A. Molchanov, Mikhail M. Mogilevski, and François Lefeuvre. 1991. “Daily 
Variations of ELF Data Observed by a Low-altitude Satellite.” Geophysical Research Letters 
18(6): 1039-42. 

Parrot, Michel, František Němec, Ondřej Santolík, and Jean-Jacques Berthelier. 2005. “ELF 
Magnetospheric Lines Observed by DEMETER.” Annales Geophysicae 23: 3301-11. 

Parrot, Michel and Youri Zaslavski. 1996. *Physical Mechanisms of Man-Made Influences on the 
Magnetosphere." Surveys in Geophysics 17: 67-100. 

Pellegrino, Fernando C. and Roberto E. P. Sica. 2004. *Canine Electroencephalographic Recording 
Technique: Findings in Normal and Epileptic Dogs." Clinical Neurophysiology 115: 477-87. 

Peratt, Anthony L. 1989a. *Plasma Cosmology. Part I. Interpretations of the Visible Universe." The 
World and I, August, pp. 294-301. 

. 1989b. *Plasma Cosmology. Part II. The Universe is a Sea of Electrically Charged 

Particles." The World and 1, September, pp. 307-17. 

. 1990. *Not with a Bang." The Sciences, January/February, pp. 24-32. 

. 1992. Physics of the Plasma Universe. New York: Springer. 

. 1995. "Introduction to Plasma Astrophysics and Cosmology." Astrophysics and Space 
Science 227: 3-11. 

Persinger, Michael A., ed. 1974. ELF and VLF Electromagnetic Field Effects. New York: Plenum. 

Persinger, Michael A., H. Wolfgang Ludwig, and  Klaus-Peter  Ossenkopp. 1973. 
“Psychophysiological Effects of Extremely Low Frequency Electromagnetic Fields: A Review." 
Perceptual and Motor Skills 36: 1131-59. 

Planté, Gaston. 1878. “Electrical Analogies with Natural Phenomena.” Nature 17: 226-29, 385-87. 

Pouillet, Claude Servais Mathias. 1853. Éléments de Physique expérimentale et de Météorologie, 6th 
ed. Paris: L. Hachette. 

Preece, William Henry. 1894. *Earth Currents." Nature 49: 554. 

Randall, Walter and Walter S. Moos. 1993. *The 11-Year Cycle in Human Births." International 
Journal of Biometeorology 37(2): 72-77. 

Randall, Walter. 1990. “The Solar Wind and Human Birth Rate: A Possible Relationship Due to 
Magnetic Disturbances.” International Journal of Biometeorology 34(1): 42-48. 














Reichmanis, Maria, Andrew A. Marino, and Robert O. Becker. 1979. *Laplace Plane Analysis of 
Impedance on the H Meridian." American Journal of Chinese Medicine 7(2): 188-93. 

Reiter, Reinhold. 1954. “Umwelteinfliisse auf die Reaktionszeit des gesunden Menschen." 
Münchener medizinische Wochenschrift 96(17, 18): 479-81, 526-29. 

. 1969. *Solar Flares and Their Impact on Potential Gradient and Air-Earth Current 

Characteristics at High Mountain Stations." Pure and Applied Geophysics 72(1): 259-67. 

. 1976. “The Electric Potential of the Ionosphere as Controlled by the Solar Magnetic Sector 
Structure." Naturwissenschaften 63(4): 192-93. 

Rheinberger, Margaret B. and Herbert H. Jasper. 1937. “Electrical Activity of the Cerebral Cortex in 
the Unanesthetized Cat.” American Journal of Physiology 119: 186-96. 

Robinson, G. H. 1966. “Harmonic Phenomena Associated with the Benmore-Haywards H.V.D.C. 
Transmission Scheme.” New Zealand Engineering, January 15, pp. 16-28. 

Roble, R. G. 1991. “On Modeling Component Processes in the Earth’s Global Electric Circuit.” 
Journal of Atmospheric and Terrestrical Physics 53(9): 831-47. 

Rooney, W. J. 1939. “Earth Currents.” In: J. A. Fleming, ed., Terrestrial Magnetism and Electricity 
(New York: McGraw-Hill), pp. 270-307. 

Rosenberg, Theodore J., Robert A. Helliwell, and John P. Katsufrakis. 1971. “Electron Precipitation 
Associated with Discrete Very-Low-Frequency Emissions.” Journal of Geophysical Research 
76(34): 8445-52. 

Ruckebusch, Y. 1963. “L’électroencéphalogramme normal du chien.” Revue de Médecine Vétérinaire 
114(1): 119-34. 

Rycroft, Michael J. 1965. “Resonances of the Earth-Ilonosphere Cavity Observed at Cambridge, 
England.” Radio Science 69D(8): 1071-81. 

. 2006. “Electrical Processes Coupling the Atmosphere and Ionosphere: An Overview.” 
Journal of Atmospheric and Solar-Terrestrical Physics 68: 445-56. 

Sa, Luiz Alexandre Nogueira de. 1990. “A Wave-Particle-Wave Interaction Mechanism as a Cause of 
VLF Triggered Emissions.” Journal of Geophysical Research 95(A8): 12,277-86. 

Schlegel, Kristian and Martin Fiillekrug. 2002. “Weltweite Ortung von Blitzen: 50 Jahre Schumann- 
Resonanzen.” Physik in unserer Zeit 33(6): 256-61. 

Schulz, Nicolas. 1961. “Lymphocytose relative et l’activité solaire." Revue médicale de Nancy 6: 
541-44. 

Schumann, Winfried O. and Herbert L. Kónig. 1954. *Über die Beobachtung von ‘Atmospherics’ bei 
geringsten Frequenzen." Naturwissenschaften 41(8): 183-84. 

Shin, Hak-Soo, Hyeon-Min Johng, Byung-Cheon Lee, Sung-Il Cho, Kyung-Soon Soh, Ku-Youn 
Baik, Jung-Sun Yoo, and Kwang-Sup Soh. 2005. “Feulgen Reaction Study of Novel Threadlike 
Structures (Bonghan Ducts) on the Surface of Mammalian Organs.” Anatomical Record 284B: 35- 
40. 

Soh, Kwang-Sup, Kyung A. Kang, and David K. Harrison, eds. 2012. The Primo Vascular System. 
New York: Springer. 

Soh, Kwang-Sup, Kyung A. Kang, and Yeon Hee Ryu. 2013. *50 Years of Bong-Han Theory and 10 
Years of Primo Vascular System." Evidence-Based Complementary and Alternative Medicine, 
article ID 587827. 

Starwynn, Darren. 2002. *Electrophysiology and the Acupuncture Systems." Medical Acupuncture 
13(1): article 7. 

Stiles, Gardiner S. and Robert A. Helliwell. 1975. “Frequency-Time Behavior of Artificially 
Stimulated VLF Emissions.” Journal of Geophysical Research 80(4): 608-18. 











Stoupel Eliyahu, J. Abramson, Stanislava Domarkiene, Michael Shimshoni, and Jaqueline Sulkes. 
1997. "Space Proton Flux and the Temporal Distribution of Cardiovascular Deaths." International 
Journal of Biometeorolgoy 40(2): 113-16. 

Stoupel, Eliyahu, Helena Frimer, Zvi Appelman, Ziva Ben-Neriah, Hanna Dar, Moshe D. Fejgin, 
Ruth Gershoni-Baruch, Esther Manor, Gad Barkai, Stavit Shalev, Zully Gelman-Kohan, Orit 
Reish, Dorit Lev, Bella Davidov, Boleslaw Goldman, and Mordechai Shohat. 2005. “Chromosome 
Aberration and Environmental Physical Activity: Down Syndrome and Solar and Cosmic Ray 
Activity, Israel, 1990-2000." International Journal of Biometeorology 50(1): 1-5. 

Stoupel, Eliyahu, Jadviga Petrauskiene, Ramuné Kalédiené, Evgeny Abramson, and Jacqueline 
Sulkes. 1995. “Clinical Cosmobiology: The Lithuanian Study 1990-1992.” International Journal 
of Biometeorology 38(4): 204-8. 

Stoupel, Eliyahu, Ramuné Kalédiené, Jadvyga Petrauskiené, Skirmanté Starkuviené, Evgeny 
Abramson, Peter Israelevich, and Jaqueline Sulkes. 2007. *Clinical Cosmobiology: Distribution of 
Deaths During 180 Months and Cosmophysical Activity. The Lithuanian Study, 1990-2004: The 
Role of Cosmic Rays." Medicina (Kaunas) 43(10): 824-31. 

Sulman, Felix Gad. 1976. Health, Weather and Climate. Basel: Karger. 

. 1980. The Effect of Air Ionization, Electric Fields, Atmospherics and Other Electric 

Phenomena on Man and Animal. Springfield, Ill.: Charles C. Thomas. 

. 1982. Short- and Long-Term Changes in Climate, 2 vols. Boca Raton, FL: CRC Press. 

Szarka, László. 1988. “Geophysical Aspects of Man-Made Electromagnetic Noise in the Earth — A 
Review." Surveys in Geophysics 9: 287-318. 

Tait, Peter Guthrie. 1884. *On Various Suggestions as to the Source of Atmospheric Electricity." 
Nature 29: 517. 

Tatnall, Adrian R. L., J. P. Matthews, Ken Bullough, and Thomas Reeve Kaiser. 1983. *Power-Line 
Harmonic Radiation and the Electron Slot." Space Science Reviews 35(2): 139-73. 

Tomizawa, Ichiro and Takeo Yoshino. 1984. *Power Line Radiation over Northern Europe Observed 
on the Balloon B15-1N." Memoirs of the National Institute of Polar Research, Special Issue 31: 
115-23. 

Tomizawa, Ichiro, Hayato Nishida, and Takeo Yoshino. 1995. *A New-Type Source of Power Line 
Harmonic Radiation Possibly Located on the Kola Peninsula." Journal of Geomagnetism and 
Geoelectricity 47: 213-29. 

Tomizawa, Ichiro, Takeo Yoshino, and Hayato Sasaki. 1985. “Geomagnetic Effect on 
Electromagnetic Field Strength of Power Line Radiation Over Northern Europe Observed on the 
Balloons B45-1N and B45-2N." Memoirs of the National Institute of Polar Research, Special Issue 


36: 181-90. 

Trakhtengerts, Victor Y. and Michael J. Rycroft. 2000. “Whistler-Electron Interactions in the 
Magnetosphere: New Results and Novel Approaches." Journal of Atmospheric and Solar- 
Terrestrial Physics 62: 1719-33. 

Tromp, Solco W. 1963. Medical Biometeorology: Weather, Climate and the Living Organism. 
Amsterdam: Elsevier. 

Trowbridge, John. 1880. “The Earth as a Conductor of Electricity." American Journal of Science, 3rd 
ser., 20: 138-41. 

Vampola, Alfred L. 1987. "Electron Precipitation in the Vicinity of a VLF Transmitter." Journal of 
Geophysical Research 92(A5): 4525-32. 

Vampola, Alfred L. and C. D. Adams. 1988. “Outer Zone Electron Precipitation Produced by a VLF 
Transmitter.” Journal of Geophysical Research 93(A3): 1849-58. 

Van Nostrand’s Engineering Magazine. 1874. “Terrestrial Electricity.” 10: 440-42. 








Villante, U., M. Vellante, A. Piancatelli, A. Di Cienzo, T. L. Zhang, W. Magnes, V. Wesztergom, and 
A. Meloni. 2004. *Some Aspects of Man-made Contamination on ULF Measurements." Annales 
Geophysicae 22: 1335-45. 

Vodyanoy, Vitaly, Oleg Pustovyy, Ludmila Globa, and Iryna Sorokulova. 2015. *Primo-Vascular 
System as Presented by Bong Han Kim.” Evidence-Based Complementary and Alternative 
Medicine, article ID 361974. 

Volland, Hans, ed. 1982. Handbook of Atmospherics, 2 vols. Boca Raton, FL: CRC Press. 

. 1987. “Electromagnetic Coupling between Lower and Upper Atmosphere.” Physica Scripta 

T18: 289-97. 

. 1995. Handbook of Atmospheric Electrodynamics, 2 vols. Boca Raton, FL: CRC Press. 

Watt, A. D. and E. L. Maxwell. 1957. “Characteristics of Atmospheric Noise from 1 to 100 KC.” 
Proceedings of the IRE 45: 787-94. 

Wei, Jianzi, Huijuan Mao, Yu Zhou, Lina Wang, Sheng Liu, and Xueyong Shen. 2012. “Research on 
Nonlinear Feature of Electrical Resistance of Acupuncture Points.” Evidence-Based 
Complementary and Alternative Medicine, article ID 179657. 

Wever, Riitger A. 1973. “Human Circadian Rhythms under the Influence of Weak Electric Fields and 
the Different Aspects of These Studies.” International Journal of Biometeorology 17(3): 227-32. 

. 1974, “ELF-Effects on Human Circadian Rhythms.” In: Michael A. Persinger, ed., ELF and 

VLF Electromagnetic Field Effects (New York: Plenum), pp. 101-44. 

. 1992. “Circadian Rhythmicity of Man under the Influence of Weak Electromagnetic Fields.” 
In: Martin C. Moore-Ede, Scott S. Campbell, and Russel J. Reiter, eds., Electromagnetic Fields 
and Circadian Rhythmicity (Boston: Birkhäuser), pp. 121-39. 

Williams, Earle R. 2009. “The Global Electrical Circuit: A Review.” Atmospheric Research 91(2-4): 
140-52. 

Wu, B., X. Hu, and J. Xu. 1993. “Effect of Increase and Decrease of Measurement Voltage on Skin 
Impedance.” Zhen Ci Yan Jiu (“Acupuncture Research”) 18(2): 104-7 (in Chinese). 

Yearby, Keith H., Andy J. Smith, Thomas Reeve Kaiser, and Ken Bullough. 1983. “Power Line 
Harmonic Radiation in Newfoundland.” Journal of Atmospheric and Terrestrial Physics 45(6): 
409-19. 

Xiang, Zhu Zong, Xu Rui Ming, Xie Jung Guo, and Yu Shu Zhuang. 1984. “Experimental Meridian 
Line of Stomach and Its Low Impedance Nature.” Acupuncture and Electro-therapeutics Research 
9(3): 157-64. 

Zhang, Weibo, Ruimin Xu, and Zongxian Zhu. 1999. “The Influence of Acupuncture on the 
Impedance Measured by Four Electrodes on Meridians.” Acupuncture and Electro-therapeutics 
Research 24(3-4): 181-88. 














Chapter 10 


Aartsma, Thijs J. and Jan Amesz. 1996. “Reaction Center and Antenna Processes in Photosynthesis 
at Low Temperature.” Photosynthesis Research 48: 99-106. 

Abdelmelek, H., A. El-May Ben Hamouda, Mohamed Ben Salem, Jean-Marc Pequignot, and 
Mohsen Sakly. 2003. “Electrical Conduction through Nerve and DNA.” Chinese Journal of 
Physiology 46(3): 137-41. 

Adey, William Ross. 1993. “Whispering Between Cells: Electromagnetic Fields and Regulatory 
Mechanisms in Tissue.” Frontier Perspectives 3(2): 21-25. 

Adler, Alan D. 1970. “Solid State Possibilities of Porphyrin Structures.” Journal of Polymer Science: 
Part C 29: 73-79. 





. 1973. “Porphyrins as Model Systems for Studying Structural Relationships." Annals of the 
New York Academy of Sciences 206: 7-17. 

Adler, Alan D., Veronika Varadi, and Nancy Wilson. 1975. “Porphyrins, Power, and Pollution.” 
Annals of the New York Academy of Sciences 244: 685-94. 

Alley, Michael C., Eva K. Killam, and Gerald L. Fisher. 1981. “The Influence of d-Penicillamine 
Treatment upon Seizure Activity and Trace Metal Status in the Senegalese Baboon, Papio Papio.” 
Journal of Pharmacology and Experimental Therapeutics 217(1): 138-46. 

Andant, Christophe, Hervé Puy, Jean Faivre, and Jean-Charles Deybach. 1998. “Acute Hepatic 
Porphyrias and Primary Liver Cancer.” New England Journal of Medicine 338(25): 1853-54. 

Apeagyei, Eric, Michael S. Bank, and John D. Spengler. 2011. “Distribution of Heavy Metals in 
Road Dust Along an Urban-Rural Gradient in Massachusetts.” Atmospheric Environment 45: 
2310-23. 

Aramaki, Shinji, Ruichi Yoshiyama, Masayoshi Sakai, and Noboru Ono. 2005. “P-19: High 
Performance Porphyrin Semiconductor for Transistor Applications.” SID 05 Digest: 296-99. 

Arnold, William. 1965. “An Electron-Hole Picture of Photosynthesis.” Journal of Physical Chemistry 
69(3): 788-91. 

Arnold, William and Roderick K. Clayton. 1960. “The First Step in Photosynthesis: Evidence for Its 
Electronic Nature.” Proceedings of the National Academy of Sciences 46(6): 769-76. 

Arnold, William and Helen K. Sherwood. 1957. “Are Chloroplasts Semiconductors?” Proceedings of 
the National Academy of Sciences 43(1): 105-14. 

Asbury, Arthur K., Richard L. Sidman, and Merrill K. Wolf. 1966. “Drug-Induced Porphyrin 
Accumulation in the Nervous System.” Neurology 16(3): 299. Abstract. 

Assaf, S. Y. and Shin-Ho Chung. 1984. “Release of Endogenous Zn?* from Brain Tissue during 
Activity.” Nature 308: 734-36. 

Athenstaedt, Herbert. 1974. “Pyroelectric and Piezoelectric Properties of Vertebrates.” Annals of the 
New York Academy of Sciences 238: 68-94. 

Barbeau, André. 1974. “Zinc, Taurine, and Epilepsy.” Archives of Neurology 30: 52-58. 

Bassham, James A. and Melvin Calvin. 1955. Photosynthesis. U.S. Atomic Energy Commission, 
report no. UCRL-2853. 

Baum, Larry, Iris Hiu Shuen Chan, Stanley Kwok-Kuen Cheung, William B. Goggins, Vincent Mok, 
Linda Lam, Vivian Leung, Elsie Hui, Chelsia Ng, Jean Woo, Helen Fung Kum Chiu, Benny 
Chung-Ying Zee, William Cheng, Ming-Houng Chan, Samuel Szeto, Victor Lui, Joshua Tsoh, 
Ashley I. Bush, Christopher Wai Kei Lam, and Timothy Kwok. 2010. “Serum Zinc is Decreased 
in Alzheimer’s Disease and Serum Arsenic Correlates Positively with Cognitive Ability.” 
Biometals 23: 173-79. 

Becker, David Morris and Sidney Kramer. 1977. “The Neurological Manifestations of Porphyria: A 
Review.” Medicine 56(5): 411-23. 

Becker, David Morris and Frederick Wolfgram. 1978. “Porphyrins in Myelin- and Non-myelin 
Fractions of Bovine White Matter.” Journal of Neurochemistry 31: 1109-11. 

Becker, Robert Otto. 1960. “The Bioelectric Field Pattern in the Salamander and Its Simulation by an 
Electronic Analog.” IRE Transactions on Medical Electronics ME-7(3): 202-7. 

. 1961a. “Search for Evidence of Axial Current Flow in Peripheral Nerves of Salamander.” 

Science 134: 101-2. 

. 1961b. “The Bioelectric Factors in Amphibian-Limb Regeneration.” Journal of Bone and 
Joint Surgery 43-A(5): 643-56. 

Becker, Robert O. and Andrew A. Marino. 1982. Electromagnetism and Life. Albany: State 
University of New York Press. 








Becker, Robert O. and Gary Selden. 1985. The Body Electric: Electromagnetism and the Foundation 
of Life. New York: William Morrow. 

Berman, J. and T. Bielicky. 1956. "Einige áufsere Faktoren in der Ätiologie der Porphyria cutanea 
tarda und des Diabetes mellitus mit besonderer Berücksichtigung der syphilitischen Infektion und 
ihrer Behandlung." Dermatologica 113: 78-87. 

Bernal, John Desmond. 1949. *The Physical Basis of Life." Proceedings of the Physical Society, 
Section A, vol. 62, part 9, no. 357A, pp. 537-58. 

Blanshard, T. Paul. 1953. “Isolation from Mammalian Brain of Coproporphyrin II and a Uro-Type 
Porphyrin.” Proceedings of the Society for Experimental Biology and Medicine 83: 512-13. 

Bonkowsky, Herbert L., Donald P. Tschudy, Eugene C. Weinbach, Paul S. Ebert, and Joyce M. 
Doherty. 1975. “Porphyrin Synthesis and Mitochondrial Respiration in Acute Intermittent 
Porphyria: Studies Using Cultured Human Fibroblasts.” Journal of Laboratory and Clinical 
Medicine 85(1): 93-102. 

Bonkowsky, Herbert L. and Wolfgang Schady. 1982. “Neurologic Manifestations of Acute 
Porphyria.” Seminars in Liver Disease 2(2): 108-24. 

Borgens, Richard B. 1982. “What is the Role of Naturally Produced Electric Current in Vertebrate 
Regeneration and Healing?" International Review of Cytology 76: 245-98. 

Borgens, Richard B., Kenneth R. Robinson, Joseph W. Vanable, Jr., and Michael E. McGinnis. 1989. 
Electric Fields in Vertebrate Repair: Natural and Applied Voltages in Vertebrate Regeneration 
and Healing. New York: Alan R. Liss. 

Boyle, Neil J. and Donal P. Murray. 1993. *Unusual Presentation of Porphyria Cutanea Tarda." 
Lancet 2: 186. 

Brodie, Martin J., George G. Thompson, Michael R. Moore, Alistair D. Beattie, and Abraham 
Goldberg. 1977. *Hereditary Coproporphyria." Quarterly Journal of Medicine 46: 229-41. 

Brown, Glenn H. and Jerome J. Wolken. 1979. Liquid Crystals and Biological Structures. New York: 
Academic. 

Burr, Harold Saxton. 1940. “Electrical Correlates of the Menstrual Cycle in Women." Yale Journal of 
Biology and Medicine 12(4): 335-44. 

. 1942. "Electrical Correlates of Growth in Corn Roots." Yale Journal of Biology and 

Medicine 14(6): 581-88. 

. 1943. *An Electrometric Study of Mimosa." Yale Journal of Biology and Medicine 15(6): 

823-29. 

. 1944a. *Moon-Madness." Yale Journal of Biology and Medicine 16(3): 249-56. 

. 1944b. "Potential Gradients in Living Systems and Their Measurements." In: Otto Glasser, 

ed., Medical Physics (Chicago: Yearbook), pp. 1117-21. 

. 1944c. *The Meaning of Bio-electric Potentials." Yale Journal of Biology and Medicine 

16(4): 353-60. 

. 1945a. *Variables in DC Measurement." Yale Journal of Biology and Medicine 17(3): 465- 




















78. 





. 1945b. “Diurnal Potentials in the Maple Tree." Yale Journal of Biology and Medicine 17(6): 
727-34. 

. 1950. “Electro-cyclic Phenomena: Recording Life Dynamics of Oak Trees.” The Yale 
Scientific Magazine, December, pp. 9-10, 32-36, 38, 40. 

. 1956. “Effect of a Severe Storm on Electrical Properties of a Tree and the Earth.” Science 
124: 1204-5. 

. 1972. Blueprint for Immortality: The Electric Patterns of Life. Saffron Walden, England: C. 
W. Daniel. 











Burr, Harold Saxton, R. T. Hill, and Edgar Allen. 1935. *Detection of Ovulation in the Intact Rabbit." 
Proceedings of the Society for Experimental Biology and Medicine 33: 109-11. 

Burr, Harold Saxton and Carl Iver Hovland. 1937. “Bio-Electric Correlates of Development in 
Amblystoma.” Yale Journal of Biology and Medicine 9(6): 541-49. 

Burr, Harold Saxton and Cecil Taverner Lane. 1935. “Electrical Characteristics of Living Systems.” 
Yale Journal of Biology and Medicine 8(1): 31-35. 

Burr, Harold Saxton and Dorothy S. Barton. 1938. “Steady-State Electrical Properties of the Human 
Organism during Sleep.” Yale Journal of Biology and Medicine 10(3): 271-74. 

Burr, Harold Saxton and Luther K. Musselman. 1936. “Bio-electric Phenomena Associated with 
Menstruation.” Yale Journal of Biology and Medicine 9(2): 155-58. 

. 1938. “Bio-Electric Correlates of the Menstrual Cycle in Women." American Journal of 
Obstetrics and Gynecology 35(5): 743-51. 

Burr, Harold Saxton, Luther K. Musselman, Dorothy S. Barton, and Naomi B. Kelly. 1937a. “Bio- 
electric Correlates of Human Ovulation.” Yale Journal of Biology and Medicine 10(2): 155-60. 

. 1937b. “A Bio-electric Record of Human Ovulation.” Science 86: 312. 

Bush, Ashley I. and Rudolph E. Tanzi. 2008. “Therapeutics for Alzheimer’s Disease Based on the 
Metal Hypothesis.” Neurotherapeutics 5(3): 421-32. 

Bush, Ashley I., Warren H. Pettingell, Gerd Multhaup, Marc d. Paradis, Jean-Paul Vonsattel, James F. 
Gusella, Konrad Beyreuther, Colin L. Masters, and Rudolph E. Tanzi. 1994. “Rapid Induction of 
Alzheimer AB Amyloid Formation by Zinc.” Science 265: 1464-67. 

Bylesj6, Ingemar. 2008. “Epidemiological, Clinical and Pathogenetic Studies of Acute Intermittent 
Porphyria.” Medical dissertation, Family Medicine, Dept. of Public Health and Clinical Medicine, 
Umea University, Sweden. 

Calvin, Melvin. 1958. “From Microstructure to Macrostructure and Function in the Photochemical 
Apparatus.” Brookhaven Symposia in Biology 11: 160-79. 

Cardew, Martin H. and Daniel Douglas Eley. 1959. “The Semiconductivity of Organic Substances. 
Part 3 — Haemoglobin and Some Amino Acids.” Discussions of the Faraday Society 27: 115-28. 
Chisolm, J. Julian, Jr. 1992. *The Porphyrias." In: Richard E. Behrman, ed., Nelson Textbook of 

Pediatrics, 14th ed. (Philadelphia: W. B. Saunders), pp. 384-90. 

Choi, D. W., M. Yokoyama, and J. Koh. 1988. *Zinc Neurotoxicity in Cortical Cell Culture." 
Neuroscience 24(1): 67-79. 

Chung, Yong-Gu, Jon A. Schwartz, Raymond E. Sawayo, and Steven L. Jacques. 1997. “Diagnostic 
Potential of Laser-Induced Autofluorescence Emission in Brain Tissue." Journal of Korean 
Medical Science 12: 135-42. 

Clayton, Roderick K. 1962. *Recent Developments in Photosynthesis." Microbiology and Molecular 
Biology Reviews 26 (2 parts 1-2): 151-64. 

Cope, Freeman Widener. 1970. *The Solid-State Physics of Electron and Ion Transport in Biology." 
Advances in Biological and Medical Physics 13: 1-42. 

. 1973. *Supramolecular Biology: A Solid State Physical Approach to Ion and Electron 

Transport." Annals of the New York Academy of Scinces 204: 416-33. 

. 1975. *A Review of the Applications of Solid State Physics Concepts to Biological 

Systems." Journal of Biological Physics 3(1): 1-41. 

. 1979. *Semiconduction as the Mechanism of the Cytochrome Oxidase Reaction. Low 

Activation Energy of Semiconduction Measured for Cytochrome Oxidase Protein. Solid State 

Theory of Cytochrome Oxidase Predicts Observed Kinetic Peculiarities." Physiological Chemistry 

and Physics 11: 261-62. 

















Crane, Eva E. 1950. “Bioelectric Potentials, Their Maintenance and Function.” Progress in 
Biophysics and Biophysical Chemistry 1: 85-136. 

Crile, George Washington. 1926. A Bipolar Theory of Living Processes. New York: Macmillan. 

. 1936. The Phenomena of Life: A Radio-Electric Interpretation. New York: W. W. Norton. 

Crist6vao, Joana S., Renata Santos, and Claudio M. Gomes. 2016. “Metals and Neuronal Metal 
Binding Proteins Implicated in Alzheimer’s Disease.” Oxidative Medicine and Cellular Longevity, 
article ID 9812178. 

Crimlisk, Helen L. 1997. “The Little Imitator — Porphyria: A Neuropsychiatric Disorder.” Journal of 
Neurology, Neurosurgery, and Psychiatry 62(4): 319-28. 

Cuajungco, Math P., Kyle Y. Fagét, Xudong Huang, Rudolph E. Tanzi, and Ashley I. Bush. 2000. 
“Metal Chelation as a Potential Therapy for Alzheimer’s Disease.” Annals of the New York 
Academy of Sciences 920: 292-304. 

Darus, Fairus Muhamad, Rabiatul Adawiyah Nasir, Siti Mariam Sumari, Zitty Sarah Ismail, and Nur 
Aliah Omar. 2012. “Heavy Metals Composition of Indoor Dust in Nursery Schools Building.” 
Procedia — Social and Behavioral Sciences 38: 169-75. 

Dolphin, David, ed. 1978-79. The Porphyrias, 7 vols. New York: Academic. 

Donald, G. F., G. A. Hunter, W. Roman, and Adelheid E. J. Taylor. 1965. “Cutaneous Porphyria: 
Favourable Results in Twelve Cases Treated by Chelation.” American Journal of Dermatology 
8(2): 97-115. 

Dorfman, W. A. 1934. “Electrical Polarity of the Amphibian Egg and Its Reversal Through 
Fertilization.” Protoplasma 21(2): 245-57. 

Downey, David C. 1992. “Fatigue Syndromes: New Thoughts and Reinterpretation of Previous 
Data.” Medical Hypotheses 39: 185-90. 

. 1994. “Hereditary Coproporphyria.” British Journal of Clinical Practice 48(2): 97-99. 

Durkó, Irene, Josef Engelhardt, Janos Szilard, Krisztina Baraczka, and Gyorgy Gal. 1984. “The 
Effect of Haemodialysis on the Excretion of the Mauve Factor in Schizophrenia.” Journal of 
Orthomolecular Psychiatry 13(4): 222-32. 

Eilenberg, M. D. and B. A. Scobie. 1960. “Prolonged Neuropsychiatric Disability and 
Cardiomyopathy in Acute Intermittent Porphyria.” British Medical Journal 1: 858-59. 

Elbagermi, M. A., H. G. M. Edwards, and A. I. Alajtal. 2013. “Monitoring of Heavy Metals Content 
in Soil Collected from City Centre and Industrial Areas of Misurata, Libya.” International Journal 
of Analytical Chemistry, article ID 312581. 

Eley, Daniel Douglas and D. I. Spivey. 1960. “The Semiconductivity of Organic Substances. Part 6 — 
A Range of Proteins.” Transactions of the Faraday Society 56: 1432-42. 

1962. “The Semiconductivity of Organic Substances. Part 8. Porphyrins and 
Dipyrromethenes.” Transactions of the Faraday Society 58: 405-10. 

Ellefson, Ralph D. and R. E. Ford. 1996. “The Porphyrias: Characteristics and Laboratory Tests.” 
1996. Regulatory Toxicology and Pharmacology 24: $119-S125. 

Felitsyn, Natalia, Colin McLeod, Albert L. Shroads, Peter W. Stacpoole, and Lucia Notterpek. 2008. 
*The Heme Precursor Delta-Aminolevulinate Blocks Peripheral Myelin Formation." Journal of 
Neurochemistry 106(5): 2068-79. 

Fisch, Michael R. 2004. Liquid Crystals, Laptops and Life. Singapore: World Scientific. 

Fishbein, Alf, John C. Thornton, Ruth Lilis, José A. Valciukas, Jonine Bernstein, and Irving J. 
Selikoff. 1980. “Zinc Protoporphyrin, Blood Lead and Clinical Symptoms in Two Occupational 
Groups with Low-Level Exposure to Lead.” American Journal of Industrial Medicine 1: 391-99. 

Flinn, J. M., D. Hunter, D. H. Linkous, A. Lanzirotti, L. N. Smith, J. Brightwell, and B. F. Jones. 
2005. “Enhanced Zinc Consumption Causes Memory Deficits and Increased Brain Levels of 











Zinc." Physiology and Behavior 83: 793-803. 

Frederickson, Christopher J., Wolfgang Maret, and Math P. Cuajungco. 2004. *Zinc and Excitotoxic 
Brain Injury: A New Model." Neuroscientist 10(1): 19-25. 

Frey, Allan H. 1971. “Biological Function as Influenced by Low Power Modulated RF Energy.” 
IEEE Transactions on Microwave Theory and Techniques MTT-19(2): 153-64. 

. 1988. “Evolution and Results of Biological Research with Low-Intensity Nonionizing 
Radiation." In: Andrew A. Marino, ed., Modern Bioelectricity (New York: Marcel Dekker), pp. 
785-837. 

Fukuda, Eiichi. 1974. “Piezoelectic Properties of Organic Polymers.” Annals of the New York 
Academy of Sciences 238: 7-25. 

Garrett, C. G. B. 1959. “Organic Semiconductors.” In: N. B. Hannay, ed., Semiconductors (New 
York: Reinhold Publishing Corp.), pp. 634-75. 

Gibney, G. N., I. H. Jones, and J. H. Meek. 1972. “Schizophrenia in association with erythropoietic 
protoporphyria — report of a case.” British Journal of Psychiatry 121: 79-81. 

Gilyarovskiy, V. A., I. M. Liventsev, Yu. Ye. Segal’, and Z. A. Kirillova. 1958. Electroson (kliniko- 
fiziologicheskoye issledovaniye). Moscow. In English Translation as Electric Sleep (A Clinical- 
Physiological Investigation). JPRS 2278. 

Goldberg, Abraham. 1959. “Acute Intermittent Porphyria: A Study of 50 Cases.” Quarterly Journal 
of Medicine 28: 183-209. 

Goldberg, Abraham and Michael R. Moore, eds. 1980. The Porphyrias. Vol. 9, no. 2 of Clinics in 
Haematology. 

Granick, S. and H. Gilder. 1945. “The Structure, Function and Inhibitory Action of Porphyrins.” 
Science 101: 540. 

Hagemann, Ole and Frederik Krebs. 2013. “Syntheses of Asymmetric Porphyrins for Photovoltaics.” 
Polymer Solar Cell Initiative, Danish Polymer Centre, Rise National Laboratory, Roskilde, 
Denmark. www.risoe.dk/solarcells. 

Halpern, R. M. and H. G. Copsey. 1946. *Acute Idiopathic Porphyria; Report of a Case." Medical 
Clinics of North America 30: 385-96. 

Hamadani, Jena D., George J. Fuchs, Saskia J. M. Osendarp, F. Khatun, Syed N. Huda, and Sally M. 
Grantham-McGregor. 2001. *Randomized Controlled Trial of the Effect of Zinc Supplementation 
on the Mental Development of Bangladeshi Infants." American Journal of Clinical Nutrition 74: 
381-86. 

Hamadani, Jena D, George J. Fuchs, Saskia J. M. Osendarp, Syed N. Huda, and Sally M. Grantham- 
McGregor. 2002. *Zinc Supplementation During Pregnancy and Effects on Mental Development 
and Behaviour of Infants: A Follow-up Study." Lancet 360: 290-94. 

Hancock, Sara M., David I. Finkelstein, and Paul A. Adlard. 2014. *Glia and Zinc in Ageing and 
Alzheimer's Disease: A Mechanism for Cognitive Decline?" Frontiers in Aging Neuroscience 6: 
137. 

Hardell, Lennart, Nils-Olof Bengtsson, U. Jonsson, S. Eriksson, and Lars-Gunnar Larsson. 1984. 
* Aetiological Aspects on Primary Liver Cancer with Special Regard to Alcohol, Organic Solvents 
and Acute Intermittent Porphyria — an Epidemiological Investigation." British Journal of Cancer 
50: 389-97. 

Hargittai, Pál T. and Edward M. Lieberman. 1991. *Axon-Glia Interactions in the Crayfish: Glial Cell 
Oxygen Consumption is Tightly Coupled to Axon Metabolism." Glia 4(4): 417-23. 

Hashim, Zawiah, Leslie Woodhouse, and Janet C. King. 1996. “Interindividual Variation in 
Circulating Zinc Concentrations among Healthy Adult Men and Women.” International Journal 
of Food Sciences and Nutrition 47: 393-90. 





Hengstman, G. H., K. F. de Laat, B. Jacobs, and B. G. van Engelen. 2009. *Sensorimotor Axonal 
Polyneuropathy without Hepatic Failure in Erythropoietic Protoporphyria." Journal of Clinical 
Neuromuscular Disease 11(2):72-76. 

Herrick, Ariane L., B. Miles Fisher, Michael R. Moore, Sylvia Cathcart, Kenneth E. L. McColl, and 
Abraham Goldberg. 1990. *Elevation of Blood Lactate and Pyruvate Levels in Acute Intermittent 
Porphyria — A Reflection of Haem Deficiency?" Clinica Chimica Acta 190(3): 157-62. 

Ho, Mae-Wan. 1993. The Rainbow and the Worm: The Physics of Organisms. Singapore: World 
Scientific. 

. 1996. “Bioenergetics and Biocommunication." In: R. Cuthbertson, M. Holcombe, and R. 

Paton, eds., Computation in Cellular and Molecular Biological Systems (Singapore: World 

Scientific), pp. 251-64. 

. 2003. “From ‘Molecular Machines’ to Coherent Organisms.” In: Francesco Musumeci, 

Larissa S. Brizhik, and Mae-Wan Ho, eds., Energy and Information Transfer in Biological Systems 

(Singapore: World Scientific), pp. 63-81. 

. 2008. The Rainbow and the Worm: The Physics of Organisms, 3rd ed. Singapore: World 
Scientific. 

Ho, Mae-Wan, Julian Haffegee, Richard Newton, Yu-Ming Zhou, John S. Bolton, and Stephen Ross. 
1996. “Organisms as Polyphasic Liquid Crystals.” Bioelectrochemistry and Bioenergetics 41: 81- 
91. 

Hoffer, A. and H. Osmond. 1963. “Malvaria: A New Psychiatric Disease.” Acta Psychiatrica 
Scandinavica 39: 335-66. 

Holtmann, W. and Ch. Xenakis. 1978. “Neurologische und psychiatrische Störungen bei Porphyria 
cutanea tarda.” Nervenarzt 49: 282-84. 

. 1979. “Stellungnahme zum Kommentar von C.A. Pierach über die Arbeit von W. Holtman 
und Ch. Xenakis: ‘Neurologische und psychiatrische Störungen bei Porphyria cutanea tarda.” 
Nervenarzt 50: 542-43. 

Hunt, Tam. 2013. “The Rainbow and the Worm: Establishing a New Physics of Life.” 
Communicative and Integrative Biology 6(2): e23149. 

Huszák, I., Irene Durkó, and K. Karsai. 1972. “Experimental Data to the Pathogenesis of 
Cryptopyrrole Excretion in Schizophrenia, I.” Acta Physiologica Academiae Scientiarum 
Hungaricae 42(1): 79-86. 

Ichimura, Shoji. 1960. “The Photoconductivity of Chloroplasts and the Far Red Light Effect.” 
Biophysical Journal 1: 99-109. 

Irvine, Donald G. and Lennart Wetterberg. 1972. “Kryptopyrrole-like Sybstance in Acute Intermittent 
Porphyria.” Lancet 2: 1201. 

Jerman, Igor. 1998. “Electromagnetic Origin of Life.” Electro- and Magnetobiology 17(3): 401-13. 

Johnson, Phyllis E., Curtiss D. Hunt, David B. Milne, and Loanne K. Mullen. 1993. “Homeostatic 
Control of Zinc Metabolism in Men: Zinc Excretion and Balance in Men Fed Diets Low in Zinc.” 
American Journal of Clinical Nutrition 57: 557-65. 

Katz, E. 1949. “Chlorophyll Fluorescence as an Energy Flowmeter for Photosynthesis.” In: James 
Franck and Walter E. Loomis, eds., Photosynthesis in Plants (Ames, IA: Iowa State College 
Press), pp. 287-92. 

Kauppinen, Raili and Pertti Mustajoki. 1988. “Acute Hepatic Porphyria and Hepatocellular 
Carcinoma.” British Journal of Cancer 57: 117-20. 

Kim, Hooi-Sung, Chun-Ho Kim, Chang-Sik Ha, and Jin-Kook Lee. 2001. “Organic Solar Cell 
Devices Based on PVK/Porphyrin System.” Synthetic Metals 117(1-3): 289-91. 














King, Janet C., David M. Shames, and Leslie R. Woodhouse. 2000. *Zinc Homeostasis in Humans." 
Journal of Nutrition 130: 13608-13668. 

Klüver, Heinrich. 1944a. *On Naturally Occurring Porphyrins in the Central Nervous System." 
Science 99: 482-84. 

. 1944b. *Porphyrins, the Nervous System, and Behavior." Journal of Psychiatry 17: 209-27. 

. 1967. *Functional Differences between the Occipital and Temporal Lobes." In: Lloyd A. 
Jeffress, ed., Cerebral Mechanisms in Behavior — the Hixon Symposium (New York: Hafner), pp. 
147-82. 

Kohl, Peter. 2003. *Heterogeneous Cell Coupling in the Heart: An Electrophysiological Role for 
Fibroblasts." Circulation Research 93: 381-83. 

Kordaé, Vaclav, Michaela Kozakova, and Pavel Martásek. 1989. *Changes of Myocardial Functions 
in Acute Hepatic Porphyrias: Role of Heme Arginate Administration." Annals of Medicine 21(4): 
273-76. 

Krijt, Jan, Pavla Stranska, Pavel Maruna, Martin Vokurka, and Jaroslav Sanitrak. 1997. *Herbicide- 
Induced Experimental Variegate Porphyria in Mice: Tissue Porphyrinogen Accumulation and 
Response to Porphyrogenic Drugs." Canadian Journal of Physiology and Pharmacology 75: 
1181-87. 

Kuffler, Stephen W. and David D. Potter. 1964. *Glia in the Leech Central Nervous System: 
Physiological Properties and Neuron-Glia Relationship." Journal of Neurophysiology 27: 290- 
320. 

Kulvietis, Vytautas, Eugenijus Zakarevičius, Juozas Lapienis, Grazina Grazeliené, Violeta 
�algevičienė, and Ričardas Rotomskis. 2007. “Accumulation of Exogenous Sensitizers in Rat 
Brain.” Acta Medica Lituanica 14(3): 219-24. 

Labbé, Robert F. 1967. “Metabolic Anomalies in Porphyria: The Result of Impaired Biological 
Oxidation?” Lancet 1: 1361-64. 

Lagerwerff, J. V. and A. W. Specht. 1970. “Contamination of Roadside Soil and Vegetation with 
Cadmium, Nickel, Lead, and Zinc.” Environmental Science and Technology 4(7): 583-86. 

Labbé, Robert F., Hendrik J. Vreman, and David K. Stevenson. 1999. “Zinc Protoporphyrin: A 
Metabolite with a Mission.” Clinical Chemistry 45(12): 2060-72. 

Laiwah, A. C. Yeung, Abraham Goldberg, and Michael R. Moore. 1983. “Pathogenesis and 
Treatment of Acute Intermittent Porphyria: Discussion Paper.” Journal of the Royal Society of 
Medicine 76: 386-92. 

Laiwah, A. C. Yeung, Graeme J. A. Macphee, P. Boyle, Michael R. Moore, and Abraham Goldberg. 
1985. “Autonomic Neuropathy in Acute Intermittent Porphyria.” Journal of Neurology, 
Neurosurgery, and Psychiatry 48: 1025-30. 

Lee, G. Richard. 1993. “Porphyria.” In: G. Richard Lee and Maxwell Myer Wintrobe, eds., 
Wintrobe’s Clinical Hematology, 9th ed. (Philadelphia: Lea & Febiger), pp. 1272-97.. 

Lehmann, Otto. 1908. Flüssige Kristalle und die Theorien des Lebens. Leipzig: Johann Ambrosius 
Barth. 

Li, Xiaoyan, Shuting Zhang, and Mei Yang. 2014. “Accumulation and Risk Assessment of Heavy 
Metals in Dust in Main Living Areas of Guiyang City, Southwest China.” Chinese Journal of 
Geochemistry 33(3): 272-76. 

Libet, Benjamin and Ralph W. Gerard. 1941. “Steady Potential Fields and Neurone Activity.” 
Journal of Neurophysiology 4(6): 438-55. 

Linet, Martha S., Gloria Gridley, Olof Nyrén, Lene Mellemkjaer, Jørgen H. Olsen, Shannon Keehn, 
Hans-Olov Admi, and Joseph F. Fraumeni, Jr. 1999. “Primary Liver Cancer, Other Malignancies, 








and Mortality Risks following Porphyria: A Cohort Study in Denmark and Sweden." American 
Journal of Epidemiology 149(11): 1010-15. 

Ling, Gilbert Ning. 1962. A Physical Theory of the Living State: the Association-Induction 
Hypothesis. Waltham, MA: Blaisdell. 

. 1965. “The Physical State of Water in Living Cell and Model Systems." Annals of the New 

York Academy of Sciences 125: 401-17. 

. 1992. A Revolution in the Physiology of the Living Cell. Malabar, FL: Krieger. 

. 1994. *The New Cell Physiology." Physiological Chemistry and Physics and Medical NMR 

26(2): 121-203. 

. 2001. Life at the Cell and Below-Cell Level: The Hidden History of a Fundamental 
Revolution in Biology. Melville, NY: Pacific Press. 

Ling, Gilbert Ning, Christopher Miller, and Margaret M. Ochselfeld. 1973. “The Physical State of 
Solutes and Water in Living Cells According to the Association-Induction Hypothesis.” Annals of 
the New York Academy of Sciences 204: 6-50. 

Livshits, V. A. and L. A. Blyumenfel’d. 1968. “Semiconductor Properties of Porphyrins.” Journal of 
Structural Chemistry 8(3): 383-88. 

Lund, Elmer J. 1947. Bioelectric Fields and Growth. Austin: University of Texas Press. 

Macy, Judy A., John Gilroy, and Jane C. Perrin. 1991. “Hereditary Coproporphyria: An Imitator of 
Multiple Sclerosis.” Archives of Physical Medicine and Rehabilitation 72(9): 703-4. 

Markovitz, Meyer. 1954. “Acute Intermittent Porphyria: A Report of Five Cases and a Review of the 
Literature.” Annals of Internal Medicine 41(6): 1170-88. 

Marshall, Clyde and Ralph G. Meader. 1937. “Studies on the Electrical Potentials of Living 
Organisms: I. Base-lines and Strain Differences in Mice.” Yale Journal of Biology and Medicine 
10(1): 65-78. 

. 1938. "Studies in the Electrical Potentials of Living Organisms: HI. Effects of Elevated 
Body Temperatures in Normal Unanesthetized Mice.” Yale Journal of Biology and Medicine 
11(2): 123-26. 

Mason, Verne R., Cyril Courville and Eugene Ziskind. 1933. “The Porphyrins in Human Disease.” 
Medicine 12(4): 355-438. 

Maxwell, Kate and Giles N. Johnson. 2000. *Chloropyll Fluorescence — a Practical Guide." Journal 
of Experimental Botany 51: 659-68. 

McCabe, Donald Lee. 1983. *Kryptopyrroles." Journal of Orthomolecular Psychiatry 12(1): 2-18. 

McGinnis, Woody R, Tapan Audhya, William J. Walsh, James A. Jackson, John McLaren-Howard, 
Allen Lewis, Peter H. Lauda, Douglas M. Bibus, Frances Jurnak, Roman Lietha, and Abram 
Hoffer. 2008a. *Discerning the Mauve Factor, Part 1." Alternative Therapies 14(2): 40-50. 

. 2008b. *Discerning the Mauve Factor, Part 2." Alternative Therapies 14(3): 50-56. 

McLachlan, D. R. Crapper, A. J. Dalton, T. P. A. Kruck, M. Y. Bell, W. L. Smith, W. Kalow, and D. 
F. Andrews. 1991. “Intramuscular Desferrioxamine in Patients with Alzheimer's Disease.” Lancet 
1: 1304-8. 

Meader, Ralph G. and Clyde Marshall. 1938. “Studies on the Electrical Potentials of Living 
Organisms: II. Effects of Low Temperatures in Normal Unanesthetized Mice.” Yale Journal of 
Biology and Medicine 10(4): 365-78. 

Mikirova, Nina. 2015. “Clinical Test of Pyrroles: Usefulness and Association with Other 
Biochemical Markers.” Clinical Medical Reviews and Case Reports 2: 027. 

Milne, David B., Janet R. Mahalko, and Harold H. Sandstead. 1983. “Effect of Dietary Zinc on 
Whole Body Surface Loss of Zinc: Impact on Estimation of Zinc Retention by Balance Method.” 
American Journal of Clinical Nutrition 38: 181-86. 




















Moore, Michael R. 1990. *The Pathogenesis of Acute Porphyria." Molecular Aspects of Medicine 
11(1-2): 49-57. 

Moore, Michael R., Kenneth E. L. McColl, Claude Rimington, and Abraham Goldberg. 1987. 
Disorders of Porphyrin Metabolism. New York: Plenum. 

Morelli, Alessandro, Silvia Ravera, and Isabella Panfoli. 2011. *Hypothesis of an Energetic Function 
for Myelin." Cell Biochemistry and Biophysics 61: 179-87. 

Morelli, Alessandro, Silvia Ravera, Daniela Calzia, and Isabella Panfoli. 2012. *Impairment of Heme 
Synthesis in Myelin as Potential Trigger of Multiple Sclerosis." Medical Hypotheses 78: 707-10. 
Morton, William E. 1995. “Redefinition of Abnormal Susceptibility to Environmental Chemicals.” 
In: Barry L. Johnson, Charles Xintaras, and John S. Andrews, Jr., eds., Hazardous Waste Impacts 

on Human and Ecological Health (Princeton, NJ: Princeton Scientific), pp. 320-27. 

1998. “Chemical-Induced Porphyrinopathy and Its Relation to Multiple Chemical 

Sensitivity (MCS).” Paper presented at Gordon Research Conference on Chemistry and Biology 

of Tetrapyrroles, Salve Regina University, Newport, RI, July 13. 

. 2000a. “The Nature of Harderoporphyria?” Paper presented at Gordon Research Conference 

on the Chemistry and Biology of Tetrapyrroles, Salve Regina University, Newport, RI, July 17. 

2000b. “Fecal Porphyrin Measurements are Crucial for Adequate Screening for 

Porphyrinopathy.” Archives of Dermatology 136: 554. 

. 2001. *Porphyrinopathy Can Explain Symptoms of Multiple Chemical Sensitivity (MCS).” 
Paper presented at MCS 2001 Conference, Santa Fe, NM, August 14. 

Nazzal, Y., Habes Ghrefat, and Marc A. Rosen. 2014. “Heavy Metal Contamination of Roadside 
Dusts: A Case Study for Selected Highways of the Greater Toronto Area, Canada Involving 
Multivariate Geostatistics.” Research Journal of Environmental Sciences 8(5): 259-73. 

Nordenstrém, Bjorn E. W. 1983. Biologically Closed Electric Circuits. Clinical, Experimental and 
Theoretical Evidence for an Additional Circulatory System. Stockholm: Nordic Medical. 

Northrop, Filmer S. C. and Harold Saxton Burr. 1937. “Experimental Findings Concerning the 
Electro-dynamic Theory of Life and an Analysis of Their Physical Meaning.” Growth 1(1): 78-88. 

Ovchinnikova, Kate and Gerald H. Pollack. 2009. “Can Water Store Charge?” Langmuir 25(1): 542- 
47. 

Painter, Joseph T. and Edwin J. Morrow. 1959. “Porphyria: Its Manifestations and Treatment with 
Chelating Agents.” Texas State Journal of Medicine 55(10): 811-18. 

Pei, Yinquan, Dayao Zhao, Jianyi Huang, and Longguan Cao. 1983. “Zinc-induced Seizures: A New 
Experimental Model of Epilepsy.” Epilepsia 24: 169-76. 

Perlroth, Mark G. 1988. “The Porphyrias.” In: Edward Rubenstein and Daniel D. Federman, eds., 
Scientific American Medicine (New York: Scientific American), 9V: 1-12. 

Peters, Henry A. 1961. “Trace Minerals, Chelating Agents and the Porphyrias.” Federation 
Proceedings 20 (3 part 2) (suppl. 10): 227-34. 

. 1993. “Acute Hepatic Porphyria.” In: Richard T. Johnson and John W. Griffin, eds., Current 
Therapy in Neurologic Disease, 4th ed. (St. Louis: B. C. Decker), pp. 317-22. 

Peters, Henry A., Derek J. Cripps, Ayhan Gécmen, George Bryan, Erdogan Ertürk, and Carl Morris. 
1987. “Turkish Epidemic Hexachlorobenzene Porphyria.” Annals of the New York Academy of 
Sciences 514: 183-89. 

Peters, Henry A., Derek J. Cripps, and Hans H. Reese. 1974. “Porphyria: Theories of Etiology and 
Treatment.” International Review of Neurobiology 16: 301-55. 

Peters, Henry A., Peter L. Eichman, and Hans H. Reese. 1958. “Therapy of Acute, Chronic and 
Mixed Hepatic Porphyria Patients with Chelating Agents.” Neurology 8: 621-32. 

















Peters, Henry A., Sherwyn Woods, Peter L. Eichman, and Hans H. Reese. 1957. “The Treatment of 
Acute Porphyria with Chelating Agents: A Report of 21 Cases.” Annals of Internal Medicine 
47(5): 889-99. 

Pethig, Ronald. 1979. Dielectric and Electronic Properties of Biological Materials. Chichester, UK: 
John Wiley & Sons. 

Petrov, Alexander G. 1999. The Lyotropic State of Matter: Molecular Physics and Living Matter 
Physics. Amsterdam: Gordon & Breach. 

Petrova, E. A. and N. P. Kuznetsova. 1972. “The Conditions of the Autonomic Nervous System in 
Patients with Porphyria Cutanea Tarda.” Vestnik Dermatologii Venerologii 46: 31-34 (in Russian). 

Pfeiffer, Carl Claus. 1975. “Mauve-factor Patients.” In: Pfeiffer, Mental and Elemental Nutrients: A 
Physician’s Guide to Nutrition and Health Care (New Canaan, CT: Keats), pp. 402-8. 

Pierach, Claus A. 1979. “Kommentar zur Arbeit von W. Holtman und Ch. Xenakis: “Neurologische 
and psychiatrische Stórungen bei Porphyria cutanea tarda.” Nervenarzt 50: 540-1. 

Pohl, Herbert A., Peter R. C. Gascoyne, and Albert Szent-Gyórgyi. 1977. “Electron Spin Resonance 
Absorption of Tissue Constituents.” Proceedings of the National Academy of Sciences 74(4): 
1558-60. 

Pollack, Gerald H. 2001. Cells, Gels, and the Engines of Life. Seattle: Ebner & Sons. 

. 2006. *Cells, Gels, and Mechanics." In: Mohammad R. K. Mofrad and Roger D. Kamm, 

eds., Cytoskeletal Mechanics (New York: Cambridge University Press), pp. 129-51. 

. 2010. *Water, Energy and Life: Fresh Views from the Water's Edge." International Journal 

of Design & Nature and Ecodynamics 5(1): 27-29. 

. 2013. The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor. Seattle: Ebner & Sons. 
Pollack, Gerald H., Xavier Figueroa, and Qing Zhao. 2009. “Molecules, Water, and Radiant Energy: 
New Clues for the Origin of Life.” International Journal of Molecular Sciences 10(4): 1419-29. 
Popp, Friz Albert, Günther Becker, Herbert L. König, and Walter Peschka, eds. 1979. 

Electromagnetic Bio-Information. München: Urban & Schwarzenberg. 

Popp, Fritz Albert, Ulrich Warnke, Herbert L. Konig, and Walter Peschka, eds. 1989. 
Electromagnetic Bio-Information, 2nd ed. München: Urban & Schwarzenberg. 

Popp, Fritz Albert and Lev Beloussov, eds. 2003. Integrative Biophysics. Dordrecht: Kluwer. 

Que, Emily L., Dylan W. Domaille, and Christopher J. Chang. “Metals in Neurobiology: Probing 
Their Chemistry and Biology with Molecular Imaging.” Chemical Reviews 108: 1517-49. 

Randolph, Theron G. 1987. Environmental Medicine — Beginnings and Bibliographies of Clinical 
Ecology. Fort Collins, CO: Clinical Ecology Publications. 

Ravera, Silvia, Martina Bartolucci, Enrico Adriano, Patrizia Garbati, Sara Ferrando, Paola Ramoino, 
Daniela Calzia, Alessandro Morelli, Maurizio Balestrino, and Isabella Panfoli. 2015. *Support of 
Nerve Conduction by Respiring Myelin Sheath: Role of Connexons." Molecular Neurobiology 
[Epub ahead of print]. 

Ravera, Silvia, Martina Bartolucci, Daniela Calzia, Maria Grazia Aluigi, Paola Ramoino, Alessandro 
Morelli, and Isabella Panfoli. 2013. “Tricarboxylic Acid Cycle-Sustained Oxidative 
Phosphorylation in Isolated Myelin Vesicles.” Biochimie 95: 1991-98. 

Ravera, Silvia, Lucilla Nobbio, Davide Visigalli, Martina Bartolucci, Daniela Calzia, Fulvia Fiorese, 
Gianluigi Mancardi, Angelo Schenone, Alessandro Morelli, and Isabella Panfoli. 2013. 
“Oxidative Phosphorylation in Sciatic Nerve Myelin and Its Impairment in a Model of 
Dysmyelinating Peripheral Neuropathy.” Journal of Neurochemistry 126: 82-92. 

Ravera, Silvia and Isabella Panfoli. 2015. “Role of Myelin Sheat Energy Metabolism in 
Neurodegenerative Diseases.” Neural Regeneration Research 10(10): 1570-71. 











Ravera, Silvia, Isabella Panfoli, Daniela Calzia, Maria Grazia Aluigi, Paolo Bianchini, Alberto 
Diaspro, Gianluigi Mancardi, and Alessandro Morelli. 2009. “Evidence for Aerobic ATP 
Synthesis in Isolated Myelin Vesicles.” International Journal of Biochemistry and Cell Biology 
41: 1581-91. 

Ravitz, Leonard J. 1953. “Electrodynamic Field Theory in Psychiatry.” Southern Medical Journal 
46(7): 650-60. 

. 1962. “History, Measurement, and Applicability of Periodic Changes in the Electromagnetic 
Field in Health and Disease.” Annals of the New York Academy of Sciences 98: 1144-1201. 

Reboul, J., H. B. Friedgood, and H. Davis. 1937. “Electrical Detection of Ovulation.” American 
Journal of Physiology 119: 387. 

Regland, B., W. Lehmann, I. Abedini, K. Blennow, M. Jonsson, I. Karlsson, M. Sjégren, A. Wallin, 
M. Xilinas, and C.-G. Gottfries. 2001. “Treatment of Alzheimer’s Disease with Clioquinol.” 
Dementia and Geriatric Cognitive Disorders 12(6): 408-14. 

Religa, D., D. Strozyk, Robert A. Cherny, Irene Volitakis, V. Haroutunian, B. Winblad, J. Naslund, 
and Ashley I. Bush. 2006. *Elevated Cortical Zinc in Alzheimer Disease." Neurology 67: 69-75. 
Riccio, P., S. Giovannelli, A. Bobba, E. Romito, A. Fasano, T. Bleve-Zacheo, R. Favilla, E. 
Quagliarello, and P. Cavatorta. 1995. “Specificity of Zinc Binding to Myelin Basic Protein.” 

Neurochemical Research 20(9): 1107-13. 

Ridley, Alan. 1969. “The Neuropathy of Acute Intermittent Porphyria.” Quarterly Journal of 
Medicine 38: 307-33. 

. 1975. “Porphyric Neuropathy.” In: Peter James Dyck, P. K. Thomas, and Edward H. 
Lambert, eds., Peripheral Neuropathy (Philadelphia: W. B. Saunders), pp. 942-55. 

Ritchie, Craig W., Ashley I. Bush, Andrew Mackinnon, Steve Macfarlane, Maree Mastwyk, Lachlan 
MacGregor, Lyn Kiers, Robert Cherny, Qiao-Xin Li, Amanda Tammer, Darryl Carrington, 
Christine Mavros, Irene Volitakis, Michel Xilinas, David Ames, Stephen Davis, Konrad 
Beyreuther, Rudolph E. Tanzi, and Colin L. Masters. 2003. “Metal-Protein Attenuation with 
Iodochlorhydroxyquin (Clioquinol) Targeting Aß Amyloid Deposition and Toxicity in Alzheimer 
Disease.” Archives of Neurology 60: 1685-91. 

Rivera, Hiram, J. Kent Pollock, and Herbert A. Pohl. 1985. “The AC Field Patterns About Living 
Cells.” Cell Biophysics 7: 43-55. 

Rock, John, Jean Reboul, and Harold C. Wiggers. 1937. “The Detection and Measurement of the 
Electrical Concomitant of Human Ovulation by Use of the Vacuum-Tube Potentiometer.” New 
England Journal of Medicine 217(17): 654-58. 

Roman, W. 1969. “Zinc in Porphyria.” American Journal of Clinical Nutrition 22(10): 1290-1303. 

Rook, Arthur and Robert H. Champion. 1960. “Porphyria Cutanea Tarda and Diabetes.” British 
Medical Journal 1: 860-61. 

Rose, Florence C. and Sylvan Meryl Rose. 1965. “The Role of Normal Epidermis in Recovery of 
Regenerative Ability in Xrayed Limbs of Triturus.” Growth 29: 361-93. 

Rose, Sylvan Meryl. 1970. Regeneration. New York: Appleton-Century-Crofts. 

. 1978. “Regeneration in Denervated Limbs of Salamanders After Induction by Applied 
Direct Currents.” Bioelectrochemistry and Bioenergetics 5: 88-96. 

Rose, Sylvan Meryl and Florence C. Rose. 1974. “Electrical Studies on Normally Regenerating, on 
X-Rayed, and on Denervated Limb Stumps of Triturus.” Growth 38: 363-80. 

Ross, Stephen, Richard Newton, Yu-Ming Zhou, Julian Haffegee, Mae-Wan Ho, John P. Bolton, and 
David Knight. 1997. “Quantitative Image Analysis of Birefringent Biological Material.” Journal 
of Microscopy 187(1): 62-67. 











Runge, Walter and Cecil J. Watson. 1962. *Experimental Production of Skin Lesions in Human 
Cutaneous Porphyria." Proceedings of the Society for Experimental Biology and Medicine 109: 
809-11. 

Saint, Eric G., D. Curnow, R. Paton, and John B. Stokes. 1954. *Diagnosis of Acute Porphyria." 
British Medical Journal 1: 1182-84. 

Sedlak, Wtodzimierz. 1970. “Biofizyczne aspekty ekologii” (“Biophysical Aspects of Ecology”). 
Wiadomości Ekologiczne 16(1): 43-53. 

. 1973. “Ochrona środowiska człowieka w zakresie niejonizującego promieniowania.” 

Wiadomości Ekologiczne 19(3): 223-37. 

. 1979. Bioelektronika: 1967-1977. Warsaw: PAX. 

. 1980. Bioelektronika — $rodowisko — Czlowiek (*Bioelectronics — Environment — Man"). 

Wrocław: Zakład Narodowy Imienia Ossolińskich. 

. 1984. Postępy fizyki życia (“Progress in the Physics of Life”) Warsaw: PAX. 

Silbergeld, Ellen K. and Bruce A. Fowler, eds. 1987. Mechanisms of Chemical-Induced 
Porphyrinopathies. Vol. 514 of Annals of the New York Academy of Sciences. 

Soldán, M. Mateo Paz and Istvan Pirko. 2012. “Biogenesis and Significance of Central Nervous 
System Myelin.” Seminars in Neurology 32(1): 9-14. 

Solomon, Harvey M. and Frank H. J. Figge. 1958. “Occurrence of Porphyrins in Peripheral Nerves.” 
Proceedings of the Society for Experimental Biology and Medicine 97: 329-30. 

Stein, Jeffrey A. and Donald P. Tschudy. 1970. “Acute Intermittent Porphyria: A Clinical and 
Biochemical Study of 46 Patients.” Medicine 49(1): 1-16. 

Sterling, Kenneth, Marvin Silver, and Henry T. Ricketts. 1949. “Development of Porphyria in 
Diabetes Mellitus.” Archives of Internal Medicine 84: 965-75. 

Szent-Györgyi, Albert. 1941. “Towards a New Biochemistry.” Science 93: 609-11. 

. 1957. Bioenergetics. New York: Academic. 

. 1960. Introduction to a Submolecular Biology. New York: Academic. 

. 1968. Bioelectronics: A Study in Cellular Regulations, Defense, and Cancer. New York: 

Academic. 

. 1969. *Molecules, Electrons and Biology." Transactions of the New York Academy of 

Sciences, 2nd ser., 31(4): 334-40. 

. 1971. “Biology and Pathology of Water.” Perspectives in Biology and Medicine 14(2): 239- 





























49. 





. 1972. The Living State: With Observations on Cancer. New York: Academic. 

. 1976. Electronic Biology and Cancer. New York: Marcel Dekker. 

. 1977. *The Living State and Cancer." Proceedings of the National Academy of Sciences 

74(7): 2844-47. 

. 1978. The Living State and Cancer. New York: Marcel Dekker. 

. 1980a. *The Living State and Cancer.” International Journal of Quantum Chemistry 18(S7): 

217-22. 

. 1980b. “The Living State and Cancer." Physiological Chemistry and Physics 12: 99-110. 

Tamrakar, Chirika Shova and Pawan Raj Shakya. 2011. *Assessment of Heavy Metals in Street Dust 
in Kathmandu Metropolitan City and Their Possible Impacts on the Environment." Pakistani 
Journal of Analytical and Environmental Chemistry 12(1-2): 32-41. 

Taylor, Caroline M., Jeffrey R. Bacon, Peter J. Aggett, and Ian Bremner. 1991. “Homeostatic 
Regulation of Zinc Absorption and Endogenous Losses in Zinc- deprived Men.” American 
Journal of Clinical Nutrition 53(3): 755-63. 

















Tefferi, Ayalew, Laurence A. Solberg, Jr., and Ralph D. Ellefson. 1994. *Porphyrias: Clinical 
Evaluation and Interpretation of Laboratory Tests." Mayo Clinic Proceedings 69: 289-90. 

Tefferi, Ayalew, Joseph P. Colgan, and Laurence A. Solberg, Jr.. 1994. *Acute Porphyrias: Diagnosis 
and Management." Mayo Clinic Proceedings 69: 991-95. 

Terzuolo, Carlo A. and Theodore H. Bullock. 1956. *Measurement of Imposed Voltage Gradient 
Adequate to Modulate Neuronal Firing." Proceedings of the National Academy of Sciences 42(9): 
687-94. 

Todd, Tweedy John. 1823. *On the Process of Regeneration of the Members of the Aquatic 
Salamander." Quarterly Journal of Science, Literature and the Arts 16: 84-96. 

Trampusch, H. A. L. 1964. *Nerves as Morphogenetic Mediators in Regeneration." Progress in Brain 
Research 13: 214-27. 

Vacher, Monique, Claude Nicot, Mollie Pflumm, Jeremy Luchins, Sherman Beychok, and Marcel 
Waks. 1984. *A Heme Binding Site on Myelin Basic Protein: Characterization, Location, and 
Significance." Archives of Biochemistry and Biophysics 231(1): 86-94. 

Vass, Imre. 2003. “The History of Photosynthetic Thermoluminescence." Photosynthesis Research 
76: 303-18. 

Vernon, Leo P. and Gilbert R. Seely, eds. 1966. The Chlorophylls. New York: Academic. 

Vgontzas, Alexandros N., Joyce D. Kales, James O. Ballard, Antonio Vela-Bueno, and Tjiauw-Ling 
Tan. 1993. “Porphyria and Panic Disorder with Agoraphobia." Psychosomatics 34(5): 440-43. 

Virchow, Rudolf Ludwig Carl. 1854. *Ueber das ausgebreitete Vorkommen einer dem Nervenmark 
analogen Substanz in den thierischen Geweben.” Archiv für pathologische Anatomie und 
Physiologie und für klinische Medicin 6: 562-72. 

Voyatzoglou, Vassilis, Theodore Mountokalakis, Vassiliki Tsata-Voyatzoglou, Anton Koutselinis, and 
Gregory Skalkeas. 1982. “Serum Zinc Levels and Urinary Zinc Excretion in Patients with 
Bronchogenic Carcinoma.” American Journal of Surgery 144(3): 355-58. 

Waldenström, Jan. 1937. “Studien über Porphyrie.” Acta Medica Scandinavica. Supplementum, vol. 
82. 





. 1957. “The Porphyrias as Inborn Errors of Metabolism.” American Journal of Medicine 
22(5): 758-72. 

Walker, Franklin D. and Walther J. Hild. 1969. “Neuroglia Electrically Coupled to Neurons.” Science 
165: 602-3. 

Watson, Cecil James and Evrel A. Larson. 1947. “The Urinary Coproporphyrins in Health and 
Disease.” Physiological Reviews 27(3): 478-510. 

Waxman, Alan D., Don S. Schalch, William D. Odell, and Donald P. Tschudy. 1967. “Abnormalities 
of Carbohydrate Metabolism in Acute Intermittent Porphyria.” Journal of Clinical Investigation 
46 (part 1): 1129. Abstract. 

Wei, Ling Y. 1966. “A New Theory of Nerve Conduction.” IEEE Spectrum 3(9): 123-27. 

Whetsell, William O., Jr., Shigeru Sassa, and Attallah Kappas. 1984. “Porphyrin-Heme Biosynthesis 
in Organotypic Cultures of Mouse Dorsal Root Ganglia: Effects of Heme and Lead on Porphyrin 
Synthesis and Peripheral Myelin.” Journal of Clinical Investigation 74: 600-7. 

With, Torben K. 1980. “A Short History of Porphyrins and the Porphyrias.” International Journal of 
Biochemistry 11: 189-200. 

Wnuk, Marian. 1987. Rola układów porfirynowych w ewolucji życia (“The Role of Porphyrin 
Systems in the Evolution of Life”). Warsaw: Akademia Teologii Katolickiej (in Polish with 
English summary). 

. 1996. Istota procesów życiowych w świetle koncepcji elektromagnetycznej natury życia: 

Bioelektromagnetyczny model katalizy enzymatycznej wobec problematyki biosystemogenezy 





(*The Essence of Life Processes in Light of the Concept of the Electromagnetic Nature of Life: 
Bioelectromagnetic Model of Enzyme Catalysis in View of the Problems of the Origin of 
Biosystems"). Lublin: John Paul II Catholic University of Lublin. 

. 2001. *The Electromagnetic Nature of Life — The Contribution of W. Sedlak to the 
Understanding of the Essence of Life." Frontier Perspectives 10(1): 32-35. 

Wong, J. W. C. 1996. *Heavy Metal Contents in Vegetables and Market Garden Soils in Hong 
Kong." Environmental Technology 17(4): 407-14. 

Wong, J. W. C. and N. K. Mak. 1997. *Heavy Metal Pollution in Children Playgrounds in Hong 
Kong and Its Health Implications." Environmental Technology 18(1): 109-15. 

Xu, Jiancheng, Qi Zhou, Gilbert Liu, Yi Tan, and Lu Cai. 2013. “Analysis of Serum and Urinal 
Copper and Zinc in Chinese Northeast Population with the Prediabetes or Diabetes with and 
without Complications." Oxidative Medicine and Cellular Longevity, article ID 635214. 

Yntema, Chester L. 1959. “Regeneration in Sparsely Innervated and Aneurogenic Forelimbs of 
Amblystoma Larvae.” Journal of Experimental Zoology 140(1): 101-24. 

Yokoyama, M., J. Koh, and D. W. Choi. 1986. “Brief Exposure to Zinc is Toxic to Cortical Neurons.” 
Neuroscience Letters 71: 351-55. 

York, J. Lyndal. 1972. The Porphyrias. Springfield, IL: Charles C. Thomas. 

Zhou, Xiaoli. 2009. “Synthesis and Characterization of Novel Discotic Liquid Crystal Porphyrins for 
Organic Photovoltaics.” Ph.D. dissertation, Kent State University, Kent, OH. 

Zon, Józef Roman. 1976. “Wpływ naturalnego środowiska elektromagnetycznego na człowieka” 
(“The Effect of the Natural Electromagnetic Environment on Man”). Roczniki Filozoficzne 23(3): 
89-100. 

. 1979. “Physical Plasma in Biological Solids: A Possible Mechanism for Resonant 

Interactions between Low Intensity Microwaves and Biological Systems.” Physiological 

Chemistry and Physics 11: 501-6. 

. 1980. “The Living Cell as a Plasma Physical System.” Physiological Chemistry and Physics 

12: 357-64. 

. 1983. “Electronic Conductivity in Biological Membranes”. Roczniki Filozoficzne 31(3): 

165-183. 

. 1986a. “Bioelectronics: A Background Area for Biomicroelectronics in the Sciences of 

Bioelectricity.” Roczniki Filozoficzne 34(3): 183-201. 

. 1986b. Plazma elektronowa w błonach biologicznych (“Electronic Plasma in Biological 

Membranes”). Lublin: Catholic University of Lublin. 

. 1994. “Bioelektromagnetyka i etyka: Niektóre kwestie moralne związane ze skażeniem 

elektromagnetycznym środowiska” (“Bioelectromagnetic and Ethics: Some Moral Questions 

Related to the Electromagnetic Pollution of the Environment”). Ethos 7(1-2): 135-50. 

. 2000. “Bioplazma i plazma fizyczna w układach żywych: Studium przyrodnicze i 
filozoficzne.” (“Bioplasma and Physical Plasma in Living Systems: A Study in Science and 
Philosophy”). Lublin: Catholic University of Lublin. 

Zon, Józef Roman and H. Ti Tien. “Electronic Properties of Natural and Modeled Bilayer 
Membranes.” In: Andrew A. Marino, ed., Modern Bioelectricity (New York: Marcel Dekker), pp. 
181-241. 

Zs.-Nagy, Imre. 1995. “Semiconduction of Proteins as an Attribute of the Living State: The Ideas of 
Albert Szent-Györgyi Revisited in Light of the Recent Knowledge Regarding Oxygen Free 
Radicals.” Experimental Gerontology 30(3/4): 327-35. 

. 2001. “On the True Role of Oxygen Free Radicals in the Living State, Aging, and 

Degenerative Disorders.” Annals of the New York Academy of Sciences 928: 187-99. 





























Sulfonal 

Bresslauer, Hermann. 1891. *Ueber die schádlichen und toxischen Wirkungen des Sulfonal." Wiener 
medizinischer Blätter 14: 3-4, 19-20. 

Erbslóh, W. 1903. *Zur Pathologie und pathologischen Anatomie der toxischen Polyneuritis nach 
Sulfonalgebrauch." Zeitschrift für Nervenheilkunde 23: 197-204. 

Fehr, Johann Heinrich Maria Christian. 1891. “Et Par Tilfzlde af Sulfonalforgiftning." Hospitals- 
Tidende, 3rd ser., 9: 1121-38. 

Geill, Christian. 1891. “Sulfonal og Sulfonalforgiftning.” Hospitals-Tidende, 3rd ser., 9: 797-812, 
821-35. 

Hammond, Greme M. 1891. “Sulfonal in Affections of the Nervous System.” Journal of Nervous 
and Mental Disease, new ser., 16: 440-42. 

Hay, C. M. 1889. “A Clinical Study of Paraldehyde and Sulphonal.” American Journal of the 
Medical Sciences, new ser., 98: 34-43. 

Ireland, W. W. 1889. “Marandon de Montyel and Others on the Dangers of Sulfonal.” London 
Medical Recorder 2: 499-500. 

Leech, D. J. 1888. “Sulfonal.” Medical Chronicle 9: 146-50. 

Marandon de Montyel, E. 1889. “Recherches cliniques sur le sulfonal chez les aliénés.” La France 
Médicale 36: 1566-70, 1577-82, 1589-93, 1602-8, 1613-17. 

Matthes, M. 1888. “Beitrag zur hypnotischen Wirkung des Sulfonals.” Centralblatt fiir Klinische 
Medicin 9(40): 723-27. 

Morel, Jules. 1893. “Accidents produits par le sulfonal.” Bulletin de la Société de Médecine Mentale 
de Belgique 68: 120-23. 

Revue des Sciences Médicales. 1889. “Thérapeutique.” 34: 502-3. 

Rexford, C. M. 1889. “Some Experiences with Sulfonal.” The Medical Record 35(13): 348. 


Chapter 11 


Abbate, Mara, Giovanni Tiné, and Luigi Zanforlin. 1996. “Evaluation of Pulsed Microwave 
Influence on Isolated Hearts." IEEE Transactions on Microwave Theory and Techniques MTT- 
44(10): 1935-41. 

Adams, Ronald L. and R. A. Williams. 1976. Biological Effects of Electromagnetic Radiation 
(Radiowaves and Microwaves) — Eurasian Communist Countries (U). Defense Intelligence 
Agency, DST-1810S-074-76. 

Afrikanova, Lena Andreevna and Yury Grigorievich Grigoriev. 1996. *Vliyanie elektromagnitnogo 
izlucheniya razlichnykh rezhimov na serdechnuyu deyatel'nost' (v ekcperimente)" (“Effects of 
various regimes of electromagnetic radiation on cardiac activity (by experiment)”). 
Radiatsionnaya biologiya. Radioekologiya 36(5): 691-99. 

Ammari, Mohamed, Anthony Lecomte, Mohsen Sakly, Hafedh Abdelmelek, and René de Séze. 
2008. “Exposure to GSM 900 MHz Electromagnetic Fields Affects Cerebral Cytochrome C 
Oxidase Activity.” Toxicology 250(1): 70-74. 

Appleby, Paul N., Margaret Thorogood, Jim I. Mann, and Timothy J. A. Key. 1999. “The Oxford 
Vegetarian Study: an Overview." American Journal of Clinical Nutrition 70(3): 525S-531S. 

Arora, Sameer, George A. Stouffer, Anna M. Kucharska-Newton, Arman Qamar, Muthiah 
Vaduganathan, Ambarish Pandey, Deborah Porterfield, Ron Blankstein, Wayne D. Rosamond, 
Deepak L. Bhatt, and Melissa C. Caughey. 2019. “Twenty Year Trends and Sex Differences in 
Young Adults Hospitalized With Acute Myocardial Infarction: The ARIC Community 
Surveillance Study.” Circulation 139: 1047-56. 


Aschenheim, Erich. 1915. “Uber Störungen der Herztätigkeit.” Münchener medizinische 
Wochenschrift 62(20): 692-93. 

Aubertin, Charles. 1916. *La récupération des faux cardiaques." Presse médicale 24: 92-93. 

Bachurin, V. I. 1979. *Influence of Small Doses of Electromagnetic Waves on Some Human Organs 
and Systems." Vrachebnoye Delo 1979(7): 95-97. JPRS 75515 (1980), pp. 36-39. 

Bajwa, Waheed K., Gregory M. Asnis, William C. Sanderson, Ahman Irfan, and Herman M. van 
Praag. 1992. *High Cholesterol Levels in Patients with Panic Disorder." American Journal of 
Psychiatry 149(3): 376-78. 

Baranski, Stanistaw and Przemystaw Czerski. 1976. “Health Status of Personnel Occupationally 
Exposed to Microwaves, Symptoms of Microwave Overexposure.” In: Baranski and Czerski, 
Biological Effects of Microwaves (Stroudsburg, PA: Dowden, Hutchinson & Ross), pp. 153-69. 

Barlow, David H. 2002. Anxiety and its Disorders, 2nd ed. New York: Guilford. 

Barron, Charles I., Andrew A. Love, and Albert A. Baraff. 1955. “Physical Evaluation of Personnel 
Exposed to Microwave Emanations.” Journal of Aviation Medicine 26(6): 442-52. 

Bates, David W., Dedra Buchwald, Joshua Lee, Phalla Kith, Teresa Doolittle, Cynthia Rutherford, W. 
Hallowell Churchill, Peter H. Schur, Mark Wener, Donald Wybenga, James Winkelman, and 
Anthony L. Komaroff. 1995. “Clinical Laboratory Test Findings in Patients with Chronic Fatigue 
Syndrome.” Archives of Internal Medicine 155(1): 97-103. 

Beall, Robert T. 1940. “Rural Electrification.” In: Gove Hambidge, ed., Farmers in a Changing 
World (Washington, DC: U.S. Department of Agriculture), pp. 790-809. 

Beattie, A. D., Michael R. Moore, Abraham Goldberg, and R. L. Ward. 1973. “Acute Intermittent 
Porphyria: Response of Tachycardia and Hypertension to Propranolol.” British Medical Journal 3: 
257-60. 

Behan, W. M. H., I. A. R. More, and P. O. Behan. 1991. “Mitochondrial Abnormalitieis in the 
Postviral Fatigue Syndrome.” Acta Neuropathologica 83: 61-65. 

Beitman, Bernard D., Imad Basha, Greg Flaker, Lori DeRosear, Vaskar Mukerji, and Joseph 
Lamberti. 1987. “Non-Fearful Panic Disorder: Panic Attacks without Fear.” Behaviour Research 
and Therapy 25(6): 487-92. 

Blank, Martin and Reba Goodman. 2009. “Electromagnetic Fields Stress Living Cells.” 
Pathophysiology 16(2-3): 71-78. 

Blom, Dirk. 2011. “Secondary Dyslipidaemia.” South African Family Practice 53(4): 317-23. 

Blom, Gaston E. 1951. “A Review of Electrocardiographic Changes in Emotional States.” Journal of 
Nervous and Mental Disease 113(4): 283-300. 

Bonkowsky, Herbert L., Donald P. Tschudy, Eugene C. Weinbach, Paul S. Ebert, and Joyce M. 
Doherty. 1975. “Porphyrin Synthesis and Mitochondrial Respiration in Acute Intermittent 
Porphyria: Studies Using Cultured Human Fibroblasts.” Journal of Laboratory and Clinical 
Medicine 85(1): 93-102. 

Bortkiewicz, A., M. Zmyslony, E. Gadzicka, and W. Szymczak. 1996. “Evaluation of Selected 
Parameters of Circulatory System Function in Various Occupational Groups Exposed to High 
Frequency Electromagnetic Fields. II. Electrocardiographic Changes." Medycyna Pracy 47(3): 
241-52 (in Polish). 

Bowen, Rudy Cecil, Ambikaipakan Senthilselvan, and Anthony Barale. 2000. “Physical Illness as an 
Outcome of Chronic Anxiety Disorders." Canadian Journal of Psychiatry 45(5): 459-64. 

Bowlby, Anthony A., Howard H. Tooth, Cuthbert Wallace, John E. Calverley, and Surgeon-Major 
Kilkelly. 1901. A Civilian War Hospital: Being an Account of the Work of the Portland Hospital, 
and of Experience of Wounds and Sickness in South Africa, 1900. London: John Murray. Pages 
128-29 on neurasthenia. 


Brasch, Dr. 1915. *Herzneurosen mit Hauthyperásthesie." Münchener medizinische Wochenschrift 
62(20): 693-95. 

Braun, Ludwig. 1915. *Ueber die Konstatierung bie Herzkranken." Wiener klinische Wochenschrift 
28(46): 1249-51. 

Brodeur, Paul. 1977. The Zapping of America. New York: W. W. Norton. 

Brown, Louis. 1999. A Radar History of World War II. Bristol, UK: Institute of Physics. 

Burr, Michael L. and Peter M. Sweetnam. 1982. “Vegetarianism, Dietary Fiber, and Mortality." 
American Journal of Clinical Nutrition 36(5): 873-77. 

Canadian Medical Association Journal. 1916. *Soldier's Heart and the Hampstead Hospital." 6(7): 
613-18. 

Caruthers, B. M., M. I. van de Sande, K. L. De Meirleir, N. G. Klimas, G. Broderick, T. Mitchell, D. 
Staines, A. C. P. Powles, N. Speight, R. Vallings, L. Bateman, B. Baumgarten-Austrheim, D. S. 
Bell, N. Carlo-Stella, J. Chia, A. Darragh, D. Jo, D. Lewis, A. R. Light, S. Marshal-Gradisbik, I. 
Mena, J. A. Mikovits, K. Miwa, M. Murovska, M. L. Pall, and S. Stevens. 2011. *Myalgic 
Encephalomyelitis: International Consensus Criteria." Journal of Internal Medicine 270(4): 327- 
38. 

Chadha, S. L., N. Gopinath, and S. Shekhawat. 1997. *Urban-Rural Differences in the Prevalence of 
Coronary Heart Disease and Its Risk Factors in Delhi." Bulletin of the World Health Organization 
75(1): 31-38. 

Chapman, William P., Mandel E. Cohen, and Stanley Cobb. 1946. *Measurements Related to Pain in 
Neurocirculatory Asthenia, Anxiety Neurosis, or Effort Syndrome: Levels of Heat Stimulus 
Perceived as Painful and Producing Wince and Withdrawal Reactions." Journal of Clinical 
Investigation 25: 890-96. 

Chernysheva, O. N. and F. A. Kolodub. 1976. “Effect of a Variable Magnetic Field of Industrial 
Frequency (50 Hz) on Metabolic Processes in the Organs of Rats." Gigiyena truda i 
professional’nyye zabolevaniya 1975(11): 20-23. In: Effects of Non-Ionizing Electromagnetic 
Radiation, JPRS L/5615, February 10, 1976, pp. 33-37. 

Chin, Kazuo, Kouichi Shimizu, Takaya Nakamura, Noboru Narai, Hiroaki Masuzaki, Yoshihiro 
Ogawa, Michiaki Mishima, Takashi Nakamura, Kazuwa Nakao, and Motoharu Ohi. 1999. 
“Changes in Intra-Abdominal Visceral Fat and Serum Leptin Levels in Patients with Obstructuve 
Sleep Apnea Syndrome Following Nasal Continuous Positive Airway Pressure Therapy.” 
Circulation 100: 706-12. 

Cleary, Stephen F., ed. 1970. Biological Effects and Health Implications of Microwave Radiation. 
Symposium Proceedings, Richmond, Virginia, September 17-19, 1969. Rockville, MD: U.S. 
Department of Health, Education and Welfare. Publication BRH/DBE 70-2. 

Cobb, Stanley, Mandel E. Cohen, and Daniel W. Badal. 1946. “Capillaries of the Nail Fold in 
Patients with Neurocirculatory Asthenia (Effort Syndrome, Anxiety Neurosis).” Archives of 
Neurology and Psychiatry 56: 643-50. 

Cohen, Anne Hamlen, ed. 2003. “In Memoriam — Mandel E. Cohen, M.D. (March 8, 1907 — 
November 19, 2000).” Annals of Clinical Psychiatry 15(3/4): 149-59. 

Cohen, Mandel Ettelson. 1949. “Neurocirculatory Asthenia (Anxiety Neurosis, Neurasthenia, Effort 
Syndrome, Cardiac Neurosis.” Medical Clinics of North America 33(9): 1343-64. 

Cohen, Mandel E., Daniel W. Badal, Alice Kilpatrick, Eleanor W. Reed, and Paul D. White. 1951. 
“The High Familial Prevalence of Neurocirculatory Asthenia (Anxiety Neurosis, Effort 
Syndrome).” American Journal of Human Genetics 3: 126-58. 

Cohen, Mandel E., Frank Consolazio, and Robert E. Johnson. 1947. “Blood Lactate Response during 
Modern Exercise in Neurocirculatory Asthenia, Anxiety Neurosis, or Effort Syndrome.” Journal 
of Clinical Investigation 26: 339-42. 


Cohen, Mandel E., Robert E. Johnson, William P. Chapman, Daniel W. Badal, Stanley Cobb, and 
Paul D. White. 1946. A Study of Neurocirculatory Asthenia, Anxiety Neurosis, Effort Syndrome. 
Final Report. Contract OEM-cmr 157. Committee on Medical Research of the Office of Scientific 
Research and Development. 

Cohen, Mandel E., Robert E. Johnson, Stanley Cobb, William P. Chapman, and Paul D. White. 1948. 
*Studies of Work and Discomfort in Patients with Neurocirculatory Asthenia." Journal of Clinical 
Investigation 27: 934. Abstract. 

Cohen, Mandel E., Robert E. Johnson, Frank Consolazio, and Paul D. White. 1946. “Low Oxygen 
Consumption and Low Ventilatory Efficiency during Exhausting Work in Patients with 
Neurocirculatory Asthenia, Effort Syndrome, Anxiety Neurosis." Journal of Clinical Investigation 
25: 920. Abstract. 

Cohen, Mandel E. and Paul D. White. 1947. “Studies of Breathing, Pulmonary Ventilaton and 
Subjective Awareness of Shortness of Breath (Dyspnea) in Neurocirculatory Asthenia, Effort 
Syndrome, Anxiety Neurosis." Journal of Clinical Investigation 26: 520-29. 

. 1951. “Life Situations, Emotions, and Neurocirculatory Asthenia (Anxiety Neurosis, 

Neurasthenia, Effort Syndrome).” Psychosomatic Medicine 13(6): 335-57. 

. 1972. *Neurocirculatory Asthenia: 1972 Concept." Military Medicine 137: 142-44. 

Cohen, Mandel E., Paul D. White, and Robert E. Johnson. 1948. *Neurocirculatory Asthenia, 
Anxiety Neurosis or the Effort Syndrome." Archives of Internal Medicine 81(3): 260-81. 

Cohn, Alfred E. 1919. “The Cardiac Phase of the War Neuroses." American Journal of the Medical 
Sciences 158(4): 453-70. 

Conner, Lewis A. 1919. “Cardiac Diagnosis in the Light of Experiences with Army Physical 
Examinations.” American Journal of the Medical Sciences 158(6): 773-82. 

Corcoran, A. P. 1917. “Wireless in the Trenches.” Popular Science Monthly 90: 795-99. 

Coryell, William, Russell Noyes, and John Clancy. 1982. “Excess Mortality in Panic Disorder.” 
Archives of General Psychiatry 39: 701-3. 

Coryell, William, Russell Noyes, and J. Daniel House. 1986. “Mortality Among Outpatients with 
Anxiety Disorders.” American Journal of Psychiatry 143(4): 508-10. 

Coryell, William. 1988. “Panic Disorder and Mortality.” Psychiatric Clinics of North America 11(2): 
433-40. 

Cotton, Thomas F., D. L. Rapport, and Thomas Lewis. 1917. “After Effects of Exercise on Pulse 
Rate and Systolic Blood Pressure in Cases of ‘Irritable Heart.’” Heart 6: 269-84. 

Coughlin, Steven R., Lynn Mawdsley, Julie A. Mugarza, Peter M. A. Calverley, and John P. H. 
Wilding. 2004. “Obstructuve Sleep Apnoea is Independently Associated with an Increased 
Prevalence of Metabolic Syndrome.” European Heart Journal 25: 735-41. 

Cowdry, Edmund V. 1933. Arteriosclerosis: A Survey of the Problem. New York: Macmillan. 

Craig, Henry R. and Paul D. White. 1934. “Etiology and Symptoms of Neurocirculatory Asthenia.” 
Archives of Internal Medicine 53(5): 633-48. 

Crimlisk, Helen L. 1997. “The Little Imitator — Porphyria: A Neuropsychiatric Disorder." Journal of 
Neurology, Neurosurgery, and Psychiatry 62: 319-28. 

Csaba, B. M. 2006. *Anxiety as an Independent Cardiovascular Risk." Neuropsycopharmacologia 
Hungarica 8(1): 5-11 (in Hungarian). 

Çuhadaroğlu, Çağlar, Ayfer Utkusavaş, Levent Öztürk, Serpil Salman, and Turhan Ece. 2009. 
“Effects of Nasal CPAP Treatment on Insulin Resistance, Lipid Profile, and Plasma Leptin in 
Sleep Apnea.” Lung 187: 75-81. 

Cutler, David M. and Elizabeth Richardson. 1997. “Measuring the Health of the U.S. Population.” 
Brookings Papers on Economic Activity 28: 217-82. 








Czerski, Przemystaw, Kazimierz Ostrowski, Morris L. Shore, Charlotte Silverman, Michael J. Suess, 
and Berndt Waldeskog, eds. 1974. Biologic Effects and Health Hazards of Microwave Radiation: 
Proceedings of an International Symposium, Warsaw, 15-18 October 1973. Warsaw: Polish 
Medical Publishers. 

Da Costa, Jacob Mendes. 1871. “On Irritable Heart: a Clinical Study of a Form of Functional Cardiac 
Disorder and its Consequences.” American Journal of the Medical Sciences, new ser., 61: 17-52. 
Daily, L. Eugene. 1943. “A. Clinical Study of the Results of Exposure of Laboratory Personnel to 

Radio and High Frequency Radar.” U.S. Naval Medical Bulletin 41(4): 1052-56. 

Dawber, Thomas R., Felix E. Moore, and George V. Mann. 1957. “Coronary Heart Disease in the 
Framingham Study.” American Journal of Public Health 47 (4 part 2): 4-24. 

Devoto, L. 1915. “Il cuore stanco nei militari poco alienati.” I! Lavoro 8: 138-47. 

Dodge, Christopher H. 1970. “Clinical and Hygienic Aspects of Exposure to Electromagnetic Fields 
(A Review of Soviet and Eatern European Literature).” In: Stephen F. Cleary, ed., Biological 
Effects and Health Implications of Microwave Radiation. Symposium Proceedings (Rockville, 
MD: U.S. Department of Health, Education and Welfare), Publication BRH/DBE 70-2, pp. 140- 
49. 

Dorkova, Zuzana, Darina Petrasova, Angela Molcanyiova, Marcela Popovnakova, and Ruzena 
Tkacova. 2008. “Effects of Continuous Positive Airway Pressure on Cardiovascular Risk Profile 
in Patients with Severe Obstructuve Sleep Apnea and Metabolic Syndrome.” Chest 134(4): 686- 
92. 

Doyle, Joseph T., A. Sandra Heslin, Herman E. Hilleboe, Paul F. Formel, and Robert F. Korns. 1957. 
*A Prospective Study of Degenerative Cardiovascular Disease in Albany: Report of Three Years' 
Experience — 1. Ischemic Heart Disease." American Journal of Public Health 47(4 part 2): 25-32. 

Drager, Luciano F., Jonathan Jun, and Vsevolod Y. Polotsky. 2010. “Obstructive Sleep Apnea and 
Dyslipidemia: Implications for Atherosclerosis.” Current Opinion in Endocrinology , Diabetes 
and Obesity 17(2): 161-65. 

Drogichina, E. A. 1960. “The Clinic of Chronic UHF Influence on the Human Organism.” In: A. A. 
Letavet and Z. V. Gordon, eds., The Biological Action of Ultrahigh Frequencies (Moscow: 
Academy of Medical Sciences), JPRS 12471, pp. 22-24. 

Drury, Alan N. 1920. “The Percentage of Carbon Dioxide in the Alveolar Air, and the Tolerance to 
Accumulating Carbon Dioxide, in Cases of So-Called ‘Irritable Heart’ of Soldiers.” Heart 7: 165- 
73. 

Dry, Thomas J. 1938. “The Irritable Heart and Its Accompaniments.” Journal of the Arkansas 
Medical Society 34: 259-64. 

Dumanskiy, Yury D. and V. F. Rudichenko. 1976. “Dependence of the Functional Activity of Liver 
Mitochondria on Microwave Radiation.” Gigiyena i Sanitariya 1976(4): 16-19. JPRS 72606 
(1979), pp. 27-32. 

Dumanskiy, Yury D. and Mikhail G. Shandala. 1974. “The Biologic Action and Hygienic 
Significance of Electromagnetic Fields of Superhigh and Ultrahigh Frequencies in Densely 
Populated Areas.” In: P. Czerski et al., eds., Biologic Effects and Health Hazards of Microwave 
Radiation: Proceedings of an International Symposium, Warsaw, 15-18 October 1973 (Warsaw: 
Polish Medical Publishers), pp. 289-93. 

Dumanskiy, Yury D. and Lyudmila A. Tomashevskaya. 1978. “Investigation of the Activity of Some 
Enzymatic Systems in Response to a Superhigh Frequency Electromagnetic Field.” Gigiyena i 
Sanitariya 1978(8): 23-27. JPRS 72606 (1979), pp. 1-7. 

. 1982. *Hygienic Evaluation of 8-mm Wave Electromagnetic Fields.” Gigiyena i Sanitariya 

1982(6): 18-20. JPRS 81865, pp. 6-9. 





Eaker, Elaine D., Joan Pinsky, and William P. Castelli. 1992. *Myocardial Infarction and Coronary 
Death among Women: Psychosocial Predictors from a 20-Year Follow-up of Women in the 
Framingham Study." American Journal of Epidemiology 135(8): 854-64. 

Eaker, Elaine D., Lisa M. Sullivan, Margaret Kelly-Hayes, Ralph B. D'Agostino, and Emilia J. 
Benjamin. 2005. “Tension and Anxiety and the Prediction of the 10-Year Incidence of Coronary 
Heart Disease, Atrial Fibrillation, and Total Mortality: The Framingham Offspring Study.” 
Psychosomatic Medicine 67: 692-96. 

Edison Electric Institute. 1940. The Electric Light and Power Industry in the United States. Year 
1939. Statistical Bulletin no. 7. 

Edison Electric Institute. 1941. The Electric Light and Power Industry in the United States. Year 
1940. Statistical Bulletin no. 8. 


Ehret, Hermann. 1915. *Zur Kenntnis der Herzschádigungen bei Kriegsteilnehmern." Münchener 
medizinische Wochenschrift 62: 689-92. 

Eilenberg, M. D. and B. A. Scobie. 1960. “Prolonged Neuropsychiatric Disability and 
Cardiomyopathy in Acute Intermittent Porphyria.” British Medical Journal 1: 858-59. 

Fang, Jing, George A. Mensah, Janet B. Croft, and Nora L. Keenan. 2008. “Heart Failure-Related 
Hospitalization in the U.S., 1979 to 2004.” Journal of the American College of Cardiology 52(6): 
428-34. 

Fattal, Omar, Jessica Link, Kathleen Quinn, Bruce H. Cohen, and Kathleen Franco. 2007. 
“Psychiatric Comorbidity in 36 Adults with Mitochondrial Cytopathies.” CNS Spectrums 12(6): 
429-38. 

Fava, G. A., C. Magelli, G. Savron, S. Conti, G. Bartolucci, S. Grandi, F. Semprini, F. M. Saviotti, P. 
Belluardo, and B. Magnani. 1994. “Neurocirculatory Asthenia: A Reassessment Using Modern 
Psychosomatic Criteria.” Acta Psychiatrica Scandinavica 89(5): 314-19. 

Feinleib, Manning, William B. Kannel, Cesare G. Tedeschi, Thomas K. Landau, and Robert J. 
Garrison. 1979. “The Relation of Antemortem Characteristics to Cardiovascular Findings at 
Necropsy: The Framingham Study.” Atherosclerosis 34: 145-57. 

Fernández-Miranda C., M. De La Calle, S. Larumbe, T. Gómez-Izquierdo, A. Porres, J. Gómez- 
Gerique, and R. Enríquez de Salamanca. 2000. *Lipoprotein Abnormalities in Patients with 
Asymptomatic Acute Porphyria." Clinica Chimica Acta 294(1-2): 37-43. 

Fisher, Irving. 1899. “Mortality Statistics of the United States Census." In: The Federal Census. 
Criticial Essays by Members of the American Economic Association, Publications of the 
American Economic Association, new ser., no. 2, March 1898, pp. 121-69. 

Flint, Austin. 1866. A Treatise on the Principles and Practice of Medicine. Philadelphia: Henry C. 
Lea. 

Fones, Edgar and Simon Wessely. 1999. *Case of Chronic Fatigue Syndrome after Crimean War and 
Indian Mutiny." British Medical Journal 319: 1645-47. 

Fox, Herbert. 1921. *Comparative Pathology of the Heart as Seen in the Captive Animals at the 
Philadelphia Zoólogical Garden." Transactions of the College of Physicians of Philadelphia, 3rd 
ser., no. 43, pp. 130-45. 

. 1923. Disease in Captive Wild Mammals and Birds. Philadelphia: J. B. Lippincott. 

Fraser, Allan and Allan H. Frey. 1968. “Electromagnetic Emission at Micron Wavelengths from 
Active Nerves.” Biophysical Journal 8: 731-34. 

Fraser, Gary E. 1999. “Associations between Diet and Cancer, Ischemic Heart Disease, and All- 
Cause Mortality in Non-Hispanic White California Seventh-day Adventists.” American Journal of 
Clinical Nutrition 70(3): 532S-538S. 

. 2009. “Vegetarian Diets: What Do We Know of Their Effects on Common Chronic 
Diseases?” American Journal of Clinical Nutrition 89(5): 1607S-1612S. 

Frasure-Smith, Nancy and Francois Lespérance. 2008. “Depression and Anxiety as Predictors of 2- 
Year Cardiac Events in Patients with Stable Coronary Artery Disease.” Archives of General 
Psychiatry 65(1): 62-71. 

Freedman, David S., Tim Byers, Drue H. Barrett, Nancy E. Stroup, Elaine Eaker, and Heather 
Monroe-Blum. 1995. “Plasma Lipid Levels and Psychologic Characteristics in Men.” American 
Journal of Epidemiology 141(6): 507-17. 

Frentzel-Beyme, R., J. Claude, and U. Eilber. 1988. “Mortality Among German Vegetarians: First 
Results after Five Years of Follow-up.” Nutrition and Cancer 11(2): 117-26. 

Freud, Sigmund. 1895. “Ueber die Berechtigung von der Neurasthenie einen be- stimmten 
Symptomencomplex als ‘Angstneurose’ abzutrennen.” Neurologisches Centralblatt 14: 50-66. 








Published in English as *On the Grounds for Detaching a Particular Syndrome from Neurasthenia 
under the Description ‘Anxiety Neurosis,’” in James Strachey, ed., The Standard Edition of the 
Complete Psychological Works of Sigmund Freud (London: Hogarth), 1962, vol. 3, pp. 87-139. 

Frey, Allan H. 1961. *Auditory System Response to Radio Frequency Energy." Aerospace Medicine 
32: 1140-42. 

. 1962. *Human Auditory System Response to Modulated Electromagnetic Energy." Journal 

of Applied Physiology 17(4): 689-92. 

. 1963. *Some Effects on Human Subjects of Ultra-High-Frequency Radiation." American 

Journal of Medical Electronics 2: 28-31. 

. 1965. *Behavioral Biophysics." Psychological Bulletin 63: 322-37. 

. 1967. “Brain Stem Evoked Responses Associated with Low-Intensity Pulsed UHF Energy.” 

Journal of Applied Physiology 23(6): 984-88. 

. 1968. “Some Effects on Human Subjects of Ultrahigh Frequency Radiation.” American 

Journal of Medical Electronics, January-March, pp. 28-31. 

. 1970. “Effects of Microwave and Radio Frequency Energy on the Central Nervous System." 

In: Stephen F. Cleary, ed., Biological Effects and Health Implications of Microwave Radiation. 

Symposium Proceedings (Rockville, MD: U.S. Department of Health, Education and Welfare), 

Publication BRH/DBE 70-2, pp. 134-139. 

. 1971. “Biological Function as Influenced by Low Power Modulated RF Energy.” IEEE 

Transactions on Microwave Theory and Techniques MTT-19(2): 153-64. 

. 1985. “Data Analysis Reveals Significant Microwave-Induced Eye Damage in Humans.” 

Journal of Microwave Power 20(1): 53-55. 

. 1988. "Evolution and Results of Biological Research with Low-Intensity Nonionizing 
Radiation." In: Andrew A. Marino, ed., Modern Bioelectricity (New York: Marcel Dekker), pp. 
785-837. 

Frey, Allan H. and Edwin S. Eichert. 1986. *Modification of Heart Function with Low Intensity 
Electromagnetic Energy." Electromagnetic Biology and Medicine 5(2): 201-10. 

Frey, Allan H. and S. R. Feld. 1975. “Avoidance by Rats of Illumination with Low Power 
Nonionizing Electromagnetic Energy." Journal of Comparative and Physiological Psychology 
89(2): 183-88. 

Frey, Allan H., Sondra Feld, and Barbara Frey. 1975. *Neural Function and Behavior: Defining the 
Relationship." Annals of the New York Academy of Sciences 247: 433-39. 

Frey, Allan H. and Rodman Messenger, Jr. 1973. *Human Perception of Illumination with Pulsed 
Ultrahigh-Frequency Electromagnetic Energy." Science 181: 356-58. 

Frey, Allan H. and Elwood Seifert. 1968. “Pulse Modulated UHF Energy Illumination of the Heart 
Associated with Change in Heart Rate.” Life Sciences 7 (part 2): 505-12. 

Frey, Allan H. and Jack Spector. 1976. “Exposure to RF Electromagnetic Energy Decreases 
Aggressive Behavior.” In: U.S. National Committee of the International Union of Radio Science, 
Program and Abstracts, URSI 1979 Spring Meeting, June 18-22 (Washington, DC: USNC-URSI), 
p. 456. 

Frey, Allan H. and Lee S. Wesler. 1979. *Modification of Tail Pinch Consummatory Behavior in 
Microwave Energy Exposure." Aggressive Behavior 12(4): 285-91. 

Friedman, Meyer. 1947. Functional Cardiovascular Disease. Baltimore: Williams and Wilkins. 

Galli, G. 1916. *Tl cuore dei soldati." I] Policlinico, Sezione Pratica 23: 489-91. 

Gardner, Ann, Anna Johansson, Rolf Wibom, Inger Nennesmo, Ulrika von Dóbeln, Lars Hagenfeldt, 
and Tore Hallstr6m. 2003. “Alterations of Mitochondrial Function and Correlations with 





























Personality Traits in Selected Major Depressive Disorder Patients." Journal of Affective Disorders 
76: 55-68. 

Gardner, Ann and Richard G. Boles. 2008. *Symptoms of Somatization as a Rapid Screening Tool 
for Mitochondrial Dysfunction in Depression." BioPsychoSocial Medicine 2: 7. 

2011. “Beyond the Serotonin Hypothesis: Mitochondria, Inflammation and 
Neurodegeneration in Major Depression and Affective Spectrum Disorders.” Progress in Neuro- 
Psychopharmocology & Biological Psychiatry 35: 730-43. 

Garssen, Bert, Mariete Buikhuisen, Doctorandus, and Richard van Dyck. 1996. “Hyperventilation 
and Panic Attacks.” American Journal of Psychiatry 153(4): 513-18. 

Gembitskiy, Ye. V. 1970. “Changes in the Functions of the Internal Organs of Personnel Operating 
Microwave Generators.” In: I. R. Petrov. ed., Influence of Microwave Radiation on the Organism 
of Man and Animals (Leningrad: “Meditsina”), in English translation, 1972 (Washington, DC: 
NASA), report no. TTF-708, pp. 106-25. 

Ghali, Jalal K., Richard Cooper, and Earl Ford. 1990. “Trends in Hospitalization Rates for Heart 
Failure in the United States, 1973-1986.” Archives of Internal Medicine 150: 769-73. 

Glaser, Zorach R. 1971-1976. Bibliography of Reported Biological Phenomena (“Effects”) and 
Clinical Manifestations Attributed to Microwave and Radio-Frequency Radiation. Bethesda, MD: 
Naval Medical Research Institute. NTIS reports nos. AD 734391, AD 750271, AD 770621, AD 
784007, AD A015622, AD A025354, and AD A029430. 

—. 1977. Bibliography of Reported Biological Phenomena (“Effects”) and Clinical 
Manifestations Attributed to Microwave and Radio-Frequency Radiation: Ninth Supplement to 
Bibliography of Microwave and RF Biologic Effects. Cincinnato, OH: National Institute for 
Occupational Safety and Health. NTIS report no. PB83176537. 

Goldberg, Abraham. 1959. “Acute Intermittent Porphyria: a Study of 50 Cases.” Quarterly Journal 
of Medicine 28: 183-209. 

Goldberg, Abraham, D. Doyle, A. C. Yeung Laiwah, Michael R. Moore, and Kenneth E. L. McColl. 
1985. “Relevance of Cytochrome-c-Oxidase Deficiency to Pathogenesis of Acute Porphyria.” 
Quarterly Journal of Medicine 57: 799. Abstract. 

Gordon, Zinaida V. 1966. Voprosy gigieny truda i biologicheskogo deistviya elektromagnitnykh polei 
sverkhvysokikh chastot. Leningrad: “Meditsina.” In English translation as Biological Effect of 
Microwaves in Occupational Hygiene (Jerusalem: Israel Program for Scientific Translations), 
1970. 

Gordon, Zinaida V., ed. 1973. O biologicheskom deystvii elektromagnitnykh poley radiochastot, 4th 
ed. Moscow. In English translation as Biological Effects of Radiofrequency Electromagnetic 
Fields, JPRS 63321 (1974). 

Gorman, Jack M., M. R. Fyer, R. R. Goetz., J. Askanazi, M. R. Liebowitz, A. J. Fyer, J. Kinney, and 
D. F. Klein. 1988. “Ventilatory Physiology of Patients with Panic Disorder.” Archives of General 
Psychiatry 45: 31-39. 

Gozal, David, Oscar Sans Capdevila, and Leila Kheirandish-Gozal. 2008. “Metabolic Alterations and 
Systemic Inflammation in Obstructuve Sleep Apnea among Nonobese and Obese Prepubertal 
Children.” American Journal of Respiratory and Critical Care Medicine 177: 1142-49. 

Grace, Sherry L., Susan E. Abbey, Jane Irvine, Zachary M. Shnek, and Donna E. Stewart. 2004. 
“Prospective Examination of Anxiety Persistence and Its Relationship to Cardiac Symptoms and 
Recurrent Cardiac Events.” Psychotherapy and Psychosomatics 73: 344-52. 

Grant, Ronald T. 1925. “Observations on the After-Histories of Men Suffering from the Effort 
Syndrome.” Heart 12: 121-42. 





Graybiel, Ashton and Paul D. White. 1935. "Inversion of the T Wave in Lead I or II of the 
Electrocardiogram in Young Individuals with Neurocirculatory Asthenia, with Thyrotoxicosis, in 
Relation to Certain Infections, and Following Paroxysmal Ventricular Tachycardia." American 
Heart Journal 10: 345-54. 

Haldane, John Scott. 1922. Respiration. New Haven: Yale University Press. 

Haldane, John Scott and John Gillies Priestley. 1935. Respiration. New Haven: Yale University 
Press. 

Hamman, Louis and Charles W. Wainwright. 1936. “The Diagnosis of Obscure Fever. I. The 
Diagnosis of Unexplained, Long-continued, Low-grade Fever.” Bulletin of the Johns Hopkins 
Hospital 58: 109-33. 

Harrison, Tinsley Randolph, F. C. Turley, Edgar Jones, and J. Alfred Calhoun. 1931. “Congestive 
Heart Failure X: The Measurement of Ventilation as a Test of Cardiac Function.” Archives of 
Internal Medicine 48(3): 377-98. 

Hartshorne, Henry. 1864. “On Heart Disease in the Army." American Journal of the Medical 
Sciences 48(7): 89-91. 

Hatano, Shuichi and Toshihisa Matsuzaki. 1977. “Atherosclerosis in Relation to Personal Attributes 
of a Japanese Populatiion in Homes for the Aged.” In: Schettler G, Y. Gogo, Y. Hata, and G. 
Klose, eds, Atherosclerosis IV: Proceedings of the Fourth International Symposium. (New York: 
Springer), pp. 116-20. 

Hay, John. 1923. “Disorders of the Cardio-Vascular System.” In: W. G. MacPherson, W. P. 
Herringham, T. R. Elliott, and A. Balfour, eds., History of the Great War (London: His Majesty’s 
Stationery Office), vol. 1, pp. 504-38. 

Hayward, Chris, C. Barr Taylor, Walton T. Roth, Roy King, and W. Stewart Agras. 1989. “Plasma 
Lipid Levels in Patients with Panic Disorder or Agoraphobia.” American Journal of Psychiatry 
146(7): 917-19. 

Healer, Janet. 1970. “Review of Studies of People Occupationally Exposed to Radio-Frequency 
Radiation.” In: Stephen F. Cleary, ed., Biological Effects and Health Implications of Microwave 
Radiation. Symposium Proceedings (Rockville, MD: U.S. Department of Health, Education and 
Welfare), Publication BRH/DBE 70-2, pp. 90-97. 

Herrick, Ariane L., B. Miles Fisher, Michael R. Moore, Sylvia Cathcart, Kenneth E. L. McColl, and 
Abraham Goldberg. 1990. “Elevation of Blood Lactate and Pyruvate Levels in Acute Intermittent 
Porphyria — A Reflection of Haem Deficiency?” Clinica Chimica Acta 190(3): 157-62. 

Hibbert, George and David Pilsbury. 1989. “Hyperventilation: Is It a Cause of Panic Attacks?” 
British Journal of Psychiatry 155(6): 805-9. 

Hick, Ford Kimmel. 1936. “Criteria of Oxygen Want with Especial Reference to Neurocirculatory 
Asthenia.” Ph.D. thesis, University of Illinois, Chicago. 

Hick, Ford Kimmel, A. W. Christian, and P. W. Smith. 1937. “Criteria of Oxygen Want, with 
Especial Reference to Neurocirculatory Asthenia.” American Journal of the Medical Sciences 
194: 800-4. 

Hill, Ian G. W. and H. A. Dewar. 1945. “Effort Syndrome.” Lancet 2: 161-64. 

Holmes, Gary P., Jonathan E. Kaplan, Nelson M. Gantz, Anthony L. Komaroff, Lawrence B. 
Schonberger, Stephen E. Straus, James F. Jones, Richard E. Dubois, Charlotte Cunningham- 
Rundles, Savita Pahwa, Giovanna Tosato, Leonard S. Zegans, David T. Purtilo, Nathaniel Brown, 
Robert T. Schooley, and Irena Brus. 1988. “Chronic Fatigue Syndrome: A Working Case 
Definition.” Annals of Internal Medicine 108: 387-89. 

Holmgren, A., B. Jonsson, M. Levander, H. Linderholm, T. Sjöstrand, and G. Ström. 1959. “Ecg 
Changes in Vasoregulatory Asthenia and the Effect of Physical Training.” Acta Medica 
Scandinavica 165(4): 259-71. 


Holt, Phoebe E. and Gavin Andrews. 1989. *Hyperventilation and Anxiety in Panic Disorder, Social 
Phobia, GAD and Normal Controls." Behaviour Research and Therapy 27(4): 453-60. 

Howell, Joel D. 1985. “‘Soldier’s Heart’: The Redefinition of Heart Disease and Specialty Formation 
in Early Twentieth-Century Great Britain." Medical History. Supplement 5: 34-52. 

Hroudová, Jana and Zdeněk Fišar. 2011. “Connectivity between Mitochondrial Functions and 
Psychiatric Disorders.” Psychiatry and Clinical Neurosciences 65: 130-41. 

Huffman, Jeff C., Mark H. Pollack, and Theodore A. Stern. 2002. “Panic Disorder and Chest Pain: 
Mechanisms, Morbidity, and Management.” Primary Care Companion, Journal of Clinical 
Psychiatry 4(2): 54-62. 

Hume, W. E. 1918. *A Study of the Cardiac Disabilities of Soldiers in France (V.D.H. and D.A.H.)." 
Lancet 1: 529-34. 

International Labour Office. 1921. Compensation for War Disabilities in Great Britain and the 
United States. Studies and Reports, ser. E, no. 4, December 30. Geneva. 

Izmerov, N. F., ed. 2005. Rossiyskaya entsiklopediya po meditsine truda (“Russian Encyclopedia of 
Occupational Medicine"). Moscow: “Meditsina.” 

. 2011a. Professional" naya patologiya: natsional’noe rykovodstvo (“Occupational Pathology: 

National Manual"). 2011. Moscow: GEOTAR-Media. 

. 2011b. Professional’nye bolezni (“Occupational Diseases”). Moscow: Academia. 

Izmerov, N. F. and E. I. Denisov, eds. 2001. Professional’niy risk (“Occupational Risk”). Moscow: 
Sotsizdat. 

Izmerov, N. F. and V. F. Kirillova, eds. 2008. Gigiyena truda (“Occupational Hygiene”). Moscow: 
GEOTAR-Media. 

Jammes, Y., J. G. Steinberg, O. Mambrini, F. Brégeon, and S. Delliaux. 2005. *Chronic Fatigue 
Syndrome: Assessment of Increased Oxidative Stress and Altered Muscle Excitability in 
Response to Incremental Exercise." Journal of Internal Medicine 257: 299-310. 

Jason, Leonard A., Karina Corradi, Sara Gress, Sarah Williams, and Susan Torres-Harding. 2006. 
“Causes of Death Among Patients with Chronic Fatigue Syndrome.” Health Care for Women 
International 27: 615-26. 

Jerabek, Jiri. 1979. “Biological Effects of Magnetic Fields.” Pracovni Lekarstvi 31(3): 98-106. JPRS 
76497 (1980), pp. 1-26. 

Johnson, George. 1868. “A Lecture on Dropsy: Its Pathology, Prognosis, and Principles of 
Treatment.” British Medical Journal 1: 213-15. 

Johnston, William J. 1880. Telegraphic Tales and Telegraphic History. New York: W. J. Johnston. 

Jones, Maxwell. 1948. “Physiological and Psychological Responses to Stress in Neurotic Patients.” 
Journal of Mental Science 94: 392-427. 

Jones, Maxwell and Veronica Mellersh. 1946. “A Comparison of the Exercise Response in Anxiety 
States and Normal Controls.” Psychosomatic Medicine 8: 180-87. 

Jones, Maxwell and Ronald Scarisbrick. 1943. “Effect of Exercise on Soldiers with Effort 
Intolerance.” Lancet 2: 331-32. 

. 1946. “The Effect of Exercise on Soldiers with Neurocirculatory Asthenia. Psychosomatic 
Medicine 8: 188-92. 

Justeson, Don R. 1979. “Behavioral and Psychological Effects of Microwave Radiation.” Bulletin of 
the New York Academy of Medicine 55(11): 1058-78. 

Kannel, William B., 1974. “The Role of Cholesterol in Coronary Atherogenesis.” Medical Clinics of 
North America 58(2): 363-79. 

Kannel, William B., Thomas R. Dawber, and Mandel E. Cohen. 1958. “The Electrocardiogram in 
Neurocirculatory Asthenia (Anxiety Neurosis or Neurasthenia): A Study of 203 Neurocirculatory 











Asthenia Patients and 757 Healthy Controls in the Framingham Study." Annals of Internal 
Medicine 49(6): 1351-60. 

Kaplan, Peter W. and Darrell V. Lewis. 1986. "Juvenile Acute Intermittent Porphyria with 
Hypercholesterolemia and Epilepsy: A Case Report and Review of the Literature." Journal of 
Child Neurology 1(1): 38-45. 

Katerndahl, David. 2004. *Panic & Plaques: Panic Disorder and Coronary Artery Disease in Patients 
with Chest Pain." Journal of the American Board of Family Practice 17(2): 114-26. 

Kawachi, Ichiro, David Sparrow, Pantel S. Vokonas, and Scott T. Weiss. 1994. “Symptoms of 
Anxiety and Risk of Coronary Heart Disease: The Normative Aging Study.” Circulation 90(5): 
2225-29. 

Key, Timothy J., Gary E. Fraser, Margaret Thorogood, Paul N. Appleby, Valerie Beral, Gillian 
Reeves, Michael L. Burr, Jenny Chang-Claude, Rainer Frentzel-Beyme, Jan W. Kusma, Jim 
Mann, and Klim McPherson. 1999. “Mortality in vegetarians and Nonvegetarians: Detailed 
Findings from a Collaborative Analysis of 5 Prospective Studies.” American Journal of Clinical 
Nutrition 70: 516S-524S. 

Keys, Ancel. 1953. “Atherosclerosis: A Problem in Newer Public Health.” Journal of the Mount 
Sinai Hospital 20(2): 118-39. 

Kholodov, Yury A. 1966. The Effect of Electromagnetic and Magnetic Fields on the Central Nervous 
System. Translation of Vliyaniye elektromagnitnykh i magnitnykh poley na tsentral’nuyu nervnuyu 
sistemu (Moscow: Nauka). NASA report no. TT-F-465. 

Klimkova-Deutschova, Eliska. 1974. “Neurologic Findings in Persons Exposed to Microwaves.” In: 
P. Czerski et al., eds., Biologic Effects and Health Hazards of Microwave Radiation: Proceedings 
of an International Symposium, Warsaw, 15-18 October 1973 (Warsaw: Polish Medical 
Publishers), pp. 268-72. 

Knickerbocker, G. G., translator. 1975. Study in the USSR of Medical Effects of Electric Fields on 
Electric Power Systems. New York: IEEE Power Engineering Society. Special Publication no. 10. 

Kochanek, Kenneth D., Sherry L. Murphy, Jiaquan Xu, and Elizabeth Arias. 2019. “Deaths: Final 
data for 2017.” National Vital Statistics Reports, vol. 68, no. 9. Hyattsville, MD: National Center 
for Health Statistics. 

Koller, F. 1962. “The Value of Anticoagulants in the Prophylaxis and Therapy of Ischaemic Heart 
Disease.” Bulletin of the World Health Organization 27(6): 659-66. 

Kolodub, F. A. and O. N. Chernysheva. 1980. “Special Features of Carbohydrate- Energy and 
Nitrogen Metabolism in the Rat Brain under the Influence of Magnetic Fields of Commercial 
Frequency.” Ukrainskiy Biokhimicheskiy Zhurnal 1980(3): 299-303. JPRS 77393 (1981), pp. 42- 
44. 

Korach, S. 1916. "Über Blutdruckmessungen bei Herzstórungen der Kriegsteilnehmer." Berliner 
klinische Wochenschrift 53(34): 944-45. 

Kordaé, Vaclav, Michaela Kozakova, and Pavel Martásek. 1989. *Changes of Myocardial Functions 
in Acute Hepatic Porphyrias: Role of Heme Arginate Administration." Annals of Medicine 21(4): 
273-76. 

Krutikov, V. N., Yu. I. Bregadze, and A. B. Kruglov, eds. 2003. Kontrol’ fizicheskikh faktorov 
okruzhayushchey sredy, opasnykh dlya cheloveka (“Control of Environmental Physical Factors 
that are Hazardous to People”). “Ekometriya” encyclopedia series. Moscow: IPK Standards Press. 

Krutikov, V. N., N. V. Rubtsova, Y. I. Bregadze, and A. B. Kruglov, eds. 2004. Vozdeystviye na 
organizm cheloveka opasnykh i vrednykh proizvodstvennykh faktorov. Mediko- biologicheskiye i 
metrologicheskiye aspekty (“The Effect of Dangerous and Injurious Occupational Factors on the 
Human Body. Medical, Biological and Metrological Aspects”). “Ekometriya” encyclopedia series, 
2 vols. Moscow: IPK Standards Press. 


Kudryashov, Yu. B., Yu. F. Perov, and A. B. Rubin. 2008. Radiatsionnaya biofizika: radiochastotnye 
i mikrovolnovye elektromagnitnye izlucheniya (“Radiation Biophysics: Radiofrequency and 
Microwave Electromagnetic Radiation"). Moscow: Fizmatlit. 

Kumar, Neelima, Sonika Sangwan, and Pooja Badotra. 2011. *Exposure to Cell Phone Radiations 
Produces Biochemical Changes in Worker Honey Bees." Toxicology International 18(1): 70-72. 
Lary, Darrel and Nora Goldschlager. 1974. “Electrocardiographic Changes during Hyperventilation 
Resembling Myocardial Ischemia in Patients with Normal Coronary Arteriograms." American 

Heart Journal 87(3): 383-90. 

Lazarev, V. L, V. F. Vinogradov, and V. V. Trotsiuk. 1989. *Blood Lipid Levels in Patients with 
Neurocirculatory Asthenia of the Cardiac Type." Kardiologiya 29(7): 74-77 (in Russian). 

Lees, Robert S., Chull S. Song, Richard D. Levere, and Attallah Kappas. 1970. “Hyperbeta- 
Lipoproteinemia in Acute Intermittent Porphyria — Preliminary Report." New England Journal of 
Medicine 282: 432-33. 

Lefebvre, B., J.-L. Pépin, J.-P. Baguet, R. Tamisier, M. Roustit, K. Riedweg, G. Bessard, P. Lévy, and 
F. Stanke-Labesque. 2008. “Leukotriene By: Early Mediator of Atherosclerosis in Obstructuve 


Sleep Apnoea?” European Respiratory Journal 32: 113-20. 

Leibowitz, Joshua Otto. 1970. The History of Coronary Heart Disease. Berkeley: University of 
California Press. 

Leonhardt, K. F. 1981. *Kardiovaskuláre Stórungen bei der akuten intermittierenden Porphyrie 
(AIP).” Wiener klinische Wochenschrift 93(18): 580-84. 

Lerner, A. Martin, Claudine Lawrie and Howard S. Dworkin. 1993. *Repetitively Negative Changing 
T Waves at 24-h Electrocardiographic Monitors in Patients with the Chronic Fatigue Syndrome." 
Chest 104(5): 1417-21. 

Letavet, A. A. and Zinaida V. Gordon, eds. 1960. O biologicheskom vozdeystvii sverkhvysokikh 
chastot. Moscow: Academy of Medical Sciences. In English translation, 1962, as The Biological 
Action of Ultrahigh Frequencies, JPRS 12471. 

Levander-Lindgren, Maj. 1962. “Studies in NeurocirculatoryAsthenia (Da Costa’s Syndrome). I. 
Variations with Regard to Symptoms and Some Pathophysiological Signs.” Acta Medica 
Scandinavica 172(6): 665-76. 

. 1963. “Studies in Neurocirculatory Asthenia. III. On the Etiology and Pathogenesis of Signs 
in the Work Test and Orthostatic Test.” Acta Medica Scandinavica 173(5): 631-37. 

Levitina, N. A. 1966. “Nonthermal Action of Microwaves on the Cardiac Rhythm of a Frog.” 
Bulletin of Experimental Biology and Medicine 62(6): 1386-87. 

Levy, Robert L., Howard G. Bruenn, and Dorothy Kurtz. 1934. “Facts on Disease of Coronary 
Arteries. Based on a Survey of Clinical and Pathologic Records of Seven Hundred and Sixty-Two 
Cases.” American Journal of the Medical Sciences 187(3): 376-90. 

Lewis, Thomas. 1918a. “Report on Neuro-Circulatory Asthenia and Its Management.” Military 
Surgeon 42: 409-26, 711-19. 

. 1918b. The Soldier s Heart and the Effort Syndrome. London: Shaw and Sons. 

. 1940. The Soldier s Heart and the Effort Syndrome, 2nd ed. London: Shaw and Sons. 

Lewis, Thomas, Thomas F. Cotton, J. Barcroft, T. R. Milroy, D. Dufton, and T. R. Parsons. 1916. 
“Breathlessness in Soldiers Suffering from Irritable Heart.” British Medical Journal 2: 517-19. 

Li, Jianguo, Laura N. Thorne, Naresh M. Punjabi, Cheuk-Kwan K. Sun, Alan R. Schwartz, Philip L. 
Smith, Rafael L. Marino, Annabelle Rodriguez, Walter C. Hubbard, Christopher P. O’Donnell, 
and Vsevolod Y. Polotsky. 2005. “Intermittent Hypoxia Induces Hyperlipidemia in Lean Mice.” 
Circulation Research 97(7): 698-706. 











Li, Jianguo, Vladimir Savransky, Ashika Nanayakkara, Phillip L. Smith, Christopher P. O'Donnell, 
and Vsevolod Y. Polotsky. 2007. *Hyperlipidemia and Lipid Peroxidation are Dependent on the 
Severity of Chronic Intermittent Hypoxia." Journal of Applied Physiology 102(2): 557-63. 

Lian, Camille. 1916. “Les palpitations par hypertension artérielle aux armées." Presse médicale, 
24(29): 228-29. 

Lin, James C. 1978. Microwave Auditory Effects and Applications. Springfield, IL: Charles C. 
Thomas. 

Logue, Robert Bruce, James Fletcher Hanson, and William A. Knight. 1944. *Electrocardiographic 
Studies in Neurocirculatory Asthenia." American Heart Journal 28(5): 574-77. 

Lopez, Alan D., Colin D. Mathers, Majid Ezzati, Dean T. Jamiston, and Christopher J. L. Murray. 
2006. Global Burden of Disease and Risk Factors. Oxford University Press. 

MacFarlane, Andrew. 1918. “Neurocirculatory Myasthenia.” Journal of the American Medical 
Association 71(9): 730-33. 

MacKenzie, James. 1916a. “The Soldier’s Heart.” British Medical Journal 1: 117-19. 

. 1916b. “Discussion on the Soldier’s Heart.” Proceedings of the Royal Society of Medicine, 
Therapeutical and Pharmacological Section, 9: 27-60. 

Makolkin, V. I., E. A. Sokova, and S. A. Abbakumov. 1984. “The Oxygen Supply in Patients with 
Neurocirculatory Asthenia during Exercise.” Kardiologiya 24(11): 71-76 (in Russian). 

Mäntysaari, Matti J., Kari J. Antila, and Tuomas E. Peltonen. 1988. “Blood Pressure Reactivity in 
Patients with Neurocirculatory Asthenia.” American Journal of Hypertension 1(2): 132-39. 

Marazziti, D., S. Baroni, M. Picchetti, P. Landi, S. Silvestri, E. Vatteroni and M. Catena Dell’Osso. 
2011. “Mitochondrial Alterations and Neuropsychiatric Disorders.” Current Medicinal Chemisry 
18: 4715-21. 

Marha, Karel. 1970. “Maximum Admissible Values of HF and UHF Electromagnetic Radiation at 
Work Places in Czechoslovakia.” In: Stephen F. Cleary, ed., Biological Effects and Health 
Implications of Microwave Radiation. Symposium Proceedings (Rockville, MD: U.S. Department 
of Health, Education and Welfare), Publication BRH/DBE 70-2, pp. 188-96. 

Marha, Karel, Jan Musil, and Hana Tuha. 1971. Electromagnetic Fields and the Life Environment. 
Berkeley: San Francisco Press. 

Maron, Barry J., Joseph J. Doerer, Tammy S. Haas, David M. Tierney, and Frederick O. Mueller. 
2009. “Sudden Deaths in Young Competitive Athletes: Analysis of 1866 Deaths in the United 
States, 1980-2006.” Circulation 119: 1085-92. 

Martens, Elisabeth J., Peter de Jonge, Beeya Na, Beth E. Cohen, Heather Lett, and Mary A. Whooley. 
2010. “Scared to Death? Generalized Anxiety Disorder and Cardiovascular Events in Patients 
with Stable Coronary Heart Disease: The Heart and Soul Study.” Archives of General Psychiatry 
67(7): 750-58. 

Martin, Linda G., Vicki A. Freedman, Robert F. Schoeni, and Patricia M. Andreski. 2009. “Health 
and Functioning Among Baby Boomers Approaching 60.” Journal of Gerontology: Social 
Sciences 64B(3): 369-77. 

Master, Arthur M. 1943. “Effort Syndrome or Neurocirculatory Asthenia in the Navy.” United States 
Naval Medical Bulletin 41(3): 666-69. 

Mathers, Colin, Ties Boerma, and Doris Ma Fat. 2008. The Global Burden of Disease, 2004 Update. 
Geneva: World Health Organization. 

McArdle, Nigel, David Hillman, Lawrie Beilin, and Gerald Watts. 2007. “Metabolic Risk Factors for 
Vascular Disease in Obstructuve Sleep Apnea.” American Journal of Respiratory and Criticial 
Care Medicine 175: 190-95. 





McCullough, Peter A., Edward F. Philbin, John A. Spertus, Scott Kaatz, Keisha R. Sandberg, W. 
Douglas Weaver. 2002. *Confirmation of a Heart Failure Epidemic: Findings from the Resource 
Utilization Among Congestive Heart Failure (REACH) Study." Journal of the American College 
of Cardiology 39(1): 60-69. 

McCully, Kevin K., Benjamin H. Natelson, Stefano Iotti, Sueann Sisto, and John S. Leigh. 1996. 
“Reduced Oxidative Muscle Metabolism in Chronic Fatigue Syndrome.” Muscle & Nerve 19: 
621-25. 

McFarland, Ross Armstrong. 1932. “The Psychological Effects of Oxygen Deprivation (Anoxemia) 
on Human Behavior.” Archives of Psychology, no. 145. 

. 1941. “The Internal Environment and Behavior.” American Journal of Psychiatry 97: 858- 





77. 

McGovern, Paul G., David R. Jacobs, Jr., Eyal Shahar, Donna K. Arnett, Aaron R. Folsom, Henry 
Blackburn, and Russell V. Luepker. 2001. “Trends in Acute Coronary Heart Disease Mortality, 
Morbidity, and Medical Care from 1985 through 1997: The Minnesota Heart Survey.” Circulation 
104: 19-24. 

McLaughlin, John T. 1962. “Health Hazards from Microwave Radiation.” Western Medicine 3(4): 
126-30. 

McLeod, K. 1898. “Tropical Heart.” Journal of Tropical Medicine 1: 3-4. 

McMurray, John J. and Simon Stewart. 2000. “Epidemiology, Aetiology, and Prognosis of Heart 
Failure.” Heart 83: 596-602. 

McRee, Donald I. “Review of Soviet/Eastern European Research on Health Aspects of Microwave 
Radiation.” 1979. Bulletin of the New York Academy of Medicine 55(11): 1133-51. 

. 1980. “Soviet and Eastern European Research on Biological Effects of Microwave 
Radiation.” Proceedings of the IEEE 68(1): 84-91. 

McRee, Donald I., Michael J. Galvin, and Clifford L. Mitchell. 1988. “Microwave Effects on the 
Cardiovascular System: A Model for Studying the Responsivity of the Autonomic Nervous 
System to Microwaves.” In: Mary Ellen O'Connor and Richard H. Lovely, eds., Electromagnetic 
Fields and Neurobehavioral Function (New York: Alan R. Liss), pp. 153-77. 

Meade, Thomas W. 2001. “Cardiovascular Disease—Linking Pathology and Epidemiology." 
International Journal of Epidemiology 30: 1179-83. 

Menawat, Anand S., R. B. Panwar, D. K. Kochar, and C. K. Joshi. 1979. *Propranolol in Acute 
Intermittent Porphyria." Postgraduate Medical Journal 55: 546-47. 

Merkel, Friedrich. 1915. *Ueber Herzstórungen im Kriege." Münchener medizinische Wochenschrift 
62(20): 695-96. 

Michaels, Leon. 1966. *ZEtiology of Coronary Artery Disease: An Historical Approach." British 
Heart Journal 28: 258-64. 

Mild, Kjell Hansson, Monica Sandstróm, and Eugene Lyskov, eds. 2001. Clinical and Physiological 
Investigations of People Highly Exposed to Electromagnetic Fields. Umea, Sweden: National 
Institute for Working life. Arbetslivsrapport 3. 

Milham, Samuel. 1979. “Cancer in Aluminum Reduction Plant Workers.” Journal of Occupational 
and Environmental Medicine 7: 475-80. 

. 1982. “Mortality from Leukemia in Workers Exposed to Electrical and Magnetic Fields.” 

New England Journal of Medicine 307(4): 249. 

. 1985a. “Mortality in Workers Exposed to Electromagnetic Fields." Environmental Health 

Perspectives 62: 297-300. 

. 1985b. “Silent Keys: Leukaemia Mortality in Amateur Radio Operators.” Lancet 1: 812. 

















1988a. "Increased Mortality in Amateur Radio Operators Due to Lymphatic and 

Hematopoietic Malignancies." American Journal of Epidemiology 127(1): 50-54. 

. 1988b. *Mortality by License Class in Amateur Radio Operators." American Journal of 

Epidemiology 128(5): 1175-76. 

. 1996. *Increased Cancer Incidence in Office Workers Exposed to Strong Magnetic Fields." 

American Journal of Industrial Medicine 30(6): 702-4. 

. 2010a. “Historical Evidence that Electrification Caused the 20th Century Epidemic of 

‘Diseases of Civilization.’” Medical Hypotheses 74: 337-45. 

. 2010b. Dirty Electricity: Electrification and the Diseases of Civilization. New York: 
iUniverse. 

Milham, Samuel and Eric M. Ossiander. 2001. “Historical Evidence that Residential Electrification 
Caused the Emergence of the Childhood Leukemia Peak.” Medical Hypotheses 56(3): 290-95. 

Miwa, Kunihisa and Masatoshi Fujita. 2009. “Cardiac Function Fluctuates during Exacerbation and 
Remission in Young Adults with Chronic Fatigue Syndrome and ‘Small Heart.’” Journal of 
Cardiology 54(1): 29-35. 

Moir, Raymond A. and K. Shirley Smith. 1946. “Cardiovascular Diseases in the British Army 
Overseas.” British Heart Journal 8(2): 110-14. 

Moore, Julie L., indexer. 1984. Cumulated Index to the Bibliography of Reported Biological 
Phenomena (“Effects”) and Clinical Manifestations Attributed to Microwave and Radio- 
Frequency Radiation, compiled by Zorach R. Glaser. Riverside, CA: Julie Moore & Associates. 

Moore, Michael R. 1990. “The Pathogenesis of Acute Porphyria.” Molecular Aspects of Medicine 
11(1-2): 49-57. 

Morris, Jeremiah Noah. 1951. “Recent History of Coronary Disease.” Lancet 1: 1-7, 69-73. 

. 1961/2. “Epidemiological Aspects of Ischaemic Heart Disease.” Yale Journal of Biology and 
Medicine 34: 359-69. 

Munroe, H. E. 1919. “Observations on Flying Sickness, with Special Reference to its Diagnosis.” 
Canadian Medical Association Journal 9(10): 883-95. 

Murphy, Sherry L., Jiaquan Xu, and Kenneth D. Kochanek. 2012. “Deaths: Preliminary Data for 
2010.” National Vital Statistics Reports, vol. 60, no. 4. Hyattsville, MD: National Center for 
Health Statistics. 

Murray, Christopher J. L. and Alan D. Lopez, eds. 1996. The Global Burden of Disease. Cambridge, 
MA: Harvard University Press. 

Myhill, Sarah, Norman E. Booth, and John McLaren-Howard. 2009. “Chronic Fatigue Syndrome and 
Mitochondrial Dysfunction.” International Journal of Clinical and Experimental Medicine 2: 1- 
16. 

Nadeem, Rashid, Mukesh Singh, Mahwish Nida, Sarah Kwon, Hassan Sajid, Julie Witkowski, 
Elizabeth Pahomov, Kruti Shah, William Park, and Dan Champeau. 2014. “Effect of CPAP 
Treatment for Obstructuve Sleep Apnea Hypopnea Syndrome on Lipid Profile: A Meta- 
Regression Analysis.” Journal of Clinical Sleep Medicine 10(12): 1295-1302. 

Naghavi, Mohsen, Haidong Wang, Rafael Lozano, Adrian Davis, Xiaofeng Liang, Maigeng Zhou, 
Stein Emil Vollset, et al. 2015. “Global, Regional, and National Age-Sex Specific All-Cause and 
Cause-Specific Mortality for 240 Causes of Death, 1990-2013: A Systematic Analysis for the 
Global Burden of Disease Study 2013." Lancet 385: 117-71. 

National Center for Health Statistics, National Vital Statistics System. 1999. *Worktable I. Deaths 
from Each Cause, by 5-Year Age Groups, Race, and Sex." Atlanta: Centers for Disease Control 
and Prevention. 

















National Center for Health Statistics, National Vital Statistics System. 2006. *Worktable I. Deaths 
from Each Cause, by 5-Year Age Groups, Race, and Sex." Atlanta: Centers for Disease Control 
and Prevention. 

National Electric Light Association. 1932. The Electric Light and Power Industry 1931. Statistical 
Bulletin no. 8. 

National Electric Light Association. 1931. The Electric Light and Power Industry 1930. Statistical 
Bulletin no. 7. 

Navas-Nacher, Elena L., Laura Colangelo, Craig Beam, and Philip Greenland. 2001. *Risk Factors 
for Coronary Heart Disease in Men 18 to 39 Years of Age." Annals of Internal Medicine 134(6): 
433-39. 

Neaton, James D. and Deborah Wentworth. 1992. *Serum Cholesterol, Blood Pressure, Cigarette 
Smoking, and Death from Coronary Heart Disease: Overall Findings and Differences by Age for 
316,099 White Men." Archives of Internal Medicine 152: 56-64. 

Neuhof, Selian. 1919. “The Irritable Heart in General Practice: A Comparison between It and the 
Irritable Heart of Soldiers." Archives of Internal Medicine 24(1): 51-64. 

Newman, Anne B., F. Javier Nieto, Ursula Guidry, Bonnie K. Lind, Susan Redline, Eyal Shahar, 
Thomas G. Pickering, and Stuart F. Quan. 2001. “Relation of Sleep-disordered Breathing to 
Cardiovascular Disease Risk Factors: The Sleep Heart Health Study.” American Journal of 
Epidemiology 154(1): 50-59. 

Nikitina, Valentina N. 2001. “Hygienic, Clinical and Epidemiological Analysis of Disturbances 
Induced by Radio Frequency EMF Exposure in Human Body.” In: Kjell Hansson Mild, Monica 
Sandström, and Eugene Lyskov, eds., Clinical and Physiological Investigations of People Highly 
Exposed to Electromagnetic Fields (Umea, Sweden: National Institute for Working life), 
Arbetslivsrapport 3, pp. 32-38. 

Njelstad, Inger, Egil Arnesen, and Per G. Lund-Larsen. 1996. “Smoking, Serum Lipids, Blood 
Pressure, and Sex Differences in Myocardial Infarction: A 12-Year Follow-up of the Finnmark 
Study.” Circulation 93: 450-6. 

Novitskiy, Yu. I., Zinaida V. Gordon, Aleksandr S. Presman, and Yury A. Kholodov. 1970. “Radio 
Frequencies and Microwaves. Magnetic and Electrical Fields.” Vol. 2, part 1, chap. 1 of Osnovy 
kosmicheskoy biologii i meditsiny (“Foundations of Space Biology and Medicine”). Moscow: 
Academy of Sciences USSR. English translation by Scientific Translation Service (Washington, 
DC: NASA), 1971, report no. TT-F-14,021. 

Nutzinger, D. O. 1992. “Hertz und Angst: Herzbezogene Angste und _ kardiovaskuldres 
Morbiditátsrisiko bei Patienten mit einer Angststórung." Der Nervenarzt 63(3): 187-91. 

Okumiya, Noriya, Kenzo Tanaka, Kazuo Ueda, and Teruo Omae. 1985. *Coronary Atherosclerosis 
and Antecedent Risk Factors: Pathologic and Epidemiologic Study in Hisayama, Japan." 
American Journal of Cardiology 56: 62-66. 

Olafiranye, O., G. Jean-Louis, F. Zizi, J. Nunes, and M. T. Vincent. 2011. “Anxiety and 
Cardiovascular Risk: Review of Epidemiological and Clinical Evidence." Mind Brain 2(1): 32-37. 

Orlova, A. A. 1960. “The Clinic of Changes of the Internal Organs under the Influence of UHF.” In: 
A. A. Letavet and Z. V. Gordon, eds. The Biological Action of Ultrahigh Frequencies (Moscow: 
Academy of Medical Sciences), JPRS 12471, pp. 30-35. 

Parikh, Nisha I., Philimon Gona, Martin G. Larson, Caroline S. Fox, Emelia J. Benjamin, Joanne M. 
Murabito, Christopher J. O’Donnell, Ramachandran S. Vasan, and Daniel Levy. 2009. “Long-term 
Trends in Myocardial Infarction Incidence and Case-Fatality in the National Heart, Lung, and 
Blood Institute’s Framingham Heart Study.” Circulation 119(9): 1203-10. 

Park, Mi Ran, Jeong Kee Seo, Jae Sung Ko, Ju Young Chang, and Hye Ran Yang. 2011. “Acute 
Intermittent Porphyria Presented with Recurrent Abdominal Pain and Hypertension.” Korean 


Journal of Pediatric Gastroenterology and Nutrition 14: 81-85. 

Parkinson, John. 1941. *Effort Syndrome in Soldiers." British Medical Journal 1: 545-49. 

Paterniti, Sabrina, Mahmoud Zureik, Pierre Ducimetiére, Pierre-Jean Touboul, Jean-Marc Féve, and 
Annick  Alpérovitch. 2001. “Sustained Anxiety and 4-Year Progression of Carotid 
Atherosclerosis." Arteriosclerosis, Thrombosis, and Vascular Biology 21(1): 136-41. 

Paul, Oglesby. 1987. *Da Costa's Syndrome or Neurocirculatory Asthenia." British Heart Journal 
58: 306-15. 

Peckerman, Arnold, John J. Lamanca, Kristina A. Dahl, Rahul Chemitiganti, Bushra Qureishi, and 
Benjamin H. Natelson. 2003. *Abnormal Impedance Cardiography Predicts Symptom Severity in 
Chronic Fatigue Syndrome." American Journal of the Medical Sciences 326(2): 55-60. 

Pervushin, V. Yu. 1957. *Changes Occurring in the Cardiac Nervous Apparatus Due to the Action of 
Ultra-High-Frequency Field." Bulletin of Experimental Biology and Medicine 43(6): 734-40. 

Peter, Helmut, Philipp Goebel, Susanne Müller, and Iver Hand. 1999. “Clinically Relevant 
Cholesterol Elevation in Anxiety Disorder: A Comparison with Normal Controls." International 
Journal of Behavioral Medicine 6(1): 30-39. 

Petrov, Ioakim Romanovich, ed. 1970a. Vliyaniye SVCh-izlucheniya na organism cheloveka i 
zhivotnykh. Leningrad: “Meditsina.” In English translation as Influence of Microwave Radiation 
on the Organism of Man and Animals (Washington, DC: NASA), report no. TTF-708, 1972. 

Phillips, Anna C., G. David Batty, Catharine R. Gale, Ian J. Deary, David Osborn, Kate MacIntyre, 
and Douglas Carroll. 2009. “Generalized Anxiety Disorder, Major Depressive Disorder, and Their 
Comorbidity as Predictors of All-Cause and Cardiovascular Mortality: The Vietnam Experience 
Study.” Psychosomatic Medicine 71: 395-403. 

Phillips, Roland L, Frank R. Lemon, W. Lawrence Beeson, and Jan W. Kuzma. 1978. “Coronary 
Heart Disease Mortality among Seventh-day Adventists with Differing Dietary Habits: A 
Preliminary Report.” American Journal of Clinical Nutrition 31 (10 suppl.): S191-S198. 

Pitts, Ferris N., Jr. and James N. McClure, Jr. 1967. “Lactate Metabolism in Anxiety Neurosis.” New 
England Journal of Medicine 277(25): 1329-36. 

Plum, William Rattle. 1882. The Military Telegraph during the Civil War in the United States, 2 vols. 
Chicago: Jansen, McClurg. 

Popular Science Monthly. 1918. “How the Zeppelin Raiders Are Guided by Radio Signals.” 92: 632- 
34. 

Presman, Aleksandr Samuilovich. 1970. Electromagnetic Fields and Life. New York: Plenum. 
Translation of Elektromagnitnye polya i zhivaya priroda (Moscow: Nauka), 1968. 

Presman, Aleksandr Samuilovich and N. A. Levitina. 1962a. “Nonthermal Action of Microwaves on 
Cardiac Rhythm. Communication I. A Study of the Action of Continuous Microwaves.” Bulletin 
of Experimental Biology and Medicine 53(1): 36-39. 

. 1962b. “Nonthermal Action of Microwaves on the Rhythm of Cardiac Contractions in 
Animals. Report II. Investigation of the Action of Impulse Microwaves.” Bulletin of Experimental 
Biology and Medicine 53(2): 154-57. 

Ratcliffe, Herbert L. 1963a. “Editorial: Environmental Factors and Coronary Disease.” Circulation 
27: 481-83. 

. 1963b. “Phylogenetic Considerations in the Etiology of Myocardial Infarction.” In: Thomas 

N. James and John W. Keyes, eds., The Etiology of Myocardial Infarction (Boston: Little, Brown), 

pp. 61-89. 

. 1965. “Age and Environment as Factors in the Nature and Frequency of Cardiovascular 

Lesions in Mammals and Birds in the Philadelphia Zoological Garden.” Comparative Cardiology 

127: 715-35. 











Ratcliffe, Herbert L. and M. T. I. Cronin. 1958. “Changing Frequency of Arteriosclerosis in 
Mammals and Birds at the Philadelphia Zoological Garden: Review of Autopsy Records.” 
Circulation 18: 41-52. 

Ratcliffe, Herbert L., T. G. Yerasimides and G. A. Elliott. 1960. “Changes in the Character and 
Location of Arterial Lesions in Mammals and Birds in the Philadelphia Zoological Garden.” 
Circulation 21: 730-38. 

Ravnskov, Uffe. 2000. The Cholesterol Myths. Washington, DC: New Trends. 

Reed Dwayne M., Jack P. Strong, Joseph Resch, and Takuji Hayashi. 1989. “Serum Lipids and 
Lipoproteins as Predictors of Atherosclerosis: An Autopsy Study.” Arteriosclerosis, Thrombosis, 
and Vascular Biology 9: 560-64. 

Reeves, William C., James F. Jones, Elizabeth Maloney, Christine Heim, David C. Hoaglin, 
Roumiana S. Boneva, Marjorie Morrissey, and Rebecca Devlin. 2007. “Prevalence of Chronic 
Fatigue Syndrome in Metropolitan, Urban, and Rural Georgia." Population Health Metrics 5: 5. 

Reyes, Michele, Rosane Nisenbaum, David C. Hoaglin, Elizabeth R. Unger, Carol Emmons, Bonnie 
Randall, John A. Stewart, Susan Abbey, James F. Jones, Nelson Gantz, Sarah Minden, and 
William C. Reeves. 2003. "Prevalence and Incidence of Chronic Fatigue Syndrome in Wichita, 
Kansas." Archives of Internal Medicine 163: 1530-36. 

Rhoads, George G, William C. Blackwelder, Grant N. Stemmermann, Takuji Hayashi, and Abraham 
Kagan. 1978. “Coronary Risk Factors and Autopsy Findings in Japanese-American Men." 
Laboratory Investigation 38(3): 304-11. 

Ridley, Alan. 1969. “The Neuropathy of Acute Intermittent Porphyria.” Quarterly Journal of 
Medicine 38: 307-33. 

. 1975. “Porphyric Neuropathy.” In: Peter James Dyck, P. K. Thomas, and Edward H. 
Lambert, eds., Peripheral Neuropathy (Philadelphia: W. B. Saunders), pp. 942-55. 

Rigg, Kathleen J., R. Finlayson, C. Symons, K. R. Hill, and R. N. T-W-Fiennes. 1960. “Degenerative 
Arterial Disease of Animals in Captivity with Special Reference to the Comparative Pathology of 
Atherosclerosis.” Proceedings of the Zoological Society of London 135(2): 157-64. 

Robey, William H. and Ernst P. Boas. 1918. “Neurocirculatory Asthenia.” Journal of the American 
Medical Association 71(7): 525-29. 

Robinson, G. V., J. C. T. Pepperell, H. C. Segal, R. J. O. Davies, and J. R. Stradling. 2004. 
“Circulating Cardiovascular Risk Factors in Obstructive Sleep Apnoea: Data from Randomised 
Controlled Trials.” Thorax 59: 777-82. 

Rodríguez-Artalejo, F., P. Guallar-Castillón, J. R. Banegas Banegas, and J. del Rey Calero. 1997. 
“Trends in Hospitalization and Mortality for Heart Failure in Spain, 1980-1993.” European Heart 
Hournal 18: 1771-79. 

Roger, Véronique L., Susan A. Weston, Margaret M. Redfield, Jens P. Hellermann- Homan, Jill 
Killian, Barbara P. Yawn, and Steven J. Jacobsen. 2004. “Trends in Heart Failure Incidence and 
Survival in a Community-Based Population.” JAMA 292(3): 344-50. 

Rothenbacher, Dietrich, Harry Hahmann, Bernd Wüsten, Wolfgang Koenig, and Hermann Brenner. 
2007. “Symptoms of Anxiety and Depression in Patients with Stable Coronary Heart Disease: 
Prognostic Value and Consideration of Pathogenetic Links.” European Journal of Cardiovascular 
Prevention and Rehabilitation 14: 547-54. 

Rothschild, Marcus A. 1930. “Neurocirculatory Asthenia.” Bulletin of the New York Academy of 
Medicine 6(4): 223-42. 

Rozanski, Alan, James A. Blumenthal, and Jay Kaplan. 1999. “Impact of Psychological Factors on 
the Pathogenesis of Cardiovascular Disease and Implications for Therapy.” Circulation 99: 2192- 
2217. 





Rural Electrification Administration, U.S. Dept. of Agriculture. January 1940. Rural Electrification 
in Utah. Washington, DC. 


. 1941. Report of the Administrator of the Rural Electrification Administration. Washington, 





DC. 

Ryle, John A. and W. T. Russell. 1949. *The Natural History of Coronary Disease." British Heart 
Journal 11(4): 370-89. 

Sadchikova, Maria N. 1960. “State of the Nervous System under the Influence of UHF.” In: A. A. 
Letavet and Z. V. Gordon, eds., The Biological Action of Ultrahigh Frequencies (Moscow: 
Academy of Medical Sciences), JPRS 12471, pp. 25-29. 

1974. “Clinical Manifestations of Reactions to Microwave Irradiation in Various 
Occupational Groups.” In: P. Czerski et al., eds., Biologic Effects and Health Hazards of 
Microwave Radiation: Proceedings of an International Symposium, Warsaw, 15-18 October 1973 
(Warsaw: Polish Medical Publishers), pp. 261-67. 

Sadchikova, Maria N. and K. V. Glotova. 1973. “The Clinic, Pathogenesis, Treatment, and Outcome 
of Radiowave Sickness.” In: Z. V. Gordon, ed. Biological Effects of Radiofrequency 
Electromagnetic Fields, JPRS 63321 (1974), pp. 54-62. 

Sadchikova, Maria N., S. F. Kharlamova, N. N. Shatskaya, and N. V. Kuznetsova. 1980. 
“Significance of Blood Lipid and Electrolyte Disturbances in the Development of Some Reactions 
to Microwaves.” Gigiyena truda i professional’nyye zabolevaniya 1980(2): 38-39. JPRS 77393 
(1981), pp. 37-39. 

Saint, Eric G., D. Curnow, and R. Paton. 1954. “Diagnosis of Acute Porphyria.” British Medical 
Journal 1: 1182-84. 

Sanders, Aaron P., William T. Joines, and John W. Allis. 1984. “The Differential Effects of 200, 591, 
and 2,450 MHz Radiation on Rat Brain Energy Metabolism.” Bioelectromagnetics 5: 419-33. 

Savransky, Vladimir, Ashika Nanayakkara, Jianguo Li, Shannon Bevans, Philip L. Smith, Annabelle 
Rodriguez, and Vsevolod Y. Polotsky. 2007. “Chronic Intermittent Hypoxia Induces 
Atherosclerosis.” American Journal of Respiratory and Critical Care Medicine 175: 1290-97. 

Scherrer, Jeffrey F., Timothy Chrusciel, Angelique Zeringue, Lauren D. Garfield, Paul J. Hauptman, 
Patrick J. Lustman, Kenneth E. Freedland, Robert M. Carney, Kathleen K. Bucholz, Richard 
Owen, and William R. True. 2010. “Anxiety Disorders Increase Risk for Incident Myocardial 
Infarction in Depressed and Nondepressed Veterans Administration Patients.” American Heart 
Journal 159(5): 772-79. 

Schott, Theodor. 1915. *Beobachtungen über Herzaffektionen bei Kriegsteilnehmern." Münchener 
medizinische Wochenschrift 62(20): 677-79. 

Scriven, George P. 1915. *Notes on the Organization of Telegraph Troops in Foreign Armies. Great 
Britain." In: Scriven, The Service of Information, United States Army, (Washington, DC: 
Government Printing Office), pp. 127-32. Reproduced in Paul J. Scheips, ed., Military Signal 
Communications (New York: Arno Press), 1980, vol. 2. 

Seldenrijk, Adrie, Nicole Vogelzangs, Hein P. J. van Hout, Harm W. J. van Marwijk, Michaela 
Diamant, and Brenda W. J. H. Penninx. 2010. *Depression and Anxiety Disorders and Risk of 
Subclinical Atherosclerosis: Findings from the Netherlands Study of Depression and Anxiety 
(NESDA)." Journal of Psychosomatic Research 69: 203-10. 

Sharrett, A. R., C. M. Ballantyne, S. A. Coady, G. Heiss, P. D. Sorlie, D. Catellier, and W. Patsch. 
2001. *Coronary Heart Disease Prediction From Lipoprotein Cholesterol Levels, Triglycerides, 
Lipoprotein(a), Apolipoproteins A-I and B, and HDL Density Subfractions: The Atherosclerosis 
Risk in Communities (ARIC) Study." Circulation 104: 1108-13. 





Shibeshi, Woldecherkos A., Yinong Young-Xu, and Charles M. Blatt. 2007. “Anxiety Worsens 
Prognosis in Patients with Coronary Artery Disease." Journal of the American College of 
Cardiology 49(20): 2021-27. 

Shiue, J. W., F. Y. Lee, K. J. Hsiao, Y. T. Tsai, S. D. Lee, and S. J. Wu. 1989. *Abnormal Thyroid 
Function and Hypercholesterolemia in a Case of Acute Intermitten Porphyria." Taiwan Yi Xue Hui 
Za Zhi (Journal of the Formosa Medical Association) 88(7): 729-31. 

Shorter, Edward. 1992. From Paralysis to Fatigue: A History of Psychosomatic Illness in the Modern 
Era. New York: Free Press. 

. 1997. A History of Psychiatry. New York: John Wiley & Sons. 

Shutenko, O. I., I. P. Kozarin and I. I. Shvayko. 1981. “Effects of Superhigh Frequency 
Electromagnetic Fields on Animals of Different Ages.” Gigiyena i Sanitariya 1981(10): 35-38. 
JPRS 81300 (1982), pp. 85-90. 

Siekierzynski, Maksymilian. 1974. “A Study of the Health Status of Microwave Workers.” In: P. 
Czerski et al., eds., Biologic Effects and Health Hazards of Microwave Radiation: Proceedings of 
an International Symposium, Warsaw, 15-18 October 1973 (Warsaw: Polish Medical Publishers), 
pp. 273-80. 

Siekierzynski, Maksymilian, Przemystaw Czerski, Halina Milczarek, Andrej Gidynski, Czestaw 
Czarnecki, Eugeniusz Dziuk, and Wieslaw Jedrzejczak. 1974. “Health Surveillance of Personnel 
Occupationally Exposed to Microwaves. II. Functional Disturbances.” Aerospace Medicine 
45(10): 1143-45. 

Sijbrands, Eric J. G., Rudi G. J. Westendorp, Joep C. Defesche, Paul H. E. M. de Meier, Augustinus 
H. M. Smelt, and John J. P. Kastelein. 2001. “Mortality Over Two Centuries in Large Pedigree 
with Familial Hypercholesterolaemia: Family Tree Mortality Study.” British Medical Journal 322: 
1019-23. 

Silverman, Charlotte. 1979. “Epidemiologic Approach to the Study of Microwave Effects.” Bulletin 
of the New York Academy of Medicine 55(11): 1166-81. 

Smart, Charles. 1888. “Cardiac Diseases.” In: Smart, The Medical and Surgical History of the War of 
the Rebellion, part III, vol. I, Medical History (Washington, DC: Government Printing Office), pp. 
860-69. 

Snowdon, David A. 1988. “Animal Product Consumption and Mortality Because of All Causes 
Combined, Coronary Heart Disease, Stroke, Diabetes, and Cancer in Seventh-day Adventists.” 
American Journal of Clinical Nutrition 48: 739-48. 

Soares-Filho, Gastão L. E, Oscar Arias-Carrión, Gaetano Santulli, Adriana C. Silva, Sergio 
Machado, Alexandre M. Valenga, and Antonio E. Nardi. 2014. “Chest Pain, Panic Disorder and 
Coronary Artery Disease: A Systematic Review." CNS & Neurological Disorders — Drug Targets 
13(6): 992-1001. 

Solberg, Lars A., Jack P. Strong, Ingar Holme, Anders Helgeland, Ingvar Hjermann, Paul Leren, and 
Svein Børre Mogensen. 1985. “Stenoses in the Coronary Arteries: Relation to Atherosclerotic 
Lesions, Coronary Heart Disease, and Risk Factors. The Oslo study.” Laboratory Investigation 53: 
648-55. 

Sonimo, N., G. A. Fava, M. Boscaro, and F. Fallo. 1998. “Life Events and Neurocirculatory 
Asthenia. A Controlled Study.” Journal of Internal Medicine 244: 523-28. 

Spinhoven, Philip, E. J. Onstein, P. J. Sterk, and D. Le Haen-Versteijnen. 1992. “The 
Hyperventilation Provocation Test in Panic Disorder.” Behaviour Research and Therapy 30(5): 
453-61. 

Stamler, Jeremiah, Deborah Wentworth, and James D. Neaton. 1986. “Is Relationship between Serum 
Cholesterol and Risk of Premature Death from Coronary Heart Disease Continuous and Graded?” 





JAMA 256(20): 2823-28. 

Stamler, Jeremiah, Martha L. Daviglus, Daniel B. Garside, Alan R. Dyer, Philip Greenland, and 
James D. Neaton. 2000. “Relationship of Baseline Serum Cholesterol Levels in 3 Large Cohorts 
of Younger Men to Long-term Coronary, Cardiovascular, and All-Cause Mortality and to 
Longevity.” JAMA 284: 311-18. 

Statistical Report of the Health of the Navy for the Year 1915. 1922. London: His Majesty's 
Stationery Office. 

Stein, Jeffrey A. and Donald P. Tschudy. 1970. *Acute Intermittent Porphyria: A Clinical and 
Biochemical Study of 46 Patients." Medicine 49(1): 1-16. 

Steiropoulous, Paschalis, Venetia Tsara, Evangelia Nena, Christina Fitili, Margarita Kataropoulou, 
Marios Froudarakis, Pandora Christaki, and Demosthenes Bouros. 2007. *Effect of Continuous 
Positive Airway Pressure Treatment on Serum Cardiovascular Risk Factors in Patients with 
Obstructuve Sleep Apnea-Hypopnea Syndrome." Chest 132(3): 843-51. 

Stephenson, G. V. and Kenneth Cameron. 1943. *Anxiety States in the Navy: A Clinical Survey and 
Impression." British Medical Journal 2: 603-7. 

Stewart, S., K. MacIntyre, M. M. C. MacLeod, A. E. M. Bailey, S. Capewell, and J. J. V. McMurray. 
2001. “Trends in Hospitalization for Heart Failure in Scotland, 1990-1996.” European Heart 
Journal 22: 209-17. 

Subbota, A. G. 1970. “Changes in Functions of Various Systems of the Organism.” In: I. R. Petrov. 
ed., Influence of Microwave Radiation on the Organism of Man and Animals (Leningrad: 
*Meditsina"), in English translation, 1972 (Washington, DC: NASA), report no. TTF-708, pp. 66- 
87. 

Suvorov, G. A. and N. F. Izmerov. 2003. Fizicheskiye faktory proizvodstvennoy i prirodnoy credy 
(“Physical Factors of Occupational and Natural Environment”). Moscow: “Meditsina.” 

Taddeini, Luigi, Karen L. Nordstrom, and C. J. Watson. 1974. “Hypercholesterolemia in 
Experimental and Human Hepatic Porphyria.” Metabolism 13: 691-701. 

Tamburello, C. C., L. Zanforlin, G. Tiné, and A. E. Tamburello. 1991. “Analysis of Microwave 
Effects on Isolated Hearts.” IEEE MTT-S Digest (IEEE Microwave Theory and Techniques 
Symposium, Boston), pp. 805-8. 

Thorogood, Margaret, Jim Mann, Paul Appleby, and Klim McPherson. 1994. “Risk of Death from 
Cancer and Ischaemic Heart Disease in Meat and Non-Meat Eaters.” British Medical Journal 308: 
1667-71. 

Thunell, Stig. 2000. “Porphyrins, Porphyrin Metabolism and Porphyrias. I. Update.” Scandinavian 
Journal of Clinical and Laboratory Investigation 60: 509-40. 

Tomashevskaya, Lyudmila A. and E. A. Solenyi. 1986. “Biologicheskoye deystviye i 
gigiyenicheskoye znacheniye  elektromagnitnogo polya,  sozdavayemogo beregovimi 
radiolokatsionnimi sredstvami” (“Biological Action and Hygienic Significance of the 
Electromagnetic Field Created by Coastal Radar Facilities”). Gigiyena i Sanitariya 1986(7): 34- 
36. 

Tomashevskaya, Lyudmila A. and Yury D. Dumanskiy. 1988. “Gigiyenicheskaya otsenka 
biologicheskogo deystviya impul’snykh elektromagnitnykh poley 850-2750 MGts” (“Hygienic 
Evaluation of the Biological Effect of Pulsed Electromagnetic Fields or 850-2750 MHz”). 
Gigiyena i Sanitariya 1988(9): 21-24. 

. 1989. “Influence of Low-Intensity 8-mm Wave EMF on Some Exchange Processes.” In: 

Fundamental and Applied Aspects of Use of Millimeter Electromagnetic Radiation in Medicine: 

Proceedings of the First All-Union Symposium with International Participation (Kiev: VNK 

“Otlik”), pp. 135-37. 





Tourniaire, A., M. Tartulier, J. Blum, and F. Deyrieux. 1961. “Confrontation des données 
fonctionnelles respiratoires et hémodynamiques cardiaques dans les névroses tachycardiaques et 
chez les sportifs.” Presse médicale 69(16): 721-23. 

Treupel, G. 1915. *Kriegsárztliche Herzfragen." Medizinische Klinik (Berlin) 62(11): 356-59. 

Tuomilehto Jaakko and Kari Kuulasmaa. 1989. “WHO MONICA Project: Assessing CHD Mortality 
and Morbidity.” International Journal of Epidemiology 18: S38-S45. 

Tyagin, Nikolay Vasil’evich. 1971. Klinicheskiye aspekty oblucheniy SVCh-diapazona (“Clinical 
Aspects of Irradiation in the SHF-range”’). Leningrad: “Meditsina.” 

Tzivoni, Dan, Zvi Stern, Andre Keren, and Shlomo Stern. 1980. “Electrocardiographic 
Characteristics of Neurocirculatory Asthenia during Everyday Activities.” British Heart Journal 
44: 426-32. 

van Rensburg, S. J., F. C. Potocnik, T. Kiss, F. Hugo, P. van Zijl, E. Mansvelt, and M. E. Carstens. 
2001. “Serum Concentrations of Some Metals and Steroids in Patients with Chronic Fatigue 
Syndrome with Reference to Neurological and Cognitive Abnormalities.” Brain Research Bulletin 
55(2): 319-25. 

Vastesaeger, Marcel M. and R. Delcourt. 1962. “The Natural History of Atherosclerosis.” Circulation 
26: 841-55. 

Verschuren, W. M. Monique, David R. Jacobs, Bennie P. M. Bloemberg, Daan Kromhout, Alessandro 
Menotti, Christ Aravanis, Henry Blackburn, Ratko Buzina, Anastasios S. Dontas, Flaminio 
Fidanza, Martti J. Karvonen, Srećko Nedeljković, Aulikki Nissinen, and Hironori Toshima. 1995. 
“Serum Total Cholesterol and Long-Term Coronary Heart Disease Mortality in Different Cultures: 
Twenty-five-Year Follow-up of the Seven Countries Study." JAMA 274(2): 131-36. 

Vogelzangs, Nicole, Adrie Seldenrijk, Aartjan T. F. Beekman, Hein P. J. van Hout, Peter de Jonge, 
and Brenda W. J. H. Penninx. 2010. “Cardiovascular Disease in Persons with Depressive and 
Anxiety Disorders.” Journal of Affective Disorders 215: 241-48. 

von Dziembowski, C. 1915. “Die Vagotonie, eine Kriegskrankheit.” Therapie der Gegenwart 56: 
405-13. 

von Romberg, Ernst. 1915. “Beobachtungen über Herz- und Gefässkrankheiten während der 
Kriegszeit." Münchener medizinische Wochenschrift 62(20): 671-72. 

Vural, M. and E. Basar. 2007. “Anxiety Disoder as a Potential for Sudden Death.” Anadolu 
Kardiyoloji Dergisi 7(2): 179-83 (in Turkish). 

Watson, Raymond C., Jr. 2009. Radar Origins Worldwide. Victoria, BC: Trafford. 

Weissman, Myrna M., Jeffrey S. Markowitz, Robert Ouellette, Steven Greenwald, and Jeffrey P. 
Kahn. 1990. “Panic Disorder and Cardiovascular/Cerebrovascular Problems: Results from a 
Community Survey.” American Journal of Psychiatry 147: 1504-8. 

Wendkos, Martin H. 1944. “The Influence of Autonomic Imbalance on the Human 
Electrocardiogram.” American Heart Journal 28(5): 549-67. 

Wheeler, Edwin O., Paul D. White, Eleanor W. Reed, and Mandel E. Cohen. 1950. *Neurocirculatory 
Asthenia (Anxiety Neurosis, Effort Syndrome, Neurasthenia): A Twenty Year Follow-up Study of 
One Hundred and Seventy-three Patients." Journal of the American Medical Association 142(12): 
878-89. 

White, Paul Dudley. 1920. *The Diagnosis of Heart Disease in Young People." Journal of the 
American Medical Association 74(9): 580-82. 

. 1938. Heart Disease, 2nd ed. New York: Macmillan. 

. 1957. “The Cardiologist Enlists the Epidemiologist.” American Journal of Public Health, 

vol. 47, no. 4, part 2, pp. 1-3. 

. 1971. My Life and Medicine: An Autobiographical Memoir. Boston: Gambit. 











Whitelaw, Andrew G. L. 1974. “Acute Intermittent Porphyria, Hypercholesterolaemia, and Renal 
Impairment.” Archives of Disability in Childhood 49: 406-7. 

Wilson, Peter W. F., Ralph B. D’Agostino, Daniel Levy, Albert M. Belanger, Halit Silbershatz, and 
William B. Kannel. 1998. “Prediction of Coronary Heart Disease Using Risk Factor Categories.” 
Circulation 97: 1837-47. 

Wilson, Robert McNair. 1916. “The Irritable Heart of Soldiers.” British Medical Journal 1: 119-20. 

Wong, Roger, Gary Lopaschuk, Gang Zhu, Dorothy Walker, Dianne Catellier, David Burton, Koon 
Teo, Ruth Collins-Nakai, and Terrence Montague. 19 92. “Skeletal Muscle Metabolism in the 
Chronic Fatigue Syndrome.” Chest 102(6): 1716-22. 

Wooley, Charles F. 1976. “Where are the Diseases of Yesteryear? DaCosta’s Syndrome, Soldier’s 
Heart, the Effort Syndrome, Neurocirculatory Asthenia — And the Mitral Valve Prolapse 
Syndrome.” Circulation 53(5): 749-51. 

. 1985. “From Irritable Heart to Mitral Valve Prolapse: British Army Medical Reports, 1860 

to 1870.” American Journal of Cardiology 55(8): 1107-9. 

. 1988. “Lewis A. Conner, MD (1867-1950), and Lessons Learned from Examining Four 
Million Young Men in World War I.” American Journal of Cardiology 61: 900-3. 

Worts, George F. 1915. “Directing the War by Wireless.” Popular Mechanics, May, pp. 647-50. 

York, J. Lyndal. 1972. The Porphyrias. Springfield, IL: Charles C. Thomas. 

Zalyubovskaya, N. P. and R. I. Kiselev. 1978. “Biological Oxidation in Cells Exposed to Microwaves 
in the Millimeter Range.” Tsitologiya i Genetika 12(3): 232-36 (in Russian). 

Zalyubovskaya, N. P., R. I. Kiselev, and L. N. Turchaninova. 1977. “Effects of Electromagnetic 
Waves of the Millimetric Range on the Energy Metabolism of Liver Mitochondria.” 
Biologicheskiye Nauki 1977(6): 133-34. JPRS 70107, pp. 51-52. 

Zhang, X., A. Patel, H. Horibe, Z. Wu, F. Barzi, A. Rodgers, S. MacMahon, and M. Woodward. 
2003. “Cholesterol, Coronary Heart Disease, and Stroke in the Asia Pacific Region.” International 
Journal of Epidemiology 32(4): 563-72. 

Zheng, Zhi-Jie, Janet B. Croft, Wayne H. Giles, and George A. Mensah. 2005. “Out-of-Hospital 
Cardiac Deaths in Adolescents and Young Adults in the United States, 1989 to 1998.” American 
Journal of Preventive Medicine 29 (5S1): 36-41. 








Chapter 12 

Allen, Frederick M. 1914. “Studies Concerning Diabetes.” Journal of the American Medical 
Association 63(11): 939-43. 

. 1915. “Metabolic Studies in Diabetes.” New York State Journal of Medicine 15(9): 330-33. 

. 1916. “Investigative and Scientific Phases of the Diabetic Question.” Journal of the 

American Medical Association 66(20): 1525-32. 

. 1922. “Observations on the Progressiveness of Diabetes.” Medical Clinics of North America 
6(3): 465-74. 

Antoun, Ghadi, Fiona McMurray, A. Brianne Thrush, David A. Patten, Alyssa C. Peixoto, Ruth S. 
Slack, Ruth McPherson, Robert Dent, and Mary-Ellen Harper. 2015. “Impaired Mitochondrial 
Oxidative Phosphorylation and Supercomplex Assembly in Rectus Abdominis Muscle of Diabetic 
Obese Individuals.” Diabetologia 58(12): 2861-66. 

Bartoni¢ek, V. and Eliska Klimkova-Deutschova. 1964. “Effect of Centimeter Waves on Human 
Biochemistry." Casopís Lékarü Ceskych 103(1): 26-30 (in Czech). English Translation in G. L. 
Khazan, ed., Biological Effects of Microwaves, ATD Report P-65-68, September 17, 1965 
(Washington, DC: Dept. of Commerce), pp. 13-14. 











Belokrinitskiy, Vasily S. 1982. “Hygienic Evaluation of Biological Effects of Nonionizing 
Microwaves.” Gigiyena i Sanitariya 1982(6): 32-34. JPRS 81865, pp. 1-5. 

Belokrinitskiy, Vasily S. and A. N. Grin’. 1983. “Nature of Morphofunctional Renal Changes in 
Response to SHF Field-Hypoxia Combination.” Vrachebnoye Delo 1983(1): 112-15. JPRS 84221, 
pp. 27-31. 

Bielski, J. and M. Sikorski. 1996. “Disturbances of Glucose Tolerance in Workers Exposed to 
Electromagnetic Radiation.” Medycyna Pracy 47(3): 227-31 (in Polish). 

Brown, John. 1790. The Elements of Medicine. Philadelphia: T. Dobson. 

Bruce, Clinton R., Mitchell J. Anderson, Andrew L. Carey, David G. Newman, Arend Bonen, 
Adamandia D. Kriketos, Gregory J. Cooney, and John A. Hawley. 2003. “Muscle Oxidative 
Capacity Is A Better Predictor of Insulin Sensitivity than Lipid Status.” Journal of Clinical 
Endocrinology and Metabolism 88(11): 5444-51. 

Brun, J. F., C. Fedou, and J. Mercier. 2000. “Postprandial Reactive Hypoglycemia.” Diabetes & 
Metabolism (Paris) 26: 337-51. 

Casson, Herbert N. 1910. The History of the Telephone. Chicago: A. C. McClurg. 

Centers for Disease Control and Prevention. 2011. “Long-Term Trends in Diagnosed Diabetes.” 
Atlanta. 

. 2014a. “Long-term Trends in Diabetes.” Atlanta. 

. 2014b. “National Diabetes Statistics Report.” Atlanta. 

. 2017. “National Diabetes Statistics Report.” Atlanta. 

Czerski, Przemystaw, Kazimierz Ostrowski, Morris L. Shore, Charlotte Silverman, Michael J. Suess, 
and Berndt Waldeskog, eds. 1974. Biologic Effects and Health Hazards of Microwave Radiation: 
Proceedings of an International Symposium, Warsaw, 15-18 October 1973. Warsaw: Polish 
Medical Publishers. 

DeLany, James P., John J. Dubé, Robert A. Standley, Giovanna Distefano, Bret H. Goodpaster, Maja 
Stefanovic-Racic, Paul M. Coen, and Frederico G. S. Toledo. 2014. “Racial Differences in 
Peripheral Insulin Sensitivity and Mitochondrial Capacity in the Absence of Obesity.” Journal of 
Clinical Endocrinology and Metabolism 99(11): 4307-14. 

Diabetes Care. 2002. “Report of the Expert Committee on the Diagnosis and Classification of 
Diabetes Mellitus.” 25 (supp. 1): S5-S20. 

Dodge, Christopher H. 1970. “Clinical and Hygienic Aspects of Exposure to Electromagnetic 
Fields.” In: Stephen F. Cleary, ed., Biological Effects and Health Implications of Microwave 
Radiation. Symposium Proceedings (Rockville, MD: U.S. Department of Health, Education and 
Welfare), Publication BRH/DBE 70-2, pp. 140-49. 

Dufty, William. 1975. Sugar Blues. Radnor, PA: Chilton. 

Dumanskiy Yury D., N. G. Nikitina, Lyudmila A. Tomashevskaya, F. R. Kholyavko, K. S. 
Zhypakhin, and V. A. Yurmanov. 1982. “Meteorological Radar as Source of SHF Electromagnetic 
Field Energy and Problems of Environmental Hygiene.” Gigiyena i Sanitariya 1982(2): 7-11. 
JPRS 81300, pp. 58-63. 

Dumanskiy, Yury D. and V. F. Rudichenko. 1976. “Dependence of the Functional Activity of Liver 
Mitochondria on Microwave Radiation.” Gigiyena i Sanitariya 1976(4): 16-19. JPRS 72606 
(1979), pp. 27-32. 

Dumanskiy, Yury D. and M. G. Shandala. 1974. “The Biologic Action and Hygienic Significance of 
Electromagnetic Fields of Superhigh and Ultrahigh Frequencies in Densely Populated Areas.” In: 
P. Czerski et al., eds., Biologic Effects and Health Hazards of Microwave Radiation: Proceedings 
of an International Symposium, Warsaw, 15-18 October 1973 (Warsaw: Polish Medical 
Publishers), pp. 289-93. 











Dumanskiy Yury D. and Lyudmila A. Tomashevskaya. 1978. "Investigation of the Activity of Some 
Enzymatic Systems in Response to a Super-high Frequency Electromagnetic Field." Gigiyena i 
Sanitariya 1978(8): 23-27. JPRS 72606 (1979), pp. 1-7. 

. 1982. *Hygienic Evaluation of 8-mm Wave Electromagnetic Fields." Gigiyena i Sanitariya 
1982(6): 18-20. JPRS 81865, pp. 6-9. 

Felber, Jean-Pierre and Alfredo Vannotti. 1964. *Effects of Fat Infusion on Glucose Tolerance and 
Insulin Plasma Levels." Medicina Experimentalis 10: 153-56. 

Flegal, Katherine M., Margaret D. Carroll, Robert J. Kuczmarski, and Clifford L. Johnson. 1998. 
“Overweight and Obesity in the United States: Prevalence and Trends, 1960-1994." International 
Journal of Obesity 22: 39-47. 

Flegal, Katherine M., Margaret D. Carroll, Cynthia L. Ogden, and Clifford L. Johnson. 2002. 
“Prevalence and Trends in Obesity Among US Adults, 1999-2000." JAMA 288(14): 1723-27. 

Flegal, Katherine M., Margaret D. Carroll, Cynthia L. Ogden, and Lester R. Curtin. 2010. 
“Prevalence and Trends in Obesity Among US Adults, 1999-2008.” JAMA 303(3): 235-41. 

Fothergill, J. Milner. 1884. *The Diagnosis of Diabetes." North Carolina Medical Journal 13: 146-47 
(reprinted from Philadelphia Medical Times). 

Gabovich, P. D., O. I. Shutenko, I. P. Kozyarin, and I. I. Shvayko. 1979. “Effects from Combined 
Exposure to Infrasound and Superhigh Frequency Electromagnetic Fields in Experiment." 
Gigiyena i Sanitariya 1979(10): 12-14. JPRS 75515 (1980), pp. 30-35. 

Gel'fon, I. A. and Maria N. Sadchikova. 1960. “Protein Fractions and Histamine of the Blood under 
the Influence of UHF and HF.” In: A. A. Letavet and Z. V. Gordon, eds., The Biological Action of 
Ultrahigh Frequencies (Moscow: Academy of Medical Sciences), JPRS 12471, pp. 42-46. 

Gembitskiy, Ye. V. 1970. “Changes in the Functions of the Internal Organs of Personnel Operating 
Microwave Generators.” In: I. R. Petrov. ed., Influence of Microwave Radiation on the Organism 
of Man and Animals (Leningrad: “Meditsina”), in English translation, 1972 (Washington, DC: 
NASA), report no. TTF-708, pp. 106-25. 

Gerbitz, Klaus-Dieter, Klaus Gempel, and Dieter Brdiczka. 1996. “Mitochondria and Diabetes: 
Genetic, Biochemical, and Clinical Implications of the Cellular Energy Circuit.” Diabetes 45(2): 
113-26. 

Gohdes, Dorothy. 1995. *Diabetes in North American Indians and Alaska Natives." In: M. I. Harris 
et al., eds., Diabetes in America, 2nd ed. (Bethesda, MD: National Institute of Diabetes and 
Digestive and Kidney Diseases), NIH publication no. 95-1468, pp. 683-702. 

Gordon, Zinaida V., ed. 1973. O biologicheskom deystvii elektromagnitnykh poley radiochastot, 4th 
ed. Moscow. In English translation as Biological Effects of Radiofrequency Electromagnetic 
Fields, JPRS 63321 (1974). 

Gray, Charlotte. 2006. Reluctant Genius: The Passionate Life and Inventive Mind of Alexander 
Graham Bell. Toronto: HarperCollins. 

Hales, Craig M., Cheryl D. Fryar, Margaret D. Carroll, David S. Freedman, and Cynthia L. Ogden. 
2018. “Trends in Obesity and Severe Obesity Prevalence in US Youth and Adults by Sex and Age, 
2007-2008 to 2015-2016.” JAMA 319(16): 1723-25. 

Harris, Maureen I., Catherine C. Cowie, Michael P. Stern, Edward J. Boyko, Gayle E. Reiber, and 
Peter H. Bennet, eds. 1995. Diabetes in America, 2nd ed. Bethesda, MD: National Institute of 
Diabetes and Digestive and Kidney Diseases. NIH publication no. 95-1468. 

Harris, Seale. 1924. “Hyperinsulinism and Dysinsulinism.” Journal of the American Medical 
Association 83(10): 729-33. 

Hirsch, August. 1883, 1885, 1886. Handbook of Geographical and Historical Pathology, 3 vols. 
London: New Sydenham Society. 





Howe, Hubert S. 1931. *Edison Lost Will to Live, Doctor Says." Pittsburgh Post- Gazette, October 
19, p. 2. 

Hurley, Dan. 2011. Diabetes Rising: How a Rare Disease Became a Modern Pandemic, and What To 
Do About It. New York: Kaplan. 

Israel, Paul. 1998. Edison: A Life of Invention. New York: Wiley. 

Jerabek, Jiri. 1979. *Biological Effects of Magnetic Fields." Pracovni Lekarstvi 31(3): 98-106. JPRS 
76497 (1980), pp. 1-25. 

Jones, Francis Arthur. 1907. Thomas Alva Edison: Sixty Years of an Inventor s Life. New York: 
Thomas Y. Crowell. 

Joslin, Elliott Proctor. 1917. The Treatment of Diabetes Mellitus, 2nd ed. Philadelphia: Lea & 
Febiger. 

. 1924. *The Treatment of Diabetes Mellitus." Canadian Medical Association Journal 14(9): 

808-11. 

. 1927. *The Outlook for the Diabetic." California and Western Medicine 26(2): 177-82, 

26(3): 328-31. 

. 1943. *The Diabetic." Canadian Medical Association Journal 48: 488-97. 

. 1950. *A Half-Century's Experience in Diabetes Mellitus." British Medical Journal 1: 
1095-98. 

Joslin Diabetes Clinic, paid advertisement. “Edison Lived His Last 50 Years with Diabetes,” 
Pittsburgh Press, April 14, 1990; October 14, 1990; Pittsburgh Post-Gazette, April 18, 1990; 
April 25, 1990; May 23, 1990; June 22, 1990; September 19, 1990; October 17, 1990. 

Josephson, Matthew. 1959. Edison: A Biography. McGraw-Hill, NY. 

Kelley, David E., Bret Goodpaster, Rena R. Wing and Jean-Aimé Simoneau. 1999. “Skeletal Muscle 
Fatty Acid Metabolism in Association with Insulin Resistance, Obesity, and Weight Loss.” 
American Journal of Physiology — Endocrinology and Metabolism 277: E1130-41. 

Kelley, David E. and Lawrence J. Mandarino. 2000. “Fuel Selection in Human Skeletal Muscle in 
Insulin Resistance: A Reexamination.” Diabetes 49: 677-83. 

Kelley, David E., Jing He, Elizabeth V. Menshikova, and Vladimir B. Ritov. 2002. “Dysfunction of 
Mitochondria in Human Skeletal Muscle in Type 2 Diabetes.” Diabetes 51: 2944-50. 

Kelley, David E. and Jean-Aimé Simoneau. 1994. “Impaired Free Fatty Acid Utilization by Skeletal 
Muscle in Non-Insulin-dependent Diabetes Mellitus.” Journal of Clinical Investigation 94: 2349- 
56. 

Kim, Juhee, Karen E. Peterson, Kelley S. Scanlon, Garrett M. Fitzmaurice, Aviva Must, Emily Oken, 
Sheryl L. Rifas-Shiman, Janet W. Rich-Edwards, and Matthew W. Gillman. 2006. “Trends in 
Overweight from 1980 through 2001 among Preschool-Aged Children Enrolled in a Health 
Maintenance Organization.” Obesity 14(7): 1-6. 

Kleinfield, N. R. 2006. “Diabetes and Its Awful Toll Quietly Emerge as a Crisis.” New York Times, 
January 9, 2006. 

Klimentidis, Yann C., T. Mark Beasley, Hui-Yi Lin, Giulianna Murati, Gregory E. Glass, Marcus 
Guyton, Wendy Newton, Matthew Jorgensen, Steven B. Heymsfield, Joseph Kemnitz, Lynn 
Fairbanks, and David B. Allison. 2011. “Canaries in the Coal Mine: a Cross-Species Analysis of 
the Plurality of Obesity Epidemics.” Proceedings of the Royal Society B 278: 1626-32. 

Klimkova-Deutschova, Eliska. 1974. “Neurologic Findings in Persons Exposed to Microwaves.” In: 
P. Czerski et al., eds., Biologic Effects and Health Hazards of Microwave Radiation: Proceedings 
of an International Symposium, Warsaw, 15-18 October 1973 (Warsaw: Polish Medical 
Publishers), pp. 269-72. 














Kochanek, Kenneth D., Sherry L. Murphy, Jiaquan Xu, and Elizabeth Arias. 2019. *Deaths: Final 
data for 2017." National Vital Statistics Reports, vol. 68, no. 9. Hyattsville, MD: National Center 
for Health Statistics. 

Kolodub, F. A. and O. N. Chernysheva. 1980. “Special Features of Carbohydrate-energy and 
Nitrogen Metabolism in the Rat Brain under the Influence of Magnetic Fields of Commercial 
Frequency.” Ukrainskiy Biokhemicheskiy Zhurnal 1980(3): 299-303. JPRS 77393 (1981), pp. 42- 
44. 

Koo, Won W. and Richard D. Taylor. 2011. *2011 Outlook of the U.S. and World Sugar Markets, 
2010-2020." Agribusiness & Applied Economics, no. 679. 

Kuczmarski, Robert J., Katherine M. Flegal, Stephen M. Campbell, and Clifford L. Johnson. 1994. 
"[ncreasing Prevalence of Overweight Among US Adults: The National Health and Nutrition 
Examination Surveys, 1960 to 1991." JAMA 272(3): 205-11. 

Kwon, Myoung Soo, Victor Vorobyev, Sami Kánnálà, Matti Laine, Juha O. Rinne, Tommi Toivonen, 
Jarkko Johansson, Mika Teräs, Harri Lindholm, Tommi Alanko, and Heikki Hämäläinen. 2011. 
“GSM Mobile Phone Radiation Suppresses Brain Glucose Metabolism.” Journal of Cerebral 
Blood Flow and Metabolism, 31(12): 2293-2301. 

Levy, Renata Bertazzi, Rafael Moreira Claro, Daniel Henrique Bandoni, Lenise Mondini, and Carlos 
Augusto Monteiro. 2012. “Availability of Added Sugars in Brazil: Distribution, Food Sources and 
Time Trends.” Revista Brasileira de Epidemiologia 15(1): 3-12. 

Li, De-Kun, Jeannette R. Ferber, Roxana Odouli, and Charles P. Quesenberry, Jr. 2012. “A 
Prospective Study of In-utero Exposure to Magnetic Fields and the Risk of Childhood Obesity.” 
Scientific Reports 2: 540. 

Lorenzo, Carlos and Steven M. Haffner. 2010. “Performance Characteristics of the New Definition of 
Diabetes: The Insulin Resistance Atherosclerosis Study.” Diabetes Care 33(2): 335-37. 

Mann, Devin M., April P. Carson, Daichi Shimbo, Vivian Fonseca, Caroline S. Fox, and Paul 
Muntner. 2010. “Impact of A1C Screening Criterion on the Diagnosis of Pre-Diabetes Among 
U.S. Adults.” Diabetes Care 33(10): 2190-95. 

Mazur, Allan. 2011. “Why Were ‘Starvation Diets’ Promoted for Diabetes in the Pre-Insulin Period?” 
Nutrition Journal 10: 23. 

Morino, Katsutaro, Kitt Falk Petersen, and Gerald I. Shulman. 2006. “Molecular Mechanisms of 
Insulin Resistance in Humans and Their Potential Links with Mitochondrial Dysfunction.” 
Diabetes 55 (suppl. 2): S9-S15. 

Morris, Jeremiah Noah. 1995. *Obesity in Britain: Lifestyle Data Do Not Support Sloth Hypothesis.” 
British Medical Journal 311: 1568-69. 

Navakatikian, Mikhail A. and Lyudmila A. Tomashevskaya. 1994. *Phasic Behavioral and Endocrine 
Effects of Microwaves of Nonthermal Intensity." In: David O. Carpenter and Sinerik Ayrapetyan, 
eds., Biological Effects of Electric and Magnetic Fields (New York: Academic), vol. 1, pp. 333- 
42. 

Nikitina, Valentina N. 2001. *Hygienic, Clinical and Epidemiological Analysis of Disturbances 
Induced by Radio Frequency EMF Exposure in Human Body." In: Kjell Hansson Mild, Monica 
Sandstróm, and Eugene Lyskov, eds., Clinical and Physiological Investigations of People Highly 
Exposed to Electromagnetic Fields (Umea, Sweden: National Institute for Working life), 
Arbetslivsrapport 3, pp. 32-38. 

Ogden, Cynthia L., Margaret D. Carroll, Brian K. Kit, and Katherine M. Flegal. 2012. “Prevalence of 
Obesity in the United States, 2009-2010.” NCHS Data Brief no. 82, January 2012. Atlanta: 
National Center for Health Statistics, Centers for Disease Control and Prevention. 

Ogden, Cynthia L., Katherine M. Flegal, Margaret D. Carroll, and Clifford L. Johnson. 2002. 
“Prevalence and Trends in Overweight Among US Children and Adolescents, 1999-2000.” JAMA 


288(14): 1728-32. 

Patti, Mary-Elizabeth and Silvia Corvera. 2010. *The Role of Mitochondria in the Pathogenesis of 
Type 2 Diabetes." Endocrine Reviews 31(3): 364-95. 

Petrov, Ioakim Romanovich, ed. 1970a. Vliyaniye SVCh-izlucheniya na organism cheloveka i 
zhivotnykh, Leningrad: “Meditsina.” In English translation as Influence of Microwave Radiation 
on the Organism of Man and Animals (Washington, DC: NASA), report no. TTF-708, 1972. 

. 1970b. “Problems of the Etiology and Pathogenesis of the Pathological Processes Caused by 
Microwave Radiation.” In: Petrov, ed., Influence of Microwave Radiation on the Organism of Man 
and Animals, pp. 147-165. 

Prentice, Andrew M. and Susan A. Jebb. 1995. “Obesity in Britain: Gluttony or Sloth?” British 
Medical Journal 311: 437-39. 

Presman, Aleksandr Samuilovich. 1970. Electromagnetic Fields and Life. New York: Plenum. 

Randle, Philip J. 1998. “Regulatory Interactions between Lipids and Carbohydrates: The Glucose 
Fatty Acid Cycle After 35 Years.” Diabetes/Metabolism Reviews 14: 263-83. 

Randle, Philip J., P. B. Garland, C. N. Hales, and E. A. Newsholme. 1963. “The Glucose Fatty-Acid 
Cycle.” Lancet 1: 785-89. 

Reynolds, C. and D. B. Orchard. 1977. “The Oral Glucose Tolerance Test Revisited and Revised.” 
CMA Journal 116: 1223-24. 

Richardson, Benjamin Ward. 1876. Diseases of Modern Life. New York: D. Appleton. 

Ritov, Vladimir B., Elizabeth V. Menshikova, Koichiro Azuma, Richard Wood, Frederico G. S. 
Toledo, Bret H. Goodpaster, Neil B. Ruderman, and David E. Kelley. 2010. “Deficiency of 
Electron Transport Chain in Human Skeletal Muscle Mitochondria in Type 2 Diabetes Mellitus 
and Obesity.” American Journal of Physiology — Endocrinology and Metabolism 298: E49-58. 

Rollo, John. 1798. Cases of the Diabetes Mellitus, 2nd ed. London: C. Dilly. 

Sadchikova, Maria N. 1974. “Clinical Manifestations of Reactions to Microwave Irradiation in 
Various Occupational Groups.” In: P. Czerski et al., eds., Biologic Effects and Health Hazards of 
Microwave Radiation: Proceedings of an International Symposium, Warsaw, 15-18 October 1973 
(Warsaw: Polish Medical Publishers), pp. 261-67. 

Sadchikova, Maria N. and K. V. Glotova. 1973. “The Clinic, Pathogenesis, Treatment, and Outcome 
of Radiowave Sickness.” In: Z. V. Gordon, ed. Biological Effects of Radiofrequency 
Electromagnetic Fields, JPRS 63321 (1974), pp. 54-62. 

Schalch, Don S. and David M. Kipnis. 1965. *Abnormalities in Carbohydrate Tolerance Associated 
with Elevated Plasma Nonesterified Fatty Acids." Journal of Clinical Investigation 44(12): 2010- 
20. 

Scriven, George P. 1915. *Notes on the Organization of Telegraph Troops in Foreign Armies. Great 
Britain." In: Scriven, The Service of Information: United States Army, (Washington, DC: 
Government Printing Office), pp. 127-32. 

Shutenko, O. L, I. P. Kozyarin, and I. I. Shvayko. 1981. "Effects of Superhigh Frequency 
Electromagnetic Fields on Animals of Different Ages." Gigiyena i Sanitariya 1981(10): 35-38. 
JPRS 81300 (1982), pp. 85-90. 

Simoneau, Jean-Aimé, Sheri R. Colberg, F. Leland Thaete, and David E. Kelley. 1995. “Skeletal 
Muscle Glycolytic and Oxidative Enzyme Capacities are Determinants of Insulin Sensitivity and 
Muscle Composition in Obese Women." FASEB Journal 9: 273-78. 

Simoneau, Jean-Aimé and David E. Kelley. 1997. *Altered Glycolytic and Oxidative Capacities of 
Skeletal Muscle Contribute to Insulin Resistance in NIDDM." Journal of Applied Physiology 83: 
166-71. 





Stalvey, Michael S. and Desmond A. Schatz. 2008. *Childhood Diabetes Explosion." In: D. LeRoith 
and A. I. Vinik, eds., Contemporary Endocrinology: Controversies in Treating Diabetes: Clinical 
and Research Aspects (Totowa, NJ: Humana), pp. 179-98. 

Starr, Douglas. 1998. Blood: An Epic History of Medicine and Commerce. New York: Knopf. 

Sydenham, Thomas. 1848. The Works of Thomas Sydenham, M.D., London: Sydenham Society. 

Syngayevskaya, V. A. 1970. “Metabolic Changes.” In: I. R. Petrov, ed., Influence of Microwave 
Radiation on the Organism of Man and Animals (Leningrad: *Meditsina"), in English translation, 
1972 (Washington, DC: NASA), report no. TTF-708, pp. 48-60. 

Thatcher, Craig D., R. Scott Pleasant, Raymond J. Geor, François Elvinger, Kimberly A. Negrin, J. 
Franklin, Louisa Gay, and Stephen R. Werre. 2009. “Prevalence of Obesity in Mature Horses: An 
Equine Body Condition Study.” Journal of Animal Physiology and Animal Nutrition 92: 222. 

The Sun. 1891. “Edison His Own Doctor.” May 10, p. 26. 

Therapeutic Gazette. 1884. *Sugar in the Urine — What Does it Signify?" 8: 180. 

Toledo, Frederico G. S., Elizabeth V. Menshikova, Koichiro Azuma, Zofia Radiková, Carol A. 
Kelley, Vladimir B. Ritov, and David E. Kelley. 2008. “Mitochondrial Capacity in Skeletal 
Muscle is Not Stimulated by Weight Loss Despite Increases in Insulin Action and Decreases in 
Intramyocellular Lipid Content.” Diabetes 57: 987-94. 

Tomashevskaya, Lyudmila A. and E. A. Solenyi. 1986. “Biologicheskoye deystviye i 
gigiyenicheskoye ^ znacheniye  elektromagnitnogo polya, sozdavayemogo _ beregovimi 
radiolokatsionnimi sredstvami” (“Biological Action and Hygienic Significance of the 
Electromagnetic Field Created by Coastal Radar Facilities”). Gigiyena i Sanitariya 1986(7): 34- 
36. 

Tomashevskaya, Lyudmila A. and Yuri D. Dumanskiy. 1988. “Gigiyenicheskaya otsenka 
biologicheskogo deystviya impul’snykh elektromagnitnykh poley” (“Hygienic Evaluation of the 
Biological Effect of Pulsed Electromagnetic Fields”). Gigiyena i Sanitariya 1988(9): 21-24. 

Welsh, Jean A., Andrea Sharma, Jerome L. Abramson, Viola Vaccarino, Cathleen Gillespie, and 
Miriam B. Vos. 2010. “Caloric Sweetener Consumption and Dyslipidemia among US Adults.” 
JAMA 303(15): 1490-97. 

Whytt, Robert. 1768. The Works of Robert Whytt, M.D. Edinburgh: J. Balfour. Reprinted by The 
Classics of Neurology and Neurosurgery Library, Birmingham, AL, 1984. 

Woodyatt, R. T. 1921. “Object and Method of Diet Adjustment in Diabetes.” Archives of Internal 
Medicine 28(2): 125-41. 

World Health Organization. 2010. Definition and Diagnosis of Diabetes Mellitus and Intermediate 
Hyperglycemia: Report of a WHO/IDF Consultation. Geneva 2010. 

. 2014. Global Status Report on Noncommunicable Diseases. Geneva. 





Bhutan 

Bhutan Broadcasting Service. 2007. *Diabetes: Emerging Non-communicable Disease in Bhutan." 
November 13. 

Chhetri, Pushkar. 2010. “ADB Grants $21.6 m for Rural Electrification.” Bhutan Observer, 
November 10. 

Choden, Tshering. 2010. “Be Wary of Lifestyle Disease.” Bhutan Times, March 21. 

Giri, Bhakta Raj, Krishna Prasad Sharma, Rup Narayan Chapagai, and Dorji Palzom. 2013. 
“Diabetes and Hypertension in Urban Bhutanese Men and Women.” Indian Journal of Community 
Medicine 38(3): 138-43. 

Pelden, Sonam. 2009. “Diabetes — The Slow Killer.” Kuensel Online (Bhutan’s daily news website), 
November 18. 


United States Agency for International Development. September 2002. Regional Hydro-power 
Resources: Status of Development and Barriers: Bhutan. Prepared by Nexant/South Asia Regional 
Initiative for Energy. 

Wangchuk, Jigme. 2011. *Bhutan Could Be Eating Itself Sick." Bhutan Observer, November 19. 

Wangdi, Tashi. 2015. “Type 1 Diabetes Mellitus in Bhutan." Indian Journal of Endocrinology and 
Metabolism 19 (suppl. 1): $14-S15. 


Chapter 13 


Acebo, Paloma, Daniel Giner, Piedad Calvo, Amaya Blanco-Rivero, Álvaro D. Ortega, Pedro L. 
Fernández, Giovanna Roncador, Edgar Fernández-Malavé, Margarita Chamorro, and José M. 
Cuezva. 2009. “Cancer Abolishes the Tissue Type-Specific Differences in the Phenotype of 
Energetic Metabolism.” Translational Oncology 2(3): 138-45. 

Adams, Samuel Hopkins. 1913. “What Can We Do About Cancer?” Ladies Home Journal, May, pp. 
21-22. 

American Lung Association. 2010. Trends in Lung Cancer Morbidity and Mortality. Washington, 
DC. 





. 2011. Trends in Tobacco Use. Washington, DC. 

Apte, Shireesh P. and Rangaprasad Sarangarajan, eds. 2009a. Cellular Respiration and 
Carcinogenesis. New York: Humana. 

. 2009b. “Metabolic Modulation of Carcinogenesis. In: Apte and Sarangarajan, eds., Cellular 
Respiration and Carcinogenesis (New York: Humana), pp. 103-18. 

Barlow, Lotti, Kerstin Westergren, Lars Holmberg, and Mats Talback. 2009. “The Completeness of 
the Swedish Cancer Register — A Sample Survey for Year 1998.” Acta Oncologica 48: 27-33. 

Briere, Jean-Jacques, Paul Bénit, and Pierre Rustin. 2009. “The Electron Transport Chain and 
Carcinogenesis.” In: Shireesh P. Apte and Rangaprasad Sarangarajan, eds., Cellular Respiration 
and Carcinogenesis (New York: Humana), pp. 19-32. 

Burk, Dean. 1942. “On the Specificity of Glycolysis in Malignant Liver Tumors as Compared with 
Homologus Adult or Growing Liver Tissues.” In: A Symposium on Respiratory Enzymes 
(Madison: University of Wisconsin Press), pp. 235-45. 

Burk, Dean, Mark Woods and Jehu Hunter. 1967. “On the Significance of Glucolysis for Cancer 
Growth, with Special Reference to Morris Rat Hepatomas.” Journal of the National Cancer 
Institute 38(6): 839-63. 

Coley, William B. 1910. “The Increase of Cancer.” Southern Medical Journal 3(5): 287-92. 

Cori, Carl F. and Gerty T. Cori. 1925. “The Carbohydrate Metabolism of Tumors. I. The Free Sugar, 
Lactic Acid, and Glycogen Content of Malignant Tumors.” Journal of Biological Chemistry 64: 
11-22. 

. 1925. “The Carbohydrate Metabolism of Tumors. II. Changes in the Sugar, Lactic Acid, and 
CO»-Combining Power of Blood Passing Through a Tumor." Journal of Biological Chemistry 65: 
397-405. 

Cuezva, José M. 2010. *The Bioenergetic Signature of Cancer." BMC Proceedings 4 (suppl. 2): 07. 

Cuezva, José M., Maryla Krajewska, Mighel López de Heredia, Stanislaw Krajewski, Gema 
Santamaría, Hoguen Kim, Juan M. Zapata, Hiroyuki Marusawa, Margarita Chamorro, and John C. 
Reed. 2002. “The Bioenergetic Signature of Cancer: A Marker of Tumor Progression.” Cancer 
Research 62: 6674-81. 

Cutler, David M. 2008. “Are We Finally Winning the War on Cancer?” Journal of Economic 
Perspectives 22(4): 3-26. 








Czarnecka, Anna and Ewa Bartnik. 2009. *Mitochondrial DNA Mutations in Tumors." In: Shireesh 
P. Apte and Rangaprasad Sarangarajan, eds., Cellular Respiration and Carcinogenesis (New York: 
Humana), pp. 119-30. 

Dang, Chi V. and Gregg L. Semenza. 1999. “Oncogenic Alterations of Metabolism.” Trends in 
Biochemical Sciences 24: 68-72. 

Fantin, Valeria R., Julie St.-Pierre, and Philip Leder. 2006. “Attenuation of LDH-A Expression 
Uncovers a Link between Glycolysis, Mitochondrial Physiology, and Tumor Maintenance.” 
Cancer Cell 9: 425-34. 

Felty, Quentin and Deodutta Roy. 2005. “Estrogen, Mitochondria, and Growth of Cancer and Non- 
Cancer Cells.” Journal of Carcinogenesis 4: 1. 

Ferreira, Tálio César and Elida Geralda Campos. 2009. “Regulation of Glucose and Energy 
Metabolism in Cancer Cells by Hypoxia Inducible Factor 1.” In: Shireesh P. Apte and 
Rangaprasad Sarangarajan, eds., Cellular Respiration and Carcinogenesis (New York: Humana), 
pp. 73-90. 

Furlow, Bryant. 2007. “VA Withholds Data From Cancer Registries Used to Track Veteran Cancer 
Rates.” Lancet Oncology 8(9): 762-63. 

Gatenby, Robert A. and Robert J. Gillies. 2004. “Why do Cancers have High Aerobic Glycolysis?” 
Nature Reviews. Cancer 4: 891-99. 

Gillies, Robert J., lan Robey, and Robert A. Gatenby. 2008. “Causes and Consequences of Increased 
Glucose Metabolism of Cancers." Journal of Nuclear Medicine 49(6) (suppl.): 24S-42S. 

Giovannucci, Edward, David M. Harlan, Michael C. Archer, Richard M. Bergenstal, Susan M. 
Gapstur, Laurel A. Habel, Michael Pollak, Judith G. Regensteiner, and Douglas Yee. 2010. 
“Diabetes and Cancer: A Consensus Report.” Diabetes Care 33(7): 1674-84. 

Goldblatt, Harry and Gladys Cameron. 1953. “Induced Malignancy in Cells from Rat Myocardium 
Subjected to Intermittent Anaerobiosis during Long Propagation In vitro." Journal of 
Experimental Medicine 97: 525-52. 

Goldblatt, Harry and Libby Friedman. 1974. “Prevention of Malignant Change in Mammalian Cells 
during Prolonged Culture In vitro." Proceedings of the National Academy of Sciences 71(5): 1780- 
82. 

Goldblatt, Harry, Libby Friedman, and Ronald L. Cechner. 1973. *On the Malignant Transformation 
of Cells during Prolonged Culture Under Hypoxic Conditions In vitro." Biochemical Medicine 7: 
241-52. 

Goldhaber, Paul. 1959. *The Influence of Pore Size on Carcinogenicity of Subcutaneously Implanted 
Millipore Filters." Proceedings of the American Association for Cancer Research 3(1): 228. 
Abstract. 

Gonzalez-Cuyar, Luis F., Fabio Tavora, Iusta Caminha, George Perry, Mark A. Smith, and Rudy J. 
Castellani. 2009. *Cellular Respiration and Tumor Suppressor Genes." In: Shireesh P. Apte and 
Rangaprasad Sarangarajan, eds., Cellular Respiration and Carcinogenesis (New York: Humana), 
pp. 131-44. 

Gordon, Tavia, Margaret Crittendon, and William Haenszel. 1961. *Cancer Mortality Trends in the 
United States, 1930-1955." In: End Results and Mortality Trends in Cancer, National Cancer 
Institute Monograph no. 6 (Washington, DC: U.S. Dept. of Health, Education, and Welfare), pp. 
131-298. 

Gover, Mary. 1939. Cancer Mortality in the United States. I. Trend of Recorded Cancer Mortality in 
the Death Registration States of 1900 from 1900 to 1935. Public Health Bulletin no. 248, U.S. 
Public Health Service. Washington, DC: Government Printing Office. 

Guan, Xiaofan and Olle Johansson. 2005. “The Sun-Shined Health.” European Biology and 
Bioelectromagnetics 1: 420-23. 


Gullino, Pietro M., Shirley H. Clark, and Flora H. Grantham. 1964. “The Interstitial Fluid of Solid 
Tumors." Cancer Research 24: 780-97. 

Hallberg, Orjan. 2009. Facts and Fiction about Skin Melamona. Farsta, Sweden: Hallberg 
Independent Research. 

Hallberg, Orjan and Olle Johansson. 2002a. “Cancer Trends during the 20th Century." Journal of the 
Australasian College of Nutrition and Environmental Medicine 21(1): 3-8. 

. 2002b. “Melanoma Incidence and Frequency Modulation (FM) Broadcasting.” Archives of 

Environmental Health 57(1): 32-40. 

. 2004a. “Malignant Melanoma of the Skin — Not a Sunshine Story!” Medical Science 

Monitor 10(7): CR336-40. 

. 2004b. “1997 — A Curious Year in Sweden.” European Journal of Cancer Prevention 13: 

535-38. 














2005. “FM Broadcasting Exposure Time and Malignant Melanoma Incidence.” 

Electromagnetic Biology and Medicine 24: 1-8. 

. 2009. “Apparent Decreases in Swedish Public Health Indicators After 1997 — Are They Due 

to Improved Diagnostics or to Environmental Factors?” Pathophysiology 16(1): 43-46. 

. 2010. “Sleep on the Right Side — Get Cancer on the Left?” Pathophysiology 17(3): 157-60. 

Hardell, Lennart. 2007. “Long-term Use of Cellular and Cordless Phones and the Risk of Brain 
Tumours.” Orebro University, power point presentation, August 31. 

Hardell, Lennart and Michael Carlberg. 2009. “Mobile Phones, Cordless Phones and the Risk for 
Brain Tumours.” International Journal of Oncology 35: 5-17. 

Hardell, Lennart, Michael Carlberg, and Kjell Hansson Mild. 2010. “Mobile Phone Use and the Risk 
for Malignant Brain Tumors: A Case-Control Study on Deceased Cases and Controls.” 
Neuroepidemiology 35: 109-14. 

. 2011a. “Pooled Analysis of Case-control Studies on Malignant Brain Tumours and the Use 

of Mobile and Cordless Phones Including Living and Deceased Subjects.” International Journal 

of Oncology 38: 1465-74. 

. 2011b. “Re-analysis of Risk for Glioma in Relation to Mobile Telephone Use: Comparison 
with the Results of the Interphone International Case-control Study.” International Journal of 
Epidemiology 40(4): 1126-28. 

Hardell, Lennart, Michael Carlberg, Fredrik Séderqvist, and Kjell Hansson Mild. 2010. “Re: Time 
Trends in Brain Tumor Incidence Rates in Denmark, Finland, Norway, and Sweden, 1974-2003.” 
Journal of the National Cancer Institute 102(10): 740-41. 

Harris, Adrian L. 2002. “Hypoxia — a Key Regulatory Factor in Tumour Growth.” Nature Reviews. 
Cancer 2: 38-47. 

Harris, David, Nora Kropp, and Paul Pulliam. 2008. “A Comparison of National Cancer Registries in 
India and the United States of America.” 3MC Conference Proceedings, Berlin. 

Highton, Edward. 1852. The Electric Telegraph: Its History and Progress. London: John Weale. 

Hirsch, August. 1886. “Cancer.” In: Hirsch, Handbook of Geographical and Historical Pathology 
(London: New Sydenham Society), vol. 3, pp. 502-9. 

Hoffman, Frederick Ludwig. 1915. The Mortality From Cancer Throughout the World. Newark: 
Prudential. 

Howlader, Nadia, Lynn A. Ries, David G. Stinchcomb, and Brenda K. Edwards. 2009. “The Impact 
of Underreported Veterans Affairs Data on National Cancer Statistics: Analysis Using Population- 
Based SEER Registries.” Journal of the National Cancer Institute 101(7): 533-36. 

International Agency for Research on Cancer. World Cancer Report 2008. Lyon, France. 














Isodoro, Antonio, Enrique Casado, Andrés Redondo, Paloma Acebo, Enrique Espinosa, Andrés M. 
Alonso, Paloma Cejas, David Hardisson, Juan A. Fresno Vara, Cristóbal Belda-Iniesta, Manuel 
González-Barón, and José M. Cuezva. 2005. *Breast Carcinomas Fulfill the Warburg Hypothesis 
and Provide Metabolic Markers of Cancer Prognosis." Carcinogenesis 26(12): 2095-2104. 

Isidoro, Antonio, Marta Martínez, Pedro L. Fernández, Álvaro D. Ortega, Gema Santamaría, 
Margarita Chamorro, John C. Reed, and José M. Cuezva. 2004. *Alteration of the Bioenergetic 
Phenotype of Mitochondria is a Hallmark of Breast, Gastric, Lung and Oesophageal Cancer." 
Biochemical Journal 378: 17-20. 

Johansen, Christoffer, John D. Boice, Jr, Joseph K. Mclaughlin, and Jgrgen H. Olsen. 2001. 
“Cellular Telephones and Cancer — a Nationwide Cohort Study in Denmark.” Journal of the 
National Cancer Institute 93(3): 203-7. 

Johansson, Olle. 2005. “The Effects of Radiation in the Cause of Cancer.” Integrative Cancer and 
Oncology News 4(4): 32-37. 

Khurana, Vini G., Charles Teo, Michael Kundi, Lennart Hardell, and Michael Carlberg. 2009. “Cell 
Phones and Brain Tumors: A Review Including the Long-Term Epidemiological Data.” Surgical 
Neurology 72(3): 205-14. 

Kidd, John G., Richard J. Winzler, and Dean Burk. 1944. “Comparative Glycolytic and Respiratory 
Metabolism of Homologous Normal, Benign, and Malignant Rabbit Tissues.” Cancer Research 4: 
547-53. 

Kim, Jung-whan and Chi V. Dang. 2006. “Cancer’s Molecular Sweet Tooth and the Warburg Effect.” 
Cancer Research 66(18): 8927-30. 

Kochanek, Kenneth D., Sherry L. Murphy, Jiaquan Xu, and Elizabeth Arias. 2019. “Deaths: Final 
data for 2017.” National Vital Statistics Reports, vol. 68, no. 9. Hyattsville, MD: National Center 
for Health Statistics. 

Kondoh, Hiroshi. 2009. “The Role of Glycolysis in Cellular Immortalization.” In: Shireesh P. Apte 
and Rangaprasad Sarangarajan, eds., Cellular Respiration and Carcinogenesis, (New York: 
Humana), pp. 91-102. 

Kondoh, Hiroshi, Matilde E. Lleonart, Jesus Gil, David Beach, and Gordon Peters. 2005. “Glycolysis 
and Cellular Immortalization.” Drug Discovery Today: Disease Mechanisms 2(2): 263-67. 

Kondoh, Hiroshi, Matilde E. Lleonart, Jesus Gil, Jing Wang, Paolo Degan, Gordon Peters, Dolores 
Martinez, Amancio Carnero, and David Beach. 2005. *Glycolytic Enzymes Can Modulate 
Cellular Life Span." Cancer Research 65(1): 177-85. 

Krebs, Hans. 1981. Otto Warburg: Cell Physiologist, Biochemist, and Eccentric. Oxford: Clarendon 
Press. 

Kroemer, G. 2006. *Mitochondria in Cancer." Oncogene 25: 4630-32. 

Lombard, Louise S. and Ernest J. Witte. 1959. “Frequency and Types of Tumors in Mammals and 
Birds of the Philadelphia Zoological Gardens.” Cancer Research 19(2): 127-41. 

López-Ríos, Fernando, María Sánchez-Aragó, Elena García-García, Álvaro D. Ortega, José R. 
Berrendero, Francisco Pozo-Rodríguez, Ángel López-Encuentra, Claudio Ballestín, and José M. 
Cuezva. 2007. “Loss of the Mitochondrial Bioenergetic Capacity Underlies the Glucose Avidity of 
Carcinomas.” Cancer Research 67(19): 9013-17. 

Malmgren, Richard A. and Clyde C. Flanigan. 1955. “Localization of the Vegetative Form of 
Clostridium tetani in Mouse Tumors Following Intravenous Spore Administration.” Cancer 
Research 15: 473-78. 

Maynard, George Darell. 1910. “A Statistical Study in Cancer Death-Rates.” Biometrika 7: 276-304. 

McFate, Thomas, Ahmed Mohyeldin, Huasheng Lu, Jay Thakar, Jeremy Henriques, Nader D. Halim, 
Hong Wu, Michael J. Schell, Tsz Mon Tsang, Orla Teahan, Shaoyu Zhou, Joseph A. Califano, 
Nam Ho Jeoung, Robert A. Harris, and Ajay Verma. 2008. “Pyruvate Dehydrogenase Complex 


Activity Controls Metabolic and Malignant Phenotype in Cancer Cells." Journal of Biological 
Chemistry 283(33): 22700-8. 

Milham, Samuel and Eric M. Ossiander. 2001. *Historical Evidence that Residential Electrification 
Caused the Emergence of the Childhood Leukemia Peak." Medical Hypotheses 56(3): 290-95. 

Moffat, Shannon. 1988. “Stanford’s Power Line Research Pioneers." Sandstone and Tile 12(2-3): 3- 
7. 

Moreno-Sánchez, Rafael, Sara Rodríguez-Enríquez, Álvaro Marín-Hernández and Emma Saavedra. 
2007. “Energy Metabolism in Tumor Cells.” FEBS Journal 274: 1393-1418. 

National Cancer Institute. 2009. “New Early Detection Studies of Lung Cancer in Non-Smokers 
Launched Today.” Press release, May 4. 

Pascua, Marcelino, Director, Division of Health Statistics, World Health Organization. 1952. 
“Evolution of Mortality in Europe during the Twentieth Century.” Epidemiological and Vital 
Statistics Report 5: 1-144. 

Pedersen, Peter L. 1978. “Tumor Mitochondria and the Bioenergetics of Cancer Cells.” Progress in 
Experimental Tumor Research 22: 190-274. 

Racker, Efraim and Mark Spector. 1956. “Warburg Effect Revisited: Merger of Biochemistry and 
Molecular Biology.” Science 213: 303-7. 

Richardson, Benjamin Ward. 1876. Diseases of Modern Life. New York: D. Appleton. 

Ristow, Michael. 2006. “Oxidative Metabolism in Cancer Growth.” Current Opinion in Clinical 
Nutrition and Metabolic Care 9: 339-45. 

Ristow, Michael and José M. Cuezva. 2009. “Oxidative Phosphorylation and Cancer: The Ongoing 
Warburg Hypothesis.” In: Shireesh P. Apte and Rangaprasad Sarangarajan, eds., Cellular 
Respiration and Carcinogenesis (New York: Humana), pp. 1-18. 

Sánchez-Aragó, María, Margarita Chamorro and José M. Cuezva. 2010. “Selection of Cancer Cells 
with Repressed Mitochondria Triggers Colon Cancer Progression.” Carcinogenesis 31(4): 567-76. 

Scatena, Roberto, Patrizia Bottoni, and Bruno Giardina. 2009. “Cellular Respiration and 
Dedifferentiation.” In: Shireesh P. Apte and Rangaprasad Sarangarajan, eds., Cellular Respiration 
and Carcinogenesis (New York: Humana), pp. 45-54. 

Scheers, Isabelle, Vincent Bachy, Xavier Stéphenne, and Étienne Marc Sokal. 2005. “Risk of 
Hepatocellular Carcinoma in Liver Mitochondrial Respiratory Chain Disorders.” Journal of 
Pediatrics 146(3): 414-17. 

Schüz, Joachim, Rune Jacobsen, Jørgen H. Olsen, John D. Boice, Jr., Joseph K. McLaughlin, and 
Christoffer Johansen. 2006. “Cellular Telephone Use and Cancer Risk: Update of a Nationwide 
Danish Cohort.” Journal of the National Cancer Institute 98(23): 1707-13. 

Semenza, Gregg L. “Foreword.” 2009. In: Shireesh P. Apte and Rangaprasad Sarangarajan, eds., 
Cellular Respiration and Carcinogenesis (New York: Humana), pp. v-vi. 

Semenza, Gregg L., Dmitri Artemov, Atul Bedi, Zaver Bhujwalla, Kelly Chiles, David Feldser, Erik 
Laughner, Rajani Ravi, Jonathan Simons, Panthea Taghavi, and Hua Zhong. 2001. “The 
Metabolism of Tumours: 70 Years Later.” In: The Tumour Microenvironment: Causes and 
Consequences of Hypoxia and Acidity. Novartis Foundation Symposium 240 (Chichester, UK: 
Wiley), pp. 251-64. 

Simonnet, Hélène, Nathalie Alazard, Kathy Pfeiffer, Catherine Gallou, Christophe Béroud, Jocelyne 
Demont, Raymonde Bouvier, Hermann Schägger, and Catherine Godinot. 2002. “Low 
Mitochondrial Respiratory Chain Content Correlates with Tumor Aggressiveness in Renal Cell 
Carcinoma.” Carcinogenesis 23(5): 759-68. 

Smith, Lloyd H., Jr. 1985. “Na*-H* Exchange, Oncogenes and Growth Regulation in Normal and 
Tumor Cells.” Western Journal of Medicine 143(3): 365-70. 


Soderqvist, Fredrik, Michael Carlberg, Kjell Hansson Mild, and Lennart Hardell. 2011. *Childhood 
Brain Tumour Risk and Its Association with Wireless Phones: A Commentary." Environmental 
Health 10: 106. 

Srivastava, Sarika and Carlos T. Moraes. 2009. *Cellular Adaptations to Oxidative Phosphorylation 
Defects in Cancer." In: Shireesh P. Apte and Rangaprasad Sarangarajan, eds., Cellular Respiration 
and Carcinogenesis (New York: Humana), pp. 55-72. 

Stein, Yael, Or Levy-Nativ, and Elihu D. Richter. 2011. “A Sentinel Case Series of Cancer Patients 
with Occupational Exposures to Electromagnetic Non-ionizing Radiation and Other Agents.” 
European Journal of Oncology 16(1): 21-54. 

Teo, Charlie. 2012. “What If Your Mobile Phone Is Giving You Brain Cancer?” The Punch, May 7. 

Teppo, Lyly, Eero Pukkala, and Maria Lehtonen. 1994. “Data Quality and Quality Control of a 
Population-Based Cancer Registry.” Acta Oncologica 33(4): 365-69. 

van Waveren, Corina, Yubo Sun, Herman S. Cheung, and Carlos T. Moraes. 2006. “Oxidative 
Phosphorylation Dysfunction Modulates Expression of Extracellular Matrix-Remodeling Genes 
and Invasion.” Carcinogenesis 27(3): 409-18. 

Vaupel, P., O. Thews, D. K. Kelleher, and M. Hoeckel. 1998. “Current Status of Knowledge and 
Critical Issues in Tumor Oxygenation.” In: Antal G. Hudetz and Duane F. Bruley, eds., Oxygen 
Transport to Tissue XX (New York: Plenum), pp. 591-602. 

Vigneri, Paolo, Francesco Frasca, Laura Sciacca, Guiseppe Pandini, and Riccardo Vigneri. 2009. 
“Diabetes and Cancer.” Endocrine-Related Cancer 16: 1103-23. 

Warburg, Otto Heinrich. 1908. “Notes on the Oxidation Processes in the Sea-Urchin’s Egg.” In: 
Warburg, The Metabolism of Tumours (London: Constable), 1930, pp. 13-25. Originally published 
as “Beobachtungen über die Oxydationsprozesse im Seeigelei,” Hoppe-Seyler’s Zeitschrift für 
physiologische Chemie 57(1-2): 1-16. 

. 1925. “The Metabolism of Carcinoma Cells.” Journal of Cancer Research 9: 148-63. 

———. 1928. “The Chemical Constitution of Respiration Ferment.” Science 68: 437-43. 

—. 1930. The Metabolism of Tumours. London: Constable. 

—. 1956. “On the Origin of Cancer Cells.” Science 123: 309-14. 

. 1966a. "Oxygen, the Creater of Differentiation." In: Nathan O. Kaplan and Eugene P. 

Kennedy, eds., Current Aspects of Biochemical Energetics (New York: Academic), pp. 103-9. 

. 1966b. The Prime Cause and Prevention of Cancer. Lecture at the meeting of the Nobel 
Laureates, Lindau, Lake Constance, Germany, June 30. English edition by Dean Burk (Würzburg: 
Konrad Triltsch), 1969. 

Warburg, Otto, Karlfried Gawehn, August-Wilhelm Geissler, Detlev Kayser, and Siegfried Lorenz. 
1965. *Experimente zur Anaerobiose der Krebszellen." Klinische Wochenschrift 43(6): 289-93. 
Warburg, Otto, August-Wilhelm Geissler, and Siegfried Lorenz. 1965. "Messung der 
Sauerstoffdrucke beim Umschlag des embryonalen Stoffwechsels in Krebs-Stoffwechsel.” 

Zeitschrift für Naturforschung 7(20b): 1070-3. 

. 1966. "Irreversible Erzeugung von Krebststoffwechsel im embryonalen Máusezellen." 
Zeitschrift für Naturforschung 7(21b): 707-8. 

Warburg, Otto, Karl Posener and Erwin Negelein. 1924. *Über den Stoffwechsel der Tumoren." 
Biochemische Zeitschrift 152: 309-44. Reprinted in English translation as “The Metabolism of the 
Carcinoma Cell” in Warburg, The Metabolism of Tumours (London: Constable), 1930, pp. 129-69. 

Warburg, Otto, Franz Wind, and Erwin Negelein. 1926. “The Metabolism of Tumors in the Body.” 
Journal of General Physiology 8: 519-30. 

Weinhouse, Sidney. 1956. “On Respiratory Impairment in Cancer Cells.” Science 124: 267-68. 
Response by Otto Warburg, pp. 269-70. Response by Dean Burk, pp. 270-71. 














Werner, Erica. 2009. *How Cancer Cells Escape Death." In: Shireesh P. Apte and Rangaprasad 
Sarangarajan, eds., Cellular Respiration and Carcinogenesis (New York: Humana), pp. 161-178. 

Williams, W. Roger. 1908. The Natural History of Cancer, with Special Reference to Its Causation 
and Prevention. New York: William Wood. 

Women's Health Policy and Advocacy Program. 2010. Out of the Shadows: Women and Lung 
Cancer. Boston: Brigham and Women's Hospital. 

Wu, Min, Andy Neilson, Amy L. Swift, Rebecca Moran, James Tamagnine, Diane Parslow, Suzanne 
Armistead, Kristie Lemire, Jim Orrell, Jay Teich, Steve Chomicz, and David A. Ferrick. 2007. 
*Multiparameter Metabolic Analysis Reveals a Close Link between Attenuated Mitochondrial 
Bioenergetic Function and Enhanced Glycolysis Dependency in Human Tumor Cells." American 
Journal of Physiology — Cell Physiology 292: C125-36. 


Fellingsbro 

Ekblom, Adolf E. 1902. “Nagot statistik fran déd- och begrafningsbóckerna i Fellingsbro 1801-1900 
jämte förslag till Sveriges läkare angående samarbete för utredande af kräftsjukdomarnas 
frekvens.” Hygiea, 2nd ser., 2(1): 11-21. 

Guinchard, J. 1914. “Telegraph Service.” In: Guinchard, Sweden: Historical and Statistical 
Handbook, 2nd ed., English issue. Stockholm: Government Printing Office, pp. 643-44. 


Radio Towers and Cancer 

Anderson, Bruce S. and Alden K. Henderson. 1986. Cancer Incidence in Census Tracts with 
Broadcasting Towers in Honolulu, Hawaii. Environmental Epidemiology Program, State of 
Hawaii Department of Health. 

Cherry, Neil. 2000. Childhood Cancer Incidence in the Vicinity of the Sutro Tower, San Francisco. 
Environmental Management and Design Division, Lincoln University, Canterbury, New Zealand. 

Dode, Adilza C., Mônica M. D. Leão, Francisco de A. F. Tejo, Antônio C. R. Gomes, Daiana C. 
Dode, Michael C. Dode, Cristina W. Moreira, Vânia A. Condessa, Cláudia Albinatti, and Waleska 
T. Caiaffa. 2011. “Mortality by Neoplasia and Cellular Telephone Base Stations in the Belo 
Horizonte Municipality, Minas Gerais State, Brazil.” Science of the Total Environment 409(19): 
3649-65. 

Dolk, Helen, Gavin Shaddick, Peter Walls, Chris Grundy, Bharat Thakrar, Immo Kleinschmidt, and 
Paul Elliott. 1997. “Cancer Incidence near Radio and Television Transmitters in Great Britain. I. 
Sutton Coldfield Transmitter.” American Journal of Epidemiology 145(1): 1-9. 

Dolk, Helen, Paul Elliott, Gavin Shaddick, Peter Walls, and Bharat Thakrar. 1997. “Cancer Incidence 
near Radio and Television Transmitters in Great Britain. II. All High Power Transmitters.” 
American Journal of Epidemiology 145(1): 10-17. 

Eger, Horst, Klaus Uwe Hagen, Birgitt Lucas, Peter Vogel, and Helmut Voit. 2004. “Einfluss der 
räumlichen Nähe von Mobilfunksendeanlagen auf die Krebsinzidenz.” Umwelt-Medizin- 
Gesellschaft 17(4): 326-32. 

Hocking, Bruce, Ian R. Gordon, Heather L. Grain, and Gifford E. Hatfield. 1996. “Cancer Incidence 
and Mortality and Proximity to TV Towers.” Medical Journal of Australia 165(11-12): 601-5. 

Morton, William and David Phillips. 1983. Radioemission Density and Cancer Epidemiology in the 
Portland Metropolitan Area. Research Triangle Park, NC: United States Environmental Protection 
Agency. 

Morton, William and David Phillips. 2000. “Cancer Promotion by Radiowave Emissions.” 
Epidemiology 11(4): S57. Abstract. 

Wolf, Ronni and Danny Wolf. 2004. “Increased Incidence of Cancer near a Cell-Phone Transmitter 
Station.” International Journal of Cancer Prevention 1(2): 123-38. 


Vatican Radio 
Agence France Presse. 2001. “Italian Minister Threatens Hunger Strike over Vatican Radio." April 
30. 





. 2003. “La Cour de Cassation Renvoie Radio Vatican Devant un Tribunal.” April 9. 

Allen, John L., Jr. 2001. “Vatican Radio Officials Charged." National Catholic Reporter, March 23. 

Bartoli, Ilaria Ciancaleoni. 2006. *I comitati contro l'elettrosmog: la Santa Sede sapeva dei rischi." E 
Polis Roma, November 24, p. 25. 

BBC News. April 11, 2003. “Vatican Radio Back in the Dock." 

. May 9, 2005. “Vatican Radio Officials Convicted.” 

Cinciripini, Giorgio. February 27, 2010. “Vatican Radio Caused Cancers, Must Compensate 
Victims.” [email protected]. 

Corriere della Sera. 2002. “In una perizia nesso ‘tra onde e casi di leucemia,’” May 10. 

Deutsche Press-Agentur. 2003. “Italian Court Okays Trial into Vatican Radio Cancer Claims.” April 
10. 

Gentile, Cecilia. 2002. “Leucemie a Cesano: ‘Colpa delle Antenne.’” La Repubblica, May 10. 

La Corte Suprema di Cassazione (Supreme Court of Cassation). 2011. Sentence no. 376/2011, 
February 24, Rome. 

La Repubblica. 2001. “Radio Vaticana ancora fuorilegge.” May 1. 

Lavinia, Gianvito. 2011. “Elettrosmog, in procura altri 23 casi di leucemia.” Corriere della Sera, 
June 8. 

Lombardi, Federico. 2001. “Vatican Radio and the Electromagnetic Pollution.” Vatican Radio, press 
release, May 4. 

Micheli, Andrea. 2010. Perizia mediante indagine epidemiologica incidente probatorio. 
Procedimento Penale 33642/03, Tribunale Penale di Roma, June 25. 

Michelozzi, Paola, Alessandra Capon, Ursula Kirchmayer, Francesco Forastiere, Annibale Biggeri, 
Alessandra Barca, and Carlo A. Perucci. 2002. “Adult and Childhood Leukemia near a High- 
power Radio Station in Rome, Italy.” American Journal of Epidmiology 155(12): 1096-1103. 

Michelozzi, Paola, Ursula Kirchmayer, Alessandra Capon, Francesco Forestiere, Annibale Biggeri, 
Alessandra Barca, C. Ancona, D. Fusco, A. Sperati, P. Papini, A. Pierangelini, R. Rondelli, and 
Carlo A. Perucci. 2001. “Mortalità per leucemia e incidenza di leucemia infantile in prossimità 
della stazione di Radio Vaticana di Roma.” Epidemiologia & Prevenzione 25(6): 249-55. 

Pierucci, Adelaide. 2006. “Elettrosmog a Radio Vaticana: perizia sulle morti di leucemia.” E Polis 
Roma, November 24. 

Stanley, Alessandra. 2001. “In Radio Feud, a Higher Kind of Superpower Irks Italy.” New York 
Times, April 13. 

Times of India. 2011. “Vatican Seeks to Stave off Trial of Top Radio Officials.” February 14. 





Chapter 14 

Austad, S. N. 1989. “Life Extension by Dietary Restriction in the Bowl and Doily Spider, Frontinella 
pyramitela." Experimental Gerontology 24(1): 83-92. 

Bacon, Francis. 1605. The Advancement of Learning. Translated and edited by Joseph Devey (New 
York: P. F. Collier and Son), 1901. 

. 1623. The History of Life and Death. In: James Spedding, Robert Leslie Ellis, and Douglas 
Denon Heath, eds., The Works of Francis Bacon (Boston: Taggard and Thompson), 1864, volume 
X, pp. 7-176. 

Beard, George Miller. 1880. A Practical Treatise on Nervous Exhaustion (Neurasthenia). New York: 
William Wood. 








. 1881a. American Nervousness: Its Causes and Consequences. New York: G. P. Putnam's 
Sons. 

Bodkin, Noni L., Theresa M. Alexander, Heidi K. Ortmeyer, Elizabeth Johnson, and Barbara C. 
Hansen. 2003. *Mortality and Morbidity in Laboratory-maintained Rhesus Monkeys and Effects 
of Long-term Dietary Restriction." Journal of Gerontology: Biological Sciences 58A(3): 212-19. 

Caratero, A., M. Courtade, L. Bonnet, H. Planel, and C. Caratero. 1998. *Effect of a Continuous 
Gamma Irradiation at a Very Low Dose on the Life Span of Mice." Gerontology 44: 272-76. 

Carlson, Loren Daniel and Betty H. Jackson. 1959. *The Combined Effects of Ionizing Radiation and 
High Temperature on the Longevity of the Sprague-Dawley Rat." Radiation Research 11: 509-19. 

Carlson, Loren Daniel, William J. Scheyer, and B. H. Jackson. 1957. “The Combined Effects of 
Ionizing Radiation and Low Temperature on the Metabolism, Longevity, and Soft Tissues of the 
White Rat." Radiation Research 7: 190-97. 

Chittenden, Russell Henry. 1907. Physiological Economy in Nutrition. New York: Frederick A. 
Stokes. 

Chou, Chung-Kwang, Arthur William Guy, Lawrence L. Kunz, Robert B. Johnson, John J. Crowley, 
and Jerome H. Krupp. 1992. “Long-term, Low-level Microwave Irradiation of Rats.” 
Bioelectromagnetics 13(6): 469-96. 

Colman, Ricki J., Rozalyn M. Anderson, Sterling C. Johnson, Erik K. Kastman, Kristopher J. 
Kosmatka, T. Mark Beasley, David B. Allison, Christina Cruzen, Heather A. Simmons, Joseph W. 
Kemnitz, and Richard Weindruch. 2009. “Caloric Restriction Delays Disease Onset and Mortality 
in Rhesus Monkeys.” Science 325: 201-4. 

Colman, Ricki J., Mark Beasley, Joseph W. Kemnitz, Sterling C. Johnson, Richard Weindruch, and 
Rozalyn M. Anderson. 2014. “Caloric Restriction Reduces Agerelated and All-cause Mortality in 
Rhesus Monkeys.” Nature Communications 5: 557. 

Condran, Gretchen A. 1987. “Declining Mortality in the United States in the Late Nineteenth and 
Early Twentieth Centuries.” Annales de démographie historique, vol. 1987, pp. 119-41. 

Cutler, Richard G. 1981. “Life-Span Extension.” In: James L. McGaugh and Sara B. Kiesler, eds., 
Aging: Biology and Behavior (New York: Academic), pp. 31-76. 

Ducoff, Howard S. 1972. “Causes of Death in Irradiated Adult Insects.” Biological Reviews 47: 211- 
40. 





. 1975. “Form of the Increased Longevity of Tribolium after X-irradiation.” Experimental 
Gerontology 10: 189-93. 

Dunham, H. Howard. 1938. “Abundant Feeding Followed by Restricted Feeding and Longevity in 
Daphnia.” Physiological Zoólogy 11(4): 399-407. 

Elder, Joseph A. 1994. “Thermal, Cumulative, and Lifespan Effects and Cancer in Mammals 
Exposed to Radiofrequency Radiation.” In: David O. Carpenter and Sinerik Ayrapetyan, eds., 
Biological Effects of Electric and Magnetic Fields (San Diego: Academic), vol. 2, pp. 279-95. 

Finot, Jean. 1906. La Philosophie de la Longévité, 11th ed. Paris: Félix Alcan. 

Fischer-Piette, Edouard. 1939. “Sur la croissance et la longevité de Patella vulgata L. en fonction du 
milieu.” Journal de Conchyliologie 83: 303-10. 

Griffin, Donald Redfield. 1958. Listening in the Dark: The Acoustic Orientation of Bats and Men. 
New Haven, CT: Yale University Press. 

Hansson, Artur, Eskil Brännäng, and Olof Claesson. 1953. “Studies on Monozygous Cattle Twins. 
XIII. Body Development in Relation to Heredity and Intensity of Rearing.” Acta Agriculture 
Scandinavica 3(1): 61-95. 

Hochachka, Peter W. and Michael Guppy. 1987. Metabolic Arrest and the Control of Biological 
Time. Cambridge, MA: Harvard University Press. 


Johnson, Thomas E., David H. Mitchell, Susan Kline, Rebecca Kemal, and John Foy. 1984. 
“Arresting Development Arrests Aging in the Nematode Caenorhabditis elegans." Mechanisms of 
Ageing and Development 28: 23-40. 

Kagawa, Yasuo. 1978. “Impact of Westernization on the Nutrition of Japanese: Changes in Physique, 
Cancer, Longevity and Centenarians.” Preventive Medicine 7: 205-17. 

Kannisto, Vàinó. 1994. Development of Oldest-Old Mortality, 1950-1990: Evidence from 28 
Developed Countries. Monographs on Population Aging, 1. Odense, Denmark: Odense University 
Press. 

Kannisto, Väinö, Jens Lauritsen, A. Roger Thatcher, and James W. Vaupel. 1994. “Reductions in 
Mortality at Advanced Ages: Several Decades of Evidence from 27 Countries.” Population and 
Development Review 20(4): 793-810. 

Kemnitz, Joseph W. 2011. “Calorie Restriction and Aging in Nonhuman Primates.” ILAR Journal 
52(1): 66-77. 

Kirk, William P. 1984. “Life Span and Carcinogenesis.” In: Joseph A. Elder and Daniel F. Cahill, 
eds., Biological Effects of Radiofrequency Radiation (Research Triangle Park, NC: U.S. 
Environmental Protection Agency), report no. EPA-600/8-83-026F, pp. 5-106 to 5-111. 

Lane, Mark A., Donald K. Ingram, and George S. Roth. 1999. “Calorie Restriction in Nonhuman 
Primates: Effects on Diabetes and Cardiovascular Disease Risk.” Toxicological Sciences 52 
(suppl.): 41-48. 

Liu, Robert K. and Roy L. Walford. 1972. “The Effect of Lowered Body Temperature on Lifespan 
and Immune and Non-Immune Processes.” Gerontologia 18: 363-88. 

Loeb, Jacques and John Howard Northrop. 1917. “What Determines the Duration of Life in 
Metazoa?” Proceedings of the National Academy of Sciences 3(5): 382-86. 

. 1917. “On the Influence of Food and Temperature upon the Duration of Life.” Journal of 
Biological Chemistry 32: 103-21. 

Lorenz, Egon, Joanne Weikel Hollcroft, Eliza Miller, Charles C. Congdon, and Robert Schweisthal. 
1955. “Long-term Effects of Acute and Chronic Irradiation in Mice. I. Survival and Tumor 
Incidence Following Chronic Irradiation of 0.11 r per Day.” Journal of the National Cancer 
Institute 15(4): 1049-58. 

Lorenz, Egon, Leon O. Jacobson, Walter E. Heston, Michael Shimkin, Allen B. Eschenbrenner, 
Margaret K. Deringer, Jane Doniger, and Robert Schweisthal. 1954. “Effects of Long-Continued 
Total Body Gamma Irradiation of Mice, Guinea Pigs, and Rabbits. III. Effects on Life Span, 
Weight, Blood Picture, and Carcinogenesis and the Role of the Intensity of Radiation." In: 
Raymond E. Zirkle, ed., Biological Effects of External X and Gamma Radiation (New York: 
McGraw-Hill), part I, pp. 24-148. 

Lyman, Charles P., Regina C. O'Brien, G. Cliett Greene, and Elaine D. Papafrangos. 1981. 
*Hibernation and Longevity in the Turkish Hamster Mesocricetus brandti." Science 212: 668-70. 

Lynn, William S. and James C. Wallwork. 1992. *Does Food Restriction Retard Aging by Reducing 
Metabolic Rate?" Journal of Nutrition 122: 1917-18. 

Mattison, Julie A., Mark A. Lane, George S. Roth, and Donald K. Ingram. 2003. *Calorie Restriction 
in Rhesus Monkeys." Experimental Gerontology 38: 35-46. 

McCarter, Roger, E. J. Masoro, and Byung P. Yu. 1985. *Does Food Restriction Retard Aging by 
Reducing the Metabolic Rate?" American Journal of Physiology — Endocrinology and Metabolism 
248: E488-90. 

McKay, Clive M. and Mary F. Crowell. 1934. “Prolonging the Life Span.” Scientific Monthly 39: 
405-14. 





McCay, Clive M., Mary F. Crowell, and Leonard A. Maynard. 1935. “The Effect of Retarded Growth 
upon the Length of Life Span and upon the Ultimate Body Size.” Journal of Nutrition 10: 63-79. 
McKay, Clive M., Leonard A. Maynard, Gladys Sperling, and LeRoy L. Barnes. 1939. “Retarded 
Growth, Life Span, Ultimate Body Size and Age Changes in the Albino Rat After Feeding Diets 

Restricted in Calories.” Journal of Nutrition 18(1): 1-13. 

McDonald, Roger B. and Jon J. Ramsey. 2010. “Honoring Clive McCay and 75 Years of Calorie 
Restriction Research.” Journal of Nutrition 140(7): 1205-10. 

Millward, Robert and Frances N. Bell. 1998. “Economic Factors in the Decline of Mortality in Late 
Nineteenth Century Britain.” European Review of Economic History 2: 263-88. 

Mitchel, Ronald E. J. 2006. “Low Doses of Radiation are Protective In vitro and In vivo: 
Evolutionary Origins.” Dose-Response 4(2): 75-90. 

Okada, M., A. Okabe, Y. Uchihori, H. Kitamura, E. Sekine, S. Ebisawa, M. Suzuki, and R. Okayasu. 
2007. “Single Extreme Low-dose/Low Dose Rate Irradiation Causes Alteration in Lifespan and 
Genome Instability in Primary Human Cells.” British Journal of Cancer 96: 1707-10. 

Ordy, J. Mark, Thaddeus Samorajki, Wolfgang Zeman, and Howard J. Curtis. 1967. “Interaction 
Effects of Environmental Stress and Deuteron Irradiation of the Brain on Mortality and Longevity 
of C57BL/10 Mice.” Proceedings of the Society for Experimental Biology and Medicine 126(1): 
184-90. 

Osborne, Thomas B., Lafayette B. Mendel, and Edna L. Ferry. 1917. “The Effect of Retardation of 
Growth upon the Breeding Period and Duration of Life of Rats.” Science 45: 294-95. 


Pearl, Raymond. 1928. The Rate of Living. New York: Alfred A. Knopf. 

Perez, Felipe P., Ximing Zhou, Jorge Morisaki, and Donald Jurivich. 2008. “Electromagnetic Field 
Therapy Delays Cellular Senescence and Death by Enhancement of the Heat Shock Response." 
Experimental Gerontology 43: 307-16. 

Pinney, Don O., D. F. Stephens, and L. S. Pope. 1972. “Lifetime Effects of Winter Supplemental 
Feed Level and Age at First Parturition on Range Beef Cows.” Journal of Animal Science 34(6): 
1067-74. 

Ramsey, Jon J., Mary-Ellen Harper, and Richard Weindruch. 2000. “Restriction of Energy Intake, 
Energy Expenditure, and Aging." Free Radical Biology and Medicine 29(10): 946-68. 

Rattan, Suresh I. S. 2004. “Aging Intervention, Prevention, and Therapy Through Hormesis.” 
Journal of Gerontology: Biological Sciences 59A(7): 705-9. 

Reimers, N. 1979. “A History of a Stunted Brook Trout Population in an Alpine Lake: A Life Span 
of 24 Years.” California Fish and Game 65: 196-215. 

Ross, Morris H. 1961. “Length of Life and Nutrition in the Rat.” Journal of Nutrition 75(2): 197-210. 

. 1972. “Length of Life and Caloric Intake.”American Journal of Clinical Nutrition 25(8): 
834-38. 

Ross, Morris H. and Gerrit Bras. 1965. “Tumor Incidence Patterns and Nutrition in the Rat.” Journal 
of Nutrition 87: 245-60. 

. 1971. “Lasting Influence of Early Caloric Restriction on Prevalence of Neoplasms in the 

Rat.” Journal of the National Cancer Institute 47(5): 1095-1113. 

. 1973. “Influence of Protein Under- and Overnutrition on Spontaneous Tumor Prevalence in 
the Rat.” Journal of Nutrition 103: 944-63. 

Rubner, Max. 1908. Das Problem der Lebensdauer. Miinchen: R. Oldenbourg. 

Rudzinska, Maria A. 1952. “Overfeeding and Life Span in Tokophyra infusionum.” Journal of 
Gerontology 7: 544-48. 

Sacher, George A. 1963. “Effects of X-rays on the Survival of Drosophila Imagoes.” Physiological 
Zoology 36(4): 295-311. 

. 1977. “Life Table Modification and Life Prolongation.” In: Caleb E. Finch and Leonard 
Hayflick, eds., Handbook of the Biology of Aging (New York: Van Nostrand Reinhold), pp. 582- 
638. 

Simmons, Heather A. and Julie A. Mattison. 2011. “The Incidence of Spontaneous Neoplasia in Two 
Populations of Captive Rhesus Macaques (Macaca mulatta).” Antioxidants & Redox Signaling 
14(2): 221-27. 

Sohal, Rajindar S. 1986. “The Rate of Living Theory: A Contemporary Interpretation.” In: K.-G. 
Collatz and R. S. Sohal, eds., Insect Aging (Berlin: Springer), pp. 23-44. 

Sohal, Rajindar S. and Robert G. Allen. 1985. “Relationship between Metabolic Rate, Free Radicals, 
Differentiation and Aging: a Unified Theory.” In: Avril D. Woodhead, Anthony D. Blackett, and 
Alexander Hollaender, eds., Molecular Biology of Aging (New York: Plenum), pp. 75-104. 

Spalding, Jonathan F., Robert W. Freyman, and Laurence M. Holland. 1971. “Effects of 800-MHz 
Electromagnetic Radiation on Body Weight, Activity, Hematopoiesis and Life Span in Mice.” 
Health Physics 20: 421-24. 

Siisskind, Charles. 1959. Cellular and Longevity Effects of Microwave Radiation. Berkeley, CA: 
University of California, Berkeley. Annual Scientific Report (1958-59) on Contract 
AF41(657)-114. Institute of Engineering Research, ser. 60, no. 241, June 30. Rome Air 
Development Center report no. RADC-TR-59-131. 

Siisskind, Charles. 1961. Longevity Study of the Effects of 3-cm Microwave Radiation on Mice. 
Berkeley, CA: University of California, Berkeley. Annual Scientific Report (1960-61) on Contract 














AF41(657)-114. Institute of Engineering Research, ser. 60, no. 382, June 30. Rome Air 
Development Center report no. RADC-TR-61-205. 

Suzuki, Masao, Zhi Yang, Kazushiro Nakano, Fumio Yatagai, Keiji Suzuki, Seiji Kodama, and 
Masami Watanabe. 1998. *Extension of In vitro Life-span of y-irradiated Human Embryo Cells 
Accompanied by Chromosome Instability." Journal of Radiation Research 39: 203-13. 

Tryon, Clarence Archer and Dana P. Snyder. 1971. “The Effect of Exposure to 200 and 400 R of 
Ionizing Radiation on the Survivorship Curves of the Eastern Chipmunk (Tamias Striatus) under 
Natural Conditions.” In: D. J. Nelson, ed., Radionuclides in Ecosystems: Proceedings of the Third 
National Symposium on Radioecology, May 10-12, 1971, Oak Ridge, Tennessee, Oak Ridge 
National Laboratory, report no. CONF-71501-P2, vol. 2, pp. 1037-41. 

Vickery, Hubert Bradford. 1944. Biographical Memoir of Russell Henry Chittenden 1856-1943. 
Washington, DC: National Academy of Sciences. 

Wachter, Kenneth W. and Caleb E. Finch, eds. 1997. Between Zeus and the Salmon: The 
Biodemography of Longevity. Washington, DC: National Academy Press. 

Walford, Roy L. 1983. Maximum Life Span, New York: Norton. 

. 1982. “Studies in Immunogerontology." Journal of the American Geriatrics Society 30(10): 
617-25. 

Weindruch, Richard and Roy L. Walford. 1988. “The Retardation of Aging and Disease by Dietary 
Restriction.” Springfield, IL: Charles C. Thomas. 

Wilkinson, Gerald S. and Jason M. South. 2002. “Life History, Ecology and Longevity in Bats.” 
Aging Cell 1: 124-31. 

Wilmoth, John R. 2000. “Demography of Longevity: Past, Present, and Future Trends.” Experimental 
Gerontology 35: 1111-29. 

Wilmoth, John R., L. J. Deegan, H. Lundström, and S. Horiuchi. 2000. “Increase of Maximum Life- 
Span in Sweden, 1861-1999.” Science 289: 2366-68. 

Wilmoth, John R. and Hans Lundström. 1996. “Extreme Longevity in Five Countries.” European 
Journal of Population 12: 63-93. 

Young, Vernon R. 1979. “Diet as a Modulator of Aging and Longevity.” Federation Proceedings 
38(6): 1994-2000. 

Yu, Byung Pal, ed. 1994. Modulation of Aging Processes by Dietary Restriction. Boca Raton, FL: 
CRC Press. 





Chapter 15 


Cell Phones and Cell Towers 

Mild, Kjell Hansson and Jonna Wilén. 2009. “Occupational Exposure in Wireless Communication.” 
In: James C. Lin, ed., Advances in Electromagnetic Fields in Living Systems, vol. 5, Health Effects 
of Cell Phone Radiation (New York: Springer), pp. 199-219. 

Tuor, Markus, Sven Ebert, Jürgen Schuderer, and Niels Kuster. 2005. “Assessment of ELF Exposure 
from GSM Handsets and Development of an Optimized RF/ELF Exposure Setup for Studies of 
Human Volunteers.” BAG Reg. No. 2.23.02.-18/02.001778. Zürich: Foundation for Research on 
Information Technologies in Society. 


Electronic Consumer Devices 
Stetzer, David A. April 2, 2000. Testimony before the Michigan Public Service Commission. 
Zyren, Jim. May 2010. “HomePlug Green PHY Overview.” Atheros Technical Paper. 


Electromodel of the Ear 


Allen, Jont B. 1980. *Cochlear Micromechanics — A Physical Model of Transduction." Journal of the 
Acoustical Society of America 68(6): 1660-70. 

Art, Jonathan J. and Robert Fettiplace. 1987. “Variation of Membrane Properties in Hair Cells 
Isolated from the Turtle Cochlea.” Journal of Physiology 385: 207-42. 

Ashmore, Jonathan F, 1987. “A Fast Motile Response in Guinea-Pig Outer Hair Cells: The Cellular 
Basis of the Cochlear Amplifier.” Journal of Physiology 388: 323-47. 

. 2008. “Cochlear Outer Hair Cell Motililty.” Physiological Reviews 88: 173-210. 

Bell, Andrew. 2000. The Underwater Piano: Revival of the Resonance Theory of Hearing. Canberra: 
Australian National University. 

. 2004. “Resonance Theories of Hearing — A History and a Fresh Approach.” Acoustics 

Australia 32(3): 95-100. 

. 2005. “The Underwater Piano: A Resonance Theory of Cochlear Mechanics.” Doctoral 

thesis, The Australian National University, Canberra. 

. 2006. “Sensors, Motors, and Tuning in the Cochlea: Interacting Cells Could Form a Surface 

Acoustic Wave Resonator.” Bioinspiration and Biomimetics 1: 96-101. 

. 2007. “Detection with Deflection? A Hypothesis for Direct Sensing of Sound Pressure by 

Hair Cells.” Journal of Biosciences 32(2): 385-404. 

. 2010. “The Cochlea as a Graded Bank of Independent, Simultaneously Excited Resonators: 

Calculated Properties of an Apparent ‘Travelling Wave.’” Proceedings of the 20th International 

Congress on Acoustics, ICA 2010, 23-27 August 2010, Sydney, Australia, pp. 1-9. 

. 2011. “How Do Middle Ear Muscles Protect the Cochlea? Reconsideration of the 

Intralabyrinthine Pressure Theory.” Journal of Hearing Science 1(2): 9-23. 

. 2012. “A Resonance Approach to Cochlear Mechanics.” PLoS ONE 7(11): e47918. 

Bell, DeLamar T., Jr. and Robert C. M. Li. 1976. “Surface-Acoustic-Wave Resonators.” Proceedings 
of the IEEE 64(5): 711-21. 

Braun, Martin. 1994. *Tuned Hair Cells for Hearing, But Tuned Basilar Membrane for Overload 
Protection: Evidence from Dolphins, Bats, and Desert Rodents." Hearing Research 78: 98-114. 
Breneman, Kathryn D., William Brownell, and Richard D. Rabbit. 2009. *Hair Cell Bundles: 

Flexoelectric Motors of the Inner Ear." PLoS ONE 4(4): e5201. 

Breneman, Kathryn D. and Richard D. Rabbit. 2009. *Piezo- and Flexoelectric Membrane Materials 
Underlie Fast Biological Motors in the Ear." Materials Research Society Symposia Proceedings 
1186E: 1186-JJ06-04. 

Brownell, William E. 2006. “The Piezoeletric Outer Hair Cell." In: Ruth Anne Eatock, Richard R. 
Fay, and Arthur N. Popper, eds., Vertebrate Hair Cells (New York: Springer), pp. 313-47. 

Brownell, William E., Charles R. Bader, Daniel Bertrand, and Yves de Ribaupierre. 1985. “Evoked 
Mechanical Responses of Isolated Cochlear Outer Hair Cells.” Science 227: 194-96. 

Canlon, Barbara, Lou Brundin, and Ake Flock. 1988. “Acoustic Stimulation Causes Tonotopic 
Alterations in the Length of Isolated Outer Hair Cells from Guinea Pig Hearing Organ.” 
Proceedings of the National Academy of Sciences 85(18): 7033-35. 

Crawford, Andrew C. and Robert Fettiplace. 1981. “An Electrical Tuning Mechanism in Turtle 
Cochlear Hair Cells.” Journal of Physiology 312: 377-412. 

de Vries, Hessel. 1948a. “Brownian Movement and Hearing.” Physica 14(1): 48-60. 

. 1948b. “Die Reizschwelle der Sinnesorgane als physikalisches Problem.” Experientia 4(6): 
205-13. 

Degens, Egon T., Werner G. Deuser, and Richard L. Haedrich. 1969. “Molecular Structure and 
Composition of Fish Otoliths.” International Journal on Life in Oceans and Coastal Waters 2(2): 
105-13. 





























Dimbylow, Peter J. 1988. “The Calculation of Induced Currents and Absorbed Power in a Realistic, 
Heterogeneous Model of the Lower Leg for Applied Electric Fields from 60 Hz to 30 MHz.” 
Physics in Medicine and Biology 33(12): 1453-68. 

Dong, Xiao-xia, Mark Ospeck, and Kuni H. Iwasa. 2002. “Piezoelectrical Reciprocal Relationship of 
the Membrane Motor in the Cochlear Outer Hair Cell.” Biophysical Journal 82(3): 1254-59. 

Fettiplace, Robert and Paul A. Fuchs. 1999. “Mechanisms of Hair Cell Tuning.” Annual Review of 
Physiology 61: 809-34. 

Ghaffari, Roozbeh, Alexander J. Aranyosi, and Dennis M. Freeman. 2007. “Longitudinally 
Propagating Traveling Waves of the Mammalian Tectorial Membrane.” Proceedings of the 
National Academy of Sciences 104(42): 16510-15. 

Gummer, Anthony W., Werner Hemmert, and Hans-Peter Zenner. 1996. “Resonant Tectorial 
Membrane Motion in the Inner Ear: Its Crucial Role in Frequency Tuning.” Proceedings of the 
National Academy of Sciences 93(16): 8727-32. 

Gummer, Anthony W. and Serena Preyer. 1997. “Cochlear Amplification and its Pathology: 
Emphasis on the Role of the Tectorial Membrane.” Ear, Nose, & Throat Journal 76(3): 151-58. 
Hackney, Carole M. and David N. Furness. 1995. “Mechanotransduction in Ververtebrate Hair Cells: 
Structure and Function of the Stereociliary Bundle.” American Journal of Cell Physiology 268: 

C1-C13. 

Hallpike, Charles Skinner and Alexander Francis Rawdon-Smith. 1934a. “The ‘Wever and Bray 
Phenomenon’: A Study of the Electrical Response in the Cochlea with Especial Reference to its 
Origin.” Journal of Physiology 81: 395-408. 

. 1934b. “The Origin of the Wever and Bray Phenomenon.” Journal of Physiology 83: 243- 





54. 

Hassan, Waled and Peter B. Nagy. 1997. “On the Low-Frequency Oscillation of a Fluid Layer 
between Two Elastic Plates.” Journal of the Acoustical Society of America 102(6): 3343-48. 

Helmholtz, Hermann Ludwig Ferdinand. 1877. Die Lehre von den Tonempfindungen als 
physiologische Grundlage ftir die Theorie der Musik. Braunschweig: Friedrich Vieweg und Sohn. 
Translation by Alexander J. Ellis, On the Sensations of Tone as a Physiological Basis for the 
Theory of Music, 4th ed. (London: Longmans, Green), 1912. 

Hoar, William Stewart and David J. Randall, eds. 1971. Fish Physiology. Vol. 5: Sensory Systems and 
Electric Organs. New York: Academic. 

Holley, Matthew C. and Jonathan F. Ashmore. 1988. “On the Mechanism of a High-Frequency Force 
Generator in Outer Hair Cells Isolated from the Guinea Pig Cochlea.” Proceedings of the Royal 
Society of London B 232: 413-29. 

Honrubia, Vicente, David Strelioff, and Stephen Sitko. 1976. “Electroanatomy of the Cochlea: Its 
Role in Cochlear Potential Measurements.” In: Robert J. Ruben, Claus Elberling, and Gerhard 
Salomon, eds. (Baltimore, MD: University Park Press), pp. 23-39. 

Hudspeth, A. James and R. S. Lewis. 1988. “A Model for Electrical Resonance and Frequency 
Tuning in Saccular Hair Cells of the Bull-Frog, Rana catesbeiana.” Journal of Physiology 400: 
275-97. 

Iwasa, Kuni H. 2001. “A Two-State Piezoelectric Model for Outer Hair Cell Motility.” Biophysical 
Journal 81(5): 2495-2506. 

Jakli, Antal. and Nandor Eber. 1993. “Piezoelectric Effects in Liquid Crystals.” In: Agnes Buka, ed., 
Modern Topics in Liquid Crystals (Singapore: World Scientific) pp. 235-56. 

Jielof, Renske, A. Spoor and Hessel de Vries. 1952. “The Microphonic Activity of the Lateral Line.” 
Journal of Physiology 116: 137-57. 


Keen, J. A. 1940. *A Note on the Length of the Basilar Membrane in Man and in Various Mammals." 
Journal of Anatomy 75: 524-27. 

Konishi, Teruzo, Donald C. Teas, and Joel S. Wernick. 1970. “Effects of Electrical Current Applied 
to Cochlear Partition on Discharges in Individual Auditory-Nerve Fibers. I. Prolonged Direct- 
Current Polarization." Journal of the Acoustical Society of America 47 (6): 1519-26. 

Kostelijk, Pieter Jan. 1950. Theories of Hearing. Leiden: Universitaire Pers Leiden. 

Lissmann, Hans W. 1958. *On the Function and Evolution of Electric Organs in Fish." Journal of 
Experimental Biology 35: 156-91. 

Mamishev, Alexander V., Kishore Sundara-Rajan, Fumin Yang, Yanqing Du, and Markus Zahn. 
2004. “Interdigital Sensors and Transducers.” Proceedings of the IEEE 92(5): 808-45. 

Moller, Peter. 1995. Electric Fishes: History and Behavior. London: Chapman & Hall. 

Mountain, David C. 1986. “Electromechanical Properties of Hair Cells.” In: R. A. Altschuler, D. W. 
Hoffman, and R. P. Bobbin, eds., Neurobiology of Hearing: The Cochlea (New York: Raven 
Press), pp. 77-90. 

Mountain, David C. and Allyn E. Hubbard. 1994. “A Piezoelectric Model of Outer Hair Cell 
Function.” Journal of the Acoustical Society of America 95(1): 350-54. 

Naftalin, Lionel. 1963. “The Transmission of Acoustic Energy from Air to the Receptor Organ in the 
Cochlea.” Life Sciences 2(2): 101-6. 

. 1964. “Reply to Criticisms by Mr. A. Tumarkin and Mr. J. D. Gray.” Journal of 

Laryngology and Otology 78: 969-71. 

. 1965. “Some New Proposals Regarding Acoustic Transmission and Transduction.” Cold 

Spring Harbor Symposia on Quantitative Biology 30: 169-80. 

. 1967. “The Cochlear Geometry as a Frequency Analyser.” Journal of Laryngology and 

Otology 81(6): 619-31. 

. 1968. “Acoustic Transmission and Transduction in the Peripheral Hearing Apparatus.” 

Progress in Biophysics and Molecular Biology 18: 3-27. 

. 1969. “A Liquid Ion-exchange Resin Microphone.” Life Sciences 8 (part 2): 223-28. 

. 1970. *Biochemistry and Biophysics of the Tectorial Membrane." In: Michael M. Paparella, 

ed., Biochemical Mechanisms in Hearing and Deafness (Springfield, IL: Charles C. Thomas), pp. 

205-10, discussion on pp. 290-93. 

. 1976. *The Peripheral Hearing Mechanism: A Biochemical and Biological Approach." 

Annals of Otology, Rhinology and Laryngology 85: 38-42. 

. 1980. “Frequency Analysis in the Cochlea and the Traveling Wave of von Békésy.” 

Physiological Chemistry and Physics 12: 521-26. 

. 1981. “Energy Transduction in the Cochlea.” Hearing Research 5: 307-15. 

Naftalin, Lionel, M. Spence Harrison and A. Stephens. 1964. “The Character of the Tectorial 
Membrane.” Journal of Laryngology and Otology 78: 1061-78. 

Naftalin, Lionel and G. P. Jones. 1969. “Propagation of Acoustic Waves in Gels with Special 
Reference to the Theory of Hearing.” Life Sciences 8 (part 1): 765-68. 

Naftalin, Lionel and Michael Mattey. 1995. “The Transmission of Acoustic Energy from Air to the 
Receptor and Transducer in the Cochlea.” Paper presented at conference on “Non-linear Coherent 
Structures in Physics and Biology,” Heriot-Watt University, Edinburgh, July 1995. 

Naftalin, Lionel, Michael Mattey, and Eve M. Lutz. 2009. “The Transmission of Acoustic Energy 
from Air to the Receptor and Transducer Structures within the Cochlea with Special Reference to 
the Tectorial Membrane.” Manuscript submitted to Hearing Research. 

Naftalin, Lionel and A. Stephens. 1966. “A Protein Electret Microphone.” Life Sciences 5(3): 223-26. 





























Neely, S. T. 1989. *A Model for Bidirectional Transduction in Outer Hair Cells." In: J. P. Wilson and 
D. T. Kemp, eds., Cochlear Mechanisms (New York: Plenum), pp. 75-82. 

Nowotny, Manuela and Anthony W. Gummer. 2006. *Nanomechanics of the Subtectorial Space 
Caused by Electromechanics of Cochlear Outer Hair Cells." Proceedings of the National Academy 
of Sciences 103(7): 2120-25. 

Offutt, George C. 1968. *Auditory Response in the Goldfish." Journal of Auditory Research 8: 391- 
400. 





. 1970. *A Proposed Mechanism for the Perception of Acoustic Stimuli near Threshold." 

Journal of Auditory Research 10: 226-28. 

. 1974. “Structures for the Detection of Acoustic Stimuli in the Atlantic Codfish, Gadus 

morhua.” Journal of the Acoustical Society of America 56(2): 665-71. 

. 1984. The Electromodel of the Auditory System. Shepherdstown, WV: GoLo Press. 

. 1986. *Wever and Lawrence Revisited: Effects of Nulling Basilar Membrane Movement on 

Concomitant Whole-Nerve Action Potential." Journal of Auditory Research 26: 43-54. 

. 1999. *New Electromodel Hearing Aid." Resonance: Newsletter of the Bioelectromagnetics 

SIG 34: 17-18. 

. 2000. *What is the Basis of Human Hearing?" Frontier Perspectives 9(2): 33-36. 

. 2002. *Energy Flow and Basilar Membrane Vibrations (Sound in the Cochlea's Fluids)." 
Presented at 25th Midwinter Research Meeting of the Association for Research in Otolaryngology, 
January. 

O'Leary, Dennis P. 1970. *An Electrokinetic Model of Transduction in the Semicircular Canal." 
Biophysical Journal 10: 859-75. 

Ozen, Siikrii 2008. “Low-frequency Transient Electric and Magnetic Fields Coupling to Child Body.” 
Radiation Protection Dosimetry 128(1): 62-67. 

Parks, Susan E., Darlene R. Ketten, Jennifer T. O’Malley, and Julie Arruda. 2007. “Anatomical 
Predictions of Hearing in the North Atlantic Right Whale.” Anatomical Record 290: 734-44. 

Pohlman, Augustus G. 1922. “Structural Factors Contributing to Acoustic Insulation of the End 
Organ.” The Anatomical Record 23:32. Abstract. 

. 1930. “Correlations Between the Acuity for Hearing Air and Bone Transmitted Sounds in 

Rinne Negative and Rinne Positive Cases.” Annals of Otology, Rhinology and Laryngology 39(4): 

927-60. 

. 1933. “A Reconsideration of the Mechanics of the Auditory Apparatus.” Journal of 

Laryngology and Otology 48: 156-95. 

. 1936. “The Present Status of the Mechanics of Sound Conduction in Its Relation to the 

Possible Correction of Conduction Deafness.” Journal of the Acoustical Society of America 8(2): 

112-17. 

. 1938. “Objections to the Accepted Interpretation of Cochlear Mechanics.” Acta Oto- 

Laryngologica 26: 162-69. 

. 1942. “Further Objections to the Accepted Interpretations of Cochlear Mechanics.” Archives 
of Otolaryngology 35: 613-22. 

Rabbit, Richard D., Harold E. Ayliffe, Douglas Christensen, Kranti Pamarthy, Carl Durney, Sarah 
Clifford, and William E. Brownell. 2005. “Evidence of Piezoelectric Resonance in Isolated Outer 
Hair Cells.” Biophysical Journal 88: 2257-65. 

Raphael, Robert M., Aleksander S. Popel, and William E. Brownell. 2000. “A Membrane Bending 
Model of Outer Hair Cell Electromotility.” Biophysical Journal 78: 2844-62. 

Richter, Claus-Peter, Gulam Emadi, Geoffrey Getnick, Alicia Quesnel, and Peter Dallos. 2007. 
“Tectorial Membrane Stiffness Gradients.” Biophysical Journal 93: 2265-76. 



































Ross, Muriel D. 1974. *The Tectorial Membrane of the Rat." American Journal of Anatomy 139: 
449-82. 

Russell, Ian J., Alan R. Cody, and Guy P. Richardson. 1986. *The Responses of Inner and Outer Hair 
Cells in the Basal Turn of the Guinea-Pig Cochlea and in the Mouse Cochlea Grown In vitro.” 
Hearing Research 22: 199-216. 

Russell, Ian J. and Peter M. Sellick. 1978. “Intracellular Studies of Hair Cells in the Mammalian 
Cochlea.” Journal of Physiology 284: 261-90. 

Santos-Sacchi, Joseph and James P. Dilger. 1988. “Whole Cell Currents and Mechanical Responses 
of Isolated Outer Hair Cells.” Hearing Research 35: 143-50. 

Spector, William S., ed. 1956. Handbook of Biological Data. Philadelphia: W. B. Saunders. Page 323 
on cochlear dimensions across species. 

Strelioff, David, Ake Flock, and Karl E. Minser. 1985. “Role of Inner and Outer Hair Cells in 
Mechanical Frequency Selectivity of the Cochlea.” Hearing Research 18: 169-75. 

Tasaki, Ichiji and César Fernandez. 1952. “Modification of Cochlear Microphonics and Action 
Potentials by KCI Solution and by Direct Currents.” Journal of Neurophysiology 15: 497-512. 

Teas, Donald C., Teruzo Konishi, and Joel S. Wernick. 1970. “Effects of Electrical Current Applied 
to Cochlear Partition on Discharges in Individual Auditory-Nerve Fibers. II. Interaction of 
Electrical Polarization and Acoustic Stimulation.” Journal of the Acoustical Society of America 
47(6): 1527-37. 

Ulfendahl, Mats and Ake Flock. 1998. “Outer Hair Cells Provide Active Tuning in the Organ of 
Corti.” Physiology 13: 107-11. 

Weitzel, Erik K., Ron Tasker, and William E. Brownell. 2003. “Outer Hair Cell Piezoelectricity: 
Frequency Response Enhancement and Resonance Behavior.” Journal of the Acoustical Society of 
America 114(3): 1462-66. 

Wever, Ernest Glen. 1966. “Electrical Potentials of the Cochlea.” Physiological Reviews 46(1): 102- 
27. 

Wever, Ernest Glen and Charles William Bray. 1930. “Action Currents in the Auditory Nerve in 
Response to Acoustical Stimulation.” Proceedings of the National Academy of Sciences 16(5): 
344-50. 

Zotterman, Yngve. 1943. “The Microphonic Effect of Teleost Labyrinths and its Biological 
Significance.” Journal of Physiology 102: 313-18. 

Zwislocki, Josef J. 1980. “Theory of Cochlear Mechanics.” Hearing Research 2: 171-82. 

Zwislocki, Josef J. and Lisa K. Cefaratti. 1989. “Tectorial Membrane II: Stiffness Measurements In 
vivo.” Hearing Research 42: 211-28. 

Zwislocki, Josef J. and My Nguyen. 1999. “Place Code for Pitch: A Necessary Revision.” Acta Oto- 
Laryngologica 119(2): 140-45. 

Zwislocki, Josef J., Norma B. Slepecky, Lisa K. Cefaratti, and Robert L. Smith. 1992. “Ionic 
Coupling Among Cells in the Organ of Corti.” Hearing Research 57: 175-94. 


Electrophonic Effect 

Adrian, Donald J. 1977. “Auditory and Visual Sensations Stimulated by Low-frequency Electric 
Currents.” Radio Science 12(6S): 243-50. 

Althaus, Julius. 1873. A Treatise on Medical Electricity, 3rd ed. Philadelphia: Lindsay and Blakiston. 

Augustin, Friedrich Ludwig. 1801. Vom Galvanismus und dessen medicinischer Anwendung. Berlin. 

. 1803. Versuch einer vollstándigen systematischen Geschichte der galvanischen Electricitát 
und ihrer medicinischen Anwendung. Berlin: Felisch. 

Bartholow, Roberts. 1881. Medical Electricity. Philadelphia: Henry C. Lea's Son. 





Bredon, Alan Dale. 1963. Investigation of Diplexing Transducers for Voice Communications. 
Electromagnetic Warfare and Communication Laboratory, Aeronautical Systems Division, Air 
Force Systems Command, Wright-Patterson Air Force Base, Ohio. Accession no. AD 400487, 
Technical Documentary Report no. ASD-TDR-63-157. 

Brenner, Rudolf. 1868. Untersuchungen und Beobachtungen über die Wirkung Elektrischer Stróme 
auf das Gehórorgan in gesunden und kranken Zustande. Leipzig: Giesecke & Devrient. 

Craik, Kenneth J. W., Alexander Francis Rawdon-Smith, and Rowan S. Sturdy. 1937. “Note on the 
Effect of A.C. on the Human Ear.” Proceedings of the Physiological Society, May 8, pp. 2P-5P. 

Eichhorn, Gustav. 1930. “The Electrostatic ‘Radiophon.’” Radio-Craft, January, p. 330. 

Einhorn, Richard N. 1967. *Army Tests Hearing Aids that Bypass the Ears." Electronic Design 
15(26): 30-32. 

Flanagan, Gillis Patrick. 1962. *Nervous System Excitation Device." U.S. Patent 3,393,279, filed 
March 13, 1962, issued July 16, 1968. 

Flies, Carl Eduard. 1801. *Versuch des Herrn Dr. Flies." In: Carl Johann Christian Grapengiesser, 
Versuche den Galvanismus zur Heilung Einiger Krankheiten anzuwenden (Berlin: Mylius), pp. 
241-52. 

Flottorp, Gordon. 1953. *Effect of Different Types of Electrodes in Electrophonic Hearing." Journal 
of the Acoustical Society of America 25(2): 236-45. 

Gersuni, Grigoryi V. and A. A. Volokhov. 1936. *On the Electrical Excitability of the Auditory Organ 
on the Effect of Alternating Currents on the Normal Auditory Apparatus.” Journal of 
Experimental Psychology 19: 370-82. 

Grapengiesser, Carl Johann Christian. 1801. Versuche den Galvanismus zur Heilung Einiger 
Krankheiten anzuwenden. Berlin: Mylius. 

Hallpike, Charles Skinner and Hamilton Hartridge. 1937. *On the Response of the Human Ear to 
Audio-Frequency Electrical Stimulation." Proceedings of the Royal Society of London B 123: 177- 
93. 

Harvey, William T. and James P. Hamilton. 1964. *Hearing Sensations in Amplitude Modulated 
Radio Frequency Fields." Master's thesis, Air Force Institute of Technology, Wright-Patterson Air 
Force Base, Ohio. Accession no. AD 608889. 

Healer, Janet. 1967. *Auditory Response to Audio-Frequency Currents." In: Healer, ed., Summary 
Report on a Review of Biological Mechanisms for Application to Instrument Design, (Washington, 
DC: National Aeronautics and Space Administration), vol. 5, pp. 5-8 to 5-13. Accession no. N67- 
40136, Document no. ARA 346-F-2, part 1. 

Hellwag, Christoph Friedrich and Maximilian Jacobi. 1802. Erfahrungen über die Heilkráfte des 
Galvanismus, und Betrachtungen über desselben chemische und physiologische Wirkungen. 
Hamburg: Friedrich Perthes. 

Hoshiko, Michael S. 1970. “Electrostimulation of Hearing." In: Norman L. Wulfsohn and Anthony 
Sances, Jr., eds., The Nervous System and Electic Currents (New York: Plenum), pp. 85-88. 

Johnson, Patrick Woodruff. 1971. *A Search for the Electrophonic Phenomena in the Microwatt 
Power Domain." Master's thesis, Naval Postgraduate School, Monterey, CA. Accession no. AD 
744911. 

Jones, H. Lewis. 1913. Medical Electricity, 6th ed. Philadelphia: P. Blakiston's Son. 

Jones, R. Clark, Stanley Stephens Stevens, and Moses H. Lurie. 1940. “Three Mechanisms of 
Hearing by Electrical Stimulation." Journal of the Acoustical Society of America 12: 281-90. 

Le Roy, Jean Baptiste. 1755. *Ou l'on rend compte de quelques tentatives que l'on a faites pour 
guérir plusieurs maladies par Électricité." Mémoires de l'Académie Royale des Sciences, pp. 60- 
98. 


Martens, Franz Heinrich. 1803. Vollständige Anweisung zur therapeutischen Anwendung des 
Galvanismus; nebst einer Geschichte dieses Heilmittels. Weiszenfels: Bose. 

Merzdorff, Johann Friedrich Alexander. 1801. Treatment of tinnitus with the galvanic current. In: 
Carl Johann Christian Grapengiesser, Versuche den Galvanismus zur Heilung Einiger Krankheiten 
anzuwenden (Berlin: Mylius), pp. 131-33. 

Morgan, Charles E. 1868. Electro-Physiology and Therapeutics. New York: William Wood. 

Moxon, Edwin Charles. 1971. *Neural and Mechanical Responses to Electrical Stimulation of the 
Cat's Inner Ear." Ph.D. dissertation, Massachusetts Institute of Technology. 

Puharich, Henry K. and Joseph L. Lawrence. 1964. Electro-Stimulation Techniques of Hearing. QRC 
Branch, Rome Air Development Center, Research and Technology Division, Air Force Systems 
Command, Griffiss Air Force Base, NY. Accession no. AD 459956, Technical Documentary 
Report no. RADC-TDR-64-18. 

Ritter, Johann Wilhelm. 1802. Beytrdge zur ndhern Kentniss des Galvanismus und der Resultate 
seiner Untersuchung, vol. 2, part 2. Jena: Friedrich Fromann. 

Salmansohn, M. 1969. Non-Acoustic Audio Coupling to the Head (NAACH). Warminster, PA: Aero- 
Electronic Technology Department, Naval Air Development Center Johnsville. Accession no. AD 
862280, Report no. NADC-AE-6922. 

Salomon, Gerhard and Arnold Starr. 1963. “Sound Sensations Arising from Direct Current 
Stimulation of the Cochlea in Man.” Danish Medical Bulletin 10(6-7): 215-16. 

Skinner, Garland Frederick. 1968. “The Trans-Derma-Phone — A Research Device for the 
Investigation of Radio-Frequency Sound Stimulation.” Master’s thesis, Naval Postgraduate 
School, Monterey, CA. 

Sommer, H. C. and Henning E. von Gierke. 1964. “Hearing Sensations in Electric Fields.” Aerospace 
Medicine 35: 834-39. 

Sprenger, Johann Justus Anton. 1802. “Anwendungsart der Galvani-Voltaischen Metall-Electricitat 
zur Abhelfung der Taubheit und Harthórigkeit." Annalen der Physik 11(7): 354-66. 

Stevens, Stanley Smith. 1937. *On Hearing by Electrical Stimulation." Journal of the Acoustical 
Society of America 8: 191-95. 

Stevens, Stanley Smith and Hallowell Davis. 1938. Hearing: Its Psychology and Physiology. New 
York: American Institute of Physics. 

Stevens, Stanley Smith and R. Clark Jones. 1939. “The Mechanism of Hearing by Electrical 
Stimulation.” Journal of the Acoustical Society of America 10(4): 261-69. 

Stevens, Stanley Smith and Fred Warshofsky. 1965. Sound and Hearing. New York: Time-Life 
Books. 

Struve, Christian August. 1802. System der medicinischen Elektrizitáts-Lehre mit Rücksicht auf den 
Galvanismus. Breslau: Wilhelm Gottlieb Korn. 

Tousey, Sinclair. 1921. Medical Electricity, Róntgen Rays and Radium, 3rd ed. Philadelphia: W.B. 
Saunders. Page 469 on auditory effects. 

Volta, Alexander. 1800. *On the Electricity excited by the mere Contact of conducting Substances of 
different Kinds." Philosophical Magazine 7 (September): 289-311. 

Wolke, Christian Heinrich. 1802. Nachricht von den zu Jever durch die Galvani-Voltaische Gehór- 
Gebe-Kunst beglükten Taubstummen und von Sprengers Methode sie durch die Voltaische 
Elekricitüt auszuüben. Oldenburg: Schulz. 


Energy Efficient Light Bulbs 
National Lighting Product Information Program. June 1999. *Screwbase Compact Fluorescent Lamp 
Products." Specifier Reports 7(1). 


National Lighting Product Information Program. May 2000. “Electronic Ballasts.” Specifier Reports 
8(1). 


Low Frequency Sounds 

Begley, Sharon. 1993. “Do You Hear What I Hear? A Hum in Taos is Driving Dozens of People 
Crazy.” Newsweek, May 3, pp. 54-55. 

Brodeur, Paul. 1977. The Zapping of America. New York: W. W. Norton. 

Cooke, Patrick. 1994. “The Hum.” Health, July/August, pp. 71-75. 

Curry, Bill P. and Gretchen V. Fleming. 2003. RF Radiation Measurements in Selected Locations in 
Kokomo, Indiana. Prepared for Acentech, Inc., Cambridge, MA, August 29. 

Deming, David. 2004. *The Hum: An Anomalous Sound Heard Around the World." Journal of 
Scientific Exploration 18(4): 571-95. 

Federation of American Scientists. 1995. Submarine Communications Master Plan. Washington, DC. 

Firstenberg, Arthur. 1999. “The Source of the Taos Hum." No Place To Hide 2(2): 3-5. 

Fox, Barry. 1989. “Low-frequency ‘Hum’ May Permeate the Environment." New Scientist, 
December 9, p. 27. 

Garufi, Frank. 1989. Loran C Field Strength Contours: Contiguous United States. Washington, DC: 
Federal Aviation Administration. Report no. DOT/FAA/CT-TN89/16. 

Hubbell, Schatzie. 1995. Hum survey results. Fort Worth, TX, October 6. 

Jansky & Bailey, Atlantic Research Corporation. 1962. The Loran-C System of Navigation. 
Washington, DC. 

Mullins, Joe H. and James P. Kelly. 1995. The Elusive Hum in Taos, New Mexico. Acoustical Society 
Newsletter 5(3): 1 ff. 

Mullins, Joe H., James P. Kelly, and Sherry Robinson. 1993. “Hum Investigation: Source Still 
Unknown, Questions Raised.” Albuquerque: University of New Mexico, August 23. 

Samaddar, S. N. 1979. “Theory of Loran-C Ground Wave Propagation — A Review.” Journal of the 
Institute of Navigation 26(3): 173-87. 

Sheppard, L. and C. Sheppard. 1993. The Phenomenon of Low Frequency Hums. Norfolk, England: 
Norfolk Tinnitus Society. 

United States Coast Guard. 1974. Loran-C User Handbooks Washington, DC. Publication no. CG- 
462. 





. 1992. Loran-C User Handbook. Washington, DC. Commandant Publication P16562.6. 


Microwave Hearing 

Chou, Chung-Kwang and Arthur William Guy. 1977. “Characteristics of Microwave-induced 
Cochlear Microphonics.” Radio Science 6(S): 221-27. 

Elder, Joseph A. and Chung-Kwang Chou. 2003. “Auditory Response to Pulsed Radiofrequency 
Energy." Bioelectromagnetics, suppl. 6: 5162-73. 

Frey, Allan H. 1961. *Auditory System Response to Radio Frequency Energy." Aerospace Medicine 
32: 1140-42. 

. 1963. *Some Effects on Human Subjects of Ultra-High-Frequency Radiation." American 

Journal of Medical Electronics, January-March 1963, pp. 28-31. 

. 1967. “Brain Stem Evoked Responses Associated with Low-intensity Pulsed UHF Energy.” 

Journal of Applied Physiology 23(6): 984-88. 

. 1970. “Effects of Microwave and Radio Frequency Energy on the Central Nervous System." 

In: Stephen F. Cleary, ed., Biological Effects and Health Implications of Microwave Radiation. 

Symposium Proceedings (Rockville, MD: U.S. Department of Health, Education and Welfare), 

Publication BRH/DBE 70-2, pp. 134-39. 














. 1971. “Biological Function as Influenced by Low-power Modulated RF Energy.” IEEE 

Transactions on Microwave Theory and Techniques MTT-19(2): 153-64. 

. 1988. “Evolution and Results of Biological Research with Low-intensity Nonionizing 
Radiation.” In: Andrew A. Marino, ed., Modern Bioelectricity (New York: Marcel Dekker, pp. 
785-837. 

Frey, Allan H. and Edwin S. Eichert II]. 1972. “The Nature of Electrosensing in the Fish.” 
Biophysical Journal 12: 1326-58. 

. 1985. “Psychophysical Analysis of Microwave Sound Perception.” Journal of Bioelectricity 
4(1): 1-14. 

Frey, Allan H. and Rodman Messenger, Jr. 1973. *Human Perception of Illumination with Pulsed 
Ultrahigh-Frequency Electromagnetic Energy." Science 181: 356-58. 

Justesen, Don R. 1975. *Microwaves and Behavior." American Psychologist 30(3): 391-401. 

Khizhnyak, E. P., V. V. Tyazhelov, and V. V. Shorokhov. 1979. *Some Peculiarities and Possible 
Mechanisms of Auditory Sensation Evoked by Pulsed Electromagnetic Irradiation.” Activitas 
Nervosa Superior 21(4): 247-51. 

Lebovitz, Robert M. and Ronald L. Seaman. 1977. “Single Auditory Unit Responses to Weak, Pulsed 
Microwave Radiation.” Brain Research 126: 370-5. 

Lin, James C. 1978. Microwave Auditory Effects and Applications. Springfield, IL: Charles C. 
Thomas. 

. 2001. “Hearing Microwaves: The Microwave Auditory Phenomenon.” [EEE Antennas and 
Propagation Magazine 43(6): 166-68. 

Seaman, Ronald L. 2002. “Transmission of Microwave-induced Intracranial Sound to the Inner Ear is 
Most Likely Through Cranial Aqueducts.” Brooks Air Force Base, TX: Walter Reed Army 
Institute of Research. 

Seaman, Ronald L. and Robert M. Lebovitz. 1989. “Thresholds of Cat Cochlear Nucleus Neurons to 
Microwave Pulses.” Bioelectromagnetics 10: 147-60. 

Sharp, Joseph C., H. Mark Grove, and Om P. Gandhi. 1974. “Generation of Acoustic Signals by 
Pulsed Microwave Energy.” IEEE Transactions on Microwave Theory and Techniques MTT- 
22(5): 583-84. 

Stocklin, Philip L. and Brian F. Stocklin. 1979. “Possible Microwave Mechanisms of the Mammalian 
Nervous System." T.-I.-T. Journal of Life Sciences 9: 29-51. 

Taylor, Eugene M. and Bonnie T. Ashleman. 1974. *Analysis of Central Nervous System 
Involvement in the Microwave Auditory Effect." Brain Research 74: 201-8. 

Tyazhelov, V. V., R. E. Tigranian, E. O. Khizhniak, and I. G. Akoev. 1979. *Some Peculiarities of 
Auditory Sensations Evoked by Pulsed Microwave Fields." Radio Science 14(6S): 259-63. 

Watanabe, Yoshiaki and Toshiyuki Tanaka. 2000. “FDTD Analysis of Microwave Hearing Effect.” 
IEEE Transactions on Microwave Theory and Techniques MTT-48(11): 2126-32. 

Wilson, Blake S. and William T. Joines. 1985. “Mechanisms and Physiologic Significance of 
Microwave Action on the Auditory System.” Journal of Bioelectricity 4(2): 495-525. 

Wilson, Blake S., John M. Zook, William T. Joines, and John H. Casseday. 1980. “Alterations in 
Activity at Auditory Nuclei of the Rat Induced by Exposure to Microwave Radiation: 
Autoradiographic Evidence Using [14C]2-deoxy-d-Glucose." Brain Reserch 187: 291-306. 











Power Line Radiation 

Kikuchi, Hiroshi. 1972. *Investigations of Electromagnetic Noise and Interference Due to Power 
Lines in Japan and Some Results from the Aspect of Electromagnetic Theory." Proceedings of the 
1972 Symposium on Electromagnetic Hazards, Pollution and Environmental Quality, Purdue 
University, Lafayette, Indiana, May 8-9, pp. 147-62. 





. 1983a. "Overview of Power-Line Radiation and its Coupling to the Ionosphere and 

Magnetosphere." Space Science Reviews 35: 33-41. 

. 1983b. *Power Line Transmission and Radiation." Space Science Reviews 35: 59-80. 

, ed. 1983c. Power Line Radiation and Its Coupling to the Ionosphere and Magnetosphere. 
Amsterdam: Reidel. 

Vignati, Maurizio and Livio Giuliani. 1997. *Radiofrequency Exposure near High-Voltage Lines." 
Environmental Health Perspectives 105 (suppl. 6): 1569-73. 








Saccular Hearing 

Akin, Faith Wurm and Owen D. Murnane. 2004. *Vestibular Evoked Myogenic Potentials (VEMP)." 
Clinical Topics in Otoneurology, a publication of GN Otometrics, Copenhagen. April issue. 

Bocca, Ettore and G. Perani. 1960. *Further Contributions to the Knowledge of Vestibular Hearing." 
Acta Oto-Laryngologica 51: 260-67. 

Cazals, Yves, Jean-Marie Aran, and Jean-Paul Erre. 1982. *Frequency Sensitivity and Selectivity of 
Acoustically Evoked Potentials After Complete Cochlear Hair Cell Destruction." Brain Research 
231: 197-203. 

. 1983. "Intensity Difference Thresholds Assessed with Eighth Nerve and Auditory Cortex 
Potentials: Compared Values from Cochlear and Saccular Responses." Hearing Research 10: 263- 
68. 

Cazals, Yves, Jean-Marie Aran, Jean-Paul Erre, Anne Guilhaume, and Catherine Aurousseau. 1983. 
“Vestibular Acoustic Reception in the Guinea Pig: A Saccular Function?” Acta Oto- 
Laryngologica 95(3-4): 211-17. 

Clarke, Andrew H., Uwe Schónfeld, and Kai Helling. 2003. *Unilateral Examination of Utricle and 
Saccule Function." Journal of Vestibular Research 13: 215-25. 

Colebatch, James G. 2006. “Assessing Saccular (Otolith) Function in Man.” Journal of the 
Acoustical Society of America, 119 (5 part 2): 3432. Abstract. 

. 2014. “Overview of VEMPs (Vestibular-Evoked Myogenic Potentials).” 30th International 
Congress of Clinical Neurophysiology, Berlin, p. 53. Abstract. 

Colebatch, James G., G. Michael Halmagyi, and Nevell F. Skuse. 1994. “Myogenic Potentials 
Generated by a Click-Evoked Vestibulocollic Reflex.” Journal of Neurology, Neurosurgery, and 
Psychiatry 57(2): 190-97. 

Didier, Anne and Yves Cazals. 1989. “Acoustic Responses Recorded from the Saccular Bundle on 
the Eighth Nerve of the Guinea Pig.” Hearing Research 37: 123-28. 

Emami, Seyede Faranak. 2013. “Is All Human Hearing Cochlear?” Scientific World Journal, article 
ID 147160. 

. 2014a. “Hypersensitivity of Vestibular System to Sound and Pseudoconductive Hearing 

Loss in Deaf Patients.” ISRN Otolaryngology, article ID 817123. 

. 2014b. “Vestibular Activation by Sound in Human.” Scholars Journal of Applied Medical 
Sciences 2(6H): 3445-51. 

Emami, Seyede Faranak and Nasrin Gohari. 2014. “The Vestibular-Auditory Interaction for Auditory 
Brainstem Response to Low Frequencies.” ISRN Otolaryngology, article ID 103598. 

Emami, Seyede Faranak, Akram Pourbakht, Kianoush Sheykholeslami, Mohammad Kamali, 
Fatholah Behnoud, and Ahmad Daneshi. 2012. “Vestibular Hearing and Speech Processing.” ISRN 
Otolaryngology, article ID 850629. 

Guinan, John J., Jr. 2006. “Acoustically Responsive Fibers in the Mammalian Vestibular Nerve.” 
Journal of the Acoustical Society of America 119 (5 part 2): 3432. Abstract. 

Igarashi, Makoto and Yuho Kato. 1975. “Effect of Different Vestibular Lesions upon Body 
Equilibrium Function in Squirrel Monkeys.” Acta Oto-Laryngolica. Supplementum 330: 91-99. 














Lenhardt, Martin L. 1999. *Stapedial-Saccular Strut and Method." U.S. Patent 6,368,267, filed 
October 14, 1999, issued April 9, 2002. 

. 2006. *Saccular Hearing: Turtle Model for a Human Prosthesis." Journal of the Acoustical 
Society of America 119 (5 part 2): 3433-34. Abstract. 

McCue, Michael P. and John J. Guinan, Jr. 1994. *Acoustically Responsive Fibers in the Vestibular 
Nerve of the Cat." Journal of Neuroscience 14(10): 6058-70. 

. 1997. *Sound-Evoked Activity in Primary Afferent Neurons of a Mammalian Vestibular 
System." American Journal of Otology 18(3): 355-60. 

Meyer, Max F. 1931. *Hearing Without Cochlea?" Science 73: 236-37. 

Reuter, Tom and Sirpa Nummela. 1998. *Elephant Hearing." Journal of the Acoustical Society of 
America 104 (2 part 1): 1122-23. 

Ribarić, Ksenija, Tine S. Prevec, and Vladimir Kozina. 1984. *Frequency-Following Response 
Evoked by Acoustic Stimuli in Normal and Profoundly Deaf Subjects.” Audiology 23(4): 388-400. 

Robertson, D. D. and Dennis J. Ireland. 1995. “Vestibular Evoked Myogenic Potentials.” Journal of 
Otolaryngology 24(1): 3-8. 

Rosengren, Sally M., Miriam S. Welgampola, and James G. Colebatch. 2010. “Vestibular Evoked 
Myogenic Potentials: Past, Present and Future.” Clinical Neurophysiology 121(5): 636-51. 

Ross, Muriel D. 1983. “Gravity and the Cells of Gravity Receptors in Mammals.” Advances in Space 
Research 3(9): 179-90. 

Sohmer, Haim, Sharon Freeman, and Ronen Perez. 2004. “Semicircular Canal Fenestration — 
Improvement of Bone- but not Air-conducted Auditory Thresholds.” Hearing Research 187: 105- 
10. 

Tait, John. 1932. “Is All Hearing Cochlear?” Annals of Otology, Rhinology and Laryngology 41: 681- 
704. 

Todd, Neil P. McAngus. 2001. “Evidence for a Behavioral Significance of Saccular Acoustic 
Sensitivity in Humans.” Journal of the Acoustical Society of America 110(1): 380-90. 

. 2006. “Is All Hearing Cochlear? — Revisited (Again).” Journal of the Acoustical Society of 
America 119 (5 part 2): 3431-32. Abstract. 

Trivelli, Maurizio, Massimiliano Potena, Valeria Frari, Tomassangelo Petitti, Valentina Deidda, and 
Fabrizio Salvinelli. 2013. “Compensatory Role of Saccule in Deaf Children and Adults: Novel 
Hypotheses.” Medical Hypotheses 80(1): 43-46. 

Wit, Hero P., J. D. Bleeker, and H. H. Mulder. 1984. “Responses of Pigeon Vestibular Nerve Fibers to 
Sound and Vibration with Audiofrequencies.” Journal of the Acoustical Society of America 75(1): 
202-8. 

Wu, Chen-Chi and Yi-Ho Young. 2002. “Vestibular Evoked Myogenic Potentials Are Intact After 
Sudden Deafness.” Ear and Hearing 23(3): 235-38. 

Young, Eric D., César Fernández and Jay M. Goldberg. 1977. “Responses of Squirrel Monkey 
Vestibular Neurons to Audio-Frequency Sound and Head Vibration.” Acta Oto-Laryngologica 
84(5-6): 352-60. 











Tinnitus 

Del Bo, Luca, Stella Forti, Umberto Ambrosetti, Serena Costanzo, Davide Mauro, Gregorio Ugazio, 
Berthold Langguth, and Antonio Mancuso. 2008. “Tinnitus Aurium in Persons with Normal 
Hearing: 55 Years Later.” Otolaryngology — Head and Neck Surgery 139: 391-94. 

Heller, Morris F. and Moe Bergman. 1953. “Tinnitus Aurium in Normally Hearing Persons.” Annals 
of Otology 62: 73-83. 

Holgers, Kajsa-Mia. 2003. “Tinnitus in 7-year-old Children.” European Journal of Pediatrics 162: 
276-78. 


Holgers, Kajsa-Mia and Jolanta Juul. 2006. “The Suffering of Tinnitus in Childhood and 
Adolescence.” International Journal of Audiology 45: 267-72. 

Holgers, Kajsa-Mia and Bo Pettersson. 2005. “Noise Exposure and Subjective Hearing Symptoms 
among School Children in Sweden.” Noise and Health 7(27): 27-37. 

Hutter, Hans-Peter, Hanns Moshammer, Peter Wallner, Monika Cartellieri, Doris-Maria Denk- 
Linnert, Michaela Katzinger, Klaus Ehrenberger, and Michael Kundi. 2010. “Tinnitus and Mobile 
Phone Use.” Occupational and Environmental Medicine 67: 804-8. 

Juul, Jolanta, Marie-Louise Barrenás, and Kajsa-Mia Holgers. 2012. “Tinnitus and Hearing in 7-year- 
old Children.” Archives of Disease in Childhood 97: 28-30. 

Kochkin, Sergei, Richard Tyler, and Jennifer Born. 2011. “MarkeTrak VIII: The Prevalence of 
Tinnitus in the United States and the Self-reported Efficacy of Various Treatments.” Hearing 
Review, November, pp. 10ff. 

Moller, Aage R., Berthold Langguth, Dirk DeRidder, and Tobias Kleinjung, eds. 2011. Textbook of 
Tinnitus. New York: Springer. 

National Center for Health Statistics. 1982-1996. “Current Estimates From the National Health 
Interview Survey.” Table 57, “Number of Selected Reported Chronic Conditions per 1,000 
Persons, by Age: United States.” Vital and Health Statistics, ser. 10, nos. 150, 154, 160, 164, 166, 
173, 176, 181, 184, 189, 190, 193, 199, 200. 

Nondahl, David M., Karen J. Cruickshanks, Guan-Hua Huang, Barbara E. K. Klein, Ronald Klein, 
Ted S. Tweed, and Weihai Zhan. 2012. “Generational Differences in the Reporting of Tinnitus.” 
Ear and Hearing 33(5): 640-44. 

Shargorodsky, Josef, Gary C. Curhan, and Wildon R. Farwell. 2010. “Prevalence and Characteristics 
of Tinnitus among US Adults.” American Journal of Medicine 123(8): 711-18. 

Wieske, Clarence W. 1963. “Human Sensitivity to Electric Fields.” Biomedical Sciences 
Instrumentation 1: 467-75. 


Ultrasonic Hearing 

Ball, Geoffrey R. and Bob H. Katz. 1998. “Ultrasonic Hearing System.” U.S. Patent 6,217,508 B1, 
filed August 14, 1998, issued April 17, 2001. 

Bance, Manohar, Osama Majdalawieh, Andrew Stewart, Michael Kiefte, and Rene van Wijhe. 2006. 
“Comparison of Air and Bone Conduction Fine Frequency Hearing Responses.” Dalhousie 
University, Nova Scotia: Ear and Auditory Research Laboratory. 

Bellucci, Richard J. and Daniel E. Schneider. 1962. “Some Observations on Ultrasonic Perception in 
Man.” Annals of Otology, Rhinology and Laryngology 71: 719-26. 

Combridge, J. H. and J. O. Ackroyd. 1945. The Design of German Telephone Subscribers’ 
Apparatus. British Intelligence Objectives Sub-Committee. BIOS Final Report no. 606. 

Corso, John F. 1963. *Bone-conduction Thesholds for Sonic and Ultrasonic Frequencies.” Journal of 
the Acoustical Society of America 35(11): 1738-43. 

Corso, John F. and Murray Levine. 1965a. “Pitch-Discrimination at High Frequencies by Air- and 
Bone-conduction.” American Journal of Psychology 78(4): 557-66. 

. 1965b. “Sonic and Ultrasonic Equal-Loudness Contours.” Journal of Experimental 
Psychology 70(4): 412-16. 

Deatherage, Bruce H., Lloyd A. Jeffress, and Hugh C. Blodgett. 1954. “A Note on the Audibility of 
Intense Ultrasonic Sound.” Journal of the Acoustical Society of America 26(4): 582. 

Dieroff, H. G. and H. Ertel. 1975. “Some Thoughts on the Perception of Ultrasonics by Man.” 
Archives of Oto-Rhino-Laryngology 209: 277-90. 

Flach, M. and G. Hofmann. 1980. *Ultraschallhóren des Menschen: Objektivierung mittels 
Hirnstammpotential." Laryngo-Rhino-Otologie. 59(12): 840-43. 





Fujisaka, Yoh-ichi, Seiji Nakagawa, and Mitsuo Tonoike. 2005. *A Numerical Study on the 
Perception Mechanism for Detecting Pitch in Bone-conducted Ultrasound." Paper presented at the 
Twelfth International Congress on Sound and Vibration, July 11-15, Lisbon, Portugal. 

Gavrilov, L. R., G. V. Gershuni, V. I. Pudov, A. S. Rozenblyum, and E. M. Tsirul'nikov. 1980. 
*Human Hearing in Connection with the Action of Ultrasound in the Megahertz Range on the 
Aural Labyrinth." Soviet Physics — Acoustics. 26(4): 290-92. 

Haeff, Andrew V. and Cameron Knox. 1963. “Perception of Ultrasound.” Science 139: 590-92. 

Hotehama, Takuya and Seiji Nakagawa. 2010. “Modulation Detection for Amplitude-modulated 
Bone-conducted Sounds with Sinusoidal Carriers in the High- and Ultrasonic-frequency Range.” 
Journal of the Acoustical Society of America 128(5): 3011-18. 

Imaizumi, Satoshi, Hiroshi Hosoi, Takefumi Sakaguchi, Yoshiaki Watanabe, Norihiro Sadato, Satoshi 
Nakamura, Atsuo Waki, and Yoshiharu Yonekura. 2001. “Ultrasound Activates the Auditory 
Cortex of Profoundly Deaf Subjects.” NeuroReport 12(3): 583-86. 

International Organization for Standardization. 2003. Normal Equal-loudness-level Contours. ISO 
226:2003 — Acoustics, 2nd ed. Geneva. 

Kietz, Hans. 1951. *Hórschwellenmessung im Ultraschallgebiet." Acta Oto-Laryngologica 39(2-3): 
183-87. 

Lenhardt, Martin L. 1999. *Upper Audio Range Hearing Apparatus and Method." U.S. Patent 
6,731,769, filed October 14, 1999, issued May 4, 2004. 

. 2003. “Ultrasonic Hearing in Humans: Applications for Tinnitus Treatment.” International 

Tinnitus Journal 9(2): 69-75. 

. 2006. “A Second Pair of Ears.” Echoes 16(4): 5-6. 

. 2008. “Ring Transducers for Sonic, Ultrasonic Hearing.” U.S. Patent 8,107,647, filed 
January 3, 2008, issued January 31, 2012. 

Lenhardt, Martin, Alex M. Clarke, and William Regelson. 1989. “Supersonic Bone Conduction 
Hearing Aid and Method.” U.S. Patent 4,982,434, filed May 30, 1989, issued January 1, 1991. 

Lenhardt, Martin L., Ruth Skellett, Peter Wang, and Alex M. Clarke. 1991. “Human Ultrasonic 
Speech Perception.” Science 253: 83-85. 

Magee, Timothy R. and Alun H. Davies. 1993. “Auditory Phenomena during Transcranial Doppler 
Insonation of the Basilar Artery.” Journal of Ultrasound in Medicine 12: 747-50. 

Maggs, James E. 1976. “Coherent Generation of VLF Hiss.” Journal of Geophysical Research 
81(10): 1707-24. 

Moller, Henrik and Christian Sejer Pedersen. 2004. “Hearing at Low and Infrasonic Frequncies.” 
Noise and Health 6(23): 37-58. 

Nishimura, Tadashi, Seiji Nakagawa, Takefumi Sakaguchi, and Hiroshi Hosoi. 2003. “Ultrasonic 
Masker Clarifies Ultrasonic Perception in Man.” Hearing Research 175: 171-77. 

Nishimura, Tadashi, Tadao Okayasu, Osamu Saito, Ryota Shimokura, Akinori Yamashita, Toshiaki 
Yamanaka, Hiroshi Hosoi, and Tadashi Kitahara. 2014. “An Examination of the Effects of 
Broadband Air-conduction Masker on the Speech Intelligibility of Speech-modulated Bone- 
conduction Ultrasound.” Hearing Research 317: 41-49. 

Nishimura, Tadashi, Tadao Okayasu, Yuka Uratani, Fumi Fukuda, Osamu Saito, and Hiroshi Hosoi. 
2011. “Peripheral Perception Mechanism of Ultrasonic Hearing.” Hearing Research 277: 176-83. 

Nishimura, Tadashi, Takefumi Sakaguchi, Seiji Nakagawa, Hiroshi Hosoi, Yoshiaki Watanabe, 
Mitsuo Tonoike, and Satoshi Imaizumi. 2000. “Dynamic Range for Bone Conduction 
Ultrasound.” In: Biomag 2000: Proceedings of 12th International Conference on Biomagnetism, 
August 13-17, 2000, Helsinki University of Technology, Espoo, Finland, pp. 125-28. 











Ohyama, Kenji, Jun Kusakari, and Kazutomo Kawamoto. 1987. “Sound Perception in the Ultrasonic 
Region." Acta Oto-Laryngolica. Supplementum. 435: 73-77. 

Oohashi, Tsutomu, Emi Nishina, Manabu Honda, Yoshiharu Yonekura, Yoshitaka Fuwamoto, Norie 
Kawai, Tadao Maekawa, Satoshi Nakamura, Hidenao Fukuyama, and Hiroshi Shibasaki. 2000. 
"[naudible High-Frequency Sounds Affect Brain Activity: Hypersonic Effect." Journal of 
Neurophysiology 83(6): 3548-58. 

Ozen, Sukru. 2008. *Low-Frequency Transient Electric and Magnetic Fields Coupling to Child 
Body." Radiation Protection Dosimetry 128(1): 62-67. 

Petrie, William. 1963. Keoeeit: The Story of the Aurora Borealis. Oxford: Pergamon Press. 

Prasch, G. and H. Siegl-Graz. 1969. "Gehórseindrücke durch Einwirkung von tonfrequenten 
Wechselstrómen und amplituden-modulierten Hochfrequenzstrómen." Archiv für klinische und 
experimentelle Ohren-, Nasen- und Kehlkopfheilkunde 194(2): 516-21. 

Pumphrey, R. J. 1950. *Upper Limit of Frequency for Human Hearing." Nature 166: 571. 

Qin, Michael K., Derek Schwaller, Matthew Babina, and Edward Cudahy. 2011. *Human Underwater 
and Bone Conduction Hearing in the Sonic and Ultrasonic Range." Journal of the Acoustical 
Society of America 129 (4 part 2): 2485. Abstract. 

Singh, D. K. and R. P. Singh. 2002. *Hiss Emissions during Quiet and Disturbed Periods." Pramana 
— Journal of Physics 59(4): 563-73. 

Stanley, Raymond M. and Bruce N. Walker. 2005. “Relative Threshold Curves for Implementation of 
Auditory Displays on Bone-conduction Headsets in Multiple Listening Environments.” Presented 
at the 11th International Conference on Auditory Display, Limerick, Ireland, July 6-9. 

Wegel, Raymond L., Robert R. Riesz, and Ralph B. Blackman. 1932. “Low Frequency Thresholds of 
Hearing and of Feeling in the Ear and Ear Mechanisms.” Journal of the Acoustical Society of 
America 4(1A): 6. 

World Health Organization. 1993. Environmental Health Criteria 137. Electromagnetic Fields (300 
Hz to 300 GHz). Geneva. 


Chapter 16 

Balmori, Alfonso. 2014. *Electrosmog and Species Conservation." Science of the Total Environment 
496: 314-16. 

. 2015. *Anthropogenic Radiofrequency Electromagnetic Fields as an Emerging Threat to 

Wildlife Orientation." Science of the Total Environment 518-519: 58-60. 





Amazon Rainforest 

da Costa, Thomaz Guedes. 2002. *Brazil's SIVAM: As It Monitors the Amazon, Will It Fulfill Its 
Human Security Promise?” ECSP Report 7: 47-58. 

Jensen, David. 2002. “SIVAM: Communication, Navigation and Surveillance for the Amazon.” 
Avionics, June 1. 

Phillips, Oliver L, Luiz E. O. C. Aragão, Simon L. Lewis, Joshua B. Fisher, Jon Lloyd, Gabriela 
López-González, Yadvinder Malhi, Abel Monteagudo, Julie Peacock, Carlos A. Quesada, Geertje 
van der Heijden, Samuel Almeida, Iêda Amaral, Luzmila Arroyo, Gerardo Aymard, Tim R. Baker, 
Olaf Bánki, Lilian Blanc, Damien Bonal, Paulo Brando, Jerome Chave, Átila Cristina Alves de 
Oliveira, Nallaret Dávila Cardozo, Claudia I. Czimczik, Ted R. Feldpausch, Maria Aparecida 
Freitas, Emanuel Gloor, Niro Higuchi, Eliana Jiménez, Gareth Lloyd, Patrick Meir, Casimiro 
Mendoza, Alexandra Morel, David A. Neill, Daniel Nepstad, Sandra Patiño, Maria Cristina 
Peñuela, Adriana Prieto, Fredy Ramírez, Michael Schwarz, Javier Silva, Marcos Silveira, Anne 
Sota Thomas, Hans ter Steege, Juliana Stropp, Rodolfo Vásquez, Przemyslaw Zelazowski, 
Ésteban Álvarez Dávila, Sandy Andelman, Ana Andrade, Kuo-Jung Chao, Terry Erwin, Anthony 


Di Fiore, Eurídice Honorio C., Helen Keeling, Tim J. Killeen, William F. Laurance, Antonio Pefía 
Cruz, Nigel C. A. Pitman, Percy Nufiez Vargas, Hirma Ramírez-Ángulo, Agustín Rudas, Rafael 
Salamáo, Natalino Silva, John Terborgh, and Armando Torres-Lezama. 2009. “Drought 
Sensitivity of the Amazon Rainforest." 2009. Science 323: 1344-47. 

Rohter, Larry. 2002. *Brazil Employs Tools of Spying to Guard Itself." New York Times, July 27, p. 
1. 

Wittkoff, E. Peter. 1999. *Amazon Surveillance System (SIVAM): U.S. and Brazilian Cooperation." 
Master's thesis, Naval Postgraduate School, Monterey, CA. 


Amphibians 

Balmori, Alfonso. 2006. *The Incidence of Electromagnetic Pollution on the Amphibian Decline: Is 
This an Important Piece of the Puzzle?" Toxicological and Environmental Chemistry 88(2): 287- 
89. 





. 2010. *Mobile Phone Mast Effects on Common Frog (Rana temporaria) Tadpole: The City 
Turned into a Laboratory." Electromagnetic Biology and Medicine 29: 31-35. 

Hallowell, Christopher. 1996. *Trouble in the Lily Pads." Time, October 28, p. 87. 

Hawk, Kathy. 1996. Case Study in the Heartland. Butler, PA. 

Hoperskaya, O. A., L. A. Belkova, M. E. Bogdanov, and S. G. Denisov. 1999. *The Action of the 
*Gamma-7N' Device on Biological Objects Exposed to Radiation from Personal Computers." 
Electromagnetic Fields and Human Health. Proceedings of the Second International Conference. 
Moscow, September 20-24, pp. 354-55. Abstract. 

Revkin, Andrew C. 2006. *Frog Killer is Linked to Global Warming." New York Times, January 12. 

Souder, William. 1996. *An Amphibian Horror Story." New York Newsday, October 15, pp. B19, 
B21. 





. 1997. *Deformed Frogs Show Rift Among Scientists." Houston Chronicle, November 5, p. 
4A. 

Stern, John. 1990. *Space Aliens Stealing Our Frogs." Weekly World News, April 17, p. 21. 

Vogt, Amanda. 1998. *Mutant Frogs Spark a Mega Mystery." Chicago Tribune, August 4, sec. 7, p. 
3j 

Watson, Traci. 1998. *Frogs Falling Silent across USA." USA Today, August 12, p. 3A. 


Birds 

Balmori, Alfonso. 2003. *Aves y telefonía móvil." El Ecologista 36: 40-42. 

. 2005. “Possible Effects of Electromagnetic Fields from Phone Masts on a Population of 
White Stork (Ciconia ciconia).” Electromagnetic Biology and Medicine 24: 109-19. 

Bigu del Blanco, Jaime. 1969. An Introduction to the Effects of Electromagnetic Radiation on Living 
Matter with Special Reference to Microwaves. Laboratory Technical Report LTR-CS-7, Control 
Systems Laboratory, Division of Mechanical Engineering, National Research Council Canada. 

. 1973. Interaction of Electromagnetic Fields and Living Systems with Special Reference to 
Birds. Laboratory Technical Report LTR-CS-113, Control Systems Laboratory, Division of 
Mechanical Engineering, National Research Council Canada. 

Bigu del Blanco, Jaime and César Romero-Sierra. 1973. Bird Feathers as Dielectric Receptors of 
Microwave Radiation. Laboratory Technical Report LTR-CS-89, Control Systems Laboratory, 
Division of Mechanical Engineering, National Research Council Canada. 

. 1975. “Microwave Pollution of the Environment and the Ecological Problem.” In: Tomas 

Dvorak, ed., Electromagnetic Compatibility 1975: 1st Symposium and Technical Exhibition on 

Electromagnetic Compatibility, Montreux, May 20-22, 1975, pp. 127-33. 











Bigu del Blanco, Jaime, César Romero-Sierra, and J. Alan Tanner. 1973a. Environmental Pollution 
by Microwave Radiation — A Potential Threat to Human Health. Laboratory Technical Report 
LTR-CS-98, Control Systems Laboratory, Division of Mechanical Engineering, National Research 
Council Canada. 

. 1973b. “Radiofrequency Fields: A New Ecological Factor" 1973 IEEE International 
Electromagnetic Compatibility Symposium Record, June 20-22, New York, pp. 54-59. 

Engels, Svenja, Nils-Lasse Schneider, Nele Lefeldt, Christine Maira Hein, Manuela Zapka, Andreas 
Michalik, Dana Elbers, Achim Kittel, P. J. Hore, and Henrik Mouritsen. 2014. *Anthropogenic 
Electromagnetic Noise Disrupts Magnetic Compass Orientation in a Migratory Bird." Nature 509: 
353-56. 

Keeton, William T. 1979. *Avian Orientation and Navigation: A Brief Overview." British Birds 
72(10): 451-70. 

Romero-Sierra, César, Carol Husband, and J. Alan Tanner. 1969. Effects of Microwave Radiation on 
Parakeets in Flight. Laboratory Technical Report LTR-CS-18. Control Systems Laboratory, 
Division of Mechanical Engineering, National Research Council Canada. 

Romero-Sierra, César, Arthur O. Quanbury, and J. Alan Tanner. 1970. Feathers as Microwave and 
Infra-Red Filters and Detectors — Preliminary Experiments. Laboratory Technical Report LTR- 
CS-40, Control Systems Laboratory, Division of Mechanical Engineering, National Research 
Council Canada. 

Romero-Sierra, César, J. Alan Tanner, and F. Villa. 1969. EMG Changes in the Limb Muscles of 
Chickens Subjected to Microwave Radiation. Laboratory Technical Report LTR-CS-16, Control 
Systems Laboratory, Division of Mechanical Engineering, National Research Council Canada. 

Tanner, J. Alan. 1966. *Effect of Microwave Radiation on Birds." Nature 210: 636. 

. 1970. “Bird Feathers as Sensory Detectors of Microwave Fields.” In: Stephen F. Cleary, ed., 
Biological Effects and Health Implications of Microwave Radiation. Symposium Proceedings 
(Rockville, MD: U.S. Department of Health, Education and Welfare), Publication BRH/DBE 70- 
2, pp. 185-87. 

Tanner, J. Alan and César Romero-Sierra. 1971. Non-Ionizing Electromagnetic Radiation and 
Pollution of the Atmosphere. Report no. DMENAE19714, Control Systems Laboratory, Division 
of Mechanical Engineering, National Research Council Canada. 

. 1982. “The Effects of Chronic Exposure to Very Low Intensity Microwave Radiation on 
Domestic Fowl.” Journal of Bioelectricity 1(2): 195-205. 

Xenos, Thomas D. and Ioannis N. Magras. 2003. “Low Power Density RF-Radiation Effects on 
Experimental Animal Embryos and Foetuses.” In: Peter Stavroulakis, ed., Biological Effects of 
Electromagnetic Fields (Berlin: Springer), pp. 579-602. 











Cedars 

Earth Link and Advanced Resources Development S. A. R. L. 2010. “Vulnerability and Adaptation 
of the Forestry Sector.” Climate Risks, Vulnerability and Adaptation Assessment, pp. 6-1 to 6-44. 
Prepared for United Nations Development Programme and Ministry of Environment of Lebanon. 

Bentouati, Abdallah and Michel Bariteau. 2006. “Réflexions sur le déperissement du Cédre de |’ Atlas 
des Aurés (Algérie)." Forét Méditerranéenne 27(4): 317-22. 

Hennon, Paul E., David V. D'Amore, Paul G. Schaberg, Dustin T. Wittwer, and Colin S. Shanley. 
2012. “Shifting Climate, Altered Niche, and a Dynamic Conservation Strategy for Yellow-Cedar 
in the North Pacific Coastal Rainforest." BioScience 62(2): 147-58. 

Hennon, Paul E., David V. D'Amore, Stefan Zeglen, and Mike Grainger. 2005. Yellow-Cedar Decline 
in the North Coast Forest District of British Columbia. Research Note PNW-RN-549. Juneau, 
AK: USDA Forest Service, Pacific Northwest Research Station. 


Hennon, Paul E. and Charles G. Shaw III. 1994. *Did Climatic Warming Trigger the Onset and 
Development of Yellow-Cedar Decline in Southeast Alaska?" European Journal of Forest 
Pathology 24: 399-418. 

Hennon, Paul E., Charles G. Shaw III, and Everett M. Hansen. 1990. *Dating Decline and Mortality 
of Chamaecyparis nootkatensis in Southeast Alaska." Forest Science 36(3): 502-15. 

Hennon, Paul E., David V. D'Amore, Dustin T. Wittwer, A. Johnson, Paul G. Schaberg, G. Hawley, 
C. Beier, S. Sink, and G. Juday. 2006. *Climate Warming, Reduced Snow, and Freezing Injury 
Could Explain the Demise of Yellow-Cedar in Southeast Alaska, USA." World Resource Review 
18(2): 427-50. 

Masri, Rania. 1995. The Cedars of Lebanon: Significance, Awareness and Management of the Cedrus 
libani in Lebanon. Lecture given at Massachusetts Institute of Technology, November 9. 

Navy Department, Bureau of Equipment. August 1, 1907. Wireless Telegraph Stations of the World. 
Washington, DC. 

Navy Department, Bureau of Equipment. Wireless Telegraph Stations of the World. Corrected to 
October 1, 1908. Washington, DC. 

United States Department of Commerce, Bureau of Navigation. July 1, 1913. Radio Stations of the 
United States. Washington, DC. 

Verstege, A., J. Esper, B. Neuwirth, M. Alifriqui, and D. Frank. 2004. “On the Potential of Cedar 
Forests in the Middle Atlas (Morocco) for Climate Reconstructions." In: E. Jansma, A. Bráuning, 
H. Gartner, and G. Schleser, eds., TRACE — Tree Rings in Archaeology, Climatology and Ecology, 
vol. 2, Proceedings of the DENDROSYMPOSIUM, May 1-3, Utrecht, The Netherlands 
(Forschungszentrum Jiilich), pp. 78-84. 


Colegio Garcia Quintana 

Santiago, Ana. 2012. “El caso Garcia Quintana cumple diez afios sin nuevos diagnósticos de cáncer." 
El Norte de Castilla, March 23. 

Diario de León. 2004. *El sexto caso de cáncer desata la alarma en un colegio de Valladolid." May 8. 

Cantalapiedra, Francisco. 2004. *Aflora otro caso de cáncer en el colegio García Quintana de 
Valladolid.” El Pais, May 8. 

El Mundo. 2004. “Un mujer diagnosticada en 2002, sexto caso de cancer en el colegio de Valladolid.” 
May 7. 


Forests 

Allen, Craig D., Alison K. Macalady, Haroun Chenchouni, Dominique Bachelet, Nate McDowell, 
Michel Vennetier, Thomas Kitzberger, Andreas Rigling, David D. Breshears, E. H. Hogg, Patrick 
Gonzalez, Rod Fensham, Zhen Zhang, Jorge Castro, Natalia Demidova, Jong-Hwan Lim, Gillian 
Allard, Steven W. Running, Akkin Semerci, and Neil Cobb. 2010. “A Global Overview of 
Drought and Heat- induced Tree Mortality Reveals Emerging Climate Change Risks for Forests.” 
Forest Ecology and Management 259: 660-84. 

Balmori, Alfonso. 2004. *;Pueden afectar las microondas pulsadas emitidas por las antenas de 
telefonía a los arboles y otros vegetales?" Ecosistemas 13(3): 79-87. 

Ciesla, William M. and Edwin Donaubauer. 1994. Decline and Dieback of Trees and Forests: A 
Global Overview. Rome: Food and Agriculture Organization of the United Nations. FAO Forestry 
Paper 120. 

Glinz, Franz. 1992. *Der Wald stirbt am Electrosmog." Auto-illustrierte 2: 1. 

Haggerty, Katie. 2010. *Adverse Influence of Radio Frequency Background on Trembling Aspen 
Seedlings: Preliminary Observations." International Journal of Forestry Research, article ID 
836278. 

Hertel, Hans Ulrich. 1991. *Der Wald Stirbt und Politiker Sehen Zu." Raum & Zeit 9(51): 3-12. 


Hommel, H. 1985. *Elektromagnetischer S$MOG - Schadfaktor und Stress?" Forstarchiv 56: 227-33. 

LeBlanc, David C., Dudley J. Raynal, and Edwin H. White. 1987. *Acidic Deposition and Tree 
Growth: I. The Use of Stem Analysis to Study Historical Growth Patterns." Journal of 
Environmental Quality 16(4): 325-40. 

Lohmeyer, Michael. 1991. *Von Mikrowellen verseuchte Umgebung; Richtfunk schneidet Schneisen 
in Walder.” Die Presse, July 31. 

Lorenz, M., V. Mues, G. Becher, Ch. Müller-Edzards, S. Luyssaert, H. Raitio, A. Fürst, and D. 
Langouche. 2003. Forest Condition in Europe. Geneva and Brussels: United Nations Economic 
Commission for Europe and the European Commission. 

Melhorn, G., B. J. Francis, and A. R. Wellburn. 1988. “Prediction of the Probability of Forest Decline 
Damage to Norway Spruce Using Three Simple Site-independent Diagnostic Parameters." New 
Phytologist 110: 525-34. 

Robbins, Jim. 2010. *What's Killing the Great Forests of the American West?" Environment 360, 
March 15. 

Schütt, Peter and Ellis B. Cowling. 1985. “Waldsterben, A General Decline of Forests in Central 
Europe: Symptoms, Development and Possible Causes.” Plant Disease 69(7): 548-58. 

Skelly, John M. and John L. Innes. 1994. “Waldsterben in the Forests of Central Europe and Eastern 
North America: Fantasy or Reality?” Plant Disease 78(11): 1021-32. 

van Mantgem, Phillip J., Nathan L. Stephenson, John C. Byrne, Lori D. Daniels, Jerry F. Franklin, 
Peter Z. Fulé, Mark E. Harmon, Andrew J. Larson, Jeremy M. Smith, Alan H. Taylor, and Thomas 
T. Veblen. 2009. *Widespread Increase of Tree Mortality Rates in the Western United States." 
Science 323: 521-24. 

Volkrodt, Wolfgang. 1989. *Electromagnetic Pollution of the Environment." In: Robert Krieps, ed., 
Environment and Health: A Holistic Approach (Aldershot, UK: Avebury), pp. 71-76. 

. 1991. *Mikrowellensmog und Waldschàden — Tut Sich Doch Noch Was in Bonn?" Raum & 

Zeit 9(52): 22-25. 

. 1992. Letter to William H. Smith, Yale University, December 26. 

Waldmann-Selsam, Cornelia and Horst Eger. 2013. *Baumscháden im Umkreis von 
Mobilfunksendeanlagen." Umwelt-Medizin-Gesellschaft 26(3): 198-208. 

Worrall, James J., Leanne Egeland, Thomas Eager, Roy A. Mask, Erik W. Johnson, Philip A. Kemp, 
and Wayne D. Shepperd. 2008. *Rapid Mortality of Populus tremuloides in Southwestern 
Colorado, USA." Forest Ecology and Management 225: 686-96. 


HAARP 

Browne, Malcolm W. 1995. *Scope System Also Offers a Tool for Submarines and Soldiers." New 
York Times, November 21, p. C10. 

Busch, Lisa. 1997. “Ionosphere Research Lab Sparks Fear in Alaska." Science 275: 1060-61. 

Microwave News. 1994. “U.S. Military Plans Powerful RF ‘Heater’ for Ionospheric Studies." 
May/June, pp. 10-11. 

Papadopoulos, Dennis, Paul A. Bernhardt, Herbert C. Carlson, Jr., William E. Gordon, Alexander V. 
Gurevich, Michael C. Kelley, Michael J. Keskinen, Roald Z. Sagdeev, and Gennady M. Milikh. 
1995. HAARP: Research and Applications. A Joint Program of Phillips Laboratory and the Office 
of Naval Research. Executive Summary. Washington, DC: Naval Research Laboratory. 

Weinberger, Sharon. 2008. “Heating Up the Heavens.” Nature 452: 930-32. 

Williams, Richard. 1988. “Atmospheric Threat.” Physics and Society 17(2): 16. 

Zickuhr, Clare and Gar Smith. 1994. “Project HAARP: The Military’s Plan to Alter the Ionosphere.” 
Earth Island Journal, Fall 1994, pp. 21-23. 








Homing Pigeons 

Armas, Genaro C. 1998. *The Homing Pigeons That Didn't." Seattle Times, October 9. 

Chaudhary, Vivek. 2004. “Phone Masts Blamed for Pigeons’ Lost Art." The Guardian, January 23. 

Elston, Laura. 2004. “Phone Masts ‘Knocking Racing Pigeons off Track.’” The Press Association 
(UK), January 23. 

Haughey, Nuala. 1997. “Mobile Phones Blamed for Poor Pigeon Performance.” Irish Times, July 21. 

Hummell, Steve. 2005. “Lost Pigeons Create Flap; Cellphone Signals Responsible for Sending Birds 
off Course, Racers Say.” Vancouver Sun, October 3. 

Indian Express. 2010. “Cellphone Towers Disorient Homer Pigeons.” December 27. 

Keeton, William T. 1972. “Effects of Magnets on Pigeon Homing.” In: S. R. Galler, K. Schmidt- 
Koenig, G. J. Jacobs, and R. E. Belleville, eds., Animal Orientation and Navigation (Washington, 
DC: Government Printing Office), NASA SP-262, pp. 579-94. 

. 1979. “Avian Orientation and Navigation: A Brief Overview.” British Birds 72(10): 451-70. 

Keeton, William T., Timothy S. Larkin, and Donald M. Windsor. 1974. “Normal Fluctuations in the 
Earth’s Magnetic Field Influence Pigeon Orientation.” Journal of Comparative Physiology 95: 95- 
103. 

New York Post. 1998. “2,400 Homing Pigeons Fly the Coop in Race.” October 8. 

Wee, Eric L. 1998. “Homing Pigeons Race Off to Oblivion.” Washington Post, October 8. 

. 1998. “Some Birds Lost During Races Are Turning Up at Area Homes, Barns and Feeders.” 

Washington Post, October 9. 








Honey Bees 

Anderson, John. 1930a. “‘Isle of Wight Disease’ in Bees. I.” Bee World 11(4): 37-42. 

. 1930b. “‘Isle of Wight Disease’ in Bees — II. A Check to the Immunity Hypothesis.” Bee 
World 11(5): 50-53. 

Bailey, Leslie 1958. “The Epidemiology of the Infestation of the Honeybee, Apis mellifera L., by the 
Mite Acarapis woodi Rennie and the Mortality of Infested Bees.” Parasitology 48(3-4): 493-506. 

. 1964. “The ‘Isle of Wight disease’: The Origin and Significance of the Myth.” Bee World 
45(1): 32-37, 18. 

Bailey, Leslie and D. C. Lee. 1959. “The Effect of Infestation with Acarapis woodi (Rennie) on the 
Mortality of Honey Bees.” Journal of Insect Pathology 1(1): 15-24. 

Bailey, Leslie and Brenda V. Ball. 1991. Honey Bee Pathology. London: Academic. 

Barrionuevo, Alexei. 2007. “Honeybees, Gone with the Wind, Leave Crops and Keepers in Peril.” 
New York Times, February 27, p. A1. 

Boecking O. and W. Ritter. 1993. “Grooming and Removal Behaviour of Apis mellifera intermissa in 
Tunisia against Varroa jacobsoni.” Journal of Apicultural Research 32: 127-34. 

Borenstein, Seth. 2007. “Honeybee Die-off Threatens Food Supply.” Washington Post, May 2. 

Calderón Rafael A., Natalia Fallas, Luis G. Zamora, Johan W. van Veen, and Luis A. Sanchez. 2009. 
“Behavior of Varroa Mites in Worker Brood Cells of Africanized Honey Bees.” Experimental and 
Applied Acarology 49(4): 329-38. 

Carr, Elmer G.. 1918. “An Unusual Disease of Honey Bees.” Journal of Economic Entomology 
11(4): 347-51. 

Dahlen, Sage. 2007. “Colony Collapse Disorder.” The Wake, Summer 2007, p. 15. 

Favre, Daniel. 2011. “Mobile Phone-induced Honeybee Worker Piping.” Apidologie 42: 270-79. 

Finley, Jennifer, Scott Camazine, and Maryann Frazier. 1996. “The Epidemic of Honey Bee Colony 
Losses during the 1995-1996 Season.” American Bee Journal 136(11): 805-8. 

Fries, Ingemar, Anton Imdorf, and Peter Rosenkranz. 2006. “Survival of Mite Infested (Varroa 
destructor) Honey Bee (Apis mellifera) Colonies in a Nordic Climate. Apidologie 37: 1-7. 








Hamzelou, Jessica. 2007. “Where Have All the Bees Gone?" Lancet 370: 639. 

Henderson, Colin, Jerry Bromenshenk, Larry Tarver, and Dave Plummer. 2007. National Honey Bee 
Loss Survey. Missoula, MT: Bee Alert Technology, Inc. 

Imms, Augustus D. 1907. *Report on a Disease of Bees in the Isle of Wight." Journal of the Board of 
Agriculture 14(3): 129-40. 

Kauffeld, Norbert M., James H. Everitt, and Edgar A. Taylor. 1976. *Honey Bee Problems in the Rio 
Grande Valley of Texas." American Bee Journal 116: 220, 222, 232. 

Kraus, Bernhard and Robert E. Page, Jr. 1995. "Effect of Varroa jacobsoni (Mesostigmata: 
Varroidae) on Feral Apis mellifera (Hymenoptera: Apidae) in California." Environmental 
Entomology 24(6): 1474-80. 

Kumar, Neelima R., Sonika Sangwan, and Pooja Badotra. 2011. *Exposure to Cell Phone Radiations 
Produces Biochemical Changes in Worker Honey Bees." Toxicology International 18(1): 70-72. 
Le Conte, Yves, Marion Ellis, and Wolfgang Ritter. 2010. *Varroa Mites and Honey Bee Health: Can 

Varroa Explain Part of the Colony Losses?” Apidologie 41(3): 353-63. 

Lee, Kathleen V., Nathalie A. Steinhauer, Karen Rennich, Michael E. Wilson, David R. Tarpy, 
Dewey M. Caron, Robyn Rose, Keith S. Delaplane, Kathy Baylis, Eugene J. Lengerich, Jeffery 
Pettis, John A. Skinner, James T. Wilkes, Ramesh Sagili, and Dennis vanEngelsdorp. 2015. “A 
National Survey of Managed Honey Bee 2013-2014 Annual Colony Losses in the USA.” 
Apidologie 46: 292-305. 

Lindauer, Martin and Herman Martin. 1972. “Magnetic Effect on Dancing Bees.” In: Sidney R. 
Galler, Klaus Schmidt-Koenig, G. J. Jacobs, and Richard E. Belleville, eds., Animal Orientation 
and Navigation, (Washington, DC: Government Printing Office), NASA SP-262, pp. 559-67. 

McCarthy, Michael. 2011. “Decline of Honey Bees Now a Global Phenomenon, Says United 
Nations.” The Independent, March 10. 

O’Hanlon, Kevin. 1997. “Few Honeybees Means Poorer Fruit, Vegetables.” Associated Press, May 
28. 

Oldroyd, Benjamin P. 1999. “Coevolution While You Wait: Varroa jacobsoni, a New Parasite of 
Western Honeybees.” Trends in Ecology and Evolution 14(8): 312-15, 1999. 

. 2007. *What's Killing American Honey Bees?” PLoS Biology 5(6): 1195-99. 

Page, Robert E. 1998. “Blessing or Curse? Varroa Mite Impacts Africanized Bee Spread and 
Beekeeping.” California Agriculture 52(2): 9-13. 

Pattazhy, Sainudeen. 2011a. Impact of Electromagnetic Radiation on the Density of Honeybees: A 
Case Study. Saarbriicken, Germany: Lambert Academic. 

. 2011b. “Impact of Mobile Phones on the Density of Honey Bees.” Munis Entomology and 

Zoology 6(1): 396-99. 

. 2012. “Electromagnetic Radiation (EMR) Clashes with Honeybees.” Journal of Entomology 
and Nematology 4(10): 1-3. 

Phillips, Ernest F. 1925. “The Status of Isle of Wight Disease in Various Countries." Journal of 
Economic Entomology 18: 391-95. 

Rennie, John, Philip Bruce White, and Elsie J. Harvey. 1921. “Isle of Wight Disease in Hive Bees: 
The Etiology of the Disease.” Transactions of the Royal Society of Edinburgh, vol. 52, part 4, no. 
29, pp. 737-79. 

Rinderer, Thomas E., Lilia I. de Guzman, G. T. Delatte, J. A. Stelzer, V. A. Lancaster, V. Kuznetsov, 
L. Beaman, R. Watts, and J. W. Harris. 2001. “Resistance to the Parasitic Mite Varroa destructor 
in Honey Bees from Far-Eastern Russia.” Apidologie 32: 381-94. 

Ruzicka, Ferdinand. 2003. *Scháden Durch Elektrosmog." Bienenwelt 10: 34-35. 

. 2006. *Scháden an Bienenvólkern." Diagnose: Funk 2006. 














Sanford, Malcolm T. 2004. *Mite Tolerance in Honey Bees." Bee Culture 132(10): 23-26. 

Science Daily. 1998. “Where Have All the Honeybees Gone?" July 6. 

. 2010. "Survey Reports Latest Honey Bee Losses." May 3. 

Seeley, Thomas D. 2004. *Forest Bees and Varroa Mites." Bee Culture, July, pp. 22-23. 

. 2007. *Honey Bees of the Arnot Forest: A Population of Feral Colonies Persisting with 
Varroa destructor in the Northeastern United States." Apidologie 38: 19-29. 

Sharma, Ved Parkash and Neelima R. Kumar. 2010. *Changes in Honeybee Behaviour and Biology 
under the Influence of Cellphone Radiations." Current Science 98(10): 1376-78. 

Spleen, Angela M., Eugene J. Lengerich, Karen Rennich, Dewey Caron, Robyn Rose, Jeffery S. 
Pettis, Mark Henson, James T. Wilkes, Michael Wilson, Jennie Stitzinger, Kathleen Lee, Michael 
Andree, Robert Snyder, and Dennis vanEngelsdorp, for the Bee Informed Partnership. 2013. *A 
National Survey of Managed Honey Bee 2011-12 Winter Losses in the United States: Results 
from the Bee Informed Partnership." Journal of Apicultural Research 52(2): 44-53. 

Steinhauer, Nathalie A., Karen Rennich, Michael E. Wilson, Dewey M. Caron, Eugene J. Lengerich, 
Jeffery S. Pettis, Robyn Rose, John A. Skinner, David R. Tarpy, James T. Wilkes, and Dennis 
vanEngelsdorp. 2014. *A National Survey of Managed Honey Bee 2012-2013 Annual Colony 
Losses in the USA: Results from the Bee Informed Partnership. Journal of Apicultural Research 
53(1): 1-18. 

Steinhauer, Nathalie, Karen Rennich, Kathleen Lee, Jeffery Pettis, David R. Tarpy, Juliana Rangel, 
Dewey Caron, Ramesh Sagili, John A. Skinner, Michael E. Wilson, James T. Wilkes, Keith S. 
Delaplane, Robyn Rose, and Dennis vanEngelsdorp. 2015. *Colony Loss 2014-2015: Preliminary 
Results." Bee Informed Partnership, UK. 

Svensson, Bórje. 2003. "Silent Spring in Northern Europe?" Bees for Development Journal 71: 3-4. 

United States Dept of Agriculture, National Agricultural Statistics Service. 2010. Honey, February. 

. 2011. Honey, February. 

Underwood, Robyn M. and Dennis vanEngelsdorp. 2007. *Colony Collapse Disorder: Have We Seen 
This Before?" Bee Culture 35(7): 13-18. 

vanEngelsdorp, Dennis, Jay D. Evans, Claude Saegerman, Chris Mullin, Eric Haubruge, Bach Kim 
Nguyen, Maryann Frazier, Jim Frazier, Diana Cox-Foster, Yanping Chen, Robyn Underwood, 
David R. Tarpy, and Jeffery S. Pettis. 2009. *Colony Collapse Disorder: A Descriptive Study." 
PLoS ONE 4(8): e6481. 

Warnke, Ulrich. 1976. *Effects of Electric Charges on Honeybees." Bee World 57(2): 50-56. 

. 2009. Bienen, Vögel und Menschen: Die Zerstörung der Natur durch “Elektrosmog.” 
Published in English as Bees, Birds and Mankind: Destroying Nature by “Electrosmog.” 
Kempten, Germany: Kompetenzinitiative. 

Wilson, William T. and Diana M. Menapace. 1979. “Disappearing Disease of Honey Bees: A Survey 
of the United States.” American Bee Journal, February, pp. 118-19; March, pp. 184-86, 217. 














House Sparrows 

ASPO/BirdLife Suisse. 2015. “Oiseau de l’année 2015: Moineau domestique” (“Bird of the Year 
2015: House Sparrow”). 

Balmori, Alfonso and Örjan Hallberg. 2007. “The Urban Decline of the House Sparrow (Passer 
domesticus): A Possible Link with Electromagnetic Radiation.” Electromagnetic Biology and 
Medicine 26: 141-51. 

Bokotey, Andrei A. and Igor M. Gorban. 2005. “Numbers, Distribution, and Ecology of the House 
Sparrow in Lvov (Ukraine).” International Studies on Sparrows 30: 7-22. 

De Laet, Jenny and James Denis Summers-Smith. 2007. “The Status of the Urban House Sparrow 
Passer domesticus in North-western Europe: A Review.” Journal of Ornithology 148 (suppl. 2): 


8275-78. 

Deccan Herald. 2010. *House Sparrow Listed as an Endangered Species." June 24. 

Dott, Harry E. M. and Allan W. Brown. 2000. *A Major Decline in House Sparrows in Central 
Edinburgh." Scottish Birds 21: 61-68. 

Eaton, Mark A., Andy F. Brown, David G. Noble, Andy J. Musgrove, Richard D. Hearn, Nicholas J. 
Aebischer, David W. Gibbons, Andy Evans, and Richard D. Gregory. 2009. “Birds of 
Conservation Concern 3.” British Birds 102: 296-341. 

Everaert, Joris and Dirk Bauwens. 2007. “A Possible Effect of Electromagnetic Radiation from 
Mobile Phone Base Stations on the Number of Breeding House Sparrows (Passer domesticus).” 
Electromagnetic Biology and Medicine 26: 63-72. 

Galbraith, Colin. 2002. “The Population Status of Birds in the U.K: Birds of Conservation Concern: 
2002-2007.” Bird Populations 7: 173-79. 

Gregory, Richard D., Nicholas I. Wilkinson, David G. Noble, James A. Robinson, Andrew F. Brown, 
Julian Hughes, Deborah Procter, David W. Gibbons, and Colin A. Galbraith. 2002. “The 
Population Status of Birds in the United Kingdom, Channel Islands and Isle of Man: An Analysis 
of Conservation Concern 2002-2007.” British Birds 95: 410-48. 

Longino, Libby. 2013. “Researchers Stumped over Decline of Sparrow Populations.” USA Today, 
October 5. 

Pattazhy, Sainudeen. 2012. “Dwindling Number of Sparrows.” Karala Calling, March, pp. 32-33. 

Prowse, Alan. 2002. “The Urban Decline of the House Sparrow.” British Birds 95: 143-46. 

Robinson, Robert A., Gavin M. Siriwardena, and Humphrey Q. P. Crick. 2005. “Size and Trends of 
the House Sparrow Passer domesticus Population in Great Britain." Ibis 147(2): 552-62. 

Sanderson, Roy F. 1995. *Autumn Bird Counts in Kensington Gardens, 1925-1995." London Bird 
Report 60: 170-76. 

Sanderson, Roy F. 2001. “Further Declines in an Urban Population of House Sparrows.” British Birds 
94: 507-8. 

Scott, Bob and Adrian Pitches. 2002. “Demise of the Cockney Sparrow.” British Birds 95: 468-70. 

Sen, Benita. 2012. “Calling Back the Sparrow.” Deccan Herald, November 26. 

Sherry, Kate. 2003. “Are Mobile Phones Behind the Decline of House Sparrows?” Daily Mail, 
January 13. 

Skorpilova, Jana, Petr Voříšek, and Alena Klvaňová. 2010. “Trends of Common Birds in Europe, 
2010 Update.” European Bird Census Council. 

Summers-Smith, James Denis. 2000. “Decline of House Sparrows in Large Towns.” British Birds 93: 
256-57. 

. 2003. “Decline of the House Sparrow: A Review.” British Birds 96: 439-46. 

. 2005. “Changes in the House Sparrow Population in Britain.” International Studies on 
Sparrow 30: 23-37. 

Times of India. 2005. “Even Sparrows Don’t Want to Live in Cities Anymore.” June 13. 

Townsend, Mark. 2003. “Mobile Phones Blamed for Sparrow Deaths.” The Observer, January 12. 








Insects 

Balmori, Alfonso. 2006. “Efectos de las radiaciones electromagnéticas de la telefonía móvil sobre los 
insectos.” Ecosistemas 15(1): 87-95. 

Barbassa, Juliana. 2006. “The Plight of the Butterfly.” New Mexican, May 11, p. D1. 

Becker, Giinther. 1977. “Communication Between Termites by Biofields.” Biological Cybernetics 
26: 41-44. 

Cammaerts, Marie-Claire and Olle Johansson. 2014. “Ants Can Be Used as Bio-indicators to Reveal 
Biological Effects of Electromagnetic Waves from Some Wireless Apparatus.” Electromagnetic 


Biology and Medicine 33(4): 282-88. 

Evans, Elaine, Robbin Thorp, Sarina Jepsen, and Scott Hoffman Black. 2008. Status Review of Three 
Formerly Common Species of Bumble Bee in the Subgenus Bombus. Portland, OR: Xerces Society 
for Invertebrate Conservation. 

Kluser, Stéphane and Pascal Peduzzi. 2007. Global Pollinator Decline: A Literature Review. Geneva: 
United Nations Environment Programme/GRID-Europe. 

Margaritis, Lukas H., Areti K. Manta, Konstantinos D. Kokkaliaris, Dimitra Schiza, Konstantinos 
Alimisis, Georgios Barkas, Eleana Georgiou, Olympia Giannakopoulou, Ioanna Kollia, Georgia 
Kontogianni, Angeliki Kourouzidou, Angeliki Myari, Fani Roumelioti, Aikaterini Skouroliakou, 
Vasia Sykioti, Georgia Varda, Konstantinos Xenos, and Konstantinos Ziomas. 2014. “Drosophila 
Oogenesis as a Bio-marker Responding to EMF Sources.” Electromagnetic Biology and Medicine 
33(3): 165-89. 

Massachusetts Division of Fisheries and Wildlife, Department of Fish and Game. 2015. 
Massachusetts List of Endangered, Threatened and Special Concern Species. Westborough, MA. 

Ministry of Environment and Forests. 2011. Report on Possible Impacts of Communication Towers 
on Wildlife Including Birds and Bees. New Delhi. 

National Research Council, Committee on the Status of Pollinators in North America. 2007. Status of 
Pollinators in North America. Washington, DC: National Academies Press. 

Panagopoulos, Dimitris J. 2011. “Analyzing the Health Impacts of Modern Telecommunications 
Microwaves.” Advances in Medicine and Biology 17: 1-55. 

. 2012a. “Effect of Microwave Exposure on the Ovarian Development of Drosophila 

melanogaster.” Cell Biochemistry and Biophysics 63: 121-32. 

. 2012b. “Gametogenesis, Embryonic and Post-Embryonic Development of Drosophila 
Melanogaster, as a Model System for the Assessment of Radiation and Environmental 
Genotoxicity.” In: M. Spindler-Barth, ed., Drosophila Melanogaster: Life Cycle, Genetics, and 
Development (New York: Nova Science), pp. 1-38. 

Panagopoulos, Dimitris J., Evangelia D. Chavdoula, Andreas Karabarbounis, and Lukas H. 
Margaritis. 2007. *Comparison of Bioactivity between GSM 900 MHz and DCS 1800 MHz 
Mobile Telephony Radiation." Electromagnetic Biology and Medicine 26: 33-44. 

Panagopoulos, Dimitris J., Evangelia D. Chavdoula, and Lukas H. Margaritis. 2010. “Bioeffects of 
Mobile Telephony Radiation in Relation to Its Intensity or Distance from the Antenna." 
International Journal of Radiation Biology 86(5): 345-57. 

Panagopoulos, Dimitris J., Evangelia D. Chavdoula, Ioannis P. Nezis, and Lukas H. Margaritis. 2007. 
“Cell Death Induced by GSM 900-MHz and DCS 1800-MHz Mobile Telephony Radiation.” 
Mutation Research 626: 69-78. 

Panagopoulos, Dimitris J., Andreas Karabarbounis, and Lukas H. Margaritis. 2004. “Effect of GSM 
900-MHz Mobile Phone Radiation on the Reproductive Capacity of Drosophila melanogaster.” 
Electromagnetic Biology and Medicine 23(1): 29-43. 

Panagopoulos, Dimitris J. and Lukas H. Margaritis. 2008. “Mobile Telephony Radiation Effects on 
Living Organisms.” In: A. C. Harper and R. V. Buress, eds., Mobile Telephones, Networks, 
Applications, and Performance (New York: Nova Science), pp. 107-49. 

. 2010. “The Identification of an Intensity ‘Window’ on the Bioeffects of Mobile Telephony 
Radiation.” International Journal of Radiation Biology 86(5): 358-66. 

Serant, Claire. 2004. “A Human Science Experiment.” New York Newsday, May 10. 

Warnke, Ulrich. 1989. “Information Transmission by Means of Electrical Biofields.” In: Fritz Albert 
Popp, Ulrich Warnke, Herbert L. König, and Walter Peschka, eds., Electromagnetic Bio- 
Information (München: Urban & Schwarzenberg), pp. 74-101. 











Williams, Paul H., Miguel B Araájo, and Pierre Rasmont. 2007. *Can Vulnerability among British 
Bumblebee (Bombus) Species be Explained by Niche Position and Breadth?" Biological 
Conservation 138: 493-505. 

Xerces Society for Invertebrate Conservation. 2015. Red List of Bees: Native Bees in Decline. 
Portland, OR. 

. 2015. Red List of Butterflies and Moths. Portland, OR. 





Konstantynów 

Flakiewicz, Wieslaw and Antonina Cebulska-Wasilewska. 1992. *Biological Effects of EM Field on 
Randomly Selected Human Population Residing Permanently Close to the High Power, Long 
Wave Radio Transmitter, and Tradescantia Plant Model System In Situ." EMC 92, Eleventh 
International Wroclaw Symposium and Exhibition on Electromagnetic Compatibility, September 
2-4, 1992, pp. 72-76. 


Mammals 

Balmori, Alfonso. 2009. "Electromagnetic Pollution from Phone Masts. Effects on Wildlife." 
Pathophysiology 16(2-3): 191-99. 

. 2010. “The Incidence of Electromagnetic Pollution on Wild Mammals: A New ‘Poison’ 
with a Slow Effect on Nature?” Environmentalist 30: 90-97. 

Magras, Ioannis N. and Thomas D. Xenos. 1997. “RF Radiation-Induced Changes in the Prenatal 
Development of Mice.” Bioelectromagnetics 18: 455-61. 





Radio Tagging Animals 

Altonn, Helen. 2002. “High-tech Tags Give Scientists Tools to Track Sea Animal Movement.” 
Honolulu Star-Bulletin, Feb 18. 

Balmori, Alfonso. 2016. “Radiotelemetry and Wildlife: Highlighting a Gap in the Knowledge on 
Radiofrequency Radiation Effects.” Science of the Total Environment 543: 662-69. 

Burrows, Roger, Heribert Hofer, and Marion L. East. 1994. “Demography, Extinction and n a Small 
Population: the Case of the Serengeti Wild Dogs.” Proceedings of the Royal Society of London B 
256: 281-92. 

. 1995. “Population Dynamics, Intervention and Survival in African Wild Dogs (Lycaon 
pictus).” Proceedings of the Royal Society of London B: 235-45. 

Caldwell, Mark. 1997. “The Wired Butterfly.” Discover Magazine, February 1. 

Godfrey, Jason D. and David M. Bryant. 2003. “Effects of Radio Transmitters: Review of Recent 
Radio-tracking Studies.” In: Williams, M., ed., Conservation Applications of Measuring Energy 
Expenditure of New Zealand Birds: Assessing Habitat Quality and Costs of Carrying Radio 
Transmitters (Wellington, New Zealand: Dept. of Conservation), pp. 83-95. 

Mech, L. David and Shannon M. Barber. 2002. A Critique of Wildlife Radio-Tracking and Its Use in 
National Parks. Jamestown, ND: U.S. Geological Survey, Northern Prairie Wildlife Research 
Center. 

Moorhouse, Tom P. and David W. Macdonald. 2005. “Indirect Negative Impacts of Radio-collaring: 
Sex Ratio Variation in Water Voles.” Journal of Applied Ecology 42: 91-98. 

Roberts, Greg. 2000. “Sick as a Parrot: Deaths Halt DNA Program.” The Age, February 8. 

Swenson, Jon E., Kjell Wallin, Göran Ericsson, Göran Cederlund, and Finn Sandegren. 1999. 
“Effects of Ear-tagging with Radiotransmitters on Survival of Moose Calves.” Journal of Wildlife 
Management 63(1): 354-58. 

Reader 5 Digest. 1998. “The Snow Tiger’s Last Stand.” November. 

Webster, A. Bruce and Ronald J. Brooks. 1980. “Effects of Radiotransmitters on the Meadow Vole, 
Microtus pennsylvanicus.” Canadian Journal of Zoology 58: 997-1001. 





Withey, John C., Thomas D. Bloxton, and John M. Marzluff. 2001. *Effects of Tagging and Location 
Error in Wildlife Radiotelemetry Studies." In: Joshua J. Millspaugh and John M. Marzluff, eds., 
Radio Tracking and Animal Populations (San Diego: Academic), pp. 43-75. 


Schwarzenburg 

Abelin, Theodor, Ekkehardt Altpeter, and Martin Róósli. 2005. *Sleep Disturbances in the Vicinity of 
the Short-Wave Broadcast Transmitter Schwarzenburg." Somnologie 9: 203-9. 

Altpeter, Ekkehardt-Siegfried, Katharina Sprenger, Katrin Madarasz, and Theodor Abelin. 1997. *Do 
Radiofrequency Electromagnetic Fields Cause Sleep Disorders?" European Regional Meeting of 
the International Epidemiological Association, Münster, Germany, September. Abstract no. 351. 

Altpeter, Ekkehardt-Siegfried, Martin Róósli. Markus Battaglia, Dominik H. Pfluger, Christoph E. 
Minder, and Theodor Abelin. 2006. *Effect of Short-Wave (6-22 MHz) Magnetic Fields on Sleep 
Quality and Melatonin Cycle in Humans: The Schwarzenburg Shut-Down Study." 
Bioelectromagnetics 27: 142-50. 

Altpeter, Ekkehardt-Siegfried, Thomas Krebs, Dominik H. Pfluger, J. von Kànel, R. Blattmann, D. 
Emmenegger, B. Cloetta, U. Rogger, H. Gerber, Bernhard Manz, R. Coray, R. Baumann, 
Katharina Staerk, Christian Griot, and Theodor Abelin. 1995. Study on Health Effects of the 
Shortwave Transmitter Station of Schwarzenburg, Berne, Switzerland. BEW Publication Series, 
Study no. 55. Federal Office of Energy, August 1995. 

Jakob, Hans-U. 2006. *Schwarzenburg — Nach 8 Jahren Geheimhaltung." Basel: Diagnose-Funk, 
June 25. 

. 2000. “State of Health after Shutdown of the Schwarzenburg Transmitter.” No Place To 
Hide 2(4): 21-22. 

Roch, Phillippe. 1996. “Health Effects of the Schwarzenburg Shortwave Transmitter,” Letter of May 
29, 1996, Bern: Federal Office of Environment, Forests and Landscape. English translation in No 
Place To Hide 1(3): 7-8. 

Stark, Katharina D. C., Thomas Krebs, Ekkehardt Altpeter, Bernhard Manz, Christian Griot, and 
Theodor Abelin. 1997. “Absence of Chronic Effect of Exposure to Short-wave Radio Broadcast 
Signal on Salivary Melatonin Concentrations in Dairy Cattle.” Journal of Pineal Research 22: 
171-76. 


Skrunda 

Balode, Zanda. 1996. “Assessment of Radio-Frequency Radiation by the Micronucleus Test in 
Bovine Peripheral Erythrocytes.” Science of the Total Environment 180: 81-85. 

Balodis, Valdis, Guntis Brimelis, Karlis Kalviskis, Olgerts Nikodemus, Didzis Tjarve, and Vija 
Znotina. 1996. “Does the Skrunda Radio Location Station Diminish the Radial Growth of Pine 
Trees?” Science of the Total Environment 180: 57-64. 

Brūmelis, Guntis, Valdis Balodis, and Zanda Balode. 1996. “Radio-frequency Electromagnetic 
Fields: The Skrunda Radio Location Station Case.” Science of the Total Environment 180: 49-50. 

Goldsmith, John R. 1995. “Epidemiologic Evidence of Radiofrequency Radiation (Microwave) 
Effects on Health in Military, Broadcasting, and Occupational Studies.” International Journal of 
Occupational and Environmental Health 1: 47-57. 

Kalnins, T., R. Krizbergs, and A. Romančuks. 1996. “Measurement of the Intensity of 
Electromagnetic Radiation from the Skrunda Radio Location Station, Latvia.” Science of the Total 
Environment 180: 51-56. 

Kolodynski, Anton and Valda Kolodynska. 1996. “Motor and Psychological Functions of School 
Children Living in the Area of the Skrunda Radio Location Station in Latvia.” Science of the Total 
Environment 180: 87-93. 





Liepa, V. and Valdis Balodis. 1994. *Monitoring of Bird Breeding near a Powerful Radar Station." 
The Ring 16(1-2): 100. Abstract. 

Magone, I. 1996. “The Effect of Electromagnetic Radiation from the Skrunda Radio Location Station 
on Spirodela polyrhiza (L.) Cultures." Science of the Total Environment 180: 75-80. 

Microwave News. 1994. “Latvia’s Russian Radar May Yield Clues to RF Health Risks." 
September/October, pp. 12-13. 

Science of the Total Environment. 1996. “Special Issue: Effects of RF Electromagnetic Radiation on 
Organisms. A Collection of Papers Presented at The International Conference on the Effect of 
Radio Frequency Electromagnetic Radiation on Organisms, Skrunda, Latvia, June 17-21, 1994.” 
180: 277-78. 

Selga, Turs and Maija Selga. 1996. “Response of Pinus sylvestris L. needles to Electromagnetic 
Fields: Cytological and Ultrastructural Aspects.” Science of the Total Environment 180: 65-73. 


Chapter 17 

Adey, William Ross. 1993. “Effects of Electromagnetic Fields. Journal of Cellular Biochemistry 51: 
410-16. 

. 1993. “Whispering Between Cells: Electromagnetic Fields and Regulatory Mechanisms in 
Tissue.” Frontier Perspectives 3(2): 21-25. 

Bas, Orhan, Osman Fikret Sönmez, Ali Aslan, Ayşe İkinci, Hatice Hancı, Mehmet Yıldırım, Haydar 
Kaya, Metehan Akça, and Ersan Odacı. 2013. “Pyramidal Cell Loss in the Cornu Ammonis of 32- 
day-old Female Rats Following Exposure to a 900 Megahertz Electromagnetic Field during 
Prenatal Days 13-21.” NeuroQuantology 11(4): 591-99. 

Bejot, Yannick, Benoit Daubail, Agnès Jacquin, Jérôme Durier, Guy-Victor Osseby, Olivier Rouaud, 
and Maurice Giroud. 2014. “Trends in the Incidence of Ischaemic Stroke in Young Adults 
Between 1985 and 2011: the Dijon Stroke Registry.” Journal of Neurology, Neurosurgery, and 
Psychiatry 85: 509-13. 

Blue Cross Blue Shield. 2019. The Health of Millennials. Washington, DC. 

Broomhall, Mark. 2017. Report Detailing the Exodus of Species from the Mt. Nardi Area of the 
Nightcap National Park World Heritage Area During a 15-Year Period (2000-2015). Report for 
the United Nations Educational Scientific and Cultural Organization (UNESCO). New South 
Wales, Australia. 

Byun, Yoon-Hwan, Mina Ha, Ho-Jang Kwon, Yun-Chul Hong, Jong-Han Leem, Joon Sakong, Su 
Young Kim, Chul Gab Lee, Dongmug Kang, Hyung-Do Choi, and Nam Kim. 2013. “Mobile 
Phone Use, Blood Lead Levels, and Attention Deficit Hyperactivity Symptoms in Children: A 
Longitudinal Study." PLoS ONE 8(3): e59742. 

Centola, G. M., A. Blanchard, J. Demick, S. Li, and M. L. Eisenberg. 2016. *Decline in Sperm Count 
and Motility in Young Adult Men from 2003 to 2013: Observations from a U.S. Sperm Bank." 
Andrology 4: 270-76. 

Cherry, Neil. 2000. Safe Exposure Levels. Lincoln University, Lincoln, New Zealand. 

. 2002. *Schumann Resonances, a Plausible Biophysical Mechanism for the Human Health 
Effects of Solar/Geomagnetic Activity." Natural Hazards Journal 26(3): 279-331. 

Dalsegg, Aud. 2002. “Far hodesmerter av mobilstraling” (“She Gets Headaches from Mobile 
Radiation”). Dagbladet, March 9. 

Grigoriev, Yury Grigorievich. 2005. “Elektromagnitnye polya sotovykh telefonov i zdorovye detey i 
podrostkov: Situatsiya, trebuyushchaya prinyatiya neotlozhnykh mer” (“The Electromagnetic 
Field of Mobile Phones and the Health of Children and Adolescents: This Situation Requires 
Urgent Action”). Radiatsionnaya biologiya. Radioekologiya 45(4): 442-50. 











. 2012. *Mobile Communications and Health of Population: The Risk Assessment, Social and 
Ethical Problems." The Environmentalist 32(2): 193-200. 

Grigoriev, Yury Grigorievich and Oleg Aleksandrovich Grigoriev. 2011. “Mobil’naya svyaz’ i 
zdorovye naseleniya: Otsenka opasnosti, sotsial’nye i eticheskiye problemi” (“Mobile 
Communication and Health of Population: Estimation of Danger, Social and Ethical Problems”). 
Radiatsionnaya biologiya. Radioekologiya 51(3): 357-68. 

. 2013. Sotovaya Svyaz’ i Zdorov’e (“Cellular Communication and Health"). Moscow: 
Ekonomika. 

Grigoriev, Yury Grigorievich and Nataliya Igorevna Khorseva. 2014. Mobil’naya Svyaz’ i Zdorov’e 
Detey (“Mobile Communication and Children’s Health”). Moscow: Ekonomika. 

Hallberg, Orjan and Olle Johansson. 2009. “Apparent Decreases in Swedish Public Health Indicators 
after 1997 — Are They Due to Improved Diagnostics or to Environmental Factors?” 
Pathophysiology 16(1): 43-46. 

Hallberg, Orjan and Olle Johansson. 2004. Glesbygd är en sjuk miljö, nu börjar även friska dö (“Say 
To Countryside Goodbye, When Even Healthy People Die”). Stockholm: Karolinska Institute, 
Experimental Dermatology Unit. Report no. 6. 

Hallberg, Örjan and Gerd Oberfeld. 2006. “Letter to the Editor: Will We All Become 
Electrosensitive?” Electromagnetic Biology and Medicine 25(3): 189-91. 

Hallman, Caspar A., Martin Sorg, Eelke Jongejans, Hank Siepel, Nick Hofland, Heinz Schwan, 
Werner Stenmans, Andreas Müller, Hubert Sumser, Thomas Hörren, Dave Goulson, Hans de 
Kroon. 2017. “More than 75 Percent Decline over 27 Years in Total Flying Insect Biomass in 
Protected Areas.” PLoS ONE 12(10): e0185809. 

Hancı, Hatice, Ersan Odacı, Haydar Kaya, Yüksel Aliyazıcıoğlu, İbrahim Turan, Selim Demir, and 
Serdar Çolakoğlu. 2013. “The Effect of Prenatal Exposure to 900-MHz Electromagnetic Field on 
the 21-old-day Rat Testicle.” Reproductive Toxicology 42: 203-9. 

Hancı, Hatice, Sibel Türedi, Zehra Topal, Tolga Mercantepe, İlyas Bozkurt, Haydar Kaya, Safak 
Ersöz, Bünyami Ünal, and Ersan Odacı. 2015. “Can Prenatal Exposure to a 900 MHz 
Electromagnetic Field Affect the Morphology of the Spleen and Thymus, and Alter Biomarkers of 
Oxidative Damage in 21-day-old Male Rats?” Biotechnic & Histochemistry 90(7). 535-43. 

Hutton, John S., Jonathan Dudley, Tzipi Horowitz-Kraus, Tom DeWitt, and Scott K. Holland. 2019. 
“Associations Between Screen-Based Media Use and Brain White Matter Integrity in Preschool- 
Aged Children.” JAMA Pediatrics 2019 Nov. 4: e193869. 

İkinci, Ayşe, Ersan Odacı, Mehmet Yıldırım, Haydar Kaya, Metehan Akça, Hatice Hancı, Ali Aslan, 
Osman Fikret Sönmez, and Orhan Baş. 2013. “The Effects of Prenatal Exposure to a 900 
Megahertz Electromagnetic Field on Hippocampus Morphology and Learning Behavior in Rat 
Pups.” Journal of Experimental and Clinical Medicine 30: 278. Abstract. 

İkinci, Ayşe, Tolga Mercantepe, Deniz Unal, Hüseyin Serkan Erol, Arzu Şahin, Ali Aslan, Orhan 
Baş, Havva Erdem, Osman Fikret Sönmez, Haydar Kaya, and Ersan Odacı. 2015. “Morphological 
and Antioxidant Impairments in the Spinal Cord of Male Offspring Rats Following Exposure to a 
Continuous 900 MHz Electromagnetic Field During Early and Mid-Adolescence.” Journal of 
Chemical Neuroanatomy [Epub ahead of print]. 

Kimata, Hajime. 2002. “Enhancement of Allergic Skin Wheal Responses by Microwave Radiation 
from Mobile Phones in Patients with Atopic Eczema/Dermatitis Syndrome.” International 
Archives of Allergy and Immunology 129(4): 348-50. 

Li, De-Kun, Hong Chen, and Roxana Odouli. 2011. “Maternal Exposure to Magnetic Fields during 
Pregnancy in Relation to the Risk of Asthma in Offspring.” Archives of Pediatrics & Adolescent 
Medicine 165(10): 945-50. 





Lister, Bradford C. and Andres Garcia. 2018. “Climate-driven Declines in Arthropod Abundance 
Restructure a Rainforest Food Web.” Proceedings of the National Academy of Sciences 115(44): 
E10397—E10406. 

Mild, Kjell Hansson, Gunnhild Oftedal, Monica Sandstróm, Jonna Wilén, Tore Tynes, Bjarte 
Haugsdal, and Egil Hauger. 1998. Comparison of Symptoms Experienced by Users of Analogue 
and Digital Mobile Phones. A Swedish-Norwegian Epidemiological Study. Umeà, Sweden: 
National Institute for Working life. Arbetslivsrapport 23. 

Mishra, Lata. 2011. *Heard This? Talking on the Phone Makes You Deaf." Mumbai Mirror, October 
26. 

Mishra, Srikanta Kumar. 2010. “Otoacoustic Emission (OAE)-Based Measurement of the 
Functioning of the Human Cochlea and the Efferent Auditory System.” Ph.D. thesis, University of 
Southampton. 

Nittby, Henrietta, Gustav Grafström, Dong Ping Tian, Lars Malmgren, Arne Brun, Bertil R. R. 
Persson, Leif G. Salford, and Jacob Eberhardt. 2008. “Cognitive Impairment in Rats After Long- 
Term Exposure to GSM-900 Mobile Phone Radiation.” Bioelectromagnetics 29: 219-32. 

Odacı, Ersan, Hatice Hancı, Ayşe İkinci, Osman Fikret Sönmez, Ali Aslan, Arzu Şahin, Haydar 
Kaya, Serdar Çolakoğlu, and Orhan Baş. 2015. “Maternal Exposure to a Continuous 900-MHz 
Electromagnetic Field Provokes Neuronal Loss and Pathological Changes in Cerebellum of 32- 
day-old Female Rat Offspring.” Journal of Chemical Neuroanatomy [Epub ahead of print]. 

Odacı, Ersan, Hatice Hancı, Esin Yuluğ, Sibel Türedi, Yüksel Aliyazıcıoğlu, Haydar Kaya, and 
Serdar Çolakoğlu. 2016. “Effects of Prenatal Exposure to a 900 MHz Electromagnetic Field on 
60-day-old Rat Testis and Epididymal Sperm Quality.” Biotechnic & Histochemistry 91(1): 9-19. 

Odacı, Ersan, Ayşe İkinci, Mehmet Yıldırım, Haydar Kaya, Metehan Akça, Hatice Hancı, Osman 
Fikret Sönmez, Ali Aslan, Mukadder Okuyan, and Orhan Baş. 2013. “The Effects of 900 
Megahertz Electromagnetic Field Applied in the Prenatal Period on Spinal Cord Morphology and 
Motor Behavior in Female Rat Pups.” NeuroQuantology 11(4): 573-81. 

Odacı, Ersan and Cansu Özyılmaz. 2015. “Exposure to a 900 MHz Electromagnetic Field for 1 Hour 
a Day over 30 Days Does Change the Histopathology and Biochemistry of the Rat Testis.” 
International Journal of Radiation Biology 91: 547-54. 

Odacı, Ersan, Deniz Ünal, Tolga Mercantepe, Zehra Topal, Hatice Hancı, Sibel Türedi, Hüseyin 
Serkan Erol, Sevdegül Mungan, Haydar Kaya, and Serdar Çolakoğlu. 2015. “Pathological Effects 
of Prenatal Exposure to a 900 MHz Electromagnetic Field on the 21-day-old Male Rat Kidney.” 
Biotechnic & Histochemistry 90(2): 93-101. 

Oktay, M. Faruk and Suleyman Dasdag. 2006. “Effects of Intensive and Moderate Cellular Phone 
Use on Hearing Function.” Electromagnetic Biology and Medicine 25: 13-21. 

Panda, Naresh K., Rahul Modi, Sanjay Munjal, and Ramandeep S. Virk. 2011. “Auditory Changes in 
Mobile Users: Is Evidence Forthcoming?” Otolaryngology — Head and Neck Surgery 144(4): 581- 
85. 

Putaala, Jukka, Antti J. Metso, Tiina M. Metso, Nina Konkola, Yvonn Kraemer, Elena Haapaniemi, 
Markku Kaste, and Turgut Tatlisumak. 2009. “Analysis of 1008 Consecutive Patients Aged 15 to 
49 with First-Ever Ischemic Stroke: the Helsinki Young Stroke Registry.” Stroke 40: 1195-1203. 

Rosengren, Annika, Kok Wai Giang, Georgios Lappas, Christina Jern, Kjell Torén, and Lena Björck. 
2013. “Twenty-four-year Trends in the Incidence of Ischemic Stroke in Sweden from 1987 to 
2010.” Stroke 44: 2388-93. 

Şahin, Arzu, Ali Aslan, Orhan Baş, Ayşe İkinci, Cansu Özyılmaz, Osman Fikret Sönmez, Serdar 
Çolakoğlu, and Ersan Odacı. 2015. “Deleterious Impacts of a 900-MHz Electromagnetic Field on 
Hippocampal Pyramidal Neurons of 8-week-old Sprague Dawley Male Rats.” Brain Research 
1624: 232-38. 


Salford, Leif G., Arne E. Brun, Jacob L. Eberhardt, Lars Malmgren, and Bertil R.R. Persson. 2003. 
*Nerve Cell Damage in Mammalian Brain after Exposure to Microwaves from GSM Mobile 
Phones." Environmental Health Perspectives 111(7): 881-83. 

Sánchez-Bayo, Francisco and Kris A. G. Wyckhuys. 2019. “Worldwide Decline of the Entomofauna: 
A Review of Its Drivers. Biological Conservation 232: 8-27. 

Shinjyo, Tetsuharu and Akemi Shinjyo. 2014. *Signifikanter Rückgang klinischer Symptome nach 
Senderabbau — eine Interventionsstudie." Umwelt-Medizin-Gesellschaft 27(4): 294-301. 

Siegel, Rebecca L., Stacey A. Fedewa, William F. Anderson, Kimberly D. Miller, Jiemin Ma, Philip 
S. Rosenberg, and Ahmedin Jemal. 2017. “Colorectal Cancer Incidence Patterns in the United 
States, 1974-2013.” Journal of the National Cancer Institute 109(8): djw322. 

Tatemichi, Masayuki, Tadashi Nakano, Katsutoshi Tanaka, Takeshi Hayashi, Takeshi Nawa, Toshiaki 
Miyamoto, Hisanori Hiro, and Minoru Sugita. 2004. “Possible Association between Heavy 
Computer Users and Glaucomatous Visual Field Abnormalities: A Cross Sectional Study in 
Japanese Workers.” Journal of Epidemiology and Community Health 58: 1021-27. 

Tibæk, Maiken, Christian Dehlendorff, Henrik S. Jørgensen, Hysse B. Forchhammer, Søren P. 
Johnsen, and Lars P. Kammersgaard. 2016. “Increasing Incidence of Hospitalization for Stroke 
and Transient Ischemic Attack in Young Adults: A Registry-Based Study.” Journal of the 
American Heart Association 5(5): e003158. 

Topal, Zehra, Hatice Hancı, Tolga Mercantepe, Hüseyin Serkan Erol, Osman Nuri Keleş, Haydar 
Kaya, Sevdegül Mungan, and Ersan Odacı. 2015. “The Effects of Prenatal Long-duration 
Exposure to 900-MHz Electromagnetic Field on the 21-day-old Newborn Male Rat Liver.” 
Turkish Journal of Medical Sciences 45(2): 291-97. 

Türedi, Sibel, Hatice Hancı, Zehra Topal, Deniz Ünal, Tolga Mercantepe, İlyas Bozkurt, Haydar 
Kaya, and Ersan Odacı. 2015. “The Effects of Prenatal Exposure to a 900-MHz Electromagnetic 
Field on the 21-day-old Male Rat Heart.” Electromagnetic Biology and Medicine 34(4): 390-97. 

Velayutham, P., Gopala Krishnan Govindasamy, R. Raman, N. Prepageran, and K. H. Ng. 2014. 
"High-frequency Hearing Loss Among Mobile Phone Users." Indian Journal of Otolaryngology 
and Head & Neck Surgery 66: S169-S172. 

Weiner, A. B., R. S. Matulewicz, S. E. Eggener, and E. M. Schaeffer. 2016. “Increasing Incidence of 
Metastatic Prostate Cancer in the United States (2004-2013). Prostate Cancer and Prostatic 
Diseases 19: 395-97. 

West, John G., Nimmi S. Kapoor, Shu-Yuan Liao, June W. Chen, Lisa Bailey, and Robert A. 
Nagourney. 2013. “Multifocal Breast Cancer in Young Women with Prolonged Contact between 
Their Breasts and Their Cellular Phones. Case Reports in Medicine, article ID 354682. 

Wiedbrauk, Danny L. 1997. “The 1996-1997 Influenza Season — A View from the Benches.” Pan 
American Society for Clinical Virology Newsletter 23(1): 1 ff. 

Wolford, Monica L., Kathleen Palso, and Anita Bercovitz. 2015. “Hospitalization for Total Hip 
Replacement Among Inpatients Aged 45 and Over: United States, 2000-2010.” NCHS Data Brief 
no. 186. 

Wong, Martin C. S., William B. Goggins, Harry H. X. Wang, Franklin D. H. Fung, Colette Leung, 
Samuel Y. S. Wonga, Chi Fai Ng, and Joseph J. Y. Sung. 2016. “Global Incidence and Mortality 
for Prostate Cancer: Analysis of Temporal Patterns and Trends in 36 Countries.” European 
Urology 70: 862-74. 

Yakymenko, I. L., E. P. Sidorik, A. S. Tsybulin, and V. F. Chekhun. 2011. "Potential Risks of 
Microwaves from Mobile Phones for Youth Health." Environment & Health 56(1): 48-51. 

Ye, Juan, Ke Yao, Dequiang Lu, Renyi Wu, and Huai Jiang. 2001. “Low Power Density Microwave 
Radiation Induced Early Changes in Rabbit Lens Epithelial Cells.” Chinese Medical Journal 
114(12): 1290-94. 


About the Author 


Arthur Firstenberg is a scientist and journalist who is at the forefront of a 
global movement to tear down the taboo surrounding this subject. After 
graduating Phi Beta Kappa from Cornell University with a degree in 
mathematics, he attended the University of California, Irvine School of 
Medicine from 1978 to 1982. Injury by X-ray overdose cut short his 
medical career. For the past thirty-eight years he has been a researcher, 
consultant, and lecturer on the health and environmental effects of 
electromagnetic radiation, as well as a practitioner of several healing arts. 

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