While Science Sleeps

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WHILE SCIENCE
SLEEPS
A Sweetener Kills
The introduction of aspartame into the food supply of the United States began
in the summer of 1981. Since that time, the incidence of Alzheimer’s deaths has
increased 100 fold (10,000%). Autism has, with no explanation, increased 25 times
(2500%). Autoimmune diseases have reached epidemic proportions, with Lupus
(SLE) up 300%, and Multiple Sclerosis, Type II Diabetes and Rheumatoid Arthritis
headed out of control. Cancers, the hallmark of formaldehyde exposure, have ex-
ploded. Skin cancer has shot up over 400%, liver cancer has tripled, kidney cancer
has doubled, and breast cancer is up 50%. The list goes on.....
This 250 page, full color book uses over 100 colorful illustrations, photographs,
tables and graphs to explain to the average person the fascinating process by
which methanol, a poison hidden in aspartame and some other foods, is converted
to formaldehyde at the very locations in the human body where these diseases
originate, revealing, for the first time, the exact details of the probable cause of
each. It is a cautionary tale of the legacy of the danger of a poisonous food additive
and the failure of a government, corrupted by greed, to safeguard the health and
welfare of its people.
This is a handbook that teaches the tools you will need to protect those you love
and inform them about the causes of a number of diseases that have, until now,
proven inexplicably elusive to a medical community beholden to Big Pharma
...While Science Sleeps.
While Science Sleeps

About the Author By Woodrow C. Monte
Dr. Woodrow C. Monte, Professor Emeritus of Food Science and Nutrition from Arizona
State University, has decades of experience in food science and nutrition as a researcher, Paperback $37.98
teacher, inventor, industry consultant and consumer advocate who is committed to food ISBN 9 781452 893679
additive safety and the prevention of food borne diseases. For over 30 years he has
studied the link between artificial sweeteners and the diseases of civilization including Kindle $9.80
Alzheimer’s, Heart Disease, Multiple Sclerosis, numerous forms of cancer, Autism and ASIN B007127OFY
other Birth Defects.
Non-Fiction, color illustrations
Dr. Monte’s testimony before Congress was instrumental in the prevention of Sulfites from
receiving status of US FDA GRAS (Generally Regarded As Safe) and the implementation
of mandatory labeling for most foods that contain this dangerous additive.
Dimensions 10 x 8 x 0.6 inches
Through his research, Dr. Monte has been awarded 22 US patents. He has shared his Now available at Amazon.com
technical expertise during hundreds of television and radio appearances including a spe-
cial feature on the CBS Evening News with Dan Rather and 60 Minutes. He is the author For further information visit
of numerous scientific publications and the book While Science Sleeps: A Sweetener Kills. whilesciencesleeps.com
While Science Sleeps© W. Monte (Prepublication) Page |1
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/

Table of Contents
Chapter 3
1 A Time When All the Easy Questions Have Been Answered 7
2 Methanol: Where Is It Found? How Can It Be Avoided? 20
3 Man And Methanol: A Tragic History of Mutation and Deceit 27
4 Formaldehyde Is The Real Problem 44
5 The Silent Battle That Turns Methanol Into Disease 64
6 How Methanol Kills 73
7 Atherosclerotic Cardiovascular Disease (Heart Disease) 94
8 Alzheimer's Disease and its Perivascular Nature 122
9 Multiple Sclerosis 136
10 Classic Autoimmune Diseases Lupus and Rheumatoid Arthritis 184
11 Cancers of Aspartame 194
12 Autism and other Birth Defects 216
Bibliography 242

Chapter 9
Multiple Sclerosis
Nature does not recognize disease; in her eyes, all has purpose, all is equal, and no one natural
process is better than another. If you seek the cause of any unknown you are wise not to impede your
vision by limiting your course of study. Learn about a natural mystery by taking it in completely; smell
and taste it if you can. You must make close acquaintance with what you study before you can hope to
see how it fits, discover its origin, and resolve how to make peace with it. View all of life’s systems as
timely events of a perfect interaction between equals – and you may begin to see their purpose. Let your
prejudice be engaged only after the whole truth is plain to you and the course is clear.
We all die. The sentence is imposed at the first beat of our anxious hearts. Few suffer a more
prolonged passing than those who succumb to multiple sclerosis (MS). The symptoms, a constant
reminder that the brain is losing control of the organism with which it was once master. The young
women who are the primary target of this tragic disorder can only cling to hope of a misdiagnosis or the
rare outcome of complete remission. We will in this chapter discuss this disease as if the cause has been
discovered and relief is on the way. I will be ridiculed for this approach, but then abuse has been the
burden of discovery since the beginning of thought.
The Conflagration That Is Multiple Sclerosis

Multiple Sclerosis was on my mind when, at the dusk of a lovely summer day on a flight over
California, I witnessed another of Nature’s catastrophes – the unforgettable sight of a forest fire
engulfing an entire mountainside. Thousands of acres of blackened bare tree trunks were outlined by a
thin encircling ring of flame where the damage effectuated. It immediately occurred to me that this was
a very powerful descriptor of MS plaque. Plaque is the anatomical equivalent of a slow forest fire, where
nerve axons are being slowly stripped bare of their insulation. It is the defining feature for which the
disease was first named by the French neurologist Jean-Martin Charcot in 1865.
I was in an introspective mood, and a stout drink or two later I began to daydream. What if, I
imagined while reminiscing about the miles of desolation, an alien space ship were to land at the scene
of this fire some time after the terrain had gone cold? What if these were brilliant alien scientists and
explorers from a planet with little oxygen in the atmosphere and, therefore, no such phenomenon as fire?
Surely their curiosity would draw them to this desolate spot that was so different from anything they had
ever experienced on their own planet. Their cargo bay would soon be loaded with samples of all manner
of charred remnants of plant and animal matter in various degrees of deterioration and decay, along with
detailed pictures of the damage done to the terrain and life forms.
As a fellow scientist now caught in such a conundrum myself I imagined their fruitless search for
the cause of this blight in the midst of a vibrant living forest, the endless rhetoric that would ensue
during their long return flight home, the search for the invisible beasts responsible, the manuscripts of
descriptive biology and theoretical speculation written after years of study and debate back on the home
planet that had no knowledge of flame. As I write this, lying on my desk, long closed, is a damaged copy
of just such a tome, the fourth edition of McAlpine’s Multiple Sclerosis,[#305] a fifteen pound, thousand
page technical masterpiece done in six colors and a print far too small to be easily read by those visually

impaired MS sufferers it purports to describe. The damage to my copy was caused by my ripping it in
half to save postage between the two continents I call home. This publication would have much in
common with the works produced by my imaginary visiting alien intellectuals. It contains a collection of
hard won scientific data, factually correct but in the end, due to just one missing bit of knowledge,
providing no help to the suffering and no answer to the most important question: Why?
McAlpine’s is not listed among the handful of literature that I classify as must reading for
someone who wishes to learn about multiple sclerosis. This compendium of the “present knowledge”
belabors the trivia of the long history of medicine’s failures with MS while incredibly failing to
encourage in any way the compelling evidence that support the possibility that an environmental poison
might just be its cause. Methanol and formaldehyde do not appear anywhere among its near million
words. The bias of the chief editor is expressed in print[#616] in his critical, unreferenced review of an
article which I hold in great esteem, authored by a good scientist who steps back and takes a careful,
thoughtful, yet critical view of his own discipline and how it connects with reality. His approach is rare,
especially among the ranks of the Delphian medical sciences. If you have MS or love someone who does
I encourage you to read the brutally honest and thought provoking twenty page review The Pathogenesis
of Multiple Sclerosis Revisited,[#615] and while you are at it take a look at What if Multiple Sclerosis isn’t
an Immunological or a Viral Disease? The Case for a Circulating Toxin.[#153] These articles will prepare
you for what I have to say about the subject.
The hostility between the various factions of those who now study multiple sclerosis may
actually be encouraged by the machinations of the major drug companies who sell extremely expensive
competing palliatives for the disease, none of which cure it. The rivalry between these companies, who
are responsible for directing most of the funding for the search for the "cure" of MS, is inspired by the
fact that even the least effective of their concoctions have proven to be billion dollar product lines, due
solely to the desperation of MS sufferers and their loved ones. To trust the cure of any disease to a group
whose existence depends upon its perpetuation seems counterintuitive, if not outright stupid. (By
“group,” I mean both the pharmaceutical companies and the various MS societies who encourage and
support each other in, to my mind, unproductive ways.)
The heated debate between the various competing groups of scientists studying MS is a debate
between those who believe that MS is a defect in the immune system, those who think it is a viral
disease, and those very few who believe that the disease is the direct result of a toxic agent from the
environment. Though it is well known that animals do not develop MS there is no consensus as to
whether animals can be used as experimental models for the disease when artificial methods are used to
induce them to lose myelin. These issues have been continually debated for over a hundred years with,
up till now, each side presenting only enough evidence to show that they may be on the right track but
not enough to assign culpability. Aside from what I will demonstrate to you in this chapter there are few
recorded instances where the incidence of MS has actually been manipulated. When Norway was
occupied during World War II food was severely restricted for several years and the incidence of MS
went down dramatically, unfortunately this has been virtually ignored.[#153]
I am not so very much interested in belaboring every detail of the slow complex conflagration
that is multiple sclerosis. My intention here is to give you what you need to know to prevent the fire
from reaching the fuel.

Listening to Nature’s Whispers

In June of 1550 the Spanish conquistador Cortez kidnapped and eventually killed the Aztec emperor
Montezuma in a successful attempt to steal the golden treasures of the Aztec people. From the time of
Columbus it was the admitted intent of European invaders to plunder the newly discovered territory of
the Americas, no matter what the cost to the “savages.” Among other bounty were the golden seeds of a
plant unknown to the conquering rabble. This was to be the first of the corn seeds from the Americas to
be received enthusiastically by the old world, but to have attached unforeseen dire consequences. The
seeds did not come with instructions. Although the Aztec people had much they could teach the
Spaniards, their traditions were not heeded. Perhaps these Europeans had such a high opinion of their
own civilization that they could not easily accept cultural knowledge from those they so easily
conquered. Whatever the case, unimaginable misery was the wage of implementing a new food without
sufficient knowledge of its safety. Pellagra, the disease of corn, was to take European scientists over 400
years to rediscover and cost millions of innocent lives to a slow and agonizing death.
Eight thousand years before the Old World finally put an end to their culture, the Aztecs had
begun experimenting with native grasses, turning them into something new to nature. They persisted,
and after generations of observation and painstaking manipulation, with careful crossing of strains, they
produced a new life form that could have never evolved naturally. It was the birth of what appeared on
first blush to be a valuable food crop – corn (maize). No record exists of who these individuals were, but
without a doubt the work that they performed was a non-invasive genetic manipulation (GM). The most
critical way that Aztec science differs from our modern GM is that the Aztecs took the ultimate
responsibility for bringing their work to completion. Over a period of years the dark side of their
unnatural invention was to present as a plague of biblical proportions. Entire villages of corn eaters
would succumb to symptoms of what must then have appeared to be many different diseases. Some
individuals would develop devastating and painful skin lesions, while others would lose all semblance of
civilization and go mad. Death would finally come to most when the heart would refuse the brain’s
signal to continue beating.
By observation, Aztec scientists were able to determine that it was the corn that was the cause of
these apocalyptic outbreaks and further, and of much greater significance, they observed that when corn
was treated overnight with powdered limestone or the ash from a wood fire the suffering would not
come. By pure and patient observation of Nature’s response to their own unnatural product these ancient
people solved the riddle of Pellagra and successfully implemented a reliable prevention. This complex
conundrum that we know now was a nutritional deficiency of niacin was laid to rest by observation,
intuition and intellect alone.
We have already discussed other ancient cultures that were adept at such research and developed
traditional adaptations of the way they prepared food to ultimately prevent premature death and
suffering caused by nutritional deficiencies and poisoning from naturally occurring toxic substances.
With the exception of the accidental discovery of antibiotics by a university microbiologist and
vaccination by a country physician who was really more of a naturalist, our modern medicine men are
wretchedly inept at discovering the cause and prevention of disease. If only we could discover what is so
very wrong with our scientific methods that makes it impossible for our researchers to tease such
revelations from Nature’s grasp! We can only guess that part of it may be that present-day medicine
appears to have no stomach for the combination of observation, intuition and common sense that ancient
peoples would have been forced to employ to come to their cures for food borne diseases. Modern
medical researchers, particularly those funded by the pharmaceutical industry, often demean such

observations by using the term “anecdotal” and employing an inflection and tenor as if they were
uttering a curse.
My use of observation, intuition and common sense, combined with careful study of the research
of many whose narrow perspectives prevented them from seeing the answers they sought, has led me to
believe that diseases of civilization (DOC) and, in particular, multiple sclerosis, were originally caused
by human meddling with the food supply. In this chapter I will apply both anecdotal observation and the
more traditional methods of modern science to point to the cause and prevention of the poisoning that
causes MS.
The Scene of the Crime

The brain, along with the rest of the central nervous system, is made up of about 50% neurons (nerve
cells) that communicate with other cells of the body via long wire-like strands called axons. Multiple
sclerosis results from the progressive deterioration of the protective myelin sheath surrounding the
axons. Axons are in many ways similar to a telephone cord, which is made up of a conductive wire
surrounded by a protective coating, without which the signal would be interrupted and muted as it
travels from the mouthpiece to the phone line. The disappearance of myelin distorts nerve cell
communication, leading to a long list of neurological symptoms including loss of sensation, muscle
spasms and weakness, fatigue, blindness, and pain. The entire collection of symptoms that constitute
multiple sclerosis can be explained by damage to the myelin sheath of specific axons in the brain and
upper spinal cord. All the symptomology deriving from the interference to the normal communication
between the brain and the rest of the body is due to what is tantamount to short circuits in axons that
transmits life sustaining information in both directions.
Specifically, damage is found around the axons that transmit signals to and from the muscles and
sensor cells. Even though the impulse that runs down the axon is not identical to the flow of electrons
that runs through an analogous electric wire, nevertheless the myelin must be insulated to provide for the
security of the messages traveling through it and to prevent the bare axons from touching and allowing
signal cross over between nerve cells or, even worse, the breaking of the unprotected axon itself. The
one major difference in the appearance of the myelin sheath when compared to the insulation on an
electrical wire is that the nerve cell’s insulation is applied in numerous evenly spaced lumps, called
nodules, that run down the length of the axon, giving a healthy axon the appearance of a strand of beads.
Each nodule consists of many layers of myelin wrapped in one continuous band around the axon it
protects.
The disease is called multiple sclerosis because usually the myelin sheath can be damaged at
multiple sites in the brain. These sites are not haphazard; they have a pattern which is characteristic of
the disease and consistent with the usual symptoms. Interestingly, these sites are identical to the sites
affected during methanol poisoning.
MS damage to the brain always begins in areas adjacent to blood vessels. Dr. James Dawson at
the University of Edinburgh in 1916 performed detailed examinations of the brains of patients who died
from MS. His meticulous descriptions of the inflammation and swelling of blood vessels and the damage
to the adjacent myelin sheath is valid to this day[#620] and again is startlingly reminiscent of the damage
caused by methanol toxicity.[#15] This presentation, consisting of the damaged vessel and many adjacent
axons which exhibit complete demylination, is plaque. These plaques radiate out from the vessels
around which they are centered. Plaques enlarge three dimensionally over time from the central vein or

small artery outward until they give the appearance of the growing limb of a tree. The analogy stretches
to the bark representing the "active" area of the plaque, where we can find macrophages busy consuming
the myelin sheaths of previously healthy axons as the plaque slowly grows with the progression of the
disease by what appears so obviously to be diffusion of a deadly poison.
Each human nerve cell has only one axon, some of which can reach over a foot in length. These
axons have to be insulated, padded, protected, and fed. Functions that are not provided directly by the
neuron (nerve cell) itself, because the distances are so great between the body of the cell and the end of
the axon. Rather, the axon is cared for by other cells of the nervous system to be found along its path in
the brain and spinal cord. It is the Schwann cell which takes it upon itself to maintain one short segment
of axon. To do this it must stretch out a thin layer of its cell membrane and grow that layer around and
around the axon many times. These windings are what become the myelin sheath. Thousands of these
Schwann cells are spaced at remarkably consistent intervals along the path of the average nerve cell
axon, giving the axon the look of a garden hose strung with evenly spaced rolls of paper towels. The
Schwann cells remain attached and are physically very close to the axon, providing life support to the
living myelin sheath. They can also act to regrow the sheath when it is in need of repair or replacement.
The regrowth is slow, but it is precisely what accounts for the periods of remittance which follow the
relapses that often occur in MS sufferers.
It is this symbiotic relationship that helps explain the major difference between Alzheimer’s
disease, which is caused by damage deep inside the axon and is irreversible, and multiple sclerosis,
which is a disease of the myelin sheath and is repairable, causing multiple cycles of exacerbation and
remission. The modus operandi of formaldehyde during the evolution of MS is identical to that of
Alzheimer’s – even to the attack on the axons of the nerve cells in close proximity to the small veins and
arteries of the circulatory system of the brain. The difference is that during Alzheimer’s, the
formaldehyde penetrates into the axon of the nerve cell itself, attacking the basic tau protein within. This
process eventually kills the entire nerve cell, which cannot be replaced. In multiple sclerosis, it is the
protein of the myelin sheath, which is actually part and parcel of the Schwann cell, that is being attacked
and consumed by the activated macrophage. The axon of the nerve cell is spared at first, just as what
happens in acute methanol poisoning. To put this simply, Alzheimer’s is a disease of the nerve cell
(neuron), while MS really begins as a disease of the Schwann cell. Eventually as MS progresses the loss
of the protective sheath will result in breakage of the axon and repair becomes impossible.
Figure 1 shows a close up diagram of what the layers of myelin look like wrapped around the
axon. It reveals what happens as the myelin is devoured by hungry macrophages layer by layer, thus
exposing once protected MBP to marauding bands of crazy hawks, leading to its modification by
formaldehyde and its eventual consumption, finally exposing the unprotected living axon of the neuron.
Some considerable time is required to finally erode away the many layers of myelin. The fascinating
thing is that many Schwann cells survive these attacks and can and do regrow their myelin sheath.
Although once considered controversial, complete remyelination of demyelinated axons within even
large plaques has recently been shown to be commonplace.[#230] This explains the often complete
disappearance of MS symptoms during remission in many MS sufferers. In most patients with MS the
disease takes an up-and-down course with long periods of remission between attacks. This implies a
valiant attempt of the Schwann cells to rebuild missing myelin sheaths consumed by the macrophages.
[#151]
If we can stop the poisoning early enough – before too many axons break and Schwann cells are
killed and the hope for complete recovery is lost – by removing from the environment and food supply
the poison that causes it, methanol, then perhaps MS can actually be cured.

Figure 1
The microphotograph of a section of a small vein in Figure 2[#517] shows clearly the plaque formation
surrounding the blood vessels in a patient with early MS. The dark spots are macrophages eating away at
myelin. Figure 3[#517] shows cross sectional views of the same tissue that can be more easily compared to
the figures in the previous chapter of perivascular Alzheimer’s plaque. As time progresses and plaques
age and become larger, the unprotected thin axons may eventually break from lack of physical
protection, cutting completely all communications and leading to the atrophy of muscles and organs and
eventually death from lack of functioning of vital tissue.
Figure 2

Figure 3
Location, Location, Location

As you now know, human blood vessels are the location of much of the alcohol dehydrogenase class I
outside of the liver (extra-hepatic ADH). The intima and media of both the veins and arteries of the
brain contain ADH,[#220] which is capable of formaldehyde production from methanol. Once produced,
formaldehyde will tirelessly search for a basic molecule with which it can react. The travel distance of
formaldehyde within the human body is limited by its extreme reactivity. The formaldehyde hawks find
much to keep them busy close to their point of origin and will not wander further than their nearest
molecular prey. Yet it must always be remembered that formaldehyde is the smallest of molecules and is
capable of going anywhere very quickly if not distracted. Much like a real hawk, formaldehyde that isn’t
reacting with something is constantly on the move. Once formaldehyde is produced from methanol it
diffuses out, mostly in the acid form (crazy hawk), into the watery world of human tissue, hunting for
prey.
What this all means is that much of the damage from methanol poisoning will be found close to
home within tissue surrounding the blood vessels and in close proximity to the ADH sources. Only a
handful of diseases are well-known to conform to this “perivascular” modus operandi with most, if not
all damage clustered in sites surrounding blood vessels and, in particular, small veins. This anatomical
behavior has always been lacking explanation. The two most important of these perivascular diseases
are multiple sclerosis[#517] and Alzheimer’s. The reason that the vascular sites of ADH formaldehyde
production are so critical to the elucidation of both these diseases of the brain is that, other than these
sites within the lining of the cerebral veins and arteries, the brain is completely free of alcohol
dehydrogenase class I.[#218] In other words, the plaques of MS and the damage of Alzheimer’s only occur
in the precise areas where the ADH that converts methanol to formaldehyde is found.
The good news for many, but obviously not all, is that the brain also has very significant,[#327] but
genetically serendipitous, distributions[#216] of the good enzyme ADH III, which can destroy

While Science Sleeps© W. Monte (Prepublication) P a g e | 10
formaldehyde, turning it into the safe formic acid before it gets a chance to attack a basic proteins.
Formaldehyde is, therefore, produced only by the ADH I found in the lining of the blood vessels of the
brain and not in brain tissue itself.[#528] It is a short journey from the blood vessel, where the
formaldehyde is produced within the lining of the vessels themselves, to the locations where MS plaque
originates on the myelin sheaths of the numerous axons crisscrossing these vessels. It is noteworthy that
some of the very first damage shown in the natural progression of MS is a swelling (edema) and
thickening of the lining of these very vessels where the formaldehyde is produced, even before the
nearby myelin appears to be affected.[#517] It is again fascinating that this damage is identical to that
found in unfortunate individuals who die slowly from acute methanol poisoning.[#15] We can take this as
an indication that formaldehyde does some damage to other proteins on its way to finding a more
desirable nesting site like myelin basic protein (MBP). In Figures 2 and 3 MS can be seen slowly
progressing along the length of these small arteries and veins throughout the brain and spinal cord.[#517]
Please try to imagine flocks of formaldehyde hawk fledglings emerging from these blood vessels
into the circuitry of the brain. Imagine wave after wave of hungry hawks looking for protein to attack,
having to go further and further as protein landing sites are lost to competitors and then eventually
consumed by macrophages, slowly but surely expanding the plaque as the years go by (Figure 7). It is
worth noting that a single drop of diet cola sweetened with aspartame contains sufficient methanol to
produce well over a hundred trillion of these damaging crazy hawks. What exactly are the crazy hawks
attacking?
Figure 7
Details of Plaque Formation

Figure 7 shows us some older MS plaque with almost all of the myelin sheaths having been eaten away
by those cute little big eyed macrophages. This forces the crazy hawks, which, if you look closely, are
emerging from the blood vessel in the foreground, to fly great distances to find more protein to attack at
the war zone at the very edges of the plaque. What are the crazy hawks trying to find, and how do we
prove that they are indeed attacking that particular protein? In order for my explanation to go further you
need to learn a little something about one additional molecule that will prove to be an extremely
important part of our chain of evidence that will establish convincingly that MS is a disease of methanol
poisoning. But first a little background.

The Look, Touch, Taste and Smell of Multiple Sclerosis

I lived what seemed a lifetime in Wellington, Colorado in the years I spent earning my master’s and
doctorate degrees in Food Science and then Nutrition at Colorado State University. It was there that I
tasted multiple sclerosis for the first time.
I met her in my Urban Renewal office, where I moonlighted from my research assistantship at
the university to earn enough extra money to lead a decent lifestyle in that rough hewn western town on
the Wyoming border. She was a striking tall blond woman with the deepest blue eyes and a blistering
temper, and we became lovers in very short order. During the length of our relationship I lived with her
multiple sclerosis in a more intimate manner than any specialist in the disease usually do. There was
always a change in her that I could detect long before her suffering began, not in her mood or her
movement, but in her taste and smell. I cannot say it was formaldehyde, but if formaldehyde had a sister
it would have been that.
There is much more to multiple sclerosis then we may ever know, and we must be open to
accepting evidence from every quarter. I doubt that Nature is an adherent to the scientific method and its
null hypothesis.
The Kitchen Autopsy
One can never forget the vision of a scientist wearing a top hat and scullery apron bent over an
oversized kitchen sink with his bare fingers thrust deep into the freshly removed brain of one of his MS
patients. Jean-Martin Charcot, the discoverer of the disease, was notorious around the saltpeter institute,
where he was chief neurologist, to have had subjected the freshly dissected brain of a patient who died
from MS to a careful screening by running his fingers through the soft custard like tissue of her
untreated brain finding the long perivascular strands of leathery plaque that gave him the idea for the
name Sclerosis (French for leather-like). The image of him doing this is reproduced in a book on the
history of MS.[#306] One can only imagine how he first encountered this extremely important telltale
feature of the disease.
As the MS plaque grows larger, the formaldehyde hydrate produced in the lining of the blood
vessels has to travel further and further to find new basic protein to bind to. The lingering of the crazy
hawk as it wends its way to the outer reaches of the older plaque provides enough dwell time for some
of the formaldehyde to react with deeper tissue within the plaque itself. This reaction of the
formaldehyde with the already demyelinated plaque gives it a strikingly hard texture that is different
from any other tissue to be found in the brain. This is what formaldehyde hydrate does to tissue and is
one of the reasons that it is used for the tanning of leather and to plasticize other substances.[#446] The
original physical description of these areas by Charcot in 1846 might have led to a quick resolution of
the cause of MS, if only formaldehyde would have been known to science at the time.
Charcot would have no idea what formaldehyde did to tissue, for unfortunately, it was not until
1868, more than twenty years later, that Hoffman was to discover and name the highly reactive
substance so easily produced by passing methanol fumes over a platinum wire, (just as in my hand
warmer). It wasn’t until Ferdinand Blum was hired by the discoverer of formaldehyde to find uses for
the extremely dangerous compound that its plasticizing effect on tissue was elucidated and exploited.
But at that time it was considered to be a laboratory oddity and not discovered as a natural substance
until years later. Much valuable time was lost to ignorance. The trail of the small molecule as the cause
of MS grew cold and to this day is rarely revisited.

The fact that brain tissue is never touched with bare hands in the modern histology laboratory,
not even after it is soaked in a solution of formaldehyde for days, makes this type of observation
unlikely and esthetically barbaric to the contemporary histologist, who rarely removes the latex gloves
from his hands. It is a sad reminder of the physical removal of modern medical practitioners from the
real world of patients.
The Cause of MS is within the Thickening Blood Vessels

We owe a great deal to Dr. James W. Dawson, the Scottish pathologist who dedicated his professional
career to the microscopic study of multiple sclerosis. Prior to his death in 1927 from a lifelong
tubercular infection he published a detailed 230 page histological examination of tissue from nine cases
of the disease. Dawson’s Histology of Disseminated Sclerosis,[#620] published in 1915, applied modern
staining techniques that brought color and greater definition to the pathology of the disease. His work
reinforced the perivascular nature of MS, along with revealing the details of the considerable thickening
and damage to the walls of the blood vessels within the plaque. This well regarded work supplemented
the microscopic analysis published by Charcot himself and numerous other scientists over the previous
fifty years. Dawson’s outstanding critical review of the scientific literature and his own summations give
us a clear understanding and insight into the thinking of the medical community as to the progression
and causation of MS during the critical early days after the first cases of MS were being reported. The
noteworthy scientists of the early Twentieth Century were convinced that MS was caused by a toxic
substance that, to their great disappointment, was invisible to them. James sums this up nicely as
follows:
The supposition of a selective poison acting through the blood-vessels, which has
received the support of most recent investigators, is justified as an hypothesis but remains
undemonstrated as a fact. …This hypothetical toxin has not been isolated, but it is
suggested that it forms in the body. …It is admitted by all, except the supporters of the
developmental nature of the process, that the distribution of the plaque areas points to
the blood-vessels as the route of conveyance of this agent, and the assumption of an
intoxication harmonizes with this relation to the blood-vessels.”[#620]
Though no animal model is reliable for studying either MS or methanol poisoning, when rabbits
(one of the few animals used successfully to study some aspects of atherosclerosis in man) were forced
to breathe methanol fumes for 8 hours a day for several months, all developed a marked increase in the
thickness of their blood vessels similar to what is consistently noted in MS pathology. Dr. Eisenberg’s
microscopic examination of the rabbits’ circulatory tissues attributed the changes to “the actual
proliferation of the fixed tissue cells, as seen by the very marked thickening of the adventitia and media
of the blood-vessels.”[#15] Most telling of all can be found in one of Oluf Roe’s ground-breaking articles,
published in the early 1940s investigating a massive outbreak of methanol poisoning that killed and
blinded numerous of his countrymen. Roe made a profound observation while investigating the optic
discs of several of his poisoned patients. These men, one of whose age was only 32 years, had survived
between 6 and 12 weeks after their acute methanol poisoning. Dr. Roe, the father of the use of ethanol to
treat methanol poisoning, states:
There was at the same time marked irregularity of the caliber of the large blood vessels
with thickening of their walls. These changes resemble those seen in the blood vessels of
the retina in arteriosclerosis.”[#49]

As is often the case it is the earliest of scientific investigators that make the real breakthroughs in
discovering the cause of diseases. It is unfortunate that these great minds of the late 19th and early 20th
Centuries did not have a way to visualize or detect formaldehyde. Although it was Charcot himself who
first noted the thickening and obstruction of the small blood vessels of the MS plaque, it was Rindfleisch
in Germany in 1863 who first identified the constant changes of the blood vessels in MS and presented
what is today called the “vascular theory of MS.” He noted the “enormous thickening” of the vessel
lining within the plaque of the MS brain and proposed that whatever was being produced within these
vessel walls was the cause of the disease.[#230] What was being produced was formaldehyde.
Symptoms Mean Little unless they are Identical in All Ways…Then They Mean Everything!
We have spent time on the symptoms of MS in Chapter 6, showing how methanol kills. In summary, the
symptoms of multiple sclerosis,[#44],[# 83],[# 85],[#169] chronic and acute methanol poisoning,[#13],[#144],[#189]
and Aspartame toxicity[#54],[# 58],[# 93],[#181] are in all ways identical. Nothing that happens to the human
body from the toxic effect of methanol has not also been expressed during the course of
MS...Nothing.[#143],[#144] This generalization extends even to the remarkable ophthalmological conditions
common to both: transitory optic neuritis and Retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally manifests as unilateral temporary
blindness.[#85],[#138],[#163] In fact, these ophthalmological symptoms have been thought for years in their
respective literatures to be “tell tale” indications for the differential diagnosis for each of these maladies
independently.[#85],[#138],[#148],[#163],[#169] The common symptoms of headache,[#13],[#83],[#181],[#189]
nervousness,[#13],[#83],[#181] depression,[#58],[#83],[#189],[#181] memory loss,[#18],[#147],[#85],[#169],[#181] tingling
sensations,[#13],[#85],[#168],[#138],[#169] pain in the extremities,[#13],[#85],[#169] optic
neuritis,[#85],[#138],[#148],[#163],[#169] bright lights in the visual field,[#139],[#83] seizures,[#21],[#83],[#160] and
inability to urinate or to keep from urinating[#139],[#146],[#167] are all shared by each of these conditions and
shared yet again by complaints from aspartame poisoning.[#54],[#58],[#93],[#181]
I take these strikingly similar symptom patterns as evidence that these disorders act on identical
components of the central nervous system and in the same way. In the early stages of MS, or when a
non-lethal dose of methanol has been administered, blindness can occur often in just one eye. Complete
recovery is a possibility. The only two afflictions for which such dramatic “remissions” are reported
from identical neuromuscular and ophthalmological damage, including “blindness,” are relapsing-
remitting multiple sclerosis [#85] and methyl alcohol poisoning.[#138],[#163] The pathology of the two
maladies is in all ways identical, particularly when it comes to destruction of the myelin sheath with no
harm to the axon itself.[#18],[#148],[#176]
It is not unusual for the modern medical practitioner to put little credence in the similarity of
symptoms between disorders, and it is indeed true that certain very common symptoms, such as
headache and depression, can be caused by all manner of bodily changes. However, the breadth of
symptomatological overlap that we are putting forth here between methanol poisoning and MS is far too
robust to put to neurological coincidence. In total, they reflect a link that cannot be refuted with any
degree of scientific vigor.
Learn a Little About Arginine

There are several important questions that need to be answered when a poison is proposed as the cause
of a disease. The first is what is the exact chemical interaction between the suspected etiologic agent and
the biological molecule or molecules that initiate the disease process, and how can it be detected? For
years the stumbling block of DOC elucidation was the inability to detect formaldehyde. An important
new tool of scientific research, however, has recently made detection possible. To understand how this
works we need to understand something about protein.
Our bodies are made of cells that are works of moveable art composed primarily of water and
protein molecules. These protein molecules are the major constituents of all earthly life. The original
recipe for each of these fascinating structures is protected deep within the nucleus of the cells, never to
leave its safe haven in our lifetime. When a new protein is needed for repair or growth, that information
can be copied directly out of the recipe book – or chromosome, as it is called – as long as the DNA that
makes up the chromosome has not been previously turned off or methylated by formaldehyde (a methyl
molecule). Just as your mom would copy a recipe from her tired old cook book onto a slip of paper and
hand it to you to for reproduction in your own kitchen, so Nature scribes and passes out of the nucleus
such individual recipes to be made into protein to build and repair your body. It is a fascinating structure
called a ribosome that has the job of making each protein from the instructions on the recipe slip, putting
together the required ingredients.
The ingredients are primarily amino acids. Floating around in the liquid of the cell (cytoplasm)
are about 20 of these different amino acids, from which the ribosome can choose. These amino acids
constitute the chemical alphabet that Nature links together for performing all of the purposes of living.
One of these amino acids is called arginine. This is the most important amino acid for those of us who
have an interest in methanol diseases, and it will be the only one that we will take the time to study here.
If you are a chemist you know about the structure of the arginine molecule, but what interests us is its
behavior. Arginine is one of only three amino acids that are basic in nature and it is the only one that can
provide three different nesting sites for our acidic crazy hawk. This means that formaldehyde can react
with arginine and methylate it one, two, or occasionally even up to three times. Arginine is considered a
formaldehyde capturer.[#225] In fact, it is more than that – it is a trap for formaldehyde, and because of
this it can be a tremendously valuable formaldehyde detector, telling us if brain tissue has made contact
with formaldehyde. Thus, a molecule invisible for a hundred and fifty years now casts a shadow that can
bear witness to its unwanted presence.
But before we can see formaldehyde’s shadow, we must have a way to detect arginine as part of
a protein. For then we could take protein from the myelin sheaths of MS sufferers and see if the arginine
it contains has been modified by formaldehyde (or “methylated”). The good news is that we now have
such a technique. The bad news is the evidence has been lost on those sleepy scientists who did not
understand its significance. The story is a sad, yet hopeful one.
Myelin Basic Protein (MBP)

Myelin basic protein (MBP) is a major component of the healthy myelin sheath and, in fact, makes up
over 35% of its total composition.[#311] For many years this particular protein has been suspected as
being the one protein most negatively affected during multiple sclerosis. Because of this it has been
extensively studied. We know the exact structure of MBP; it is made up of 170 amino acids, 19 of which
are arginine molecules. MBP contains a higher percentage of arginine than any other human protein.
This extremely high percentage of arginine is what gives MBP its very basic nature[#41] and from whence
it’s name is derived. The Crazy Hawk, formaldehyde hydrate, is acidic and acids and bases will interact
if given the opportunity. The Crazy Hawk would be naturally attracted to MBP, bonding to its arginine
and eventually methylating it and leaving behind an excellent record of its presence as described above.

Even though changes in the MBP composition of the MS brain are considered the most
important chemical milestones of the disease’s progression, neurologists were surprised to discover that
MBP often completely disappears from the center of the MS plaque itself.[#707] Of greater significance
was the discovery of an incredible selective loss of this basic protein in otherwise normal appearing
tissue up to about a millimeter and a half beyond the edge of these plaques.[#311] If you use your
imagination to visualize the flight of the Crazy Hawks outward from their source in the vessels at the
center of the plaque, if the formaldehyde modification of MBP would activate macrophages, then its
phagocytosis (consumption) could account elegantly for the selective disappearance of MBP from
surrounding tissue.
Looking for the Shadow of Formaldehyde

A few years ago while living in a small oceanfront New Zealand village with a population of less than
100 souls, I met a young German couple, both PhD chemists, who rented a home down the street from
my cottage. We were quick to be friends and got together from time to time to discuss the chemistry of
methanol and formaldehyde. The young woman was kind enough to translate some of the early German
work done on methanol toxicity that I had in my almost complete collection of scientific literature on the
subject. New Zealand happens to be one of those countries of the world with an extremely high rate of
Multiple Sclerosis (the reason for which we will explain later), and so inevitably one day the topic of our
discussion turned to MS.
I explained how I believed that the disease could be caused by methanol’s transformation within
the lining of the veins into formaldehyde, which then modified the basic protein of the myelin sheath,
marking it for destruction by activated macrophages. I ended the monologue with my usual complaint
that the reason this had not been discovered was the absence of a reliable way to determine that a protein
had been modified by the little formaldehyde molecule. Without any hesitation my translator’s husband
informed me that in fact a new analytical method had been developed that could take large protein
molecules, break them up into smaller bits and determine accurately if a change had been made by even
a single formaldehyde molecule (one carbon atom) in any of the pieces.[#706] The equipment (an ion trap
storage/reflection time-of-flight mass spectrometer) was expensive, and it would not be easy to get time
on it, but he had a friend at a German university who had access to one and for such a purpose he was
sure he could schedule us the use of it. We immediately began putting together an experimental design
that could prove or disprove once and for all if methanol was the cause of MS.
The brain tissue of MS sufferers could be compared to brain tissue from normal individuals. If
we could show that the MBP from the normal brains contained arginine with little or no nesting crazy
hawks (methylation) and, therefore, prove they had not been attacked by formaldehyde, this would be
the first step. The second and most important step would be to test MBP from the areas close to and in
the direct path of plaque formation in the MS brain to see if indeed more methylation of the arginine
would be found there, giving us conclusive proof of formaldehyde modification. With that kind of
evidence, surely the methanol hypothesis would be impossible to ignore.
We would have to apply to tissue banks around the world that stored frozen brain tissue from the
cadavers of deceased MS patients and describe to their scientific committees our need for samples of
their valuable tissue to perform our experiment. We would then use this fascinating new analysis method
to determine if formaldehyde was setting the stage for the damage that became MS. Nothing else would
be as effective in determining whether formaldehyde was altering the brains of MS patients as
evaluating their brains for methylated arginine. Finally, we had found a way to prove methanol’s

formaldehyde as the cause of an important disease of civilization. We parted in a state of great

excitement. The real work started the very next day, with both of us hitting the computer and launching
an intense review of the literature so that we would be able to write out proposals to the laboratories
whose cooperation would be vital for us to carry out our research.
“Woody…They Have Done Our Experiment for Us.… But they Just Don’t Get It!”
I will never forget the call I received the very next day. My friend was so excited that he spoke in
German, and at first I couldn’t understand what he was trying to get across. I only knew it had to do with
what we had discussed the previous evening. The good news was that my German friend had found a
reference that led him to believe that our experiment had been performed eight years before, in 2002,
just as we had designed it. I asked him to email me the reference to the article so that I could read it for
myself. The title was indeed titillating: An Important Role for…Modifications of MBP in the
Pathogenesis of MS.[#224] The bad news turned out to be that those doing the study had not a clue of the
scientific significance or impact of what they had discovered. They had found gold and reported the
glitter, but they had no use for it. But the results will not be lost on your prepared minds, I promise!
Finding the Shadow of Formaldehyde in the MS Brain: The Smoking Gun (a triple blind study)
Although it is tragic when lives are lost to ignorance, Nature is, by definition, uncompromising and has
no inclination to follow the simplistic paradigms of man’s seriously flawed scientific didacticisms. The
natural world cannot be expected to be completely understood by even the most competent individual
investigator if that investigator is only trained in science, but not nature. Thus the results of any
scientific study can have many interpretations, the least reliable of which is very often the conclusion of
the extremely prejudiced corresponding author of the manuscript in which it is reported. Scientists often
only report what they were actually expecting to find, leaving any troublesome “outlying” data and
conclusions that may offend their peers in the editorial trash bin. This is why the more removed the
scientist is from the interpretation of his own data the better.
A single blind study is a scientific study performed on human subjects that are purposely kept in
the dark as to whether or not they are part of the experimental group (usually a group being given a
study medication or treatment, or suffering from the disease being studied) or the control group (usually
a group being given a placebo or a group that is reflective of the general population). In other words,
only the subjects are “blind” and, therefore, unable to purposefully or subconsciously act to skew the
results. When the researchers are also kept from knowing this information until after the interpretation of
the data, we have what is called a “double blind” study because both the researchers and the subjects are
“blind,” preventing either party from acting to affect the results. When researchers stumble on a result
that they were not expecting and that they cannot explain, I call that a “triple blind” study because all
pre-conception, prejudicial design, and ability to skew results has been removed, and the data is pure.
Just as a double blind study is better than a single blind study, I consider a triple blind study to bear the
most important fruit of all.
The original discoveries of the U-shaped curve that proved the protective effect of low levels of
alcohol consumption against various diseases of civilization were all reported reluctantly by researchers
who had discovered this association with no prior intent or expectation. These and other such
discoveries have been invaluable in the development of my own view of Nature. The collaborative work
done on MS brain tissue at the Department of Chemistry at the University of Michigan and the Hospital

for Sick Children in Toronto will probably be the most important of all such studies, and it appears that
their reporting was complete and flawless.[#224] They were merely looking for changes – any changes –
in the chemical composition of MBP between the brains of normal individuals and those with MS. Of
the hundreds of changes they could have found, the only ones worth reporting were the ones that
happened to show conclusively that formaldehyde was present in higher concentrations in the brains of
those who had died with the disease than in the brains of the control group.
The researchers gathered the MS tissue for their study from brain tissue banks in Canada and
Colorado. They carefully matched control cadaver samples by age and sex to normal brain samples
obtained from violent or sudden cardiac deaths not involving brain injury. The samples gathered from
the brain tissue of MS sufferers had well over twice the number of “Crazy Hawks” attached to the
arginine that made up its MBP as the control samples. The results were astounding and went beyond our
wildest dreams, for not only was the presence of formaldehyde verified by the large increase in arginine
methylation,[#200] but also another completely unsuspected outcome was reported. The phosphorylation
of the MBP was “dramatically reduced” by over 90%, going from 60 sites in the normal brain MBP to
only 4 in the MS samples. It is well known that formaldehyde inhibits phosphorylation at extremely low
concentrations.[#113], [#404]
Do you remember the young black girl whose tragic death gave us the critical number for the
minimum lethal dose of methanol in humans? Her dreadful last gasp for breath, which froze in vigor for
all eternity, was caused by the ability of formaldehyde to destroy the enzymes in her mitochondria that
cause the phosphorylation of ADP. By so doing, it robbed her of her ability to distribute life giving
energy from her metabolism. No other phenomenon can explain both of these astounding changes to
MBP in the MS brain; it can only be explained by the direct intervention of formaldehyde. It is well
known that the mitochondria in the axons of multiple sclerosis plaque show significant signs of damage
and oxidative stress[#481] similar to that presented during methanol poisoning.[#482]
Let me close this with a paraphrased quote from the authors of this revealing article that will help
you tie together the last two chapters.
Although we do not have an explanation for the state of hypophosphorylation (reduced
phosphorylation) at this time, studies in Alzheimer’s disease demonstrated that
uncoupling of mitochondrial oxidative phosphorylation resulting in decreased amounts of
ATP-activation… and other forms of phosphorylation in the Alzheimer’s brain.[#224]
Tragically the good scientists who performed our experiment for us knew nothing of the ways of the
Crazy Hawk. Perhaps if they had, their good work would have led to the end of the mystery of the cause
of MS and the beginning of the implementation of a real cure. Maybe now it can.
Evidence That Methanol Causes MS

MS Researchers Can Only Agree on One Cause for Multiple Sclerosis: Smoking
Science has been seeking the cause of multiple sclerosis for 150 years. In the early days of the disease it
was repeatedly suggested that significant evidence implicated a small toxic molecule[#153],[#185] – perhaps
a solvent.[#74],[#140] Methanol is the smallest of solvents and one whose poisoning symptoms are identical
to those of MS.
I will not take the time to go over all of the culprits that have been evaluated as a possible cause
for multiple sclerosis. Bacteria, viruses, and most disease-causing agents known to man have at one time

or another come under fruitless scrutiny. To this day, some still believe that MS is caused by a disorder
of the immune system itself or by a sexually transmitted entity.[#184] It is important to understand that for
very good reasons the original researchers in the field, well into the early 20 th Century, all held to the
belief that MS was caused by a circulating toxin which they could not detect or identify.[#153] Presently,
however, the most regarded theory of causation puts full blame on the darling little macrophage.
The good scientists who held that the cause was a circulating toxin were at great disadvantage.
Not only was methanol considered safer than ethanol at the time they were doing their laboratory work,
but also formaldehyde had not yet been discovered. Even after the discovery of formaldehyde,
researchers remained without any animal test subject for studying methanol poisoning and no way to
detect the chemical changes made by formaldehyde to protein. Thus, even if it had occurred to them to
do so, it was impossible to test the link between MS and methanol in the laboratory environment. In the
article that I mentioned in the previous chapter by the neurologist Dr. Fredrick Wolfgram, he asks his
collogues to reevaluate looking for a toxic cause for MS. The very last sentence of his conclusion is
noteworthy, valid and insightful to this day: “Do we have any evidence as to whether there is or isn’t a
low-molecular-weight compound in the brains of MS patients that disrupts myelin? The answer is: ‘No,’
because no one has ever bothered to look.” [#153]
It is of the utmost importance that you understand the significance of the fact that during the last
hundred and fifty years the search for a cause of MS has found only one culprit. The screening of
literally thousands of viruses, bacteria and toxic chemical substances has to this day elucidated only one
universally accepted causative agent for MS: cigarette smoking. Most significant of all, this one
etiologic agent also just happens to be an important source of methanol. Tobacco smoke has been shown
to cause both new cases of MS[#67-70],[#337],[#338],[#339],[#340],[#71] and to induce the relapse of MS in patients
who suffered from the disease but were in remission, transforming a relapsing-remitting clinical course
into a much more serious and deadly secondary progressive course.[#69]
Understanding where the methanol comes from in cigarettes requires some knowledge of how
tobacco leaves are processed into cigarettes. The leaves of the tobacco plant contain large amounts of
pectin; and although most scientists are unaware of this, tobacco leaves are left in barns to ferment for
weeks.[#61],[#62],[#66] This fermentation releases some of the available methanol from the pectin into the
leaf. Wood is then burned to flue-cure the tobacco. The smoke makes direct contact with the tobacco its
methanol-laden smoke soaking into the leaf, as the heat turns the tobacco a brilliant golden color before
it is sold to be made into cigarettes.[#65] Additional methanol is generated in the smoldering cigarette
itself as the leaf is burned. Consequently, methanol is one of the most abundant poisons found in
cigarette smoke.[#63] Methanol has been detected in human breath following smoking,[#64] indicating its
absorption by the lungs and presence in the blood.
Looking back to the first discovery of MS it would certainly be difficult to link the disease to
cigarette smoke, since the manufactured cigarette was not available in Europe until some time after
1860, when they were first being sold commercially in the United States. More important than this is the
reality that many of those who develop MS, even today, do not smoke and in many cases never have. It
is clear, therefore, that methanol has more sources than this one but smoking should be considered a
reliable source of methanol.

The Etiology of Multiple Sclerosis – Follow the Methanol

Every Disease has a Beginning, a First Performance – Just How Old is MS?
When an individual is suffering from the early stages of MS, it could easily be mistaken for many other
diseases; however, the ultimate symptoms and unusual gate of the full-blown disease are unique,
unmistakable, and so tragic as to still bring a tear even to my trained eye. Nevertheless, medical texts
from the Middle Ages contain no descriptions of any disease which would be recognizable as MS.[#230]
The fact that this obvious severe symptomology is completely absent from any historical or even biblical
literature is telling. Wolfgram even noted during his plea for the search of a small solvent as the cause of
MS that “there is a curious lack of reference to the obvious symptoms of MS in the medical literature
prior to the middle of the nineteenth century.”[#151] This is all proof that MS is indeed a disease of
modern civilized man.
It was the discovery of the controlled use of fire that brought man and methanol into potentially
dangerous proximity. In chapter two you learned that the smoke produced from the burning of plant
material contains methanol. The impact of this methanol was probably minimal, depending on the
relationship between various cultures and how they chose to use fire – and more importantly, its smoke.
The smokeless flame of a clean burning wood fire contains no detectable methanol, as the blue flame
represents the burning off of methanol. Charcoal is wood that has been heat treated in such a way as to
remove all methanol and is safely used by many cultures for indoor cooking with no methanol risk. The
cultures that developed a taste for food smoked for preservation purposes were probably the first to feel
the sting of methanol disease, in the same way that today individuals who smoke cigarettes laden with
methanol notoriously suffer from a higher incidence of all DOC.
It was not until the development of the canning of fruits and vegetables in the early eighteen
hundreds that methanol was to begin its slow progression toward becoming a daily component of the
diet of the civilized world. The daily consumption of methanol would be an important prerequisite for
the continuous, unrelenting demylination that consistently exceeds the ability of the Schwann cell to
rebuild itself, eventually leading to the complete removal of axon protection that presents as MS.
The History of Man’s Methanol Consumption Corresponds to the History of MS

It is the Frenchman Nicolas Appert, the inventor of canning in 1807, who must take responsibility for
beginning a process that was to eventually bring methanol into every civilized household throughout the
mechanized world. By following the ebb and flow of the canning industry and the consumption trends of
canned fruits and vegetables since those early years we can learn a great deal about the evolution of MS.
The first canning factory was fully operational in England by 1813.[#46] Due to the expense
involved in the production of the cans themselves, early canning was undertaken primarily with high
value meats, which have no pectin content and, therefore, would not have caused methanol
accumulation. Canning of fruits and vegetables, however, quickly followed as the wealthy acquired a
taste for these products out of season. Over time canning became more prevalent and less expensive,[#46]
and the per capita consumption of canned plant material skyrocketed – as did the incidence of multiple
sclerosis. As the canning industry flourished so did the practice of incorporating into recipes the
“natural,” methanol-laden juices from canned fruits and vegetables rather than discarding them.
Canned fruits and vegetables were, for many years, the major food source of methanol in the
human diet. In the years that have passed since caning's humble beginnings, MS has transformed from a
medical curiosity to one of the most important and common of the DOC. For 150 of the last 200 years
the very best indicator of incidence of the disease in a population would have been the weight of canned
fruits and vegetables consumed by the average citizen of the country being surveyed.
The incidence of MS increased slowly after its symptoms were first put to pen in the diary of the
grandson of King George III in 1822. We see no official mention of the disease again until ten years
later, when its anatomical details are depicted in a book of medical illustrations published in England by
Robert Carswell in 1832. This was a time when canned fruits and vegetables were quite expensive and
available particularly to the rich. The first officially documented case of multiple sclerosis was reported
nearly 35 years later by Jean-Martin Charcot in a lecture in 1868 (discussed below),[#45] although it is
generally agreed that the “first identifiable instance of MS” was that of Augustus d’Este, whose
symptoms started between 1822 and 1843.[#45] During the 19th Century MS was considered “quite rare,”
with Charcot reporting fewer than 40 cases during his long career.[#45] Increasing numbers of cases were
reported in the late 19th Century.[#45]
During this same period it was discovered that if wood was heated in a large metal container it
would produce a smoke that could be condensed into a dark foul smelling liquid called wood alcohol,
the original name for methanol. The use of wood alcohol as a solvent for many industrial uses as a
replacement for the much more expensive ethanol began about that time and, in fact, Paris was the first
large city that would take advantage of the convenience of this liquid fuel, which was easier to transport
than wood and could be used as a cooking fuel. It wasn’t long before the rich had methanol burning
stoves which, under conditions of poor ventilation, were responsible for exposing kitchen help to
methanol fumes. It may not have been a coincidence that the first time multiple sclerosis was to be
described in detail in a scientific publication was in 1865 by Jean Charcot of France. His first case was
his own kitchen servant, whom he had convinced to donate her body, after her death, to his research.
The Early Years of the Multiple Sclerosis Timeline

 No evidence exists to suggest that MS is an ancient malady.
 MS was unknown until some time after Nicolas Appert of France invented canning in 1807.
 The first identifiable instance of MS was not until around 1822 (Augustus d’Este, Grandson of
George III).
 MS was first illustrated in drawings done by Carswell in 1831.
 MS was first described in detail, but as a “rare” disease, in 1865 by Jean Charcot of France.
 MS remained uncommon until the 1890s, when the combination of several factors that increased
contact with methanol coincided with the disease becoming common, with variable frequency.
 The beginning of the epidemic of MS over “the last 30 years” coincides with the introduction of
Aspartame.
An Explosion of Methanol and Disease: The Turn of the 19th Century

The year 1865 was a noteworthy year for methanol in that it marked the end of the Civil War in the
United States. It was during this long war that Union troops were often fed canned fruits and vegetables
as sustenance while they were in the field. This was their first introduction to such delicacies, and they

were greatly impressed. When the war was finally over, the soldiers brought home with them a ready
appetite and market for the fledgling canning industry.
The invention of automatic machines that could make canned fruits and vegetables faster and
cheaper than ever before slowly brought canned methanol-contaminated plant products into every home
of the United States. It was at this time that the Ball family developed heat resistant jars that could be
used by any homemaker to put away fruits and vegetables from their own gardens. Add to this the
discovery in 1895 of a method for making the bad-smelling and -tasting wood alcohol look and taste just
like ethanol. Subsequently, this new methanol began to be used as a substitute for ethanol in many
industrial applications, such as in solvents used to make fast drying glues for the leather and shoe
industry, and as an additive in many cough syrups and foods extracts, such as vanilla. It is easy to see a
correlation between the steady acceptance of MS as a “common” disease during the first twenty years of
the 20th Century and the steady increase in the methanol in the environment and the diet during the very
same period of time. Meanwhile, some of the most intensive testing of the safety of methanol was being
conducted in laboratories throughout the world, on every animal except man, and they all proved that
methanol was safer than any other alcohol.
Up until the early 1880s the cigarette was a specialty item made by hand, sold for a penny
apiece, and very much the stepchild of other tobacco products, such as snuff. But in 1883, an automated
cigarette rolling machine, developed by James Bonsack, was put into use, revolutionizing cigarette
production. The retail price was cut in half, and volume, which in pre-machine days had never exceeded
500 million, leapt to 10 billion by 1910 in the United States alone. There is no doubt that these few years
between the nineteenth and twentieth centuries saw a sudden explosion in the incidence of all of the
diseases of civilization, of which MS is a prominent member. This was also a time when the
consumption of methanol, not merely from cigarette smoking, but from many different sources,
increased dramatically in both the diet and the environment.
Innovations at the Turn of the 19th-20th Century that Increased Contact with Methanol
 Use of methanol for heating in Paris kitchens replaced dangerous wood burning stoves.
 Machine-rolled cigarettes increased smoking by a factor of 20 in less than thirty years.
 Use of methanol as a solvent for fast drying glues in the leather and shoe industries rose dramatically
in shoe making centers such as Italy and New York.
 Home canning of fruits and vegetables was becoming extremely popular after the American Civil
War; the returning troops loved the idea of eating fruits and vegetables in winter.
 Machines made cans extremely inexpensive and plentiful, and canned fruits and vegetables cheaper
than fresh and available all year long.
 Tests on all animals proved methanol was safer to drink than ethanol.
 Methods for purifying and removing bad odor and taste of wood alcohol were developed.
 Methanol was allowed and frequently used in place of ethanol in food extracts, many medicines, and
body salves, including witch hazel and other body ointments.
A Food Scientist’s Nightmare Called Aspartame

The symptoms of multiple sclerosis, chronic and acute methanol toxicity, and aspartame poisoning are
in all ways identical because they all reflect slight variations on the same theme. Nothing happens to the
human body from the toxic effect of methanol that is not also expressed during the course of MS – not
one thing.
Thirty years ago as Professor and Director of the Food Science and Nutrition Laboratory of
Arizona State University I was unwittingly thrust into the aspartame debate with a great deal of publicity
that accomplished only two good things. First, it brought to the public’s attention the fact that a problem
of some kind was associated with the new artificial sweetener. Second, it established me as a contact
person with whom the public could share their experiences and information.
The calls from consumers started coming to my office at such a rate that for over six months I
had to enlist student volunteers to man my telephone when I was in class or working in my laboratory.
By far the preponderance of complaints were from women, and these reports consisted mostly of the
classic symptoms of early MS.[#58] Some even sent me MRIs depicting images one would expect of MS.
I would talk directly to as many as my schedule would allow and encourage all who complained to stop
their consumption of aspartame, suggesting that if they felt brave enough, that they wait a month and
then resume consumption and share with me the result. Nearly every time, the symptoms disappeared
within a week after aspartame consumption was stopped. Those who had the courage to retest all
reported a return of symptoms in varying degrees of severity.
On one very notable occasion I was sent a clean MRI from a girl who had stopped diet soda for a
year and whose prior MRI showed massive signs of MS. By the way, MRIs taken in the early stages of
MS do not show demylination; they show edema in places where the high-fat brain tissue is being
displaced by the microglia (the brain’s macrophage) and the liquid of inflammation. That was what this
girl’s initial MRI had shown. At that time, MS was not within my scope of research, so when I had
heard enough I made contact with the headquarters of the National Multiple Sclerosis Society in New
York City and got the ear of their director of research. I shared with him, with the enthusiasm of a young
scholar, why I thought that methanol might be the cause of MS. He asked me to send him what evidence
I had, which I did with dispatch. To make a long story short, I never received even the courtesy of a
reply to my extensive report and was never allowed to talk to him directly again. Medical researchers
hate anecdotal information. The reasons for this are clouded in the evolution of a scientific mindset that
specifies data must be generated in the perfect laboratory environment. Unfortunately, this approach
does not work well in the absence of suitable animal test subjects in the laboratory.
In 1984, I published my first scientific article about the sweetener: Aspartame; Methanol and the
Public Health.[#1] In the article, I voiced my concern about the new sweetener and the fact that it was
increasing the methanol content of the food supply – but made no mention of multiple sclerosis.
Publication of the article, along with more publicity over my lawsuit against the Food and Drug
Administration (FDA) (which eventually made its way to the US Supreme Court), brought a flood of
additional calls and letters to my office from individuals who thought that they had been poisoned by the
product. Many of these individuals also had symptoms of multiple sclerosis and some, in fact, were
being tested for the disease. A local doctor also visited me to ask whether I thought his patients’
consumption of large quantities of diet sodas in the intolerably hot Phoenix summers might be
connected to their complaints about symptoms of MS.
Looking into the scientific literature I discovered several articles suggesting that I was not the
first to identify methanol as the possible cause of multiple sclerosis. Dr. Hugo Henzi, a Swiss physician
who, during his long career, cared for many MS patients, had been struck by the similarities of the

symptoms of methanol poisoning and MS. Henzi’s work consisted of a book published in 1980[#5] and
three scientific articles[#6],[#8],[#10] that have never been referenced in any MS publication, save my own. I
realized that aspartame had provided us with a way to track the public health to the quantitative change
of methanol in the food supply. For all intents and purposes, aspartame was methanol, and I had
consumption numbers for it. Ending the circumstantial nature of the etiological basis of methanol as the
cause of MS would serve as good news for the future of world health, though it would provide little
comfort for the innocent populations that had submitted to the Mangle-like enterprise that was the
aspartame industry.
Unfortunately, it would take many years for the MS disease statistics from increasing aspartame
consumption to build. When the data became available I was ready. I procured from the Centers for
Disease Control its multiple sclerosis incidence data for the United States during the period that
consumption of aspartame was building. This was data that could have quickly been made available to
the Multiple Sclerosis Society. Figure 4 plots the data in a linear manner just as we did for Alzheimer’s
disease in the last chapter. The data certainly appears to indicate a marked upward trend in the incidence
rate of MS beginning early in the 1980s. In order to get some indication of the strength of this trend I
have created another graph of the same data.
Figure 4
In Figure 5 I have had the computer draw a trend line, sometimes called a linear regression line, in
heavy black that shows more clearly the direction of the trend of the incidence of multiple scleroses
during that important period of time. Just as I had feared, the incidence had gone up 60% during the first
decade following the introduction of aspartame.
Figure 5

MS usually takes about ten years from first onset of symptoms to reportable diagnosis of the
disease.[#86],[#167] This early reporting was evidence, to me, of much worse to follow. How long did it
take before the deaths from MS caught up to the consumption of methanol from aspartame? The issue of
the death rate from MS has been a very important topic in neurology, particularly with the report of the
steady decrease in MS deaths that was observed in the United States during the entire 1970s.[#710] This
decline would reflect a continuing decrease in smoking among young adults, as well as a clear change in
preference of US consumers for cleverly marketed and delicious frozen fruits and vegetables, which
began attracting consumers’ attention away from the high methanol canned alternatives, beginning in
earnest in the 1960s. The neurological community was taken aback by the clear and apparent reversal of
this trend during ten-year study period beginning in 1990, with a dramatic and steady increase in the
death rate of MS throughout the period. Their concerns were justified, considering, as the investigators
themselves noted, that the treatment of the disease had actually improved since the earlier study.[#214]
What they do not mention is that their study was performed just ten years after the introduction of what
would be the most important source of methanol in the human diet. This allowed for plenty of time for
the added methanol to take its toll on those already suffering from the disease.
I have plotted the data from this study on our usual graph so we can compare the death rate from
MS, as we did from Alzheimer’s, with the consumption of aspartame. The results are again breathtaking.
The mirroring of the two curves is obvious, although expressing a gap of ten years as compared to the 14
years it took Alzheimer’s deaths to catch up with increased methanol consumption from aspartame. You
will notice that the MS death curve is not quite as smooth as the Alzheimer’s curve, but this comes from
the much lower number of people who die each year from MS as compared to Alzheimer’s, which has a
death rate over ten times higher than that of MS. One can, however, have absolutely no doubt as to the
strong upward trend throughout the entire study period.
Figure 6
MS: A Disease of Colder Climates and Flush Toilets – Before Aspartame

A number of unusual theories about the origin of Multiple Sclerosis have come directly from the
scientific literature. To my mind the silliest of all is the present speculation being acted upon by some of
the most influential of the world’s pharmaceutical companies: that the innate immune system is its
cause. Let me volunteer here, in the spirit of full disclosure, that some of my very closest friends are
macrophages, a fact which I admit may cloud my thinking. But in all seriousness when a scientific thesis
known as the sanitation hypothesis[#85] comes right out and faults proper sanitation as the royal road to
multiple sclerosis and correlates the number of flush toilets in a community to the long term disease
incidence, it should give one pause. This is particularly the case when the assumptions on which it is

based appear to be, etiologically, the most reliable proposed to date by the sum total of the neurological
research establishment. If this scares you, then you may not have the stomach to be an MS scholar. No
matter how misguided, the present medical establishment will consistently reference the most
challenged of theories of MS origin – so long as those theories have nothing, whatsoever, to do with a
food origin for the disorder. This prejudice against the dietary origin of this disease (or any disease) has
always been a serious handicap of the medical community.
By now, if you have read the supporting literature referenced here, the most skeptical among you
would have to find at least some merit in the possibility that methanol just might be the cause of MS. I
will not waste time reiterating the massive amount of literature on this disease. Other fascinating facts
about its distribution across geographical locations, occupations and gender need explaining, along with
the changes in all of these categories that have accompanied the revolutionary introduction of the
sweetener aspartame. This evidence is circumstantial, but still has considerable merit and is worthy of
both your time and consideration.
One thing that you can take away from the latter part of this chapter is important: MS was once
considered to be a “rich man’s disease” in that its prevalence was positively correlated with the
trappings of civilization, including modern sanitation practices.[#85] It is a universal truth that the
economically poorest among us – those who cannot afford toilet paper, let alone toilets themselves,
those who farm only or forage for all of their sustenance and cannot afford canned fruits or vegetables or
cigarettes or diet soda or any other methanol-containing mark of civilization, those poorest of the poor
who still make up an alarmingly large percentage of the world’s population – are free from autoimmune
diseases such as MS.[#168]
A World Awash in MS After Aspartame

Aspartame and cigarettes have two ignoble distinctions that they share. The first is the inordinate
amount of money spent by their manufacturers for seriously compromised science,[#249] political
influence and extravagant advertising campaigns to assure the public of their safety. The other is both
are substantial sources of methanol without any significant redeeming ethanol protection. They stand out
in this latter regard, as no other such naked methanol sources could be listed as common consumables.
The epidemic of multiple sclerosis and other autoimmune disease throughout the world over the
last 30 years cannot be denied.[#79],[#337-346],[# 80],[# 347-349],[# 81],[#350],[# 82] Multiple sclerosis, once almost
unknown in Japan,[#44],[# 85],[#168] has now risen to menace a large portion of the population.[#81],[#350] The
lower latitudes and warmer climates, which once “mysteriously” protected people from the full brunt of
this tragically debilitating disease,[#83],[#85],[#168] have seen incidence and prevalence of MS climb to as
much as four times what they were in the days before summer drinks were sweetened with
Aspartame.[#79],[#338],[#340],[#342],[#343],[#344],[#345],[#80],[#347],[#348],[#349] The United States, which has long had a
relatively high MS incidence, has seen at least a 50% increase.[#77] Medical journals in Australia[#82] and
New Zealand[#90] both report unexplainable increases in their inordinately high[#168] “infection” rates.
I believe that just telling you this information is not going to convince you. My experience has
shown that for most people, that is just so many words. In order for you to be convinced of something as
important as the methanol theory of MS causation you need to take a little walk in my shoes. What I
have done is put together a short slide show, reproduced as Appendix 1, in which I present the literature
that I just described above, in an annotated fashion, right out of their respective scientific journals. You
will find their reference numbers in parentheses on the lower left corner of each slide. Please take the

time right now to read through this personal slide show made just for you, and I will be waiting right
here for you when you return.
As you can see, all the available data does show that the incidence of MS in the United States,
and eventually the rest of the developed world, has clearly increased, and that increase appears to have
begun with the introduction of the methanol-containing sweetener aspartame in July of 1981.[#194][#586]
Spend some time reviewing the maps done by Dr. John F. Kurtzke on slides 10, 11 and 12. John is a
physician whose life work has been the epidemiology of MS. He drew these maps at different times
during his career. When dealing with such depictions of data, it is a very important consideration that
they are all produced by the same competent individual and to the same standard. We will talk more
about John’s work on the Faroe Islands later. Pay particular attention to the increase in MS incidence in
the warmer climates. The growth of the disease into Mexico and South America is easier to see, but have
a close look at Europe, where the entire northern Mediterranean basin is now an area of high frequency,
and where all of Italy and both Portugal and Greece are now also subject to a high frequency in the
disease.[#195] John calls this “diffusion,” and that is very descriptive, but to my mind it is all linked
directly to the success of the marketing of carbonated diet beverages containing aspartame throughout
all of Europe and, interestingly enough, the Netherlands. The second largest aspartame production plant
in the world (Japan has the largest) had to be built in Italy in 1985 to supply the tremendous demand for
the methanol-containing products by the burgeoning European market.
One last word about the marketing of diet soda – the advertising blitz throughout the South
American countries of Brazil and Argentina was noteworthy and appealed quickly to the narcissistic
tendencies of those countries’ weight-conscious populations, a fact which probably accounts for the
increase in their MS statistics. The enhanced importance of this unexpected increased incidence[#77] is
that it reversed a clear trend that had been going on for ten years during the entire 1970s[#214] which,
looking back, appeared as an apparent consequence of the reduction of smoking with the increased
awareness of the health implications of tobacco smoke (which, as mentioned in Chapter 2, is the only
known cause of MS). It took about eight years of exposure to aspartame before the death rate from MS
began to dramatically reflect the increase in incidence.[#214] The increase in death rate is an eerie mirror
image of the graph of the increase in the consumption rate of aspartame and, therefore, of methanol (see
Figure 6).
The only logical explanation for an increase in multiple sclerosis in the warmer climates would
be an increase in the exposure to the causative agent. If that cause was methanol, then that implies that
something consumed in warm climates would have to have had its methanol content increased
dramatically. Before the summer of 1981 no diet drinks contained any methanol. Beginning that
summer, only powdered drinks had aspartame and, therefore, methanol added to them. These drinks had
to be mixed with water and were marketed mostly to women who had a kitchen available to them most
of the day. In the fall of 1983, after I lost my bid to prevent aspartame from being approved for uses as
an artificial sweetener in carbonated beverages,[#56] the methanol content of diet drinks began an upward
trend which was eventually to lead to their exposing consumers to more methanol than canned fruits and
vegetables[#1] – or any other food, for that matter. This trend definitely increased the general
consumption of methanol in warm climates.

Change in Frequency of MS by Sex: The Methanol Source – Food or Smoke – Makes All the
Difference
Modern women bear the brunt of the multiple sclerosis epidemic.[#351],[#352],[#353] Presently three or four
women get the disease for every man who does. We have become used to the reality that MS is a
women’s disease and, as you saw in the slide show, it is becoming more and more of a women’s disease
as time passes. It appears that each survey that is done and each study that is repeated finds ever greater
numbers of women over men who suffer from the malady.[#91] It has not always been this way, and the
ratios appear to have changed considerably over time with no apparent reason; however, an explanation
is indeed easy if methanol is what causes MS.
Well into the turn of the 20th Century, with the concomitant introduction of methanol into the
environment and food supply, the incidence of MS had already grown from that of a rare disease and
medical oddity to one of greater prevalence. Before long, it became the subject of much organized
medical research and discussion. The group of nine neurologists who made up the New York
Neurological Society met to discuss MS in 1902. Recorded in the minutes of that meeting was a general
agreement that MS was a rare disease in New York.[#153] MS increased dramatically (over 140%) in
Germany and Switzerland between 1906 and 1940.[#153] In 1921 this sea change prompted the American
Association for Research in Nervous and Mental Diseases (ARNMD) to theme its annual meeting in
New York City Current Knowledge and Research on Multiple Sclerosis.[#306] The two day meeting
featured presentations on the pathology, epidemiology, etiology and clinical features of the disease and
were published the following year. The organization also captured a consensus of the understanding and
state of medical research on MS presented by the gathered researchers and clinicians. The conclusions
emphasized that MS was among the most common organic disease of the nervous system and that its
cause was some “unknown toxin.” Most important of all the organization concluded that “males are
attacked more often, with a male: female ratio of 3:2” and that the disease occurs more in “skilled
manual workers than laborers.” It was at this meeting that it was also first noticed that MS is more
frequent in the colder climates of both the United States and Europe.[#306]
How methanol gets to the brain makes all the difference. If you were a skilled leather worker
employed in one of the many shoe or leather factories in New York City or other major industrial
centers of the Unites States during the early 1900s, methanol would be an ingredient in the glue and
treatments you used and you would be breathing in these fumes during the work day. This would also be
the case if you were a painter or one of any number of other occupations which used cheap methanol as
a solvent or to clean surfaces before finishing. If you smoked cigarettes, as many men did during this
time period when cigarette smoking was increasing tremendously with the advent of cheap addictive
automatically-rolled cigarettes, then you would also be exposed to steady amounts of methanol. These
occupational and recreational sources of environmental methanol would supplement the methanol to
which both you and your wife were exposed at the evening meal when she opened up a few cans of
vegetables and heated them up with the juices for your supper.
The details of how methanol reaches your brain differ, depending on whether you are getting
your methanol via your lungs or in your diet. It is this difference that accounts for all of this tweaking of
the sexual ratios of MS and some of the other DOC. All is sexually equal when methanol comes from
cigarettes or exposure in the workplace air supply or via environmental fumes. Methanol entering the
lungs goes directly into the bloodstream equally in both sexes. It is when methanol enters the body via
the food supply that things get really interesting, and is what accounts for the difference across sexes in
incidence of MS.

A modern study published in the New England Journal of Medicine[#94] reports the result of
biopsies of the gastric lining of men and women. The astonishing result proved that the concentration of
ADH in the gastric lining of men was much higher than that in women. Men, therefore, have the
advantage of having large supplies of ADH busily removing methanol from their food at a rate that is
four times faster on an equal-body-size basis than women’s bodies can remove dietary methanol. [#94]
The methanol that men consume, both in the food they eat and the diet soda they drink, is four times
more likely to be removed from the blood before it ever reaches their brains. The male brain is spared
the onslaught by the Crazy Hawks because the methanol is metabolized to formaldehyde in the gut
where it can reap its havoc on a more forgiving organ that has a considerably greater regenerative
capacity. Finally, we have an explanation for the disparity between men’s and women’s reactions to
methanol poisoning and the diseases it causes. This may also help to explain why men have more
gastrointestinal complaints from both methanol and Aspartame consumption.[#93],[# 99]
The importance of this cannot be overstated. Those presenting their patient reports at the
ARNMD meeting were reporting on a preponderance of victims from the occupational exposure to
methanol in the workplace and smoking. Certainly, women were suffering from their dietary exposure,
but their disadvantage to methanol toxicity was overshadowed by the industrial exposure and smoking to
which their male counterparts were much more likely to make contact. During this time the use of
methanol in the workplace was being investigated and was receiving considerable negative press, with
the result that laws were eventually passed restricting its use and requiring warning labels be placed in
plain site wherever it was stored.[#17] As time passed methanol was reduced in the workplace but,
unfortunately, not banned completely. The consumption of canned fruits and vegetables literally
skyrocketed as canned foods became less expensive and more acceptable. Additionally, home canning
of all manner of plant produce increased between and during the two world wars.
In the 1940s, just two decades after the ARNMD meeting, the National Multiple Sclerosis
Society found the incidence of the disease to be virtually equally distributed between the sexes. In the
1960s, professor Schumacher found that slightly more women than men were contracting MS.[#306] The
‘70s reversed completely the ARNMD ratios, with every series reporting women being more frequently
affected than men, with the usual ratio being three woman to two men.[#169] By the early 1980s the
number of women with the disease rose just a little higher with 1.7 women to each man who had the
disease.[#166]
But the real sea change in the incidence of MS in women did not come until after the
introduction of a brand new methanol source never before known on our planet or found in our food
supply. A can of diet soda sweetened with aspartame has up to four times the amount of methanol as a
can of green beans. Worse than that and of much greater significant is that while one would have
difficulty consistently consuming six cans of green beans or tomato sauce a day for any length of time,
in places like Arizona, Australia or Mexico such consumption of thirst quenching, good-tasting calorie
free liquid would be commonplace and has now become customary. The great human health experiment
that was begun in 1981 took a great leap forward with the sweetener’s allowance as an ingredient in
carbonated beverages in 1984, and is going strong right now with aspartame costing much less than
sugar to sweeten. The result of all of this was presented at the 59th annual meeting of the American
Academy of Neurology in Boston on April 26, 2007.[#351] Dr. Gary Cutter, professor of Biostatistics at
the University of Alabama, said women are now four times as likely as men to get multiple sclerosis: “It
started at two-to-one and is now four-to-one.”
The increase is more pronounced in younger people, with young women especially contracting it
at an accelerating rate. “This rapid change suggests that it’s not just the disease behaving as usual,”

Cutter said. “It is unfortunate, but it is an opportunity and we can use this information to learn what
directions we ought to pursue.” Nicholas LaRocca, a VP at the National MS Society, said, “This is an
interesting phenomenon, and I’m not sure anyone knows why it’s happening.”
MS is going through the roof and nobody knows why! As a statistician, Professor Cutter deals
with numbers. We thank him for his fine research. But to the victims of this dread plague it’s more than
“unfortunate,” and more than “an opportunity” or “an interesting phenomenon.”[#91]
It is interesting to note here that 3:1 is the sexual ratio represented by adverse reactors to
aspartame reported by the US Center for Disease Control in its study of serious aspartame health related
reactions in 1984.[#58] The Center found three women to every man whose aspartame consumption
complaints were serious enough to warrant investigation.[#93] Women’s complaints also more frequently
involve serious neurological complications that are identical to those of MS. The Centers for Disease
Control could not put 2 and 2 together and claimed they could not see a “constellation” of symptoms
that would cause them any concern about the new additive. This was after a very unusual two month
delay in the release of the report to accommodate an emergency “executive review” of the original
document. The executive review has never been released.
Can Methanol Really Cause MS?

The evidence that the formaldehyde produced from methanol causes multiple sclerosis is overwhelming
and would be very difficult to refute, particularly if you are debating me, but unfortunately it can be
ignored – and has been.
Back in 1990, after the Federation of American Societies for Experimental Biology refused to
allow me to give an oral presentation at its annual meeting, I agreed to present a poster session showing
a rat model of MS using methanol to damage axons.[#2] I decided I would personally give the
presentation, not wanting to put any of my graduate students in a position to take the heat for something
that was not merely controversial, but perhaps more importantly, something which could impact the
financial stability of many junk food and pharmaceutical goliaths. I had prepared myself to face the
toughest questions and was, in fact, anxious to debate the issue as to whether methanol was indeed the
cause of multiple sclerosis. To my surprise, however, I was relegated to what turned out to be a very
remote corner of a satellite presentation hall with a few dozen foreign graduate students, none of which
could converse easily in English – and no one came. It was as if my presentation had a little note
attached that warned of the possibility that serious bodily harm would come to any who attended. Our
data was submitted to various research publications, in one case several times, but was always refused
without consistently remediable comment.
The fact is, sufficient information already exists in the scientific literature to show convincingly
that long term exposure to methanol will invariably increase the incidence of MS in human populations,
and conversely, to show that the absence of methanol is an important precursor to an MS-free
population. Let’s take a look at that fascinating data and you can decide for yourself.
MS Can be Found in Some Places, but Cannot be Found in Others

Places Where MS Isn’t on the Menu
You can find locations on this planet where MS simply does not exist. This alone should give hope to
those who have the disease. The people who occupy these special places are, for all intents and

purposes, made of the same stuff as those who are prone to contracting MS. It has been shown that when
they immigrate, at an early enough age, to environments that do foster the disease and they eat the food
and drink the water and breath the air of their new environment, they acquire the same risk of the disease
as everyone else.[#44] The good news from this is that it isn’t you. It is something in what you eat, drink
and breathe that is the cause of this disease.
The places where MS is nonexistent or extremely rare can change rather quickly, as we have
seen happen over “the last thirty years.” This is even more evidence that the disease is not part and
parcel of the sunlight or the geography of these sanctuaries, but is strictly part of the changeable
environment of food and air. We know that MS is absent from places where the majority of the
population lives directly from nature with little or no access to or need for canned fruits and vegetables
or diet products containing aspartame. Though the scientific literature points to tropical areas or areas of
extreme poverty (where the laughable but statistically valid sanitation theory was born), these MS-free
zones have never been strictly limited to the warmer, poorer countries of the world. The exceptions are
glaring and can teach us something about MS.
Although central Africa,[#184] Mexico, South and Central America, and good part of India did fit
into the MS-free category in 1979 when Dr. Kurtzke produced his excellent MS distribution map,
important exceptions to the warm climate rule could still be found. The Inuit or Eskimo people of
extreme northern Canada have rarely known MS, and those who still maintain their customary diet
remain free of the disease.[#169] Japan is an example of a country which once enjoyed the lowest MS rate
of any civilized country in the entire world, and yet it is extremely affluent, without a tropical climate,
and has extremely high standards of sanitation.
All we need do is take a look at the diet of the Japanese people and we can lay to rest this whole
muddled issue of the epidemiology of MS. The Japanese are sticklers for eating fruits and vegetables
fresh and in season. They would not even consider opening a can of green beans or any other such
canned plant product. Even though they do have a thriving canned food industry, it is primarily the
canned fish and marine mammals that are canned for domestic consumption. The canned fruit and
vegetable products make up a small part of the industry and are essentially all produced for export.
Furthermore, the Japanese consume a consistent quantity of fermented foods which are abundant in
ethanol, another great advantage that protects the population from methanol. In 1960 the prevalence of
MS in Japan was a little over 2 per 100,000 population. Compare that to an island at the same latitude,
England, at about the same time, where the MS rate was over 50 per 100,000.[#169]
In January of 1985 I received a call from a colleague at MIT asking if I had time for a meeting
with an important Japanese scientist and his translators. He was consulting for a major food cooperative
in Tokyo, one of the biggest in the country. In Japan, if you have a product that you want the Japanese to
consume it must be carried by one of these cooperatives, and they are very strict about what they allow
into their stores. Aspartame was at the gate and the Japanese were concerned about what my friend was
saying about the possibility that it was causing seizures.[#368] When he showed them my article warning
of the dangers of methanol consumption and exposure, they immediately wanted to see me. To make a
long story short, we did meet and I did what I could to supply him with numerous articles and evidence
that I had uncovered up to that time, but my efforts were fruitless. The fix was in. Ajinomoto, the
Japanese chemical giant, had made a deal with Donald Rumsfeld’s company and agreed to participate in
the mass production of aspartame to supply a market that was expanding faster than anyone’s wildest
dreams. No one could have stopped the approval of aspartame in Japan with Ajinimoto behind it. To this
day the company bears a heavy burden for using extreme political pressure and far worse to protect
aspartame from proper scrutiny. Aspartame entered the almost perfect Japanese food supply shortly

thereafter, and as the article that constitutes slide number 14 in the slide show indicates, the prevalence
rate of MS in Japan has remarkably quadrupled “in the past 30 years.”[#81]
A Group of Islands called Faroe where a Lack of Trees Prevented MS

A group of 17 islands in the North Atlantic has played an inordinately important role in the history and
study of multiple sclerosis. A number of medical professionals have made a name for themselves
fruitlessly pursuing the cause of MS in those islands – to the point that the island government no longer
appears to be interested in proffering its citizenry as guinea pigs for a failed cause.[#195]
The Faroese are a semi-independent part of the Kingdom of Denmark. They are located as far
away from Japan as one can get without heading back closer. This small group of islands is situated in
the stormiest part of the North Atlantic, midway between Scotland and Iceland. The weather is cloudy
and windy throughout the year and the summers are cool and sunless. Daily sunshine in the summer
months averages only about four hours a day. If ever a place could be found that would be perfect for
disproving the vitamin D deficiency theory of the cause MS, this would be it. The meticulously kept
medical history of the native-born residents of this land of over 44,000 in population has been searched
back to before the 19th Century began, without finding one single case of MS – until July of 1943. What
makes this truly amazing is that this location could be considered to be the geographical heart of MS
country. The nearest land masses have MS prevalence rates that are the highest on the planet. Scotland
has 62 per 100,000, Iceland has 72, Orkney Island has 108, Shetland Island approaches 300, and so
on.[#169] All these countries and islands were originally settled during the same Nordic migrations, thus
ensuring populations of similar genetic descent, making the conundrum even more interesting.
The event that occurred that apparently triggered the first case of MS on the Faroe Islands was
the occupation of the islands by British military forces for five years during World War II, beginning in
April of 1940 and ending in September of 1945. This event is believed to have triggered the “epidemic”
of MS on the Faroes. The epidemic began in 1943, after two years of contact with the troops or
something they brought with them, and consisted of 21 patients. It is generally believed that the troops
brought either an infection or a toxin that was to cause the disease.[#195] A careful study has revealed that
those individuals most affected were those who had been in direct contact with the troops and who lived
in close proximity to their numerous bases.[#168] It is at this point where the silliness begins, culminating
in a scientific piece accusing MS of being a “sexually transmitted infection.”[#184] The toxin idea was put
to rest early on when it was clear that the disease didn’t go away after the troops left and subsequent
“epidemics” occurred.
In a review written in 2003 by a man who had spent years on the island looking for the cause of
MS, Dr. John Kurtzke explains the phenomenon in an important paragraph which I will quote here
exactly.
The troops therefore brought something to the Faroes which later resulted in an
epidemic of clinical MS. This had to be either an infection or toxin, with either one
geographically widespread on the islands from 1941. Now a toxin could not be
responsible for later epidemics. Therefore, if there are such (and there are), then there
must have been an infection carried by a large proportion of British troops (because of
its wide distribution) in asymptomatic fashion (because they were healthy troops). This
must be a persistent infection which takes time (here two years) to be transmitted to a
naïve populace, the Faroese. As noted, we call this agent the primary multiple sclerosis

affection, which have defined as a specific, but unknown, widespread, persistent

infection that will only rarely lead to clinical neurologic MS years after its
acquisition.[#195]
I can’t emphasize enough the importance of this paragraph, which exemplifies the extent to which
physicians will go to try and show that all disease is caused by bacteria, virus or some other living thing,
no matter how far they have to reach. This is the medical mindset and it has cost literally millions of
lives to poisonings and nutrient deficiencies throughout the ages. This is not John’s fault; this is the fault
of his medical training.
The most egregious misstatement in John’s paragraph is, “Now a toxin could not be responsible
for later epidemics.” The troops brought with them items such as canned foods, fruit preserves,
marmalades and other rations, along with the ubiquitous cigarette, all of which would be very desirable
to the island people, especially during time of war. It is very possible that any of these methanol-
containing treats were traded or gifted to the locals, who acquired a taste for, or, in the case of cigarettes,
an addiction to them and subsequently became a staple after the troops departed. If this was the case,
then of course the “toxin” would have lingered.
To me, the methanol explanation makes much more sense than the strange-new-alien-disease-
causing factor, of which the good doctor and all of his many colleagues have never actually been able to
find even a trace. Because of the preponderance of physician investigators with preconceived
expectations, the diet of the islanders was essentially ignored during the early years when good data
could have been gathered from the population while the occupation was still fresh in their memories. In
the more than 60 years since MS mysteriously found the Faroes, only one scientist has put any effort
into looking at the diet of the islands and has studied seriously the food consumption of the Faroes and
its relationship to MS. His work was not published until 1989 and is actually a review of cook books and
importation records of foods to the islands before the occupation and shortly afterward. He stresses that
until the war, the traditional diet was indigenous and based primarily on fish, as well as mutton, whale,
wild birds, and potatoes. This very limited diet is still maintained to some extent, particularly in the
smaller villages, which are still free from MS.[#82] This scientist does confirm that after the war, a
“rapid” evolution introduced many new food products into the diet, though unfortunately he is not
specific about which foods were introduced.[#82]
The truly fascinating angle that the author, Klaus Lauer, takes on the Faroe diet may, in fact,
explain exactly why they had been completely exempt from MS all throughout its dramatic increase in
the rest of the civilized world and, in particular, their close neighbors during the early 1900s: the
complete absence of smoking. By that, I do not mean cigarette smoking, but rather the smoking of fish
and other meat products. Unlike the traditions of the islands’ neighbors, smoking of meats is not
practiced as a traditional method of food preservation in the Faroes.[#82] They preserve fish and other
meats by air drying, as is done with cod in many cultures. Their cook books describe in detail salting
and wind drying, but do not mention smoking. Outside the Faroes, that area of the world is famous for
its smoked foods. The Scots and Icelanders, for instance, have perfected the art of preservation by
smoking and it is not unusual for them to offer smoked fish along with their jams and preserves with
every meal.[#487] The Shetland Islands have a special process called “reesting” in which they smoke their
food slowly over a peat fire.[#82] Unfortunately, the smoke from burning peat contains three times the
methanol level of wood smoke.[#180] This could help explain why the Shetland Islands have the dubious
honor of having the highest incidence of MS in the world, approaching 300 per 100,000 and
climbing.[#169] But what these other cultures have that Faroes do not is trees and/or peat bogs to provide
the heat, smoke and methanol to make the food smoking process work. The North Atlantic archipelago

is known for its treelessness. Climatic and geographic conditions and centuries of sheep-breeding have
left the Faroe islands all but treeless.
After publishing the Faroe diet article, Lauer published an article attempting to link the disparate
incidence of MS in various provinces of France and Switzerland to the use of wood smoke to preserve
meat.[#69] He made a convincing story of the high incidence of MS in populations that would
customararily smoke meats as compared to to those who air dried their meats. Though he was not aware
of the possible impact of methanol at the time, it is interesting and important that he put to pen a clear
association between MS and diet that needed exposure. His writings have been largely ignored by the
medical community.
Methanol consumption was overlooked as a factor in all the studies done on the Faroes. The fact
is that even after the work of Henzi, methanol has never been seriously explored as the possible cause of
MS. The Scandinavian countries and portions of the Slavic nations have some of the highest incidence
of MS of any population in the world.[#354],[#168] In these countries consumption of both commercial- and
home-canned fruits and vegetables is high, as is consumption of smoked food as describe above.
Moreover, methanol can be found in traditional liquors made from rotted fruit culled off the ground
during harvest and rotted in barrels for months. Some of these liquors have a high enough methanol
content to exclude them from international commerce. It may not be a coincidence that the highest
incidence of MS is found in cultures which had the potential for very high methanol consumption even
before the advent of aspartame.
The Little Village Of Wellington: The World’s Highest MS Incidence Rate

It seems like many significant things in my life happen in towns called Wellington. I met MS in
Wellington, Colorado. I discovered the very rare dark side of the little country of New Zealand in its
capital of Wellington. And as you soon will probably agree, the most interesting Wellington of all was
one where I have never been and have no desire to ever visit, the Village of Wellington, Ohio. It isn’t
that I have anything against Wellington, Ohio. It’s just that it appears that an old enemy of mine,
multiple sclerosis, chose to take up residency there for a time.
The real mystery of this story is how I discovered this little burg in the first place. With a
population of 4600 people – one tenth that of the Faroes, and with absolutely nothing of great
importance ever having happened within 100 miles of the place since the last Ice Age, we have the
Internet to thank for bringing us together. The juxtaposition of the word’s methanol and multiple
sclerosis plugged into the Environmental Protection Agency’s website brought up something I had never
seen before: a Health Consultation. It seems that it is type of investigation done by a group that serves
under the US Centers for Disease Control called the Agency for Toxic Substances and Disease Registry.
The study was conducted in 2005, during the George Bush administration.
I knew the chances of the work being slanted toward industry and away from the public health
were strong. I went to the report’s conclusions first, just as one would look ahead to see whether a cheap
novel had a good ending before deciding whether to waste much time reading it. As I suspected, it was
clear that the anonymous researchers who had conducted the study (none of their names were attached to
the document) were themselves unwilling to make a difference. The conclusion began with “no
significant contaminants of concern were identified in human exposure pathways.” Reading further,
however, there appeared a bit of a surprise that made my heart skip a beat or two: “The causes of MS,
the primary health concern in this community, are unknown; the disease is believed to be caused by a

combination of genetic and environmental factors.” Then this highly unusual statement: “This
evaluation did not suggest any additional hypotheses for the cause of MS.”[#578] Obviously, this little
town had suffered a serious outbreak of MS, but the population was very small and it was located in the
middle of farm country, surrounded by rolling hills of grass. The researchers could only point to a
mysterious environmental factor, but could not identify the cause of the outbreak.
The other promised word I had entered into my search criteria, methanol, was nowhere to be
found in the conclusion. This often happens with modern search engines finding every use of the word. I
am often disappointed to find “methanol” being something less than important in the documents found
by such searches, with the only use of the word in some minor subscript. Throwing my concern for the
forests aside I quickly printed out the entire document and devoured and annotated it in what seemed
like no time at all. The document, hidden in the archives of a government agency under siege during the
worst of years for public safety issues, contained information that was enlightening and extremely
helpful and confirmed my fears of what could/would happen to a population that was consistently dosed
with small amounts of methanol over a long period of time. Unlike aspartame, this methanol came from
the air.
The report was oddly written as if by someone who was new at such things. It did not disclose
exactly why the federal government was called in to investigate this outbreak of MS until halfway
through the report itself. Under the topic of “Community Health Concerns” I found that the Ohio
Department of Health had, in 1998, identified enough cases of MS in this little community to give
Wellington an MS prevalence rate of 600 cases per 100,000. To put this into perspective, this gave
Wellington the dubious honor of having the highest MS rate ever recorded in the entire world, worse
even than that of the Shetland Islands, which had not yet reached 300. For twenty five people in this
little community to have been diagnosed in a period of less than ten years with multiple sclerosis was
bad enough, but it did not end there. The incidence of other suspected autoimmune diseases and cancer
had also risen to the point of great concern to local authorities. The other disease that most interested me
was lupus, another methanol disease which we will discuss in the next chapter.
By the time I got to this earth-shattering bit of information, which was treated with the greatest
of nonchalance, I had already learned that the EPA did not arrive at Wellington until September 4-5,
2003 – a year after what it turns out was the offending foundry had fired its workers and closed its doors
for the last time, thereby limiting the chances of gleaning any valuable information from the fresh
memories of its disgruntled former employees. It seemed, in fact, that this group of Washington
bureaucrats came to this village to allay fears and participate in a cover-up of a major cluster of MS that
could have done for them precisely what their conclusion said it did not do: “suggest an additional
hypothesis for the cause of MS” – Methanol. For you see, the only chemical that this group’s
investigation found that was being flagrantly dumped into the environment and that could have caused
this tremendous increase in the MS rate of this little community was methanol.
The report contains a review of the literature in which the researchers admit knowing “a weak
association between solvent exposure and the development of MS may exist,” but the statement is
couched in such a way as to make it appear that the anonymous authors are essentially attempting to
cover their own rear ends, since at the same time they also recognize the fact that methanol can cause
“damage to the central nervous system” without any reflection whatsoever on the situation at hand. In
this age of computerized searches, the literature review by all rights should have mentioned the works
by Henzi that clearly and specifically implicated methanol as a causative agent for MS. Obviously, they
chose not to mention this, for any competent researcher would have stumbled across Henzi’s work and
included it. But then how would they not then be required to explain away the possible association

between the methanol exposure in the little town and the resulting MS epidemic. I have always
wondered whether the individuals that write such reports are actually clones, created in a mysterious
laboratory some place where they are kept dormant and benign until a truly misguided politician comes
along who wants a scientific-sounding paper generated that will hide the truth and forward a wrong-
sided agenda. Certainly Hitler had no difficulty rounding up as many of these pseudo-researchers as he
needed to get his dirty little jobs done. They are also at work at the EPA and, rare as they may be in New
Zealand, even its Wellington has its share of them. What a terrible shame.
It would be far too easy to get carried away with politics at this point; suffice it to say, it is clear
to me that if this Health Consultation is anything it is a political piece. The long and short of it is that
methanol is at the very heart of the health problems that confront the people of this little Ohio
community. This methanol came from Sterling Foundry, which was located on the very southwest edge
of the city limits of Wellington, just a few hundred feet from the drinking water plant and reservoir for
the town. In 1990, new owners bought the foundry out of bankruptcy and it appears that the trouble
began at around that time. The prevailing wind in this area of Ohio blows out of the southwest and it
wasn’t long before townspeople began complaining of “odors” emanating from the plant.
The State of Ohio Environmental Protection Agency investigated the facility in 1995 and
discovered the plant was operating without any effective air pollution control equipment, all of which
had stopped working during the time the plant was in bankruptcy and out of commission. The plant had
“unregulated on-site storage facilities” for large amounts of methanol, with between 20 and 40 tons of it
stored on site, outside the plant proper. Nothing anywhere in the report indicates exactly what the
intended use of the methanol was, although usually in such facilities it is used to clean freshly cast metal
work as it comes out of hot molds. This process usually takes place in outdoor areas to prevent the
buildup of dangerous vapors. We can only guess at this point why the foundry workers were never asked
by researchers how the methanol was used or why such enormous amounts of methanol were kept on the
property at any one time.
After the first Ohio EPA investigation in 1995 the plant was required to keep records of the
amount of methanol it kept in storage and to “estimate” the evaporative losses from these storage
facilities. The self-reported Toxic Release Inventory from the Sterling Foundry facility in the last three
years before it closed (the only inventory available) indicated an annual leakage from storage to the air
on-site as 5000 pounds a year. The Ohio EPA admitted that this was evidently not regulated or
monitored and never itself did any testing of the atmosphere or verification of any kind. The researchers
mentioned this methanol leakage and restated that “methanol can be toxic to humans, targeting the
central nervous system.” The same paragraph, without scientific reference, states that methanol released
into the atmosphere is “rapidly oxidized to carbon dioxide,” thus justifying the next statement that the
data does not necessarily mean that off-site residents were exposed to methanol at concentrations that
would amount to any health concern. The first statement is a lie and the second is silly.
Methanol is very stable in the air and its oxidation to carbon dioxide requires it be burned or the
presence of a very special bacterium not found in the atmosphere.[#723] I believe the smells from the
foundry that for years had instigated complaints from the townspeople located downwind from it were in
part methanol that was leaking from those storage facilities and being used for some unknown purpose
outside the facility. The very sad thing is that we could have had a very good idea of just how much
methanol was going into the air of Wellington. The foundry was buying its methanol from somewhere
and the companies that sell such dangerous substances keep good records of those sales. Why didn’t the
CDC “investigators” track down Starling’s methanol source and ask the right questions? The only
possible answer is that they just didn’t want to know. Sadly, the only thing we do know is that it was

enough methanol to raise the rate of MS of the citizens of Wellington to a level higher than anywhere
else in the world.
Industrial Exposure to Methanol – Jobs that can Last for an Eternity

Organic Solvents and the Risk of MS: Only One Solvent at Cause
According to a review article published in 1996, the theory that prolonged contact with organic solvents
can cause MS was first proposed in 1982.[#74] This theory is correct and this book backs it up fully. Only
one problem remains, and it brings us to a very important issue. Only one organic solvent, methanol, is
the cause of MS. The other few thousand organic solvents have nothing to do with MS. More important
of all, only one other organic solvent, ethanol, can, if properly applied, stop or even cure MS, by
preventing methanol from transforming into formaldehyde and, therefore, preventing symptoms. This
means if you wanted to prove the theory, disprove the theory or reverse the theory you know how that
can be done by carefully picking you organic solvent.
It was clear in the early 1900s that more workers in the leather and the shoe-making industries
developed multiple sclerosis than in other industries.[#59] The major reason that MS was considered a
disease of men in the early 1900s was because methanol was used freely in industry, particularly in the
manufacture of glues and many other sorts of liquids used by businesses that hired only men. Methanol
was common in industry for two important reasons. First of all, methanol is an outstanding solvent,
better than ethanol for use in all manner of glues, paints and varnishes. Second, it has a lower boiling
point than ethanol and evaporates off much more quickly, drying paint or hardening the glue faster and
reducing labor costs. Methanol is also an outstanding and very inexpensive solvent for cleaning and
removing stains and oily contaminants.
I mentioned the association between exposure to solvents in general and incidents of multiple
sclerosis in the previous section. The scientific literature is peppered with articles on the pro and con
side of this issue, and now that you know more about methanol than the average scientist you can see
that the premise is correct, but only for methanol and no other solvent. Knowing that all solvents are not
equal when it comes to causing MS you can wade through the industrial solvent MS literature and cull
the useless articles from the others.
The removal of methanol from industrial glues has been a very slow process since the
advantages are so great. The shoe industry was the last to convert to other solvents, although records are
difficult to obtain on such industrial secrets as the exact makeup of this type of product. Unfortunately,
the MS rate of a particular factory is the most reliable indication as to whether methanol is being used as
a solvent or not. The first published study addressing the question of MS and solvent exposure found
that in the late 1970s, the incidence of MS among workers in the shoe and leather industry in Florence,
Italy was five times higher than that of the general population.[#245] Another Italian prevalence study
done in the mid 1980s reported a prevalence of MS among shoe workers of over three times above the
general Italian population, a number that was still extremely high but probably reflecting a reduction in
methanol use by the leather industry around the world.
The fact of the matter is that in modern times the danger associated with methanol contact with
industrial personnel and the large number of deaths from industrial accidents caused by improper use of
methanol has limited the number of occupations and industries where workers make contact with this
dangerous organic solvent. Painters were often exposed to methanol in the old days, but again methanol
has slowly been removed from most paints due to the danger of both its manufacture and its ultimate

use. Its presence in paint is bound to account for the twofold increase in risk of MS in painters over
construction and food processing workers found during a study of 50,000 workers followed over a 16
year period in Norway beginning in 1970.[#480]
Industrial Contact with Methanol

These days warning signs abound and the use of methanol in all industries and even science laboratories
is accompanied with stern visible and documented warnings of blindness, irreversible neurological
damage and birth defects associated with methanol. In fact, a definite disconnect seems to prevail. The
only individuals who seem not to be take methanol seriously are the bureaucrats working at the Food
Safety Authority of New Zealand or the Food and Drug Administration of the United States or even the
European Food Safety Authority, where I am consistently and repeatedly told that “there is nothing to
worry about because methanol is a food.” Of course, I tell myself that these dim-witted incompetents are
all mere toadies for the powerful food lobbies that proffer them with god-knows-what recompense,
either real or implied. It is still painfully insufficient consolation to me, especially when I have no
recourse. At any rate, the workplaces of the modern world treat methanol with great respect and it is
difficult today to find any profession in which individuals daily and consistently make contact with
methanol. Two exceptions, however, help prove my point.
Those Who Work With Hot Wood

The paper and wood industry have a great deal to fear if methanol is banned completely from the
workplace,[#553] as it must eventually be, because it can actually be produced as a byproduct of these
industries’ general operations. Methanol is, after all, just another name for wood alcohol. The heat
required to release methanol from wood as a gas into the environment is not as great as one would
suspect. No flame is required, and the temperatures at which paper is made from scrap wood fall well
within the methanol production range. Even the heat produced from the friction of the blade of a
chainsaw can produce methanol when trees are felled. The paper industry does not like to talk publically
about methanol, although we know that all 300 paper mills throughout the world produce what they call
internally a “methanol-water waste stream,” and each must find a way to dispose of it. Some do much
better than others. This stream, which comes off the processing wood pulp, is often exposed to the
atmosphere, where it releases both methanol and a group of sulfur-containing compounds called
mercaptans that smell very bad (like some paper mills). Chances are very good if you smell a paper mill,
you are also smelling some methanol.
Some mills incinerate the methanol streams to destroy the methanol, while others turn the
methanol into formaldehyde for sale to other industries.[#70] Methanol produced by paper mills and wood
processing plants is not carefully regulated by most governmental agencies, due most likely to the
political power of organizations such as the American Forest & Paper Association, which collects and
uses large sums of money from its members for the purpose of lobbying, much like the methanol and
formaldehyde lobbying groups we discussed earlier. Keep in mind that any process that heats wood to
high temperatures can and does produce methanol. With the proper precautions, plants can be and have
been designed to keep this methanol from causing harm to their employees or the nearby community.
Sweden sets a good example of how paper can be made safely.
In a fascinating epidemiological study a number of industrial activities in four European
countries were randomly screened to determine if any of them had higher risk than any other for their

workers developing multiple sclerosis. Paper manufacturing was by far statistically the most closely
associated with MS in all countries tested except for Sweden. Paper manufacturing was followed by
wood processing in Norway and Switzerland and leather processing in those same two countries. The
author points out that the “association between MS and paper manufacturing is all the more surprising,
since this industry played only a minor role in the respective countries.”[#13] This study is in agreement
with the high correlation of MS with the felling of coniferous trees in Norway and earlier observations
of a high MS rate associated with wood processing occupations in Europe.[#334] This data would mean
little if other industries showed a high correlation to MS. The fact is that multiple sclerosis is found
more frequently in industries where methanol is used or made as a byproduct that can contaminate the
working environment.
It would be ideal to find an occupation that would not be considered one in which practitioners
would normally make contact with any toxic chemicals except for methanol. Then we could look at
health records and see just what happens to these people in the course of their working lives. It sounds
like a scientists daydream - and yet we have done just that in the next section.
Teachers’ Paradigm
Methanol is a powerful killer of humans. Our tolerance to acute dosages is low, much lower that the
toxicology literature reflects. This discrepancy is due primarily to the accompanying ethanol that is
almost always co-administered with the methanol, either as a portion of the lethal concoction or as an
attempt at life saving that goes hand-in-hand with dialysis. A patient who survives the first week of an
acute bout of methanol poisoning may not always enjoy a complete recovery but the patient usually
lives. We don’t know experimentally what chronic administration of methanol over a long period does
because it can only be tested on humans. To my mind the perfect human testing has already been done
by the double blind introduction of aspartame to the world’s food supply. I have shown you where that
testing has gone, but due to the magnitude of my claims I felt it important to find another human study
group with another approach to the administration of methanol – one that allows for consistent
administration of methanol on as regular a basis as would be feasible with a human test population while
at the same time limiting the contact these individuals might have with other dangerous industrial
chemicals. Where was I to find such an idyllic study group who would stand still and expose themselves
willingly for their entire careers to this dangerous poison? Little did I imagine that this perfect
experimental study group would turn out to be one of which I was a member for a number of years.
A Cold Awakening in Riverton

I woke up with a start in the middle of a wintry New Zealand night late one July with something on my
mind. I ran to my office without properly protecting myself from the cold, turned on my computer,
which seemed to take forever to find the Internet, and, teeth chattering, I inputted the key word, “Ditto.”
I had started teaching right after graduating from the New Mexico Institute of Mining and
Technology. My high school chemistry and physics teacher and mentor, Oscar Weisberg, was not about
to allow his protégé to get killed in Viet Nam. Oscar had heard that I was back in New Jersey staying at
my parents’ summer home at the Shore. He called, and after we had a good catch-up he summoned me
to his laboratory. Although Oscar was essentially a high school teacher, he was also a brilliant scientist
who was exempted from service during the Second World War to work on the atomic bomb. The short
story is that he would be taking a sabbatical and I was the only one he was willing to trust to teach his

flock while he was gone. I told him I was a scientist and had no intention of teaching, having taken not
one class that would count toward a teaching certificate. All he had to say was, “Well, you are going to
let me down then.”
Somehow he managed to obtain an emergency certification for me that would allow me to teach
in my old high school while he was gone. After a little initial awkwardness teaching a summer school
class in chemistry for practice, I found that I loved the experience enough to begin taking night school
classes that would allow me to continue teaching for a few years. Eventually, I was lucky enough to get
a fantastic job at one of the best teaching establishments in the world, a private school called Colorado
Academy just outside of Denver. In all, I taught young kids in secondary schools for five years before I
went on to earn my Doctorate and return to University.
So why am I telling you this? Part and parcel of learning to teach, particularly in secondary
schools with large classes, was learning and gaining proficiency in the care and use of a device called a
Ditto machine. The dream I had many years later on that chilly Riverton morning was one of me back in
New Jersey working in the faculty lounge at my high school. I was retrieving a rectangular one gallon
metal can of liquid from a closet stacked high with such cans. In my dream I was looking at the label
and, sure enough, it was Ditto fluid. I turned it over to view the contents declaration. What woke me up
was the horror of seeing only a brightly colored cautionary skull and crossbones and noticing that one of
the eyes in the skull was looking back at me with a slow, menacing wink. Fear quickly turned into
curiosity and my search began.
A Ditto machine (also referred to as a spirit duplicator) is a low-volume, very inexpensive
printing method used by primarily by schools. The term “spirit duplicator” comes from the alternative
term for alcohol, which is “spirits.” Methyl alcohol was the only component of the liquid in that can. It
is used as a solvent to transfer inks from a template typed by the teacher onto the blank paper that would
become the handout for the students in class that day. The spirit duplicator was invented in 1923 by
Wilhelm Ritzerfeld. The best-known manufacturer in the United States was Ditto Corporation of
Illinois, hence that name. My search turned up some amazing information about this ubiquitous
secondary teaching tool. By ubiquitous I mean that the duplicators were everywhere, but particularly in
the teachers’ lounges of every school where I ever taught or visited. Our school had four of them, and
they were always kept in tip top shape. While other teachers were having a coffee or chatting or
preparing for their next classes, someone was usually busy in the background inserting their templates
and running off purple copies.
I taught secondary science classes that required numerous handouts, as do most secondary school
classes. I remember doing some presentations in the primary school on occasion and having to wait in
line at their one and only machine. It sounds silly, I know, but this bit of information will turn out to be
important very soon. Even the advent of the Xerox machine didn’t change this; because of the
inexpensiveness of the Ditto machine copies and of the machines themselves, teachers even today are
encouraged to use the Ditto to make the copies for their classes. The copies that come from the Ditto
machine have a distinctive light blue print and a strong methyl alcohol smell that some find appealing. I
can’t tell you how many times I would watch as my colleagues would pick up a ream of Ditto copies and
fan them in front of their face and smell to see if they were dry enough not to smear as they handed them
to their class that day. Often the pages coming off the machine would be saturated with methanol and
would have to sit on a desk in the faculty lounge to “dry.” The reason that ethanol would not work as a
substitution for methanol in these machines was that it would take too long to evaporate and was not a
satisfactory solvent for the ink that was impregnated into the original template.

All this methanol – but what was it doing to these poor teachers? I would like you to see what I
saw as I progressed through my literature review. The slide show in Appendix 2 is an abbreviation of
what I found and may mean more to many of you than my discussion. Please take the time right now to
read through it.
Safety Studies – but Nothing Changes!

My computer search of Ditto machines brought up some fascinating information and good evidence that
over the years, concerns have been raised about the methanol from these machines and just how
dangerous exposure to it might be. These machines have been used in schools since the 1930s. The first
investigation was by the Connecticut State Department of Health, which found that the average Ditto
machine, without a great deal of use, could easily evaporate up to a gallon of methanol a day, all of
which was subsequently vaporized and went into the atmosphere of the room in which the machine was
located. Researchers measured methanol concentrations of well over 200 parts per million in the air of
the rooms that contained heavily used Ditto machines.
Researchers warned of this in the 1948 issue of the Industrial Hygiene Newsletter and again in
1954 in an article entitled, “Exposure To Methanol from Spirit Duplicating Machines,” which was
published in The Industrial Hygienist.[#411] This article was specific and stated that “this type of
duplicating machine is in common use in schools and business offices.” The article further stressed that
all of the duplicating fluids contain methanol, with some being made up of 100% of this solvent and
rarely any containing less than 40%. One gallon of the fluid can produce between 8,000 to 12,000 copies
with wide variability. The paper came out of the machine wet with methanol and, as the copies were
handled or riffled, large volumes of methanol vapor rapidly evaporated into the room air and the lungs
of the operator, who was often exposed to concentrations of over 1000 parts per million of the poisonous
substance. They warned that they tested the air in one very large 5000 square foot office with a 10 foot
high ceiling, even leaving the door in the room open during the run. This decreased the methanol
concentrations, but even so, they remained above the allowable limit. In the end, researchers
recommended that all such machines be hooded and vented out of the building.[#411] I taught in several
schools between 1967- 71 (twenty years later) and visited many others, and I can attest to the fact that I
never saw a single vented Ditto machine until in 1997, when ASU began a program to put vents above
all spirit duplicator machines in the University, including the one in our department.
This was not the end of the warnings. Again in 1980 and 1981the US National Institute for
Occupational Safety and Health (NIOSH) was called in to investigate two major cases involving
numerous complaints. The first was in the Everett School District in Everett, Washington, where
operators of spirit duplicators throughout the very large public school district were reporting MS-like
symptoms and blaming it on the duplicators. Then they were called in to do another extensive Health
Hazard Evaluation Report for very similar complaints, this time to the main campus of the University of
Washington.[#208] These cases were the most extensive studies done to date on the exposure risks of
individuals operating Ditto machines, researchers verified that within just 15 minutes of operation, 75%
of the duplicators they tested produced concentrations of methanol that were well over 1100 parts per
million. They also noted that 45% of the operators experienced symptoms such as blurred vision,
headache, nausea, dizziness and eye irritation, all of which are consistent with the toxic effect of methyl
alcohol. The conclusion was that “a health hazard due to excessive exposure to methyl existed in the
operation of spirit duplicators.”

Teachers, it seems, had been exposed to methanol for their entire careers. This has been going on
certifiably since at least 1948. But when did it stop? On March 21, 1995 the nationwide newspaper, USA
Today published an article entitled “Ditto Sheets in Schools Hazardous.”[#209] The piece was written as a
result of the release of a study done by the American Federation of Teachers at the request of numerous
member teachers complaining of health problems that they had linked to their use of Ditto machines.
The article starts, “Those smelly, purple-ink sheets that teachers regularly crank out on low-tech ditto
machines may be hazardous to everyone’s health.” The study revealed that a spot check of schools from
all over the country, including the most populous states of California, Pennsylvania and Michigan, found
that the Ditto machines are still in frequent use. Most important, the study showed that exposure to
methanol in schools can be much higher than levels allowed in workplaces by the Occupational Safety
and Health Administration. The article goes on to reveal that methanol has a “high odor threshold,” and
by the time you smell it, “you’ve already been overexposed.”
Teachers Become the Perfect Test Animal for Methanol Poisoning

We can document that at least in the United States, most teachers have been exposed to methanol on a
workday basis for their entire careers. We can’t say that they received equal doses as we could if we
were experimenting with rats in a controlled laboratory environment, but we can make up for that by
having a large population of exposed teachers over a very long period of time. We know a little more
about our subjects as well; we know that those who teach on the secondary level have been consistently
exposed to more methanol than the average primary school teacher, who has need for fewer handouts.
We know that some equanimity may be found among these two classes of teachers because even though
some teachers have used more handouts than others, the machines have usually traditionally been
located in the teachers’ lounges, thus exposing even those teachers who didn’t do many handouts.
The Diseases of Teaching

While still in secure self exile in New Zealand I continued my literature review, looking to see if
teachers’ health was any different from that of the general public. The results of my search shook me
seriously to my very core. It was while still in lovely Riverton among my many Kiwi friends that I really
did begin to wonder whether some sort of conspiracy could have been involved in the fact that science
seemed to have entirely missed the connection between methanol exposure and MS. The title of this
book, “While Science Sleeps,” was thus born, as was my determination to circumvent the establishment
and bring all of my findings directly to the public – the people who needed it most.
The first article I remember reading was a review that described a French survey which had the
perfect title: Do teachers have more health problems?[#215] Sure enough, the author admitted that the
literature comparing diseases between teachers and the general public was rare, but he pointed me in the
right direction to other articles that have shown an increased incidence in breast and thyroid cancers in
the teaching population, two methanol-sensitive organs that we will talk about in the cancer chapter. The
“Eureka!” moment, however, came when I read this phrase: “and surprising enough, there is an
association between school teaching and mortality from autoimmune diseases.” I just wanted to stop
right there, go no further, and avoid the risk that the reference was a weak one or poorly done, or worse,
that it had a strange sample selection. I think that I floated on the little bit of good news for at least an
hour before I built up the courage to look up the reference number in the bibliography.

When I did finally look it up I was both relieved and pleasantly surprised. The article had been
published in one of the few journals in the area that I regarded as both untouchable and prestigious; I
would trust the results of any article its editors selected to publish. The Journal of Rheumatology
published only the best work, and now I couldn’t wait to get the article into my shaking hands. When I
did, I was blown away by it, and I think you will be, as well.
Excess Autoimmune Disease Mortality Among School Teachers

The name of the article was “Excess Autoimmune Disease Mortality Among School Teachers.”[#210] The
work was faultless and the data was conservatively compiled from the death certificates of all deaths in
the US for the ten year period between 1985-95. School teacher deaths were compared to those of
persons in other professional occupations. The conclusion: “Our results substantiate excess mortality
from autoimmune diseases among teachers and suggest that, relatively early in their careers, teachers
experience an occupational exposure that increases the risk of autoimmune diseases.” They found that
“excess mortality was significantly greater in secondary teachers than elementary teachers.” Most
astonishing of all, “the greatest relative excess in autoimmune disease mortality among teachers
occurred for multiple sclerosis.”
In fact, the rate of multiple sclerosis among secondary school teachers was almost twice that of
their professional counterparts. “The autoimmunity disease mortality was most strongly elevated among
secondary school teachers. In particular, significant excess mortality from multiple sclerosis and lupus
occurred in the 35-44 age interval of secondary school teachers.” We will discuss lupus and the other
autoimmune diseases that this study found associated with secondary school teaching in the next chapter
and the cancers of methanol in the chapters after that. The one other statistically significant statement
that can be taken directly from this study was that “among white males teaching was associated with
excess mortality from multiple sclerosis.”
In explaining the rationale behind doing this study the investigators said that the National
Institute for Occupational Safety and Health had produced a survey of occupational mortality that
unexpectedly pointed to elevated autoimmune disease mortality among school teachers during the 1984-
88 period. “Our results show that significant elevated mortality also occurred in the subsequent 1989-95
period.”
MS Treatment – Pharmaceutical Placeboes or Perhaps Worse

All modern treatments for MS and all treatments that are in “the pipeline” are dangerous and should be
avoided at all cost. MS has no known cure, and after reading about all of the many modern
treatments,[#615] I can only conclude from the evidence provided that over the last 50 years the only one
that showed statistically valid improvement in double-blind studies, albeit for a relatively short period of
time, is plasmapheresis.[#186] Plasmapheresis involves removing the liquid portion (plasma) of a patient’s
blood, then returning the red and white blood cells to the patient without the plasma. The reason this
procedure has a positive effect may very well be something other than the official reason it is performed;
you see, the process could be expected to remove much of the methanol from the bloodstream, reducing
its concentration substantially in the tissues. Transfusions seem also to have similar effect.[#43] I cannot
recommend these two treatments because it would be far easier to just avoid methanol.

Conclusion and Review

You can see for yourself now that the daily administration of methanol to the human organism does not
go unnoticed by the immune system. The evidence is simply far too overwhelming for the
pharmaceutical industries to credibly justify ignoring it any longer. As a scientist I can do little more
than present a coherent molecular theory, and then prove the hypothesis using three paradigms with two
distinct methods of methanol administration. Viewing methanol toxicity as the etiologic cause of MS
answers all of the nagging questions and unexplained anomalies that have stalled the search for the
cause of this disease. I realize that absolutely nothing can convince the pharmaceutical giants, who are
now heavily invested in developing their own useless palliatives for MS, to give them up and rally
around the methanol hypothesis. In the end, however, I believe that the truth will win out. Henry Miller
prophesied over 50 years ago:
It is possible that the cause of multiple sclerosis lies buried somewhere in these lengthy
protocols waiting to be found by someone ingenious enough to unearth it.[#306]
Review
1. MS is a disease that begins around brain blood vessels, adjacent to the exact locations where
methanol converts to formaldehyde, very much like Alzheimer’s Disease.
2. MS was first discovered long before formaldehyde, making the determination of its cause
impossible.
3. The vast majority of early researchers believed that the cause of MS was a “toxic substance” that
forms in and is distributed via the blood vessels of the brain. “Whatever is being produced within
the vessel walls is the cause of the disease.”
4. All symptoms of MS can be found during the course of methanol poisoning if the patient lives long
enough.
5. Myelin Basic Protein (MBP) is the protein of the myelin sheath that is removed during MS plaque
development. MBP contains a high percentage of arginine, which acts as a trap for formaldehyde.
The MBP of MS patients has been shown to have reacted with formaldehyde and cause a marked
increase of the methylation of its arginine.
6. The MBP of MS brain tissue has been shown to be severely deficient in phosphorylation, which
we know can be caused by formaldehyde.
7. The Smoking Paradigm: Cigarette smoke is high in methanol and is the only etiological cause of
MS that is generally accepted by the scientific community.
8. Consistent circumstantial evidence links increases in methanol-containing food consumption and
in industrial use of methanol to corresponding increases in MS incidence during the transition from
the 19th century into the 20th century.
9. The advent of aspartame, a methanol carrier, has introduced an opportunity to quantify additional
methanol in the food supply since 1981.
10. The Aspartame Paradigm: statistics show convincingly that as more and more aspartame is
consumed by the US population the incidence of – and perhaps more importantly the death rate
from – MS has also increased dramatically.

11. The higher incidence of MS in colder climates was due to the higher consumption levels of canned
fruits and vegetables in temperate climates. This began reversing shortly after methanol-containing
diet sodas and other thirst quenching products became popular and inexpensive in the tropics.
12. MS was at one time a disease of men when it was caused by industrial contact. It is increasingly
more of a women’s disease. When methanol is inhaled as a gas during cigarette smoking or
industrial contamination the distribution tends to be equal between the sexes. The stomach of the
man, however, has 4 or 5 times more ADH in its lining than that of a woman. When methanol is
consumed via diet soda, the ADH removes methanol before it can get to the brain, so less of it
reaches men’s brains than women’s brains. As more and more methanol has become a dietary
poison, the shift from male to female disease has followed.
13. The Faroe Islands are surrounded by countries with very high incidence of MS, yet the country
traditionally did not have the disease represented in its population until after the occupation of
large numbers of British Troops during the Second World War. Faroes have no trees or peat
deposits and, therefore, developed methods to salt and air dry fish and other meats for
preservation, unlike its neighbors, who dine on smoked foods at each meal. The indigenous diet of
the Faroans contains no methanol.
14. The Village of Wellington, Ohio experienced an epidemic of MS that should have been traced to
the escape of methanol fumes from a foundry, affecting the populace located downwind of it.
15. Professions such as shoe making and papermaking that have been shown to have high incidence of
MS can also be shown to have exposes their workers to levels of methanol.
16. The Teaching Paradigm: The US teaching profession might just be the best profession to use to
link methanol exposure to increased incidence of MS. Secondary school teachers suffer an
incidence of MS almost twice as high as their professional counterparts. They also can be shown to
have had consistent workday exposure to methanol fumes by the ubiquitous use of Ditto machines
that use high concentrations of methanol as a print transfer agent.
It has been over 30 years since I heard my first unsolicited plea for help from an aspartame
consumer who had linked consumption of the product to her suffering. My first thought after an hour’s
listening was that this courageous young woman would soon be diagnosed with Multiple Sclerosis. It is
in her honor and in the memory of my friend from Wellington, Colorado that I seek to explain the
compelling link between methanol and MS.
____________________________________________________________________________
Post Script:
A Word About Depression, a Common Complaint of Methanol Poisoning and all the DOC
We have charted two methanol diseases that have long gestation periods. However, methanol poisoning,
MS and aspartame consumption have one symptom that is a quick responder (24-48 hours) that
permeates the literature of both methanol poisoning and MS and is a constant anecdotal complaint from
aspartame consumers. Depression was the second most reported complaint from aspartame consumers,
next to headaches, in the study done by the CDC when it finally took a cursory and shallow look at the
health impact of aspartame in a very conflicted and highly unusual report published by them in 1984.[#58]

A comprehensive double-blind crossover study designed to ascertain whether individuals with mood
disorders were vulnerable to developing depression after consumption of moderate amounts of
aspartame concluded that "individuals with mood disorders are particularly sensitive to this artificial
sweetener and its use in this population should be discouraged"[#54] The result of this experiment were
statistically significant even though the experiment was halted prematurely by the Ohio Universities
College of Medicine Institutional Review Board due to the severity of reactions within the group of
patients with a history of depression. Such major reactions are uncommon in the aspartame toxicity
literature. The reason for this may have to do with the difficulty in procuring the chemical for testing
purposes without having to rely on the honesty of the manufacturer. Dr. Ralph G. Walton chairman of
the department of Psychiatry first author of the article explains in his own words what he went through.
"Nutrasweet Company did try very hard to prevent me from getting aspartame for our double blind
study. The company had stated that they would supply aspartame and placebo capsules free of charge to
any "legitimate researcher." As a full professor and chairman of a department at a major medical school
I think I qualified as "legitimate" but they refused to provide it to me. When I pressed they said it was
"unnecessary" research. At that point I said I was willing to buy it from them rather than have it
provided free. They still refused. I then turned to bottlers of diet soda and was told that they had been
instructed by the company not to sell it to me. We did eventually obtain aspartame, but only after a
world-wide search. In retrospect I am glad that I did not get the aspartame or placebos from the
company - who knows what they would have sent me?"
As a teacher, I immediately noticed that college students and teenagers, in particular, were quick
to pick up on the great-tasting aspartame sweetened diet sodas as a way to keep their weight down. I
asked the CDC for the data it had collected on successful suicides of teenagers during the years after
aspartame was added to carbonated beverages and its consumption exploded. The response was
startling. Figure 6 represents this data in the usual fashion. Unlike Alzheimer’s, with a 14-year delay
until death, the teen suicide rate of this important period spirals around the aspartame consumption curve
like the two snakes slithering up the caduceus.* This quick response would be expected since the mood
alterations generated by both methanol and aspartame take hours, not years. There is also some evidence
that the anhedonia produced by methanol may be identical to that induced by alcohol withdrawal and
linger for some time.[#38] This striking yet tragic illustration required the deaths of 1600 teenagers above
the normal rate in the US to generate. Their parents would not consider their loss anecdotal.
Figure 7

* The caduceus the magic wand of the Greek god Hermes (Mercury) and is used by the medical
pharmaceutical establishment as their symbol. Hermes is considered the protector of merchants and
thieves.
BIBLIOGRAPHY
(1) Monte WC. Aspartame; Methanol and the Public Health. Journal of Applied Nutrition
1984;36(1):42-58.
(2) Monte W, Glanzman D, Johnston C. Methanol as a Model Etiologic Agent in Multiple Sclerosis.
FASEB 1990;26(4(3)):Abstract.
(3) Roe O. Methanol Poisoning Its clinical course pathogenesis and treatment. Acta Medica
Scandinavica 1946;126:1-252.
(4) Kallen R, Jencks W. Equilibria for the Reaction of Amines with Formaldehyde and Protons in
Aqueous Solution. J Biol Chem 1966;241(24):5864.
(5) Henzi H. The Methanol Hypothesis A New Concept of Multiple Sclerosis:. M Sr N ed. Zurich:
Juris Druck; 1980.
(6) Schwyzer R, Henzi H. Multiple Sclerosis: Plaques Caused by 2-Step Demyelination? Med
Hypothesis 1983;12:129-42.
(7) Trocho C, Pardo R, Fafecas I, Virgili J, Remesar X, Fernandez-Lopez JA, et al. Formaldehyde
derived from dietary aspartame binds to tissue components in vivo. Life Sci 1988;63(5):337-
49.
(8) Henzi H. Chronic Methanol Poisoning with the Clinical and Pathologic-Anatomical Features of
Multiple Sclerosis Medical Hypothesis. Med Hypothesis 1984;13:63-75.
(9) Hazra D, Seth H, Mathur K, Wahal P, Prakash V, Maheshwari B, et al. Electrocardiographic

Changes in Acute Methanol Poisoning. J.Assoc.Physicians India 1974;22:409-13.
(10) Schwyzer R, Henzi H. Multiple Sclerosis: Prevention of Serious Illness - Vision of a Desired
Future for Newly Ascertained Patients. Med Hypothesis 1992;37:115-8.
(11) Rousseau M, Straif K, Siemiatycki J. IARC Carcinogen Update(Formaldehyde now Class 1

carcinogen). Environmental Health Perspectives 2005;113(9):A580.
(12) Apol A. Health Hazard Evaluation Report. PB82-19464 8. University of Washington Seattle.
Washington. NIOSH U. S .Dept. of Health and Human Services; 1981.

(13) Lauer K. Risk of multiple sclerosis in relation to industrial activities: an ecological study in four
European countries. Neuroepidemiology 1989;8(1):38-42.
(14) G.D. Searle Co. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and
Development. Petition submitted to the US Food and Drug Administration. United States Food
and Drug Administration; 1983.
(15) Eisenberg A. Visceral Changes in Wood Alcohol Poisoning by Inhalation. American Journal of
Public Health 1917;7:765-71.
(16) Bennett I, Cary F, Michell G, Cooper M. Acute Methyl Alcohol Poisoning; A Review Based on
Experience in an Outbreak of 323 Cases. Medicine 1953;32:431-57.
(17) Wimer W, Russell J, Kaplan H. Alcohols Toxicology History. Southwest Research Institute San
Antonio TX: Noyes Data Corporation.; 1983.
(18) Gaul H, Wallace C, Auer R. MR findings in methanol intoxication. Am J Neuroradiol

1995;16:1783-6.
(19) Francot P, Geoffroy P. Le Methanol dans les jus de fruits. les boissons. fermentees. les alcools et
spiritueux. Revue Des Fermentations Et Des Industries Alimentaires. 1956;11:279-86.
(20) Davoli F, Cappellini L, Airoldi L, Fanelli R. Serum methanol concentrations in rats and in men
after a single dose of aspartame. Food Chem Toxicol. 24(3):187 1986;24(3):187.
(21) Schneck S. Methyl alcohol. In: Vinken P, Bruyn G, editors. Handbook of Clinical Neurology.
Amsterdam: North-Holland; 1989. p. 351-60.
(22) Weisberger A, MacLaughlin J. Electrocardiographic Changes Associated with Methyl Alcohol

Poisoning. American Heart Journal 1946;33:27-33.
(23) Horiuchi S, Takata K, Morino Y. Scavenger Receptor for Aldehyde-modified Proteins. The
Journal of Biological Chemistry 1986;261(11):4962.
(24) Horiuchi S, Takata K, Morino Y. Purification of a Receptor for Formaldehyde-treated Serum

Albumin from Rat Liver. The Journal of Biological Chemistry. 260(1):482 1985;260(1):482-
88.
(25) Horiuchi S, Takata K, Morino Y. Characterization of a Membrane-associated Receptor from Rat

Sinusoidal Liver Cells That Binds Formaldehyde-treated Serum Albumin. The Journal of
Biological Chemistry 1985;260(1):475-81.
(26) Metz B, Jiskoot W, Hennink W, Crommelin D, Kersten G. Physicochemical and

immunochemical techniques predict the quality of diphtheria toxoid vaccines. Vaccine
2003;22:156-67.

(27) Means G, Feeney R. Chemical Modification of Proteins (formaldehyde hydrate). Francisco, CA.:
Holden-Day, Inc; 1971.
(28) Kirchner J, Miller J. Volatile Water-Soluble and Oil Constituents of Valencia Orange Juice.
Agricultural and Food Chemistry 1957;5(4):283.
(29) Lund E, Kirkland C, Shaw P. Methanol. Ethanol. and Acetaldehyde Contents of Citrus Products.
Agricultural and Food Chemistry 1981;29:361.
(30) Koivusalo M. Studies on the Metabolism of Methanol and Formaldehyde in the Animal
Organism. Acta Physiologica Scandinavica 1956;39:1.
(31) Buys C, De Jong C, Bouma J, Gruber M. Rapid Uptake by Liver Sinusoidal Cells of Serum
Albumin Modified with Retention of its Compact Conformation. Biochimica Et Biophysica
Acta 1975;392:95.
(32) Buys C, Elferink G, Bouma J, Gruber M, Nieuwenhuis P. Proteolysis of Formaldehyde-treated

Albumin in Kupffer Cells and Its Inhibition by Suramin. Journal of the Reticuloendothelial
Society 1973;14:209.
(33) Gruner O, Bilzer N. Methanol content of fruit-juices. Its significance in congener analysis.
Blutalkohol 1983;20:241.
(34) Casey J, Self R, Swain T. Origin of Methanol and Dimethyl Sulphide from Cooked Foods. Nature
1963;200:885.
(35) Braverman J, Lifshitz A. Pectin Hydrolysis in Certain Fruits during Alcoholic Fermentation. Food
Technology 1957(July):356-58.
(36) Campbell L, Palmer G. Pectin. In: Spiller G, Amen R, editors. Topics in Dietary Fiber Research.
New York: Plenum Press.; 1994. p. 105.
(37) Fink W. The ocular pathology of methyl-alcohol poisoning. Amer J Ophthal 1942;26:694.
(38) Millman R. Alcohol; The Friendly Foe. In: Science Year. The World Book Science Annual; 1982.
p. 112-20.
(39) Gordon G. NutraSweet Questions Swirl (How Sweet It Isn’t a UPI Investigative Report ). Seattle
Times. Seattle, Wash. Oct 13, 1987. p. F1: United Press International; 1987.
(40) Tephly T. Comments on the purported generation of formaldehyde from the sweetener aspartame
[letter: not peer-reviewed]. Life Sci 1999;65:157-60.
(41) Lutton J, Winston R, Rodman T. Multiple Sclerosis: Etiological Mechanisms and Future
Directions. Experimental Biology and Medicine 2004;229:12-20.

(42) Heinzow B. Formic acid in urine--a significant parameter in environmental diagnosis? Zentralbl
Hyg Umweltmed 1992;192(5):455-61.
(43) Alexander L, Berkeley A, Alexander A. Multiple Sclerosis Prognosis and Treatment. Illinois:
Charles C .Thomas Publisher; 1961.
(44) Hallpike J, Adams C, Tourtellotte W. Multiple Sclerosis, Pathology, diagnosis and management.
Baltimore: Williams & Wilkins.; 1983.
(45) Multiple Sclerosis Trust. History of MS. 2007. Available from: URL:
http://www.mstrust.org.uk/information/a2z/history.jsp
(46) Westler Foods Corp. The History of Food Canning. 2007. Available from: URL:
http://www.westlerfoods.com/pdf/canning_process.pdf
(47) Gold M. Scientific Abuse in Methanol / Formaldehyde Research related to Aspartame 2008.
Available from: URL: http://www.holisticmed.com/aspartame/abuse/methanol.html
(48) G.D. Searle Co. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and
Development. Petition submitted to the US FDA. United States Food and Drug Administration;
1983.
(49) Westline T. Methanol Warning Sign.: T&B Westline; 1965.
(50) Soffritti M, Belpoggi F, Tibaldi E, Espost iD, Lauriola M. Lifespan Exposure to Low Doses of
Aspartame Beginning During Prenatal Life Increases Cancer Effects in Rats. Environmental
Healt Perspectives, National Institute of Health 2007.
(51) Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C. Results of Long-Term

Results of Long-Term Experimental Studies on the Carcinogenicity of Methyl Alcohol and
Ethyl Alcohol in Rats. N.Y. Acad. Sci. 2002;982:46.
(52) Roe O. Species Differences in Methanol Poisoning. I. Minimal Lethal Doses. Symptoms. and
Toxic Sequelae of Methanol Poisoning in Humans and Experimental Animals. CRC Critical
Reviews in Toxicology 1982;18:376-90.
(53) Rao K, Aurora A, Muthaiyan S, Ramakrishnan S. Methanol toxicity - an experimental study. Bull
Jawaharlal Inst Post-Grad Med Educ Res 1977;2:1.
(54) Walton RG, Hudak R, Green-Waite R. Adverse Reactions to Aspartame: Double-Blind Challenge
in Patients from a Vulnerable Population. Biological Psychiatry 1993;34:13.
(55) Smith E, Taylor R. Acute Toxicity of Methanol in the Folate-Deficient Acatalasemic Mouse.
Toxicology 1982;25:271.
(56) Thomas P. Aspartame: The Shocking Story of the World’s Bestselling Sweetener. The Ecologist

2005;36(Sept.).
(57) Nauta W, Lampert P, Yount V. Decision of the Public Board of Inquiry ,Department of Health
and Human Services. 44 Fed. Reg. 31716: U.S. Food and Drug Administration; 1979.
(58) Center for Disease Control. Center for Disease Control 1984. Evaluation of Consumer
Complaints Related to Aspartame Use. Morbidity and Mortality Weekly Report. 33:605. 1984.
(59) Center for Disease Control. Center for Disease Control 1976. Occupational Exposure to Methyl
Alcohol. U.S. Department of Health. Education. and Welfare.; 1976.
(60) Hodgson P. Office of Hon Pete Hodgson. NZ Minister of Health. 2007. Personal
Communication.; 2007.
(61) Frankenburg W. Chemical Changes in the Harvested Tobacco Leaf. Part II. Chemical and
Enzymic Conversions during Fermentation and Aging. Advances in Enzymology. 10:351
1950;10:351.
(62) Neuberg C, Kobel M. Uber die encymatische Abspaltung von Methylalkohol aus Pektin durch ein
Ferment dis Tabaks. Zeitschrift Für Lebensmitteluntersuchung Und -Forschung A
1939;77(3):272.
(63) Newsome J, Normal V, Keith C. Vapor Phase Analysis of Cigarette Smoke. Tobacco Science
9:102 1965;9:102.
(64) Larsson B. Gas Chromatography of Organic Volatiles in Human Breath and Saliva. Acta
Chemica Scandinavica 1965;19:159-64.
(65) Fellenberg T. Uber den Nachweis und die Bestimmung des Methylalkohols. sein Vorkommen in
den verschiedenen Nahrungsmitteln und das Verhalten der methylalkoholhaltland. Biochem Z
1918;85:45-117.
(66) Kertesz Z. The Pectic Substances. New York: Interscience Publishers Inc.; 1951.
(67) Hernan M, Olek M, Ascherio A. Cigarette Smoking and Incidence of Multiple Sclerosis.
American Journal of Epidemiology 2001;154(1):69-74.
(68) Hernan M, Jick S, Logroscino G, Olek M, Ascherio A, Jick H. Cigarette smoking and the
progression of multiple sclerosis. Brain 2005;128(6):1461-65.
(69) Lauer K. Multiple sclerosis in relation to meat preservation in France and Switzerland.
Neuroepidemiology 1989;8(6):308-15.
(70) In Tech. Turning Waste To Profit. 2001. Available from: URL:

http://www.allbusiness.com/manufacturing/computer-electronic-product-
manufacturing/1075167-1.html

(71) Nortvedt M, Riise T, Maeland J. Multiple sclerosis and lifestyle factors: The Hordaland Health
Study. Neurol Sci 2005;26:334-39.
(72) Bamford R, Sibley W, Thies C. Seasonal variation of multiple sclerosis exacerbations in Arizona.
Neurology 1983;33:697-701.
(73) Hardy C, Palmer B, Muir K, Sutton A, Powell R. Smoking history. alcohol consumption. and
systemic lupus erythematosus: a case-control study. Ann Rheum Dis 1998;57:451-5.
(74) Landtblom A, Flodin U, Sodeifeldt B, Wolfson C, Axelson O. Organic Solvents and Multiple
Sclerosis: A Synthesis of the Current Evidence. Epidemiology 1996;7(4):429-33.
(75) Grabenstein J. ImmunoFacts: Vaccines & Immunologic Drugs. St. Louis. MO.: Wolters Kluwer
Health Inc.; 2006.
(76) Weiner H, Dau P, Khatri B, Petajan J, Birnbaum G, McQuillen M, et al. Double-blind study of
true vs. sham plasma exchange in patients treated with immunosuppression for acute attacks of
multiple sclerosis. Neurology. 1989;39(9):1143-9.
(77) Hirtz D, Thurman D, Gwinn-Hardy K, Mohamed M, Chaudhuri A, Zalutsky R. How common are
the “common” neurologic disorders? Neurology 2007;68:326-37.
(78) Monte W. Sickly Sweet: Is your Diet Sweetener Killing You? Fitness Life 2007;33:30-3.
(79) Corona T, Roman G. Multiple Sclerosis in Latin America. Neuroepidemiology 2005;26:1-3.
(80) Grimaldi L, Palmeri B, Salemi G, Giglia G, D’Amelio M, Grimaldi R. High prevalence and fast
rising incidence of multiple sclerosis in Caltanissetta. Sicily. southern Italy.
Neuroepidemiology. 2007;28(1):28-32.
(81) Kira J. Epidemiology of multiple sclerosis in Japanese: with special reference to opticopsinal
multiple sclerosis. Rinsho Shinkeigaku. 2006;46(11):859-62.
(82) Lauer K. Ditary Changes in Temporal Relation to Multiple Sclerosis in the Faroe Islands: An
Evaluation of Literary Sources. Neuroepidemiology 1989;8:200-6.
(83) Lazoff M. Multiple Sclerosis Symptoms. 2005. Available from: URL:

www.emedicine.com/emerg/topic321.htm#section%7Eauthor_information
(84) Waksman B. Mechanisms in multiple sclerosis. Nature 1985;318:104.
(85) Leibowitz U, Alter M. Multiple Sclerosis: Clues to its cause.: North-Holland Publishing Co.;
1973.
(86) Saha A, Khudabaksh A. Aberrations Induced by Methanol in Germinal Cells of Grasshopper.

Oxya velox Fabricius. Indian J Exper Biol 1974;12:72.
(87) DeLuca J. Alcohol and Health. Fourth Special Report to the U.S. Congress Secretary of Health
and Human Services. Secretary of Health and Human Services; 1981.
(88) Roe O. The Metabolism and Toxicity of Methanol. Parmacological Review 1955;7:399-412.
(89) Bingham E. Expert Panel Report, Human Reproductive and Developmental Toxicity of Methanol
Toxicity of Methanol. Draft with important internal comment. http://cerhr.niehs.nih.gov: U.S.
Department of Health & Human Services National Toxicology Program; 2001.
(90) Gallegher L, Lea R. The epidemiology of multiple sclerosis in New Zealand. The New Zealand
Medical Journal 2005;118:1212-3.
(91) Boyles S. MS Increasingly a Woman’s Disease. MedicineNet.com

Changes in the Sex Ratio over Time in Multiple Sclerosis, 59th Annual meeting of the
American Academy of Neurology, Boston Cutter, G. et al 2007. Available from: URL:
www.medicinenet.com/script/main/art.asp?articlekey=80722
(92) Burbacher T, Grant K, Shen D. Reproductive and offspring Developmental Effects Following
Maternal Inhalation Exposure to Methanol in Nonhuman Primates. Health Effects Institute;
1999.
(93) Shelby M. NTP-CERHR Monograph on the Potential Human Reproductive and Developmental
Effects of Methanol. 2003. U.S. Department of Health and Human Services; 2003.
(94) Frezza M, di Padova C, Pozzato G, Terpin M, Baraona E, Lieber C. High blood alcohol levels in
women. The role of decreased gastric alcohol dehydrogenase activity and first-pass
metabolism. N Engl J Med. 1990;322(2):95-9.
(95) Christenson L, Borrowman T, Vachon C, Tollefson M, Otley C, Weaver A, et al. Incidence of

Basal Cell and Squamous Cell Carcinomas in a Population Younger Than 40 Years. JAMA
2005;294(6):681-90.
(96) Mahalik M, Gautieri R. Reflex Responsiveness of CF-1 Mouse Neonates Following Maternal
Aspartame Exposure. Res Commun in Psych 1984;9:385.
(97) Dahl O, Aarseth J, Myhr K, Nyland H, Midgard R. Multiple sclerosis in Nord-Trondelag County.
Norway. A prevalence and incidence study. Acta Neurol Scand 2003;109(6):378-84.
(98) Fighting Autism. Number of Cases 2001. Available from: URL:

http://www.fightingautism.org/idea/autism.php?
(99) Gettler A, St.George A. Wood Alcohol Poisoning. Journal of the American Medical Association
1918;70:145.

(100) Sturtevant F. Use of Aspartame in Pregnancy. Int J Fertil 1985;30(1):85.
(101) Anonymous. Therapeutic claims in multiple sclerosis.: National Multiple Sclerosis Society;
1982.
(102) Sturtevant F. Does Aspartame Cause Methanol Toxicity? Fd Chem Toxic 1985;23(10):961.
(103) Infurna R, Weiss B. Neonatal Behavioral Toxicity in Rats Following Prenatal Exposure to
Methanol. Teratology 33:259-265 1986;33:259-65.
(104) Bolon B, Dorman D, Janszen D, Morgan K, Welsch F. Phase-specific developmental toxicity in

mice following maternal methanol inhalation. Fundam Appl Toxicol 1993;21(4):508-16.
(105) Dorman D, Bolon B, Struve M, LaPerle K, Wong B, Elswick B, et al. Role of formate in
methanol-induced exencephaly in CD-1 mice. Teratology 2005;51(1):30-40.
(106) Potts A, Praglin J, Farkas J, Orbison L, Chickering D. Studies on the Visual Toxicity of
Methanol. VIII. Additional Observations on Methanol Poisoning in the Primate Test Object.
Am J Ophthalmol. 1955;40(5 part 2):76-83.
(107) Kavet R, Nauss K. The Toxicity of Inhaled Methanol Vapors. Critical Reviews in Toxicology
1090;21(1):21-50.
(108) Rabinowitch I. Biochemical Studies in a Fatal Case of Methyl Alcohol poisoning. Archives of
Internal Medicine Chicago 1922;29:821-27.
(109) Kane R, Talbert W, Harlan J, Sizemore G, Cataland S. A methanol poisoning outbreak in

Kentucky. A clinical epidemiological study. Arch Environm Hlth 1968;17:119.
(110) Menne F. Acute Methyl Alcohol Poisoning. a Report of Twenty-Two Instances with
Postmortem Examinations. Archives of Pathology. 26:77 1935;26:77-92.
(111) Altman L. Two Win Nobel Prize for Discovering Bacterium Tied to Stomach Ailments. New
York Times 2005;Sect. Science.
(112) Kini M, Cooper J. Biochemistry of Methanol Poisoning-III; The Enzymic Pathway for the
Conversion of Methanol to Formaldehyde. Biochemical Pharmacology 1961;8:207.
(113) Kini M, Cooper J. Biochemistry of Methanol Poisoning; The Effect of Methanol and its
Metabolites on Retinal Metabolism. Biochemical Journal 1962;82:164.
(114) French D, Edsall J. The Reactions of Formaldehyde with Amino Acids and Proteins. Adv
Protein Chem 1945;2:277-335.
(115) Leaf G, Zatman L. A Study of the Conditions Under Which Methanol May Exert a Toxic
Hazard in Industry. British Journal of Industrial Medicine 1952;9:19.

(116) Cooper J, Kini M. Biochemical Aspects of methanol Poisoning. Biochemical Pharmacology

1962;11:405.
(117) Cooper J, Felig P. The Biochemistry of Methanol Poisoning. II. Metabolic Acidosis in the
Monkey. Toxicol.Appl.Pharmacol 1961;3:202.
(118) Clay K, Murphy R, Watkins W. Experimental Methanol Toxicity in the Primate; Analysis of
Metabolic Acidosis. Toxicol.Appl.Pharmacol 1975;34:49.
(119) McLean D, Jacobs H, Mielke B. Methanol Poisoning A Clinical and Pathological Study. Annals
of Neurology 1979;8:161.
(120) Posner H. Posner HS. 1975. Biohazards of Methanol in Proposed New Uses. J Toxicol Environ
Health 1975;1:153.
(121) Tephly T, McMartin K. Methanol metabolism and toxicity. In: Stegink L, Filer L, editors.
Aspartame: Physiology and Biochemistry. New York: Marcel Dekker Inc.; 1984. p. 111-40.
(122) von Oettingen W. The Aliphatic Alcohols Their Toxicity and Potential Dangers in Relation to
Their Chemical Constitution and Their Fate in Metabolism. Public Health Bulletin 1943;281:8.
(123) Schink B, Zeikus J. Microbial Methanol Formation: A Major End product of pectin Metabolism.
Current Microbiology 1980;4:387-89.
(124) Nelson B, Brightwell W, MacKenzie D, Khan A, Burg J, Weigel W, et al. Teratological

Assessment of Methanol and Ethanol at High Inhalation Levels in Rats. Fundam Appl Toxicol
1985;5:727.
(125) Sollmann T. Studies of chronic intoxications on albino rats. II. Alcohol; Methyl. ethyl. “wood”
and acetone. J Pharmacol Exper Therap 1920;16:291.
(126) Victor M. Some Observations on the Neurological Effects of Alcohol Intoxication and
Withdrawal. In: Roizin L, Shiraki H, Grcevic N, editors. Neurotoxicology. New York: Raven
Press; 1977. p. 517-27.
(127) Smith S, Smith S, Buckley B. Combined Formate and Lactate Acidosis in Methanol Poisoning.
Lancet 1981;2(8258):1295-6.
(128) Fulop M. Methanol Intoxication. Lancet 1982;1(8267):338.
(129) Roe O. The Ganglion Cells of the Retina in Cases of Methanol Poisoning in Human Beings and
Experimental Animals. Acta Opthalmologica 1948;26:169-82.
(130) Potts A. The Aliphatic Alcohols, Chapter 15. In: Sears M, editor. “Pharmacology of the Eye” -
Handbook of Experimental Pharmacology Vol. 69: XXV. Berlin, Heidelberg, New York,

Tokyo: Springer-Verlag New York, LLC; 1984. p. 639-53.
(131) Martin-Amat G, McMartin K, Hayreh S, Hayreh M, Tephly T. Methanol Poisoning Ocular

Toxicity Produced by Formate. Toxicology and Applied Pharmacology 1978;45:201-8.
(132) Makar A, Tephly T, Mannering G. Methanol Metabolism in the Monkey. Molecular

Pharmacology 1968;4:471-83.
(133) Majchrowicz E. Biochemical Pharmacology of Ethanol. New York: Plenum Press; 1973.
(134) Majchrowicz E, Mendelson J. Blood Methanol Concentrations During Experimentally Induced

Ethanol Intoxication in Alcoholics. The Journal of Pharmacology and Experimental
Therapeutics 1971;179:293-300.
(135) Magrinat G, Dolan J, Biddy R, Miller L, Korol B. Ethanol and Methanol Metabolites in Alcohol
Withdrawal. Nature 1973;244:234-5.
(136) Walder A, Redding J, Faillace L, Steenberg W. Rapid Detoxification of the Acute Alcoholic
with Hemodialysis. Surgery 1969;66:201-7.
(137) Guggenheim M, Couch J, Weinberg W. Motor Dysfunction as a Permanent Complication of

Methanol Ingestion. Archives of Neurology 1971;24:550-4.
(138) Scott E, Helz M, McCord C. The Histopathology of Methyl Alcohol Poisoning. American
Journal of Clinical Pathology 1933;3:311-19.
(139) Keyvan-Larijarni H, Tannenberg A. Methanol Intoxication; Comparison of Peritoneal Dialysis

and Hemodialysis Treatment. Arch Intern Med 1974;134:293-6.
(140) Gronning M, Albrektsen G, Kvale G, Moen B, Aarli J, Nyland H. Organic solvents and multiple
sclerosis: a case-control study. Acta Neurol Scand 1993;88:247-50.
(141) Agner K, Hook O, von Porat B. The Treatment of Methanol Poisoning with Ethanol. With
Report of Two Cases. Quarterly Journal of Studies on Alcohol 1949;9:515-22.
(142) Roe O. The roles of Alkaline salts and Ethyl Alcohol in the treatment of Methanol Poisoning.
Quart.J.Stud.Alcohol 1950;11:107-12.
(143) Erlanson P, Fritz H, Hagstam K, Liljenberg B, Tryding N, Voigt G. Severe Methanol

Intoxication. Acta Medica Scandinavica 1965;177(4):393-408.
(144) Browning E. Methanol Toxicology. In: Browning E, editor. Toxicity and Metabolism of
Industrial Solvents. New York: Elsevier Publishing Company; 1965. p. 315-23.
(145) Humphries P, Pretorius E, Naud H. Direct and indirect cellular effects of aspartame on the brain.
Eur J Clin Nutr 2007;8:1-12.

(146) Isaacs R. Acute Methyl Alcohol Poisoning. JAMA 1920;75:718-21.
(147) Pick L, Bielschowsky M. Ueber histologische Befunde im Auge and im Zentralnervensystem

des Menschen bei akuter todlicher Vergiftung mit Methylalkohol. Klin Wschr 1912;49:888-93.
(148) Sharpe J, Hostovsky M, Bilbao J, Rewcastle N. Methanol optic neuropathy; A histopathological

study. Neurology 1982;32:1093-100.
(149) Waksman B, Reynolds W. Multiple Sclerosis as a Disease of Immune Regulation. Proceedings

of the Society for Experimental Biology and Medicine 1984;175:282-94.
(150) Pohl J. Ueber die Oxydation des Methyl Und Aethylalkohols im Thierkorper. Naunyn-
Schmiedeberg’s Arch Exp Path Pharmak 1893;31:281-302.
(151) Anderson C, Rubinstein D, Filley C, Stears J. MR enhancing brain lesions in methanol

intoxication. J Comput Assist Tomogr 1997;21(5):834-6.
(152) Fackelmann K. Myelin on the Mend: Can antibodies reverse the ravages of multiple sclerosis?
Science News 1990;137:218-9.
(153) Wolfgram F. What if Multiple Sclerosis isn’t an Immunological or Viral Disease? The Case for
a Circulating Toxin. Neurochemical Research 1979;4:1-14.
(154) Adams C. Histochemical Contributions to the Study of Multiple Sclerosis. In: Stoward P, Polak
J, editors. Histochemistry: The Widening Horizons: John Wiley & Sons Ltd.; 1981. p. 163-81.
(155) Giulisni G., Brizoli E., Angeleri VA., Caraffa 0., Foschih N., Speranzini C. The organic glue
solvents in the pathogenesis of multiple sclerosis: an
http://www.stuff.co.nz/environment/rena-crisis/5789174/Deliberate-course-sent-Rena-to-
reefEpidemiological study. (Battaglia MA., Crimi G., eds. International Multiple Sclerosis
Conference, Rome,Sept. 14-17,1988; 1988 Sep 14-17; Rome. An Update on Multiple Sclerosis
(International Congress Series).
(156) Brown M, Goldstein J. Lipoprotein Metabolism in the Macrophage; Implications for Cholesterol
Deposition in Atherosclerosis. Annu Rev Biochem 1983;52:223-61.
(157) Tephly T. Factors in Responses to the Environment. Introduction. Federation Proceedings

1977;36(5):1627.
(158) Blundell J, Hill A. Paradoxical Effects of an Intense Sweetener (Aspartame) on Appetite. Lancet
1986;1:1092.
(159) Coulombe R, Sharma R. Neurobiochemical Alterations Induced by the Artificial Sweetener

Aspartame (NutraSweet). Toxicology and Applied Pharmacology 1986;83:79-85.

(160) Walton R. Seizure and Mania After High Intake of Aspartame. Journal of the Academy of
Psychosomatis Medicine 1986;27:218-20.
(161) Roak-Foltz RI, Leveille G. Projected Aspartame Intake: Daily Ingestion of Aspartic Acid.
Phenylalanine. and Methanol In AspartameAspartame. In: Stegink L, Filer L, editors.
Aspartame: Physiology and Biochemistry. New York: Marcel Dekker; 1984. p. 201-5.
(162) Main R, Barry M. On The Toxicity of Methyl Alcohol in Extracts and Medicine. Illinois
(163) Koller C. Poisoning by Wood Alcohol: A case of Complete Blindness (Transitory) with
Recovery of Vision. Medical Record 1905;68(1):10-2.
(164) Stedman T. The Wood Alcohol Question. Medical Record 1905;67:59,102,381.
(165) Wood C. Death and Blindness as a Result of Poisoning by Methyl Alcohol or Wood Alcohol
and Its Various Preparations. International Clinics; A Quarterly of Clinical Lectures
1906;16:68.
(166) Kritchevsky M. Multiple Sclerosis. In: Wigbert CW, MD., editor. Neurology for Non-
Neurologists. Philadelphia: Grune & Stratton; 1988. p. 177-87.
(167) Blaivas J. Evaluation of Urinary Bladder Symptoms in Multiple Sclerosis. In: Poser C, editor.
The Diagnosis of Multiple Sclerosis. New York: Thieme - Stratton Inc.; 1984.
(168) Kurtzke J. Epidemiologic contributions to multiple sclerosis; An overview. Neurology

1980;30(7):61-79.
(169) Matthews B. Multiple Sclerosis: The Facts. New York Toronto: Oxford University Press; 1978.
(170) Mawdsley C, Mayer R. Nerve Conduction in Alcoholic Polyneuropathy. Brain 1965;88:335-56.
(171) Benton C, Calhoun F. The Ocular Effects of Methyl Alcohol Poisoning. Report of a Catastrophe
involving Three Hundred and Twenty Persons. Trans Amer Acad Ophthal Otolaryng
1952;56:875-85.
(172) Yano K, Rhoads G, Kagan A. Coffee. Alcohol and Risk of Coronary Heart Disease Among
Japanese Men Living in Hawaii. NEJM 1977;297(8):405-9.
(173) Lester D. Endogenous Ethanol: A Review. Quarterly Journal of Studies on Alcohol

1961;22:555-74.
(174) Lester D. The Concentration of Apparent Endogenous Ethanol. Q J Stud Alcohol 1962;23:17.
(175) Lieber C, DeCarli L. Hepatic Microsomal Ethanol-Oxidizing System. In vitro characteristics and
adaptive properties in vivo. The Journal of Biological Chemistry 1970;245(10):2505-12.

(176) Klatsky A, Friedman G, Siegelaub A. Alcohol and Mortality. Annals of Internal Medicine
1981;95:139-45.
(177) Hoque M., Monte WC., Black L., Johnston CS. Methanol Neuropathy and Teratology A
Histological Study on Long-Evans Rats. FASEB 1988;25(2(6)):A513.
(178) Benditt E. The Origin of Atherosclerosis. Scientific American 1994;236(2):74-85.
(179) Metz B, Kersten G, Jong A, Meiring H. Identification of formaldehyde-induced modifications in

proteins: reactions with diphtheria toxin 2005. Available from: URL: http://igitur-
archive.library.uu.nl/dissertations/2005-0303-105230/c7.pdf
(180) Christian T, Kleiss B, Yokelson R, Holzinger R, Crutzen P, Hao W, et al. Comprehensive

laboratory measurements of biomass-burning emissions: 1. Emissions from Indonesian,
African, and other fuels. J Geophys Re 2003;108(D23):4719-32.
(181) Grey D. Summary of Adverse Reactions Attributed to Aspartame. US Department of Health and
Human Services; 1995.
(182) Criqui M, Wallace R, Heiss G, Mishkel M, Schonfeld G, Jones G. Cigarette smoking and
plasma high-density lipoprotein cholesterol. The Lipid Research Clinics Program Prevalence
Study. Circulation 1980;62(4 Pt 2):70-6.
(183) Parthasarathy N, Kumar R, Manikandan S, Devi R. Methanol-Induced Oxidative Stress in Rat

Lymphoid Organs. J Occup Health 2006;48:20-7.
(184) Hawkes C. Is multiple sclerosis a sexually transmitted infection? Journal of Neurology

Neurosurgery and Psychiatry 2002;73(4):439-43.
(185) Kantarci O, Wingerchuk D. Epidemiology and natural history of multiple sclerosis: new
insights. Curr Opin Neurol 2006;19:248-54.
(186) Dahshan A, Donovan K. Auto-Brewery Syndrome in a Child With Short Gut Syndrome: Case
Report and Review of the Literature. Journal of Pediatric Gastroenterology and Nutrition
2001;33:214-15.
(187) Borras E, Coutelle C, Rosell A, Fernandez-muixi F, Broch M, Crosas B. Genetic Polymorphism

of Alcohol Dehydrogenase in Europeans: The ADH2*2 Allele Decreases the Risk for
Alcoholism and Is Associated With ADH3*1. Hepatology 2000;31(4):984-89.
(188) Erickson S, Kulkarni AB. Methanol in Normal Human Breath. Science 1963;141:639-40.
(189) Wood C, Buller F. Poisoning by Wood Alcohol: Cases of Death and Blindness from Columbian
Spirits and other Nethylated Preparations. JAMA 1904;43:972-77, 1058-62,1117-23,1213-
21,1289-95.

(190) Kingsbury K. The Changing Face Of Breast Cancer. TIME 2007;107(16):36-40.
(191) Gram I, Braaten T, Terry P, Sasco A. Breast Cancer Risk Among Women Who Start Smoking as
Teenagers. Cancer Epidemiology Biomarkers & Prevention 2005;14(1):61-6.
(192) Nagata C, Mizoue T, Tanaka K, Tsuji I. Tobacco Smoking and Breast Cancer Risk: An
Evaluation Based on a Systematic Review of Epidemiological Evidence among the Japanese
Population. Jpn J Clin Oncol 2006;36(6):387-94.
(193) Kingsbury K. The Changing Face Of Breast Cancer. TIME Magazine 2007;107(16):36.
(194) Monte W. A Deadly Experiment: MS & Aspartame Are They Linked? Fitness Life 2007;34:36-
43.
(195) Kurtzke J. Epidemiology and multiple sclerosis a personal review 2003. Available from: URL:
http://www.direct-ms.org/pdf/EpidemiologyMS/EpidemiologyMS.pdf
(196) Godish T. Formaldehyde Exposures from Tobacco Smoke: A Review. American Journal of
Public Health 1989;79(8):1044-45.
(197) Bressler J. The Bressler Report. United States Food and Drug Administration; 1977.
(198) Puchtler H, Meloan S. On the chemistry of formaldehyde fixation and its effect on
immunohistochemical reactions. Histochemistry 1985;82:201-4.
(199) Taskinen HK., Kyyronen P, Sallmen M, Virtanen S, Liukkonen T, Huida O. Reduced Fertility
Among Female Wood Workers Exposed to Formaldehyde. American Journal of Industrial
Medicine 1999;36:206-12.
(200) Metz B., Kersten G, Hoogerhout P, Brugghe H, Timmermans H. Identification of

Formaldehyde-induced Modifications in Proteins. The Journal of Biological Chemistry
2004;279(8):6235-43.
(201) Hansen J, Contreras K, Harris C. Methanol. Formaldehyde. and Sodium Formate Exposure in
Rat and Mouse Conceptuses: A Potential Role of the Visceral Yolk Sac in Embryotoxicity.
Birth Defects Research (Part A) 2004;73:72-82.
(202) Monte W. Bittersweet: Aspartame Breast Cancer Link. Fitness Life 2008;34:21-2.
(203) Anonymous. Definition of Adenocarcinoma. 2001. Available from: URL:

http://www.healthlike.com/galecontent/adenocarcinoma>
(204) Darwish A., Roth C, Duclos P, Ohnd S, Nassar A. Investigation into a cluster of infant deaths
following immunization: evidence for methanol intoxication. Vaccine 20 2002;20:3585-89.

(205) Shahangian S, Ash O. Formic and Lactic Acidosis in a Fatal Case of Methanol Intoxication. Clin
Chem 1986;32(2):295-97.
(206) Rogers J, Brannen K, Barbee B, Zucker R, Degitz S. Methanol Exposure During Gastrulation
Causes Holoprosencephaly. Facial Dysgenesis. and Cervical Vertebral Malformations in
C57BL/6J Mice. Birth Defects Research 2004;71:80-8.
(207) Abbott B, Ebron-McCoy M, Andrews J. Cell death in rat and mouse embryos exposed to
methanol in whole embryo culture. Toxicology 1994;97:159-71.
(208) Arigeleri F., Bollettini 0., Brizoli E., Giuliani 0., Scarpino 0. A prevalence study of multiple
sclerosis in the Regiorse Marchi, Italy. (Battaglia MA., Crimi G., eds. International Multiple
Sclerosis Conference, Rome,Sept. 14-17,1988; 1988 Sep 14-17; Rome.
(209) Henry T. Ditto-machine fluid harmful. Union charges. USA Today 1995 Mar 22;Sect. F:F-2.
(210) Walsh S, DeChello L. Excess Autoimmune Disease Mortality Among School Teachers.
Rheumatology 2001;28:1537-45.
(211) Kruse J. Methanol poisoning. Intensive Care Med 1992;18:391-7.
(212) d’Alessandro A, Osterloh J, Chuwers P, Quinlan P, Kelly T, Becker C. Formate in Serum and
Urine after Controlled Methanol Exposure at the Threshold Limit Value. Environmental Health
Perspectives 1994;102(2):178-81.
(213) Bernstein L, Allen M, Anton-Culver H, Deapen D, Horn-Ross P. High breast cancer incidence
rates among California teachers: results from the California Teachers Study (United States).
Cancer Causes and Control 2002;13:625-35.
(214) Redelings M, McCoy L, Sorvillo V. Multiple Sclerosis Mortality and Patterns of Comorbidity in
the United States from 1990 to 2000. Neuroepidemiology 2006;26:102-07.
(215) Becker C. Methanol Poisoning. Journal of Emergency Med 1983;1:51-8.
(216) Crabb D, Matsumoto M, Chang D, You M. Overview of the role of alcohol dehydrogenase and
aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology.
Proceedings of the Nutrition Society 2004;63:49-63.
(217) King A, Threlfall W, Band P, Gallagher R. Mortality Among Female Registered Nurses and
School Teachers in British Columbia. American Journal of Industrial Medicine 1994;26:125-
32.
(218) Mori O, Haseba T, Kameyama K, Shimizu H. Histological distribution of class III alcohol
dehydrogenase in human brain. Brain Research 2000;852:186-90.
(219) Labreche F, Goldberg M. Exposure to Organic Solvents and Breast Cancer in Women: A

Hypothesis. American Journal of Industrial Medicine 1997;32:1-14.
(220) Allili-Hassani A, Martinez S, Peralba J. Alcohol dehydrogenase of human and rat blood vessels.
FEBS Letters 1997;405:26-30.
(221) Buehler R, Hess M, Wartburg J. Immunohistochemical Localization of Human Liver Alcohol

Dehydrogenase in Liver Tissue. Cultured Fibroblasts. and HeLa Cells. American Association
of Pathologists 1982;108(1):89-99.
(222) Alemany M. Open Letter To Hawaii House Committee on Health. Maria Alemany Professor of
Nutrition and Food Science University of Barcelona. Spain.; 2008 Feb 12.
(223) Stegink L. Aspartame Metabolism in Humans: Acute Dosing Studies. In: Stegink L, Filer L,
Tephly T, editors. Aspartame Physiology and Biochemistry. New York: Marcel Dekker; 1984.
p. 509-54.
(224) Kim J, Mastronardi F, Wood D, Lubman D, Zand R, Moscarello M. Multiple Sclerosis: An

important role for post-translational modifications of myelin basic protein in pathogenesis.
Molecular & Cellular Proteomics 2003;2(7):453-62.
(225) Szende B, Tyihak E., Trez L. Role of arginine and its methylate derivatives in cancer biology
and treatment. Cancer Cell International 2001;1(3):1-5.
(226) Joiris N. Le Scotome central positif et Transitoire signe de weekers) dans la nevrte optique
Retrobulbaire. au cours de L’intoxication aigue par l’alcool methylique. Arch Dophtalmolojie
1935;1:52.
(227) Mumford P. Two Forms of Dermatitis Due to the Use of Methylated Spirit Externally. British
Medical Journal 1925;2:607.
(228) Novick N. Aspartame-Induced Granulomatous Panniculitis. Annals of Internal Medicine

1985;102(2):206-7.
(229) Rao K, McConnell R, Waisman HA. 52 Week Oral Toxicity Study in the Infant Monkey (SC-
18862). In: Searle Research and Development, editor. Docket File. Aspartame for use as a
Sweetener in Carbonated Beverages.. Petition submitted to the United States Food and Drug
Administration - FAP Part of 2A3661; 1972.
(230) Kesselring J. Multiple Sclerosis.: Cambridge University Press; 1997.
(231) Obeid R, Kasoha M, Knapp J, Kostopoulos P. Folate and Methylation Status in Relation to
Phosphorulated Tau Protein and Amyloid in Cerebrospinal Fluid. 53(6):1129-1136. Clinical
Chemistry 2007;53(6):1129-36.
(232) Staehelin H. Micronutrients and Alzheimer’s disease. Proceedings of the Nutrition Society
2005;64:565-70.

(233) Yang C, Otsuka M, Ohama E. An Immunohistochemical Study of Perivascular Plaque in

Alzheimer’s Disease and Cerevral Amyloid Angiopathy. Yongo Acta Medica 2003;46:9-16.
(234) Nie C, Wei Y, Chen X, Liu Y, Dui W, Liu Y, et al. Formaldehyde at Low Concentration Induces
Protein Tau into Globular Amyloid-Like Aggregates In Vitro and In Vivo. PLoS ONE
2007;2(7:e629):1-13.
(235) Nie C, Wang X, Liu Y, Perrett S, He R. Amyloid-like aggregates of neuronal tau induced by
formaldehyde promote apoptosis of neuronal cells. BMC Neuroscience 2007;8(9):1-16.
(236) Köppel C, Baudisch H, Schneider V, Ibe K. Suicidal ingestion of formalin with fatal
complications. Intensive Care Med 1990;16(3):212-4.
(237) Andersen K, Launer L, Dewey M, Letenneur L, Ott A, Copeland J. Gender differences in the
incidence of AD and vascular dementia: The EURODEM Studies. Neurology
1999;53(9):1992-7.
(238) Palmisano J, Gruver C, Adams N. Absence of anion gap metabolic acidosis in severe methanol
poisoning: a case report and review of the literature. Am J Kidney Dis 1987;9(5):441-4.
(239) Hovda K, Munda lH, Urdal P., McMartin K, Jacobsen D. Extremely slow formate elimination in
severe methanol poisoning: a fatal case report. Clin Toxicol (Phila) 2007;45(5):516-21.
(240) Alemany M. Open Letter To The Public. Maria Alemany Professor of Nutrition and Food
Science University of Barcelona. Spain. http://www.mpwhi.com/hhc-malemany.pdf:; 2008.
(241) Zheng T, Holford T, Taylor Mayne S, Luo J. A case-control study of occupation and breast-
cancer risk in Connecticut. J Cancer Epidemiol Prev 2002;7(1):3-11.
(242) Stürmer T, Wang-Gohrke S, Arndt VB, H., Kong X, Kreienberg R, Brenner H. Interaction
between alcohol dehydrogenase II gene, alcohol consumption, and risk for breast cancer. Br J
Cancer 2002;87(5):519-23.
(243) Mann K, Dengler W. Changes in the central nervous system of alcohol dependent patients.
Research Society of Alcoholism 2005;29(5):896-901.
(244) Naya M, Nakanishi J. Risk assessment of formaldehyde for the general population in Japan.
Regul Toxicol Pharmacol 2005;43(3):232-48.
(245) Amaducci L., Arfaoi0li C., Inzircari D., Marci M. Multiple sclerosis among shoe and leather
workers: an epidemiological survey in Florence. Acta Neurol Scand 1982;65:94-103.
(246) Kurtzke J. Epidemiologic evidence for multiple sclerosis as an infection. Clin Microbiol Rev
1993;6(4):382-427.

(247) Monte WC. Aspartame News Articles and other stuff.; 2009.
(248) Kurtzke J. Kurtzke JF. 2005. Epidemiology and etiology of multiple sclerosis. Phys Med
Rehabil Clin N Am 2005;16(2):327-49.
(249) Ong E, Glantz S. Tobacco industry efforts subverting International Agency for Research on
Cancer’s second-hand smoke study. Lancet 2000;355:1253-9,1197-9.
(250) Krieger N. Is breast cancer a disease of affluence. poverty. or both? The case of African
American women. Am J Public Health 2002;92(4):611-13.
(251) Kahn A, Blum D. Methyl alcohol poisoning in an 8-month-old boy: an unusual route of
intoxication. J Pediatr 1979;94(5):841-3.
(252) Anonymous. Spirit Duplicators. 2001. Available from: URL:

http://www.earlyofficemuseum.com/copy_machines.htm
(253) McCoy H, Cipolle R, Ehlers S, Sawchuk R, Zaske D. Severe Methanol Poisoning: Application
of a Pharmacokinetic Model for Ethanol Therapy and Hemodialysis. Amer J Med
1979;67:604-7.
(254) Roy M, Bailey B, Chalut D, Senécal P, Gaudreault P. What are the adverse effects of ethanol
used as an antidote in the treatment of suspected methanol poisoning in children? 41(2):155-
61. J Toxicol Clin Toxicol 2003;41(2):155-61.
(255) Medinsky M, Dorman D. Recent developments in methanol toxicity. Toxicology Letters

1955;82(83):707-11.
(256) Sakanashi T, Rogers J, Fu S, Connelly L, Keen C. Influence of maternal folate status on the
developmental toxicity of methanol in the CD-1 mouse. Teratology 1996;54(4):198-206.
(257) Thrasher J, Broughton A, Micevich P. Antibodies and immune profiles of individuals

occupationally exposed to formaldehyde: six case reports. Am J Ind Med 1988;14(4):479-88.
(258) Khoury S, Guttmann C, Orav E, Kikinis R, Jolesz F, Weiner H. Changes in Activated T Cells in
the Blood Correlate With Disease Activity in Multiple Sclerosis. Archives of Neurology
2000;57:1183-89.
(259) Makar A, Tephly T, Sahin G, Osweiler G. Formate metabolism in young swine. Toxicol Appl
Pharmacol 1990;105(2):315-20.
(260) Dorman D, Dye J, Nassise M, Ekuta J, Bolon B, Medinsky M. Acute Methanol Toxicity in
Minipigs. Fundam Appl Toxicol 1993;20(3):341-7.
(261) Tephly T, Green M, Gamble J. Formate metabolism in micropig. Toxicol Appl Pharmacol
1992;116(1):142-5.

(262) Anonymous. The History of MS. 2001. Available from: URL:

http://www.nationalmssociety.org/download.aspx?id=32
(263) Anonymous. Acting Positively: Strategic Implications of the Economic costs of Multiple
Sclerosis in Australia 2005. Available from: URL:
www.ms.org.au/msinformation/articles/MSFINALREPORTWINTER2005.pdf
(264) Paasma R, Hovda K, Tikkerberi A, Jacobsen D. Methanol mass poisoning in Estonia: outbreak
in 154 patients. Clin Toxicol (Phila) 2007;45(2):152-7.
(265) Hernández M, Holanda M, Tejerina E, González C. Methanol poisoning and heparin: a

dangerous couple? Am J Emerg Med 2004;22(7):620-21.
(266) Finkelstein Y, Vardi J. Progressive parkinsonism in a young experimental physicist following

long-term exposure to methanol. Neurotoxicology 2002;23:521-5.
(267) Belson M, Morgan B. Methanol Toxicity in a Newborn. J Toxicol Clin Toxicol 2004;42(5):673-
7.
(268) Kaphalia B, Carr J, Ansari G. Increased endobiotic fatty acid methyl esters following exposure
to methanol. Fundam Appl Toxicol 1995;28(2):264-73.
(269) Verhelst D, Moulin P, Haufroid V, Wittebole X, Jadoul M, Hantson P. Acute renal injury
following methanol poisoning: analysis of a case series. J Toxicol 2004;23(4):267-73.
(270) Bessell-Browne R, Bynevelt M. Two cases of methanol poisoning: CT and MRI features.
Australas Radiol 2007;51(2):175-8.
(271) Salzman M. Methanol Neurotoxicity. Clin Toxicol (Phila) 2006;44(1):89-90.
(272) Tephly T. The Toxicity of Methanol. Life Sciences 1991;48:1031-41.
(273) Tephly T. Comments on the purported generation of formaldehyde and adduct formation from
the sweetener aspartame. Life Sciences 1999;65(13):157-60.
(274) McMartin K, Martin-Amat G, Noker P, Tephly T. Lack of a role for formaldehyde in methanol
poisoning in the monkey. Biochem Pharmacol 1979;28(5):645-9.
(275) Thun M, Peto R, Lopez A, Monaco J, Henley S, Heath C. Alcohol consumption and mortality
among middle-aged and elderly U.S. adults. N Engl J Med 1997;337(24):1705-14.
(276) Ernstgård L, Shibata E, Johanson G. Uptake and disposition of inhaled methanol vapor in
humans. Toxicol Sci 2005;88(1):30-8.
(277) Hamilton R. Final Diagnosis - Multiple Sclerosis. 2001. Available from: URL: Search Result

http--path_upmc_edu-cases-case79-images-micro6_jpg
(278) Bolon B, Welsch F, Morgan K. Methanol-induced neural tube defects in mice: pathogenesis
during neurulation. Teratology 1994;49(6).
(279) Kloner R, Rezkalla S. Kloner RA. Rezkalla SH. 2007. To drink or not to drink? That is the
question. Circulation 2007;116(11):306-17.
(280) Vliegenthart R, Oei H, van den Elzen A, van Rooij F, Hofman A, Oudkerk M, et al. Alcohol
consumption and coronary calcification in a general population. Arch Intern Med
2004;164(21):2355-60.
(281) Akechi T, Asaki M, Uchitomi Y, Tsugane S. Alcohol consumption and suicide among middle-
aged men in Japan. Brit J of Psychiatry 2006;188:231-36.
(282) Woodward M, Tunstall-Pedoe H. Alcohol consumption. diet. coronary risk factors. and
prevalent coronary heart disease in men and women in the Scottish heart health study. J
Epidemiol Community Health 1995;49(4):354-62.
(283) Wei M, Gibbons L, Mitchell T, Kampert J, Blair S. Alcohol intake and incidence of type 2
diabetes in men. Diabetes Care 2000;23(1):16-21.
(284) Vahtera J, Poikolainen K, Kivimäki M, Ala-Mursula L, Pentti J. Alcohol intake and sickness
absence: a curvilinear relation. Am J Epidemiol 2002;156(10):969-76.
(285) Turvey C, Schultz S, Klein D. Alcohol use and health outcomes in the oldest old. Subst Abuse
Treat Prev Policy 2006;29(1):1-8.
(286) Mukamal K, Chung H, Jenny N, Kuller L, Longstreth W, Mittleman M, et al. Alcohol use and
risk of ischemic stroke among older adults: the cardiovascular health study. Stroke
2005;36(9):1835-6.
(287) McMartin K, Martin-Amat G, Tephly T. The Monkey as a Model in Methanol Poisoning. In:
Thurman R, editor. Alcohol and Aldehyde Metabolizing Systems.Volume II Enzymology and
Subcellular Organelles. San Diego, CA: Academic Press; 1977. p. 419-28.
(288) Lang I, Wallace R, Huppert F, Melzer D. Moderate alcohol consumption in older adults is
associated with better cognition and well-being than abstinence. Age Ageing 2007;36(3):256-
61.
(289) Koppes L, Dekker J, Hendriks H, Bouter L, Heine R. Moderate alcohol consumption lowers the
risk of type 2 diabetes: a meta-analysis of prospective observational studies. Diabetes Care
2005;28(3):719-25.
(290) Schwarzmann A. Methylalkoholvergiftung, chronische, durch Einatmen von Methyl-alkohol-

haltigen Formaldehyddarnpfen, Samml. Vergiftungsf. 1934;5(129):A 442-61.

(291) Medinsky M, Dorman D. Recent developments in methanol toxicity. Toxicology Letters

1995;82-83:707-11.
(292) Brenner H, Arndt V, Rothenbacher D, Schuberth S, Fraisse E, Fliedner T. The association

between alcohol consumption and all-cause mortality in a cohort of male employees in the
German construction industry. Int J Epidemiol 1997;26(1):85-91.
(293) Pedersen J, Heitmann B, Schnohr P, Grønbaek M. The combined influence of leisure-time

physical activity and weekly alcohol intake on fatal ischaemic heart disease and all-cause
mortality. Eur Heart J 2008;29(2):204-12.
(294) Hougaku H, Fleg J, Lakatta E, Scuteri A, Earley C, Najjar S, et al. Effect of light-to-moderate
alcohol consumption on age-associated arterial stiffening. Am J Cardiol 2005;95(8):1006-10.
(295) Mukamal K, Robbins J, Cauley J, Kern L, Siscovick D. Alcohol consumption. bone density. and
hip fracture among older adults: the cardiovascular health study. Osteoporos Int
2007;18(5):593-602.
(296) Thomsen J. Atherosclerosis in alcoholics. Forensic Sci Int 1995;75(2-3):121-31.
(297) Beulens J, Kruidhof J, Grobbee D, Chaturvedi N, Fuller J, Soedamah-Muthu S. Alcohol

consumption and risk of microvascular complications in type 1 diabetes patients: the
EURODIAB Prospective Complications Study. Diabetologia 2008;51(9):1631-8.
(298) Duffy J. Alcohol consumption and all-cause mortality. Int J Epidemiol 1995;24(1):100-5.
(299) Marmot M, Rose G, Shipley M, Thomas B. Alcohol and mortality: a U-shaped curve. Lancet
1981;1(8220 Pt1):580-83.
(300) Mänttäri M, Tenkanen L, Alikoski T, Manninen V. Alcohol and coronary heart disease: the roles
of HDL-cholesterol and smoking. J Intern Med 1997;241(2):157-63.
(301) Rouillier P, Boutron-Ruault M, Bertrais S, Arnault N, Daudin J, Bacro J, et al. Alcohol and
atherosclerotic vascular disease risk factors in French men: relationships are linear, J-shaped,
and U-shaped. Alcohol Clin Exp Res 2005;29(1):84-8.
(302) Wang J, Tung T, Yin W, Huang C, Jen H, Wei J, et al. Effects of moderate alcohol consumption
on inflammatory biomarkers. Acta Cardiol 2008;63(1):65-72.
(303) Kikuchi S, Nakajima T, Kobayashi O, Yamazaki T, Kikuichi M, Mori K. U-shaped effect of

drinking and linear effect of smoking on risk for stomach cancer in Japan. Jpn J Cancer Res
2002;93(9):953-59.
(304) Vanheusden K, van Lenthe F, Mulder C, van der Ende J, van de Mheen D. Patterns of
association between alcohol consumption and internalizing and externalizing problems in

young adults. J Stud Alcohol Drugs 69(1):49-57 2008;69(1):49-57.
(305) Compston A, Confavreux C, Lassmann H, McDonald I, Miller D, Noseworthy J, et al.

McAlpine’s Multiple Sclerosis. Fourth Edition. 4 ed. London: Churchill Livingston - Elsevier.;
2005.
(306) Murray T. Multiple Sclerosis - The History of a disease. New York: Demos Medical Publishing;
2005.
(307) McAlpine D, Lumsden C. Multiple Sclerosis: A Reappraisal. Edinburgh London: E. & S.

Livingston; 1968.
(308) Shephard S. Pickled, Potted, and Canned. New York: Simon & Shuster Paperbacks; 2000.
(309) Klaassen C. Casarett & Doull’s Toxicology The Basic Science of Poisons. 6 ed. New York:
McGraw-Hill; 2001.
(310) Wilson C, Trotter C. Scottish Heritage Food and Cooking. London: Lorenz Books; 2005.
(311) Wolfgram F, Ellison G, Stevens J, Andrews J. Multiple Sclerosis - Immunology, Virology and
Ultrastructure. New York: Academic Press; 1972.
(312) Anonymous. The Canned Food Reference Manual 1939-942-1947. New York: American Can
Company; 1950.
(313) Anonymous. New Zealand Briefing on Aspartame.; 2008.
(314) Anonymous. A History of the Canning and Freezing industry in New York State - 75th
Anniversary. The New York State Canners and Freezers Association; 1960.
(315) Bitting A. Appertizing - The Art of Canning Its History and Development.: The Trade
Pressroom; 1937.
(316) Burks J, Johnson K. Multiple Sclerosis - Diagnosis, Medical Management and Rehabilitation.
New York: Demos; 2000.
(317) Hayes A. Hayes AW. 1982. Principles and Methods of Toxicology. Raven Press. ISBN 0-
89004-470-8. New York: Raven Press; 1982.
(318) Hoshing S. The Canning industry of Japan. Tokyo: The Foreign Relations Council The Japan
Economic Federation; 1940.
(319) Beniac D, Wood D, Palaniyar N, Ottensmeyer F, Moscarello M, Harauz G. Marburg’s variant of

multiple sclerosis correlates with a less compact structure of myelin basic protein. Mol Cell
Biol Res Commun 1999;1(1):48-51.

(320) Anonymous. The ABC’s of Canned Foods. New York: National Canners Association; 1955.
(321) Oguma K, Lee J. Authors’ Reply. Microbiology 2006;152:1895-97.
(322) Atassi M. On the enhancement of anti-neurotoxin antibody production by subcomponents HA1

and HA3b of Clostridium botulinum type B 16S toxin-haemagglutinin. Microbiology
2006;152:1891-95.
(323) Weinshenker B. Therapeutic Plasma Exchange for Acute Inflammatory Demyelinating

Syndromes of the Central Nervous System. Journal of Clinical Apheresis 1999;14:144-48.
(324) Linseisen J, Rohrmann S, Norat T, Gonzalez C. Dietary intake of different types and
characteristics of processed meat which might be associated with cancer risk--results from the
24-hour diet recalls in the European Prospective Investigation into Cancer and Nutrition
(EPIC). Public Health Nutr 9(4):449-64 2005;9(4):449-64.
(325) Anonymous. US Department of Vital Statistics/Center for Disease Control Leading causes of
Death 1900 - 1998.; 2000.
(326) Chen J, Haley R, Hidestrand M, Shankar K. Estradiol Protects Against Ethanol-Induced Bone
Loss by Inhibiting Up Regulation of RANKL in Osteoblasts. 2006. Available from: URL:
JPET Fast Forward DOI:10.1124/jpet.106.109454 JPET #109454
(327) Beisswenger T, Holmquist B, Vallee B. Chi-ADH is the sole alcohol dehydrogenase isozyme of
mammalian brains: implications and inferences. Proc Natl Acad Sci 1985;82(24):8369-73.
(328) Jacob SE., Stechschulte S. Formaldehyde, aspartame, and migraines: a possible connection.
Dermatitis 2008;19(3):E10-11.
(329) Olney J, Farber N, Spitznagel E, Robins L. Increasing brain tumor rates: is there a link to
aspertame. J Neuropathol Exp Neurol 1996;11:1115-23.
(330) Launer L, Andersen K, Dewey M. Rates and risk factors for dementia and Alzheimer’s disease.
Neurology 52: 78-84 1999;52:78-84.
(331) Brey RL. Cigarette smoking and MS: Yet another reason to quit. Neurology 2003;61(8):E11-2.
(332) Costenbader K, Karlson E. Cigarette smoking and autoimmune disease: what can we learn from
epidemiology? Lupus 2006;15(11):737-45.
(333) Riise T, Nortvedt M, Ascherio A. Smoking is a risk factor for multiple sclerosis. Neurology
2003;61(8):1122-24.
(334) Behrend RC. Multiple sclerosis in Europe. Eur Neurol 1969;2(3):129-45.
(335) Ogawa G, Mochizuki H, Kanzaki M, Kaida K, Motoyoshi K, Kamakura K. Seasonal variation of

multiple sclerosis exacerbations in Japan. Neurol Sci 2003;24:417-19.
(336) Abella-Corral J, Prieto J, Dapena-Bolaño D, Iglesias-Gÿ3mez S, Noya-García M, Lema M.

Seasonal variations in the outbreaks in patients with multiple sclerosis. Rev Neurol
2005;40(7):394-96.
(337) Celius E, Vandvik B. Multiple sclerosis in Oslo. Norway: prevalence on 1 January 1995. and
incidence over a 25-year period. European Journal of Neurology 2001;8(5):463-74.
(338) Barnett M, Williams D, Day S, Macaskill P, McLeod J. Progressive increase in incidence and
prevalence of multiple sclerosis in Newcastle. Australia: a 35-year study. J Neurol Sci
2003;213:1-6.
(339) Sumelahti M, Tienari P, Wikström J, Palo J, Hakama M. Increasing prevalence of multiple

sclerosis in Finland. Acta Neurol Scand 2001;103(3):153-58.
(340) Pugliatti M, Sotgiu S, Solinas G, Castiglia P, Pirastru M, Murgia B, et al. Multiple sclerosis
epidemiology in Sardinia: evidence for a true increasing risk. Acta Neurol Scand.
2001;103(1):20-6.
(341) Sundström P, Nyström L, Forsgren L. Incidence (1988-97) and prevalence (1997) of multiple
sclerosis in Västerbotten County in northern Sweden. J Neurol Neurosurg Psychiatry
2003;74(1):29-32.
(342) Pugliatti M, Riise T, Sotgiu M, Sotgiu S, Satta W, Mannu L, et al. Increasing incidence of
multiple sclerosis in the province of Sassari. northern Sardinia. Neuroepidemiology
2005;25(3):129-32.
(343) Pozzilli C, Romano S, Cannoni S. Epidemiology and current treatment of multiple sclerosis in
Europe today. J Rehabil Res Dev 2002;39(2):175-85.
(344) Pugliatti M, Sotgiu S, Rosati G. The worldwide prevalence of multiple sclerosis. Clin Neurol
Neurosurg 2002;104(3):182-91.
(345) Wald N, Hackshaw A. Cigarette smoking: an epidemiological overview. Brit. Med. Bull
1996;52(1):3-11.
(346) Ranzato F, Perini P, Tzintzeva E, Tiberio M. Increasing frequency of multiple sclerosis in

Padova. Italy: a 30 year epidemiological survey. Mult Scler 2003;9(4):387-92.
(347) Netter F. The CIBA Collection of Medical Illustrations. Summit New Jersey: CIBA
Pharmaceutical Company; 1962.
(348) Granieri E, Casetta I, Govoni V, Tola M, Marchi D, Murgia S, et al. The increasing incidence
and prevalence of MS in a Sardinian province. Neurology 2000;55:842-47.

(349) Grimaldi L, Salemi G, Grimaldi G, Rizzo A, Marziolo R, Lo Presti C., et al. High incidence and
increasing prevalence of MS in Enna (Sicily). southern Italy. Neurology 2001;57(10):1891-3.
(350) Tanaka K, Kujuro Y, Suzuki S, Tanahashi N, Hamada J, Nogawa S, et al. Clinical and
laboratory features of in-patients with multiple sclerosis in a University Hospital in Tokyo
from 1988-2002. Intern Med 2005;44(6):560-66.
(351) Alonso A, Hernán M. Temporal trends in the incidence of multiple sclerosis: a systematic
review. Neurology 2008;71:129-35.
(352) Hernán M, Olek M, Ascherio A. Geographic variation of MS incidence in two prospective

studies of US women. Neurology 1999;53:1711-18.
(353) Noonan C, Kathman S, White M. Prevalence estimates for MS in the United States and evidence
of an increasing trend for women. Neurology 2002;51(1):136-38.
(354) Rosati G. The prevalence of multiple sclerosis in the world: an update. Neurol Sci 2001;22:117-
39.
(355) Pugliatti M, Sotgiu S, Solinas G, Castiglia P, Rosati G. Multiple sclerosis prevalence among
Sardinians: further evidence against the latitude gradient theory. Neurol Sci 2001;22(2):163-
65.
(356) Centers for Disease Control and Prevention (CDC). Update: trends in fetal alcohol syndrome--
United States, 1979-1993. MMWR Morb Mortal Wkly Rep 1995;44(13):249-51.
(357) Coutelle C. Risk Factors in Alcohol Associated Breast Cancer: Alcohol Dehydrogenase
Polymorphism and Estrogens. International Journal of Oncology 2004;25:1127-32.
(358) Triano E, Slusher L, Atkins T, Beneski J, Gestl S. Class I Alcohol Dehydrogenase Is Highly
Expressed in Normal Human Mammary Epithelium but not in Invasive Breast Cancer:
Implications for Breast Carcinogenesis. Cancer Research Arch 2003;63:3092-100.
(359) Poschl G, Seitz H. Alcohol and Cancer (Review). Alcohol & Alcoholism 2004;39(3):155-65.
(360) McAlpine D, Lumsden C. Multiple Sclerosis: A Reappraisal. Second Edition. 2 ed. London:
Churchill Livingston; 1972.
(361) McAlpine D, Compston N, Lumsden C. Multiple Sclerosis. First Edition. 1 ed. London: E. & S.
Livingston; 1955.
(362) Kirchner J, Miller J, Rice R, Keller G, Fox M. Volatile Water-Soluble Constituents of Grapefruit
Juice. Journal of Agricultural and Food Chemistry 1953;1(7):510-11.
(363) Turner C, Spanel P, Smith D. A longitudinal study of ethanol and acetaldehyde in the exhaled
breath of healthy volunteers using selected-ion flow-tube mass spectrometry. Rapid Commun

Mass Spectrom 2006;20:61-8.
(364) Joshi R, Jan S, Wu Y, MacMahon S. Global Inequalities in Acess to Cardiovascular Health Care
- Our Greatest Challenge. Journal of the American College of Cardiology 2008;52(23):1817-
25.
(365) Irving GW. Evaluation of the Health Aspects of Formic Acid, Sodium Formate, and Ethyl
Formate as Food Ingredients. Bethesda Md: Federation of American Societies for
Experimental Biology; 1974 No.: NTIS Doc PB-266 282, 1976. (NTIS Doc PB-266 282,
1976).
(366) Chang M, Olin K, Tsoi C, Wight T, Chait A. Human monocyte-derived macrophages secrete
two forms of proteoglycan-macrophage colony-stimulating Factor That Differ in their Ability
to Bind Low Density Lipoproteins. J Biol Chem 1998;273(26):15985-92.
(367) Yant W, Schrenk H. Distribution of methanol in dogs after inhalation and administration by
stomach tube and subcutaneously. J Ind Hyg Toxicol 1937;19:337-45.
(368) Wurtman R. Aspartame; Possible Effect on Seizure Susceptibility. Lancet 1985;2:8463:1060.
(369) Wood D, Moscarello M. Is the Myelin Membrane Abnormal in Multiple Sclerosis? Journal of
Membrane Biology 1984;79:195-201.
(370) Tephly T, Parks R, Mannering G. Methanol Metabolism in the Rat. Journal of Pharmacology
and Experimental Therapeutics 1964;143:292-300.
(371) Walrath J, Fraumeni J. Proportionate Mortality among New York Embalmers. In: Gibson J,
editor. Formaldehyde Toxicity. Washington: Hemisphere Publishing Corporation; 1994. p.
227-36.
(372) Wallace R, Lynch C, Pomrehn P. Alcohol and Hypertension; Epidemiologic and Experimental
Considerations. The Lipid Research Clinics Program. Circulation 64:III41 1981;64(suppl.
III):41-7.
(373) Von Wartburg JP, Buehler R. Biology of Disease - Alcoholism and Aldehydism: New
Biomedical Concepts. Laboratory Investigation 1984;50(1):5-15.
(374) Trumper M. The Antifreeze Methanol Hazard. International Clinics; A Quarterly of Clinical
Lectures 1931(March):84-8.
(375) Swenberg J, Gross E, Martin J, Popp J1M. Mechanisms of Formaldehyde Toxicity. In: Gibson J,
editor. Formaldehyde Toxicity. Washington: Hemisphere Publishing Corp; 1983. p. 132-47.
(376) Battey L, Patterson J, Heyman A. Effects of Methyl Alcohol on Cerebral Blood Flow and
Metabolism Observations During and after Acute Intoxication. A.M.A.Archives of Neurology
and Psychiatry 1956;23:252-56.

(377) Sturtevant F. Aspartame--A New Food Ingredient Reply to the Critical Comments of Woodrow
C. Monte. J.Environ.Sci.Health 1985;20(8):863.
(378) Johnson R, Richardson E. The Neurological Manifestations of Systemic Lupus Erythematosus.

Medicine. 1968;47(4):337-69.
(379) Anonymous. Methanol Health Effects. 4100 North Fairfax Drive, Suite 740, Arlington, VA
22203: Methanol Institute; 2008.
(380) Pearsall N, Weiser R. The Macrophage. Philadelphia: Lea and Febiger Publishing Corp.; 1970.
(381) Jornvall H, Hempel J, von Bahr-Lindstrom H, Vallee B. Alcohol and Aldehyde Dehydrogenases
Structures of the Human Liver Enzymes, Functional Properties and Evolutionary Aspects.
Alcohol & Alcoholism 1987(Suppl.1):13-23.
(382) Makar A, Mannering G. Role of Intracellular Distribution of Hepatic Catalase in the

Peroxidative Oxidation of Methanol. Molecular Pharmacology 1968;4:484-91.
(383) Majchrowicz E. Metabolic Correlates of Ethanol. In: Majchrowicz E, editor. Biochemistry and
Pharmacology of Ethanol Volume 2. New York: Plenum Press; 1973. p. 122-40.
(384) Majchrowicz E. Reversal in central nervous system function during ethanol withdrawal in
humans and experimental animals. Federation Proceedings 1981;40(7):2065-40.
(385) Smith C. Pathophysiology of the Alcohol Withdrawl Syndrome. Med Hypothesis. 7:231
1981;7:231-49.
(386) Jacob M, Sellers E. Emergency Management of Alcohol Withdrawal. Drug Therapy Hospital.
1977;7(April):26-32.
(387) Liskow B, Rinck C, Campbell J, DeSouza C. Alcohol Withdrawl in the Elderly. Journal of
Studies on Alcohol. 50:414 1989;50(5):414-21.
(388) Cohen G, Collins M. Alkaloids from Catecholamines in Adrenal Tissue Possible Role in
Alcoholism. Science. Science 1970;167:1749-51.
(389) Jones A. Elimination Half-life of Methanol During Hangover. Pharmacology & Toxicology
1987;60:217-20.
(390) Lieber C, Seitz H, Garro A. Alcohol-Related Diseases and Carcinogensis. Cancer Research
1979;39:2863-86.
(391) Ostrovsky Y, Pronko P, Shishkin S, Kolesnikov V, Volynets S. An Attempt to Evaluate

Diagnostic and Prognostic Significance of Blood Endogenous Ethanol in Alcoholics and Their
Relatives. Alcohol. 6:97 1989;6:97-102.

(392) Breeden J. Alcohol, Alcoholism, and Cancer. Medical Clinics of North America
1984;68(1):163-77.
(393) Smythies J. The Transmethylation and One-Carbon Cycle Hypotheses of Schizophrenia.

Psychological Medicine 1983;13:711-14.
(394) Davis V, Walsh M. Alcohol, Amines, and Alkaloids A Possible Biochemical Basis for Alcohol
Addiction. Science 1970;167:1005-7.
(395) Collins M, Cohen G. Isoquinoline Alkaloid Biosynthesis from Adrenal Catecholamines during
C14 Methyl Alcohol Metabolism in Rats. Federation Proceedings 1970;29:608.
(396) Ismail L, Sargent T, Dobson E, Pollycove M. Altered Metabolism of the Methionine Methyl
Group in the Leukocytes of Patients with Schizophrenia. Biological Psychiatry
1978;13(6):649-59.
(397) Cohen G, Barrett R. Fluorescence Microscopy of Catecholamine-Derived

Tetrahydroisoquinoline Alkaloids Formed During Methanol Intoxication. Federation
Proceedings 1969;28:288.
(398) Cohen G. Alkaloid Products in the Metabolism of Alcohol and Biogenic Amines. Biochemical
Pharmacology 1976;25:1123-28.
(399) Price J. Methylation in Schizophrenics: A Pharmacogenetic Study. Journal of Psychiatry

Research 1972;9:345-51.
(400) Koivusalo M. Methanol. In: Tremolieres J, editor. Alcohols and Derivatives, vol 2. London:
Pergamon Press; 1970. p. 465-505.
(401) Gosselin R. Ethyl Alcohol/Ethylene Glycol/Methyl Alcohol. In: Gosselin R, editor. Clinical
Toxicology of Commercial Products. Baltimore, Maryland: Williams & Wilkins; 1981. p. 229-
33.
(402) Eells J, McMartin K, Black K, Viravan V, Tisdell R, Tephly T. Formaldehyde Poisoning; Rapid
Metabolism to Formic Acid. JAMA 1981;246(11):1237-37.
(403) Kendal L, Ramanathan A. Excretion of Formate After Methanol Ingestion in Man. Biochemical
Journal 1953;54:424-26.
(404) Kini M, Cooper J. The Biochemistry of Methanol Poisoning I. Phosphorylation Coupled to the
Mitochondrial Oxidation of Formaldehyde. Biochim Biophys Acta 1960;44:599-601.
(405) Lope V., Pollán M., Gustavsson P, Plato N., et. al. Occupation and thyroid cancer risk in
Sweden. J Occup Environ Med. 2005 Sep;47(9):948-57. 2005;47(9):948-57.

(406) see 108. See 108.
(407) Mannering GP, RE.Tephly, TR. Comments of a Recent Publication by Kini and Cooper which
Purports to Show that Alcohol Dehydrogenase is Responsible for the Physiological Oxidation
of Methanol. Biochem. Pharmacol 1962;11:677-79.
(408) Miller T, Wolin M. Oxidation of Hydrogen and Reduction of Methanol to Methane is the Sole
Energy Source for a Methanogen Isolated from Human Feces. Journal of Bacteriology
1983;153(2):1051.
(409) Lester D, Greenberg L. The Inhalation of Ethyl Alcohol by Man. Quarterly Journal of Studies on
Alcohol 1951;12:167-78.
(410) Myddleton G1. Tobacco and Mortality. Lancet 1985;2:1430-31.
(411) McAllister R. Exposure to Methanol from Spirit Duplicating Machines. American Industrial
Hygiene Association Quarterly 1954;15:26-8.
(412) Mendelson J, Wexler D, Leiderman P, Solomon P. A Study of Addiction to Nonethyl Alcohols

and Other Poisonous Compounds. Quarterly Journal of Studies on Alcoholism 1957;18:561-
80.
(413) Krolman G, Pidde W. Acute Methyl Alcohol Poisoning. Canadian Journal of Ophthalmology
1968;3:270-78.
(414) Krishnamurthi M, Natarajan A, Shanmugasundaram K, Fadmanabhan K, Nityanandan K. Acute

Methyl Alcohol Poisoning. The Journal of the Association of Physicians of India 1968;16:801-
05.
(415) Keeney A, Mellinkoff S. Methyl alcohol poisoning. Ann Intern Med 1951;34:331-38.
(416) Jacobson B, Russell H, Grimm J, Fox E. Acute Methyl Alcohol Poisoning: Report of Eighteen
Cases. Naval Medical Bulletin 1945;44(1):1099-106.
(417) Martensson E, Olofsson A. Clinical and Metabolic Features of Ethanol-Methanol Poisoning in

Chronic Alcoholics. Lancet 1988;1:327-28.
(418) Branch A, Tonning D. Acute methyl alcohol poisoning. Observations in some thirty cases.
Canad J Publ Hlth 1945;36:147-51.
(419) see 132. See 132.
(420) McMartin K, Makar A, Martin-Amat G, Palese M, Tephly T. Methanol Poisoning. I. The Role
of Formic Acid in the Development of Metabolic Acidosis in the Monkey and the Reversal by
4-Methylpyrazole. Biochemical Medicine 1975;13:319-33.

(421) McMartin K, Martin-Amat G, Makar A, Tephly T. Methanol Poisoning. V. Role of Formate

Metabolism in the Monkey. Journal of Pharmacology and Experimental Therapeutics
1977;201(3):564-72.
(422) Baumbach G, Cancilla P, Martin-Amat G, Tephly T, McMartin K, Makar A, et al. Methyl

Alcohol Poisoning. IV. Alterations of the Morphological Findings of the Retina and Optic
Nerve. Arch Ophthalmol 1977;95:1859-65.
(423) Makar A, Tephly T. Folate Deficiency and Methanol Poisoning In the Rat. In: Thurman R,
editor. Alcohol and Aldehyde Metabolizing Systems.Volume II Enzymology and Subcellular
Organelles. San Diego, CA: Academic Press. Inc.; 1977. p. 413-18.
(424) Nachevski V. Testing of Some Plum Varieties Suitable for Industrial Use. Lozar Vinar
1980;29(4):19.
(425) Self R, Casey J, Swain T. The Low-Boiling Volatiles of Cooked Foods. Chemistry and Industry
1963(May 25):863-64.
(426) Manning D. Cheddar Cheese Flavour Studies. I. Production of Volatiles and Development of
Flavour During Ripening. Journal of Dairy Research 1978;45(3):479-90.
(427) Norman S, Craft C. Production of Ethanol. Acetaldehyde. and Methanol by Intact Oranges
During and After Nitrogen Storage. Journal of the American Society for Horticulutral Science
1971;96(4):464-67.
(428) Bigelow W, Cathcart P. Relation of Processing to the Acidity of Canned Foods. In: Goldblith S,
Joslyn M, Nickerson J, editors. An Anthology of Food Science. Volume I - An Introduction to
Thermal Processing of Foods. Berkeley, CA: AVI Publishing Co.; 1961. p. 579-600.
(429) Anonymous. Treatment of Multiple Sclerosis. and also Methanol Poisoning. Lancet 1983(Apr
23):909-10.
(430) Johnson K. Cerebrospinal fluid and blood assays of diagnostic usefulness in multiple sclerosis.
Official Journal of the American Academy of Neurology. Neurology 1980;30(2):106-9.
(431) Kinnunen E. Multiple Sclerosis in Finland; Evidence of Increasing Frequency and Uneven
Geographic Distribution. Neurology 1984;34:457-61.
(432) Larsen J, Aarli J, Nyland H, Riise T. Western Norway. a high-risk area for multiple sclerosis; A
prevalence incidence study in the county of Hordaland. Neurology 1984;34:1202-7.
(433) Paty D, Poser C. Clinical Symptoms and Signs of Multiple Sclerosis. In: Poser C, editor. The
Diagnosis. Multiple Sclerosis.A Guide for Patients and Their Families. New York: Thieme-
Stratton Inc.; 1984. p. 23-43.
(434) McFarlin D, McFarland H. Medical Progress - Multiple Sclerosis. Part I. New England Journal

of Medicine 1982;307(19):1183-88.
(435) Kurtzke J. Epidemiological Findings Indicating An Exogenous Cause of MS. In: Boese A,
editor. Search for the Cause of Multiple Sclerosis and Other Chronic Diseases of the Central
Nervous System. Weinheim-Deerfield Beach. Florida-Basel: Verlag Chemie; 1979.
(436) Kuroiwa Y. Does Asian MS Favor an Exogenous Agent as the Cause? In: Boese A, editor.
Search for the Cause of Multiple Sclerosis and other Chronic Diseases of the Central Nervous
System.Florida-Basel. Weinheim-Deerfield Beach-Florida-Basel.: Verlag Chemie; 1979. p.
405-13.
(437) Chatard H, Gimbert E. Methanol dermatitis: Some reflections on its clinical and medico-legal
aspects. Archives Des Maladies Professionnelles De Medicine Du Travail Et Securite Sociale
1951;12:436-38.
(438) Dean J, Murray M, Ward E. Toxic Responses of the Immune System. In: Casarett and Doull’s
Toxicology; The Basic Science of Poisons. New York: Macmallan Publishing Inc.; 1994. p.
245-85.
(439) Zatman L. The Effect of Ethanol on the Metabolism of Methanol in Man. Biochem J
1946;40:67.
(440) see 141. See 141.
(441) Keeser E. Toxicity. Etiology and Therapeutic Control of Specific Toxicity of Methanol. Archive
Fur Exper Pathund Pharmakol 1931;160:687-91.
(442) Pohl J. About the oxidation of methyl and ethyl alcohol within the animal body. Naunyn-
Schmiedeberg’s Arch Exp Path Pharmak 1893;31:281-302.
(443) Orthner H. Methyl Alcohol Poisoning With Marked Cerebral Changes: Pathology of Cerebral
Permeability. Virchows Archiv 1953;323:442-64.
(444) Diefenbach W. Methyl Alcohol Poisoning: Diagnosis and Treatment. Mississippi Valley
Medical Journal 1953;75:129-31,159-60.
(445) Patterson R, Pateras V., Grammer LC., Harris KE. Human Antibodies Against Formaldehyde-
Human Serum Albumin Conjugates or Human Serum Albumin in Individuals Exposed to
Formaldehyde. Int Archs Allergy Appl Immunol 1986;79:53-9.
(446) Newell G. Overview of Formaldehyde. In: Gibson J, editor. Formaldehyde Toxicity.

Washington DC: Hemisphere Publishing Corporation; 1994. p. 3-35.
(447) Heslinga F, Deierkauf F. The Action of Formaldehyde Solutions on Human Brain Lipids.
Journal of Histochemistry and Cytochemistry 1962;10:704-9.

(448) Kline B. Formaldehyde Poisoning: With report of a fatal case. Archives of Internal Medicine
1925;36:220-28.
(449) Grafstrom R, Fornace A, Autrup H, Lechner J, Harris C. Formaldehyde Damage to DNA and
Inhibition of DNA Repair in Human Bronchial Cells. Science 1983;220:216-18.
(450) Gottschling L, Beaulieu H, Melvin W. Monitoring of Formic Acid in Urine of Humans Exposed
to Low Levels of Formaldehyde. American Industrial Hygiene Association Journal
1984;45(1):19-23.
(451) Marshall E. EPA Indicts Formaldehyde. 7 Years Later. Science 1987(April 24):381.
(452) Anonymous. Mobil Oil Advertisement. Time Magazine 1989(Aug 28):7.
(453) Stirling J. Amblyopia due to Methyl Alcohol. Ophthalmic Review 1905;24:38-40.
(454) Nagel. CSG. Methyl Alcohol Amblyopia with Special Reference to Optic Nerve: Report of
Case. Journal of the American Medical Association 1905(Nov. 18):1560-62.
(455) McGregor I. A Study of the Histopathological Changes in the Retina and Late Changes in the
Visual Field in acute Methyl Alcohol Poisoning. British Journal of Ophthalmology 27:523
1943;27:523-43.
(456) Gilger A, Potts A. Studies on the Visual Toxicity of Methanol V. The Role of Acidosis in
Experimental Methanol Poisoning. American Journal of Opthamology 1955;39ii:63-85.
(457) Potts A. Dr. Potts is designated as the 1961 laureate for The Jonas S. Friednwald Memorial
Lectureship. Investigative Ophthalmology 1962;1(3):283-5.
(458) Potts A. Retinotoxic and Choroidotoxic Substances: The Jonas S. Friednwald Memorial Lecture.
Investigative Ophthalmology 1962;1(3):290-303.
(459) Van Slyke D. Donald D. Van Slyke: On His 80th Year:. Clin Chem 1963;9(6):646-63.
(460) Van Slyke D, Palmer W. Studies of acidosis. XVI. The titration of organic acids in urine. J. Biol.
Chem. 1920;41:567-85.
(461) Ruedemann A. The Electroretinogram in Chronic Methyl Alcohol Poisoning in Human Beings.
American Ophthalmological Society Annual Meeting 1961;59:480-529.
(462) see 106. See 106.
(463) Audet J. Alcool Methilique et Atrophie Optique. Laval Medical 10:446 1945;10:446-51.
(464) Duke-Elder S. Textbook of Ophthalmology. Vol. VI. Injuries.; 1954.

(465) Clarren S, Smith D. The Fetal Alcohol Syndrome. N Engl J Med 1978;298:1063-67.
(466) Shepard T. Catalog of Teratogenic Agents. 2 ed. Baltimore London: The John Hopkins
University Press; 1976.
(467) Jones K, Smith D, Ulleland C, Streissguth A. Pattern of Malformation in Offspring of Chronic

Alcoholic Mothers. Lancet 1973;7815(June 9):1267-71.
(468) Levy L. A form of Immunological Atherosclerosis. In: Advances in Experimental Medicine and
Biology. New York.: Plenum Publishing Corp.; 1967. p. 426-32.
(469) Hennekens C, Rosner B, Cole D. Daily Alcohol Consumption and Fatal Coronary Heart
Disease. American Journal of Epidemiology. 1978;107(3):196-200.
(470) Castelli W. Epidemiology of Coronary Heart Disease; The Framingham Study. American
Journal of Medicine 1984(Feb 27):4-12.
(471) Lipton R, Newman L, Solomon S. Aspartame and Headache. N Engl J Med 1988;318(18):1200-
02.
(472) Smith R. Aspartame Approved Despite Risks. Science 1981;213(28):986-87.
(473) Dickson D. Aspartame sugar substitute. New court overruled. Nature 292:283 1981;292(July
23):283.
(474) Ranney R. The Metabolism of the Methyl Moiety of Aspartame. Methanol Metabolism in the
Monkey. In: Searle Data Submitted For Aspartame Petition. Document No.MRC-751-0022 (E-
92). Chicago: G.D. Searle Inc.; 1963.
(475) Eng L. Localizations of Spacific Brain Antigens. In: Boese A, editor. Search for the Cause of
Multiple Sclerosis and other Chronic Diseases of the Central Nervous System. Basel: Verlag
Chemie; 1980. p. 15-460.
(476) Cooper G, Miller F, Pandey J. The Role of Genetic Factors in Autoimmune Disease:
Implications for Environmental Research. Environmental Health Perspectives 107(5):693
1999;107(5):693-700.
(477) Main R. On the Toxicity of Methyl Alcohol in Extracts and Medicines. The Quarterly Journal of
Inebriety 1904;26:146-51.
(478) Jelliffe S. Multiple Neuritis in Wood Alcohol Poisoning. Medical News 1905(Mar 4):387-90.
(479) Hufferd R. Optic Neuritis Due to Intoxication With Wood Alcohol. American Pharmaceutical
Association 1932;21:548.
(480) Atchinson J. Methyl (Wood) Alcohol. New York State Journal of Medicine 1905;5:127-28.

(481) Burhans E. Methyl Alcohol Poisoning. Clinical and Pathological Study of 11 Cases. Illinois
(482) Takagi S, Ryoko I, Yamauchi R, Kojima S, Yasuno S, Baba T. Aldehyde Dehydrogenase 2

Gene Is a Risk Factor for Myocardial Infarction in Japanese Men. Hypertens Res
2002;25(5):677-81.
(483) Hines LM., Meir S, Stampfer J, Jingma H, Gaziano M. Genetic Variation in Alcohol
Dehydrogenase and the Beneficial effect of Moderate Alcohol Consumption on Myocardial
Infarction. N Engl J Med 2001;344(8):549-55.
(484) Freiberg M, Samet J. Alcohol and Coronary Heart Disease - The Answer Awaits a Randomized
Controlled Trial. Circulation 2005;112:1379-81.
(485) Klatsky A. Alcohol, wine, and vascular diseases - an abundance of paradoxes. Am J Physiol
Heart Circ Physiol 2008;294:582-83.
(486) Eaton S, Eaton S, Konner M. Paleolithic nutrition revisited- A twelve-year retrospective on its
nature and implications. Review EJCN 1997;51:207-16.
(487) Macdonald L. The Best of Scottish Food and Drink,. London: Little, Brown and Company;
1996.
(488) Hunt R. The Toxicity of Methyl Alcohol. John Hopkins Hospital Bulletin. 13:213 1902;13:213-
25.
(489) Bergeron R, Cardinal J, Geadah D. Prevention of Methanol Toxicity by Ethanol Therapy. N

Engl J Med 1982;307(24):1528.
(490) see 144. See 144. In:: Elsevier Publishing Company.
(491) Giolli R, Pope J. The Mode of Innervation of the Dorsal Lateral Geniculate Nucleus and the
Pulvinar of the Rabbit by Axons Arising from the Visual Cortex. Journal of Comparative Neur
1973;147:129-43.
(492) Able EL. Fetal alcohol syndrome: the ‘American Paradox’. Alcohol & Alcoholism
1998;33(3):195-201.
(493) McCord C. Toxicity of Methyl Alcohol (Methanol) Following Skin Absorption and Inhalation.
Industrial and Engineering Chemistry 1931;23(8):931-36.
(494) see 88. See 88.
(495) Roe O. Past. Present and Future Fight Against Methanol Blindness and Death. 1970;89:235-42.

(496) Monte W. Personal Communication. 2006. Bill Richardson Governor of New Mexico.
1/1/2006.; 2006.
(497) Denton J. Part II Technical Support Document for Describing Available Cancer Potency Factors.
California Environmental Protection Agency, Office of Environmental Health Hazard
Assessment.; 2002.
(498) Egg C. Zur Kenntnis der Methylalkohol-Wirkung. Schweizerische Medizinische Wochenschrift

1927;57:5-7.
(499) Flury F, Wirth W. Methyl Alcohol and Poisoning Methyl Compounds. Archiv fur
Gewerbepathologie und Gewerbehygiene 7:221. Archiv Fur Gewerbepathologie Und
Gewerbehygiene 1936;7:221-26.
(500) Keeser E, Vincke E. Uber die Bildung von Formaldehyd Beim Abbau des Methylalkohols.
Klin.Wochenschr 1940;19:583-85.
(501) Terry M, Gammon M, Zhang F, Knight J, Wang Q, Britton J, et al. ADH3 genotype, alcohol
intake and breast cancer risk. Carcinogenesis. Carcinogenesis 2006;27(4):840-47.
(502) Terry M, Gammon M, Zhang F, Vaughan T, Chow W, Risch H, et al. Alcohol dehydrogenase 3
and risk of esophageal and gastric adenocarcinomas. Cancer Causes Control 2007;18(9):1039-
46.
(503) Estonius M, Svensson S, Höög J. Alcohol dehydrogenase in human tissues: localisation of

transcripts coding for five classes of the enzyme. FEBS Lett. 1996;397:338-42.
(504) Seitz H, Egerer G, Simanowski U, Waldherr R, Eckey R, Agarwal D, et al. Human gastric
alcohol dehydrogenase activity: effect of age, sex, and alcoholism. Gut 1993;34:1433-37.
(505) Duester G, Farrés J, Felder M, Holmes R, Höög J, Parés X, et al. Recommended nomenclature
for the vertebrate alcohol dehydrogenase gene family. Biochem Pharmacol 1999;58(3):389-95.
(506) Luo Y, Ingram V. Uncoupling of mitochondria activates protein phosphatases and inactivates
MBP protein kinases. J Alzheimers Dis 2001;3(6):593-98.
(507) Kawamura M, Heinecke J, Chait A. Increased uptake of alpha-hydroxy aldehyde-modified low

density lipoprotein by macrophage scavenger receptors. J Lipid Res. 41(7):1054
2000;41(7):1054-59.
(508) Fogelman A, Shechter I, Seager J, Hokom M, Child J, Edwards P. Malondialdehyde alteration of

low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-
macrophages. Proc Natl Acad Sci. 1980;77(4):2214-8.
(509) Armstrong S. Ethanol: Brief Report on its use in Gasoline. Cambridge MA.: Cambridge
Environmental, Inc. Cambridge MA.; 1999.

(510) Allen N, Beral V, Casabonne D, Kan S, Gillian K, Reeves G, et al. Moderate Alcohol Intake and
Cancer Incidence in Women. JNCI 2009;101:296-305.
(511) Anton A, Smith D. Breath Analysis for Clinical Diagnosis And Therapeutic Monitoring.
Singapore: World Scientific Publishing Company; 2005.
(512) Jelski W, Szmitkowski M. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase

(ALDH) in the cancer diseases. Clin Chim Acta 2008;395(1-2):1-5.
(513) Iribarren C, Tekawa I, Sidney S, Friedman G. Effect of cigar smoking on the risk of
cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men. N Engl J
Med. 1999;340(23):1773-80.
(514) Kinne R, Bräuer R, Stuhlmüller B, Palombo-Kinne E, Burmeste rG. Macrophages in rheumatoid

arthritis. Arthritis Res 2000;2(3):189-202.
(515) Roman M, Shanker B, Davis A, Lockshin M, Sammaritano LNE. Prevalence and correlates of
accelerated atherosclerosis in systemic lupus erythematosus. N Engl J Med
2003;349(25):2399-406.
(516) Salmon J, Roman M. Subclinical atherosclerosis in rheumatoid arthritis and systemic lupus
erythematosus. Am J Med 2008;21(10 Suppl 1):S3-8.
(517) Gay F, Drye T, Dicdk W, Esiri M. The application of multifactorial cluster analysis in the
staging of plaques in early multiple sclerosis. Identification and characterization of the primary
demyelinating lesion. Brain 1997;120(Pt 8):1461-83.
(518) Gay F. Early cellular events in multiple sclerosis. Intimations of an extrinsic myelinolytic
antigen. Clin Neurol Neurosurg 2006;108(3):234-40.
(519) Katsiari C, Liossis S, Sfikakis P. The Pathophysiologic Role of Monocytes and Macrophages in
Systemic Lupus Erythematosus; A Reappraisal. Semin Arthritis Rheum 2009(Jan 14):1-13.
(520) Sherer Y, Gorstein A, Fritzler M, Shoenfeld Y. Autoantibody explosion in systemic lupus

erythematosus; more than 100 different antibodies found in SLE patients. Semin Arthritis
Rheum 2005;34(2):501-37.
(521) Kahlert H, Grage-Griebenow E, Stüwe H, Cromwell O, Fiebig H. T cell reactivity with

allergoids: influence of the type of APC. J Immunol 2000;165(4):1807-15.
(522) Marsh D, Lichtenstein L, Campbell D. Studies on “allergoids” prepared from naturally occurring
allergens. I. Assay of allergenicity and antigenicity of formalinized rye group I
component.(5);705-22. Immunology 1970;18(5):705-22.
(523) Holgate S. Asthma and allergy--disorders of civilization? QJM 1998;91(3):171-84.

(524) Herbert M, Russo J, Yang S, Roohi J, Blaxill M, Kahler S, et al. Autism and environmental
genomics. Neurotoxicology 2006;27(5):671-84.
(525) Blaxill M. What’s going on? The question of time trends in autism. Public Health
2004;119(6):536-51.
(526) Kern J. Purkinje cell vulnerability and autism: a possible etiological connection. Brain Dev
2006;25(6):377-82.
(527) Jepson B. Changing the Course of Autism: A Scientific Approach for Parents and Physicians.
Boulder, Colorado: Sentient Publications; 2007.
(528) Galter D, Carmine A, Buervenich S, Duester G, Olson L. Distribution of class I, III and IV
alcohol dehydrogenase mRNAs in the adult rat, mouse and human brain. Eur J Biochem
2003;270(6):1316-26.
(529) McCarver D, Thomasson H, Martier S, Sokol R, Li T. Alcohol dehydrogenase-2*3 allele

protects against alcohol-related birth defects among African Americans. J Pharmacol Exp Ther
1997;283(3):1095-101.
(530) McCarver D. ADH2 and CYP2E1 Genetic Polymorphisms: Risk Factors for
Alcohol-Related Birth Defects. Drug Metabolism and Disposition 2001;29(4-2):562-65.
(531) Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health
2006;29(4):245-54.
(532) Yusuf S, Ounpuu S, Anand S. The global epidemic of atherosclerotic cardiovascular disease.
Med Princ Pract 2002;11(Suppl 2):3-8.
(533) Waldman M. Are We Experiencing an Alzheimer’s Epidemic? Presentation (Abstract 90)

[AD/PD 2009: 9th International Conference on Alzheimer’s and Parkinson’s Diseases:].
http://www.medscape.com/viewarticle/590106; 2009.
(534) Sink K. Moderate Alcohol Consumption May Lower Dementia Risk in Cognitively Normal
Elderly. Presentation. Alzheimer’s Association 2009 International Conference on Alzheimer’s
Disease (ICAD); ; Vienna. www.medscape.com: medscape; 2009.
(535) Mehlig K, Skoog I, Guo X, Schütze M, Gustafson D, Waern M, et al. Alcoholic Beverages and
Incidence of Dementia: 34-Year Follow-up of the Prospective Population Study of Women in
Göteborg. Am J Epidemiol 2008;167(6):684-91.
(536) Uramoto K, Michet C, Thumboo J, Sunku J, O’Fallon W, Gabriel S. Trends in the incidence and
mortality of systemic lupus erythematosus, 1950-1992. Arthritis Rheum 1999;42(1):46-50.
(537) Anonymous. Methanol, IPCS. Geneva: International Programme On Chemical Safety World

Health Organization; 1997.
(538) Burbacher T, Grant K, Shen D, Sheppard L, Damian D, Ellis S, et al. Chronic maternal
methanol inhalation in nonhuman primates (Macaca fascicularis): reproductive performance
and birth outcome. Neurotoxicol Teratol 2004;26(5):639-50.
(539) Bartzokis G, Cummings J, Sultzer D, Henderson V, Nuechterlein K, Mintz J. White Matter

Structural Integrity in Healthy Aging Adults and Patients With Alzheimer Disease. Arch
Neurol 2003;60(3):393-8.
(540) Casserly I, Topol E. Convergence of atherosclerosis and Alzheimer’s disease: inflammation,

cholesterol, and misfolded proteins. Lancet 2004;363(9415):1139-46.
(541) Main R. Death from Poisoning by Methyl Alcohol. The Learned Coroner. Illinois Medical
Journal 1904;27:146-54.
(542) Mathews W. McAlpine’s Multiple Sclerosis, Fourth Edition. 4 ed.; 2005.
(543) Stechschulte S, Jacob S. Formaldehyde, aspartame, migraines: a possible connection.(author

reply). Dermatitis 2009;20(3):177-9.
(544) Abegaz E, Bursey R. Formaldehyde, aspartame, migraines: a possible connection.(comment on).

Dermatitis 2009;20(3):176-7.
(545) Hill A, Belsito D. Systemic contact dermatitis of the eyelids caused by formaldehyde derived
from aspartame? Contact Dermatitis 2003;49(5):258-9.
(546) Chapman L. Experimental Induction of Hangover. Q J Stud Alcohol 1970;5:67-86.
(547) Oppermann JA, Muldoon E, Ranney R. Metabolism of Aspartame in Monkeys. Journal of

Nutrition 1973;103(10):1454-59.
(548) Bouchard M, Brunet R, Droz P, Carrier G. A Biologically Based Dynamic Model for Predicting
the Disposition
Of Methanol and Its Metabolites in Animals and Humans. Toxicological Sciences
2001;64:169-84.
(549) Nabors LOB. Calorie Control Council Objections to NTP-CERHR 2002, Letter September
7,2001. In: NTP-CERHR Monograph on the Potential Human Reproductive and
Developmental Effects of Methanol. 2003. http://cerhr.niehs.nih.gov: U.S. Department of
Health and Human Services; 2001.
(550) Sandler J. PETA, People for the Ethical Treatment of Animals Objections to NTP-CERHR
2002. Letter dated June 8, 2002. In: NTP-CERHR Monograph on the Potential Human
Reproductive and Developmental Effects of Methanol. 2003. http://cerhr.niehs.nih.gov: U.S.
Department of Health and Human Services; 2003.

(551) Davis J, Barone S. Dr. Davis and Dr. Barone, CERHR committie members, object to Bias of
final report. NTP-CERHR 2002. Letters dated July 3 - 8 2002. In: NTP-CERHR Monograph
on the Potential Human Reproductive and Developmental Effects of Methanol. 2003.
http://cerhr.niehs.nih.gov: U.S. Department of Health and Human Services; 2003.
(552) Lynn J. Methanol Institute Objections to NTP-CERHR 2002.Letter dated July 3, 2002. In: NTP-
CERHR Monograph on the Potential Human Reproductive and Developmental Effects of
Methanol. 2003. http://cerhr.niehs.nih.gov: U.S. Department of Health and Human Services;
2003.
(553) Festa J. American Forest Paper Association Objections to NTP-CERHR 2002. Letter dated July
8, 2002. In: NTP-CERHR Monograph on the Potential Human Reproductive and
Developmental Effects of Methanol. 2003. http://cerhr.niehs.nih.gov: U.S. Department of
(554) Matthews W. McAlpine’s Multiple Sclerosis. Second Edition. 2 ed. London: Churchill
Livingston - Elsevier.; 1991.
(555) Adams D. The Granulomatous Inflammatory Response: A Review. American Journal of

Pathology 1976;41(1):164-92.
(556) Williams G, Williams W. Granulomatous inflammation--A review. J Clin Pathol

1983;36(7):723-33.
(557) Purdue M, Beane Freeman L, Anderson W, Tucker M. Recent Trends in Incidence of Cutaneous
Melanoma among US Caucasian Young Adults. Journal of Investigative Dermatology (2008)
128, 29052908; Doi:10.1038/Jid.2008.159; Published Online 10 July 2008 2008;128(12):2905-
08.
(558) Nagarajan R, Patzel K, Martin M, Yasui D, Swanberg S, Hertz-Picciotto I, et al. MECP2

promoter methylation and X chromosome inactivation in autism. Autism Research
2008;1(3):169-78.
(559) Nagarajan R, Hogart A, Gwye Y, Martin M, LaSalle J. Reduced MeCP2 expression is frequent
in autism frontal cortex
And correlates with aberrant MECP2 promoter methylation. Epigenetics 2006;1(4):e1-11.
(560) Sadikovic B, Al-Romaih K, Squire J, Zielenska M. Cause and consequences of genetic and
epigenetic alterations in human cancer. Curr Genomics 2008;9(6):394-408.
(561) Selye H. Further sutdies concerning the participation of the Adrenal Cortex in the Pathogenesis
of Arthritis. British Medical Journal 1949;19(2(4637)):1129-35.
(562) Gardner. DL. The Experimental Production of Arthritis. Ann Rheum Dis 1960;19(4):297-317.

(563) Scott B, Weisbrot L, Greenwood J, Bogoch E, Paige C, Keystone E. Rheumatoid Arthritis

Synovial Fibroblast and U937 Macrophage/Monocyte Cell Line Interaction In Cartilage
Degradation. 2005;40(3):490-98.
(564) Siragusa R, Cerda J, Baig M, Burgin C, Robbins F. Methanol production from the degradation
of pectin by human colonic bacteria. Am J Clin Nutr 1988;47:848-51 1988;47:848-51.
(565) Pine S, Sanchez B. The Formic Acid-Formaldehyde Methylation of Amines. J Org Chem
1971;36(6):829-43.
(566) Fu S, Sakanashi T, Rogers J, Hong K, Keen C. Influence of dietary folic acid on the
developmental toxicity of methanol and the frequency of chromosomal breakage in the CD-1
mouse. Reproductive Toxicology 1996;10(6):455-63.
(567) Olek S, Maier S, Olek K, Olek A. Digitizing Molecular Diagnostics: Current and Future
Aplications of Epigenome Technology. In: Beck S, Olek A, editors. The Epigenome.
Weinheim: Wiley-VCH; 2003. p. 153-70.
(568) Aziz M, Agrawal A, Adhami V, Ali M, Baig M, Seth P. Methanol-induced neurotoxicity in pups
exposed during lactation through mother: Role of folic acid. Neurotoxicology and Teratology
2002;24(4):519-27.
(569) Huanga Y, Heldb G, Andrewsb J, Rogersb J. C14 methanol incorporation into DNA and proteins
of organogenesis stage mouse embryos in vitro. Reproductive Toxicology 15 (2001) 429435
2001;15:429-35.
(570) Mitchell S, Reiss A, Tatusko D, Ikuta I, Kazmerski D, Botti J, et al. Neuroanatomic alterations
and social and communication deficits in monozygotic twins discordant for autism disorder.
Am J Psychiatry 2009;166(8):917-25.
(571) Webb S, Sparks B, Friedman S, Shaw D, Giedd J, Dawson G, et al. Cerebellar vermal volumes
and behavioral correlates in children with autism spectrum disorder. Psychiatry Res
2009;172(1):61-7.
(572) Indredavik M, Brubakk A, Romundstad P, Vik T. Prenatal smoking exposure and psychiatric
symptoms in adolescence. Acta Paediatr 2007;96(3):377-82.
(573) Hultman C, Sparén P, Cnattingius S. Perinatal risk factors for infantile autism. Epidemiology
2002;13(4):417-23.
(574) Croghan I, Pruthi S, Hays J, Cha S, Johnson R, Kosel M, et al. The role of smoking in breast
cancer development: an analysis of a Mayo Clinic cohort. Breast J 2009;15(5):489-95.
(575) Reynolds P, Hurley S, Goldberg D, Anton-Culver H, Bernstein L, Deapen D, et al. Active

smoking, household passive smoking, and breast cancer: evidence from the California
Teachers Study. J Natl Cancer Inst 2004 Jan 7;96(1):29-37 2004;96(1):29-37.

(576) American Cancer Society. Breast Cancer Facts & Figures 2007-2008. Atlanta, GA: American
Cancer Society, Inc.; 2008.
(577) Horner M, Ries L, Krapcho M, Neyman N, Aminou R, Howlader N, et al. SEER Cancer
Statistics Review, 1975-2006, National Cancer Institute. Bethesda, MD,
http://seer.cancer.gov/csr/1975_2006/, based on November 2008 SEER data submission,
posted to the SEER web site, 2009. Bethesda, MD: National Cancer Institute.; 2008.
(578) Agency for Toxic Substances and Disease Registry. Health Consultation; Village of Wellington,
Environmental Contamination Concerns. Ohio Department of Health: U.S. Department of
(579) Agency for Toxic Substances and Disease Registry. Petitioned Public Health Assessment,
LaFarge Corporation - Alpena Plant, Alpena, Alpena County, Michigan. U.S. Department of
(580) Riise T, Moen B, Kyvik K. Organic solvents and the risk of multiple sclerosis. Epidemiology
2002;13(6):718-20.
(581) Witte M, Bø L, Rodenburg R, Belien J, Musters R, Hazes T, et al. Enhanced Number and
Activity of Mitochondria in Mutiple Sclerosis Lesions. J Pathol 2009;219(2):193-204.
(582) Seme M, Summerfelt P, Neitz J, Eells J, Henry M. Differential Recovery of Retinal Function
after Mitochondrial Inhibition by Methanol Intoxication. Invest Ophthalmol Vis Sci
2001;42(3):834-41.
(583) Miller A, To T, Baines C, Wall C. The Canadian National Breast Screening Study-1: breast
cancer mortality after 11 to 16 years of follow-up. A randomized screening trial of
mammography in women age 40 to 49 years. Ann Intern Med 2002;137(5 Part 1):305-12.
(584) Zampolla T, Spikings E, Zhang T, Rawson D. Effect of methanol and Me2SO exposure on
mitochondrial activity
And distribution in stage III ovarian follicles of zebrafish (Danio rerio). Cryobiology
2009;59:188-98.
(585) Hoffmann D, Hoffmann I. Chapter 5; The Changing Cigarette: Chemical Studies and Bioassays.
In:Shopland D, Burns D, Benowitz N, Amacher R, editors. Risks Associated with Smoking
Cigarettes with Low Machine-Measured Yields of Tar and Nicotine - Monograph No. 13 U.S.
Department of Health and Human Services: National Cancer Institute, U. S. National Institutes
of Health; 2001. p. 160-70. (Smoking and Tobacco Control Monographs; vol. 13).
(586) Monte W. Methanol: A chemical Trojan horse as the root of the inscrutable U. Med Hypotheses
2010;74(3):493-6.
(587) Hayflick L. The Quest for Immortality:Science at the Frontiers of Aging. Radiation Research

2001;156(3):334-36.
(588) Lin JC, GC. Associations of Sugar and Artificially Sweetened Soda with Albuminuria and
Kidney Function Decline in Women.[Epub ahead of print] doi: 10.2215/CJN.03260410. Clin J
Am Soc Nephrol. 2010(Sep 30).
(589) Altaweel M, Hanzlik R, Ver Hoeve J, Eells J, Zhang B. Ocular and systemic safety evaluation of
calcium formate as a dietary supplement. J Ocul Pharmacol Ther 2009;25(3):223-30.
(590) Kamino K, Nagasaka K, Imagawa M, Yamamoto H, Yoneda H, Ueki A, et al. Deficiency in

mitochondrial aldehyde dehydrogenase increases the risk for late-onset Alzheimer’s disease in
the Japanese population. Biochem Biophys Res Commun 2000;273(1):192-6.
(591) Tong Z, Zhang J, Luo W, Wang W, Li F, Li H, et al. Urine formaldehyde level is inversely
correlated to mini mental state examination scores in senile dementia. Neurobiol Aging 2009.
(592) Ohsawa I, Kamino K, Nagasaka K, Ando F, Niino N, Shimokata H, et al. Genetic deficiency of
a mitochondrial aldehyde dehydrogenase increases serum lipid peroxides in community-
dwelling females. J Hum Genet 2003;48(8):404-9.
(593) Fox C, Johnson F, Whiting J, Roller P. Formaldehyde Fixation. J Histochem Cytochem

1985;33(8):845-53.
(594) Levy M. The Acidity of Formaldehyde and the end point of the Formol Titration. J Biol Chem
1933;105(1):157-65.
(595) Casanova M, Heck H, Janszen D. Comments on ‘DNA-protein crosslinks, a biomarker of

exposure to formaldehyde--in vitro and in vivo studies’ by Shaham et al. Carcinogenesis
1996;17(9):2097-101.
(596) Shaham J, Bomstein Y, Meltzer A, Kaufman Z, Palma E, Ribak J. DNA--protein crosslinks, a

biomarker of exposure to formaldehyde--in vitro and in vivo studies. Carcinogenesis. 1996
Jan;17(1):121-5. 1996;17(1):121-5.
(597) Offit P, Jew R. Addressing parents’ concerns: do vaccines contain harmful preservatives,
adjuvants, additives, or residuals? Pediatrics. 2003 Dec;112(6 Pt 1):1394-7 2003;112(6 Pt
1):1394-7.
(598) Park A. Autism Numbers Are Rising. The Question is Why? Time 2009;2009(21):55-6.
(599) Schechter R, Grether J. Continuing increases in autism reported to California’s developmental

services system: mercury in retrograde. Arch Gen Psychiatry 2008;65(1):19-24.
(600) Rutter M. Incidence of autism spectrum disorders: changes over time and their meaning. Acta
Paediatr. 2005 Jan;94(1):2-15. 2005;94(1):2-15.

(601) Anonymous. Histone demethylation 2009 [cited 12/25/2009]. Available from: URL:
http://www.abcam.com/index.html?pageconfig=resource&rid=11182&pid=5
(602) Bannister A, Schneider R, Kouzarides T. Histone methylation: dynamic or static? Cell. 2002 Jun
28;109(7):801-6 2002;109(7):801-6.
(603) Kutschera U. Plant-Associated Methlobacteria as Co-Evolved Phytosymbionts. Plant Signaling

& Behavior 2007;2(2):74-8.
(604) Pham M, Lemberg D, Day A. Probiotics: sorting the evidence from the myths. Med J Aust
2008;188:304-8.
(605) Trager R. Formaldehyde politics block research chief joining EPA.

http://www.rsc.org/chemistryworld/News/2009/October/13100902.asp: RSC Advancing the
Chemical Sciences; 2009.
(606) Kiernan J. Formaldehyde, formalin, paraformaldehyde and glutaraldehyde:

What they are and what they do. Microscopy Today 2000;00(1):8-12.
(607) Lehninger A. Biochemistry, The Molecular Components of Cells pp. 80. 2 ed. New York, New
York: Worth Publishers, Inc.; 1975.
(608) McDonald W. The mystery of the origin of MS. Journal of Neurology, Neurosurgery, and
Psychiatry 1986;49:113-23.
(609) Putnam T. The Centenary of Miltiple Sclerosis. Arch Neurol Psychiatry 1938;40(4):806-13.
(610) Lucas A, Greaves D. Atherosclerosis: role of chemokines and macrophages. Expert Rev Mol
Med 2001;3(25):1-18.
(611) Pisarik P, Kai D. Vestibulocochlear toxicity in a pair of siblings 15 years apart secondary to
aspartame: two case reports. Cases Journal 2009, 2:9237 2009;2:9237.
(612) Rowley B, Lund D, Richardson T. Reductive Methylation of Lactoglobulin with Formaldehyde.

J Dairy Sci 62:533--536 1979;62:533-36.
(613) Kim H, Cho E, Bae J, Yu D, Oh S, Kang H, et al. Recent trend in the incidence of premalignant
and malignant skin lesions in Korea between 1991 and 2006. J Korean Med Sci.
2010;25(6):924-29.
(614) Sicotte N, Kern K, Giesser B, Arshanapalli A, Schultz A, Montag M, et al. Regional

hippocampal atrophy in multiple sclerosis. Brain 2008;131(Pt 4):1134-41.
(615) Behan P, Roep B. The pathogenesis of multiple sclerosis revisited. J R Coll Physicians Edinb
2002;32:244265.

(616) Compston A. Revisiting The pathogenesis of multiple sclerosis revisited. Int MS J.

2003;10(1):29-31.
(617) Halldorsson T, Strøm M, Petersen S, Olsen S. Intake of artificially sweetened soft drinks and
risk of preterm delivery: a prospective cohort study of 59,334 Danish pregnant women. Am J
Clin Nutr Doi:10.3945/Ajcn.2009.28968 2010.
(618) Rico E, Rosemberg D, Senger M, Arizi MB, Bernardi G, Dias R, et al. Methanol alters ecto-
nucleotidases and acetylcholinesterase in zebrafish brain. Neurotoxicol Teratol
2006;28(4):489-96.
(619) Simintzi I, Schulpis K, Angelogianni P, Liapi C, Tsakiris S. The effect of aspartame on

acetylcholinesterase activity in hippocampal homogenates of suckling rats. Pharmacol Res.
2007;56(2):155-9.
(620) Dawson J. The Histology of Disseminated Sclerosis. Trans Royal Soc Edin 1916;50:517-740.
(621) Hitler A. Mein Kampf.: Project Gutenberg of Australia eBook; 2002.
(622) Allen G., Courchesne E. Differential effects of developmental cerebellar abnormality on

cognitive and motor functions in the cerebellum: an fMRI study of autism. Am J Psychiatry
2003;160(2):262-73.
(623) Simintzi I, Schulpis K, Angelogianni P, Liapi C, Tsakiris S. The effect of aspartame on

acetylcholinesterase activity in hippocampal homogenates of suckling rats. Pharmacol Res.
2007;56(2):155-9.
(624) Tsakiris S, Schulpis K. Answer to letter sent by A.G. Renwick related to Simintzi et al. report
published in Food and Chemical Toxicology 2007;45(12):2397-401. Food Chem Toxicol.
2008;46:1208-09.
(625) Tsakiris S, Schulpis K. Answer to letter sent by E. Abegaz and R. Bursey Ajinimoto Corporation
Washington USA related to Simintizi et al report published in Pharmacol Res 2007;56155-9.
Pharmocol Res. 2008;57:89-90.
(626) Dorman D, Welsch F. Developmental Toxicity of Methanol in Rodents. Chemical Industry

Institute of Toxicology Activities 1996;16(2):1-7.
(627) Shelby M. NTP-CERHR Expert Panel report on the reproductive and developmental toxicity of
methanol. Reproductive Toxicology 2004;18:303-90.
(628) Holahan CJ., Schutte KK., Brennan PL., Holahan CK., Moos BS., Moos RH. Late-Life Alcohol
Consumption and 20-Year Mortality. Alcohol Clin Exp Res, Vol 34, No 11, 2010: Pp 111
2010;34(11):1-11.
(629) Fediuk K. Vitamin C in the Intuit diet: past and present. McGill University, Montreal: School of

Dietetics and Human Nutrition; 2000.
(630) Castanedo-Tardan MP., González ME., Connelly EA., Giordano K., Jacob SE. Systematized
contact dermatitis and montelukast in an atopic boy. Pediatr Dermatol 2009;26(6):739-43.
(631) Verhelst D., Moulin P., Haufroid V., Wittebole X., Jadoul M., Hantson P. Acute renal injury
following methanol poisoning: analysis of a case series. Int J Toxicol 2004;23(4):267-73.
(632) Lee E., Brady AN., Brabec MJ., Fabel T. Effects of methanol vapors on testosterone production
and testis morphology in rats. Toxicol Ind Health 1991;7(4):261-75.
(633) Saha AK., Khudabaksh AR. Chromosome aberrations induced by methanol in germinal cells of
grasshopper, Oxya velox Fabricius. Indian J Exp Biol. 1974;12(1):72-5.
(634) Rincÿ3n ID., Williams K., Stern MP., Freeman GL., Escalante A. High Incidence of
Cardiovascular Events in a Rheumatoid Arthritis Cohort Not Explained by Traditional Cardiac
Risk Factors. Arthritis & Rheumatism 2001;44(12):2737-45.
(635) Myasoedova E., Crowson CS., Kremers HM., Therneau TM., Gabriel SE. Is the incidence of
rheumatoid arthritis rising?: results from Olmsted County, Minnesota, 1955-2007. Arthritis
Rheum 2010;62(6):1565-7.
(636) Deltour L., Haselbeck RL., Ang HL., Duester G. Localization of Class I and Class IV Alcohol
Dehydrogenases in Mouse Testis and Epididymis: Potential Retinol Dehydrogenases for
Endogenous Retinoic Acid Synthesis. Biology of Reproduction 1997;56(1):102-9.
(637) Bühler R., Pestalozzi D., Hess M., Von Wartburg JP. Immunohistochemical localization of
alcohol dehydrogenase in human kidney, endocrine organs and brain. Pharmacol Biochem
Behav. 1983;18 Suppl 1:55-9 1983;18(Suppl 1):55-9.
(638) Petersen BJ., Cornell NW., Veech RL. Alcohol dehydrogenase in cultured human skin
fibroblasts. Human fibroblast alcohol dehydrogenase. Adv Exp Med Biol 1980;132:533-41.
(639) Poon R., Chu I., Bjarnason S., Potvin M., Vincent R., Miller RB., et al. Inhalation toxicity study
of methanol, toluene, and methanol/toluene mixtures in rats: effects of 28-day exposure.
Toxicol Ind Health. 1994 May-Jun;10(3):231-45 1994;10(3):231-45.
(640) Smith M., Hopkinson DA., Harris H. Developmental changes and polymorphism in human
alcohol dehydrogenase. Ann Hum Genet 1971;34(3):251-71.
(641) COPD International. COPD Statistical Information 2010. Available from: URL:
http://www.copd-international.com/library/statistics.htm
(642) Maxwell JR., Gowers IR., Moore DJ., Wilson AG. Alcohol consumption is inversely associated
with risk and severity of rheumatoid arthritis. Rheumatology 2010;49(11).

(643) Almeida OP., Hulse GK., Lawrence D., Flicker L. Smoking as a Risk Factor for Dementia and
Cognitive Decline: A Meta-Analysis of Prospective Studies. Addiction 2002;97(1):15-28.
(644) Hultman CM., Sparén P., Cnattingius S. Perinatal risk factors for infantile autism.
Epidemiology. 2002 Jul;13(4):417-23. 2002;13(4):417-23.
(645) De Hertog SA., Wensveen CA., Bastiaens MT., Kielich CJ., Berkhout MJ., Westendorp RG., et
al. Relation between smoking and skin cancer. J Clin Oncol 2001;19(1):231-8.
(646) Chow WH., Devesa SS., Warren JL., Fraumeni JF Jr. Rising incidence of renal cell cancer in the
United States. JAMA. 1999;281(17):1628-31.
(647) Schulze MB, Manson JE., Ludwig DS., Colditz GA., Stampfer MJ., Willett WC., et al. Sugar-
sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged
women. JAMA 2004;292(8):927-34.
(648) Willi C., Bodenmann P., Ghali WA., Faris PD., Cornuz J. Active smoking and the risk of type 2
diabetes: a systematic review and meta-analysis. JAMA 2007;298(22):2654-64.
(649) Pinhas-Hamiel O., Dolan LM., Daniels SR., Standiford D., Khoury PR., Zeitler P. Increased
incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr 1996;128(5
Pt. 1):608-15.
(650) Magis DC., Jandrain BJ., Scheen AJ. Alcohol, insulin sensitivity and diabetes. Rev Med Liege
2003;58(7-8):501-7.
(651) Ejerblad E., Fored CM., Lindblad P., Fryzek J., Dickman PW., Elinder CG., et al. Association
between smoking and chronic renal failure in a nationwide population-based case-control
study. J Am Soc Nephrol 2004;15(8):2178-85.
(652) Hunt JD., van der Hel OL., McMillan GP., Boffetta P., Brennan P. Renal cell carcinoma in
relation to cigarette smoking: Meta-analysis of 24 studies. Int J Cancer. 2005 Mar
10;114(1):101-8. 2005;114(1):101-8.
(653) Asztalos E. The need to go beyond: evaluating antenatal corticosteroid trials with long-term
outcomes. J Obstet Gynaecol Can 2007;29(5):429-32.
(654) Shiono PH., Klebanoff MA., Rhoads GG. Smoking and drinking during pregnancy. Their effects
on preterm birth. JAMA 1986;255(1):82-4.
(655) Thun MJ., Lally CA., Flannery JT., Calle EE., Flanders WD., Heath CW Jr. Cigarette smoking
and changes in the histopathology of lung cancer. J Natl Cancer Inst 1997;89(21):1580-6.
(656) Navab R., Bandarchi B., Tsao M-S. Carcinoma-Associated Fibroblasts in Lung Cancer. In:
Keshamouni V., Arenberg D., Kalemkerian G, editors. Lung Cancer Metastasis; Novel
Biological Mechanisms and Impact on Clinical Practice. DOI: 10.1007/978-1-4419-0772-

1_10: SpringerLink; 2009. p. 193-215.
(657) Soffritti M., Belpoggi F., Manservigi M., Tibaldi E., Lauriola M., Falcioni L., et al. Aspartame
Administered in Feed, Beginning Prenatally Through Life Span, Induces Cancers of the Liver
and Lung in Male Swiss Mice. Am J Ind Med 2010.
(658) Nielsen NM., Rostgaard K., Rasmussen S., Koch-Henriksen N., Storm HH., Melbye M, et al.
Cancer risk among patients with multiple sclerosis: a population-based register study. Int J
Cancer 2006;118(4):979-84.
(659) Martins MRI., Azoubel R. Effects of Aspartame on Fetal Kidney: A Morphometric and
Stereological Study. Int J Morphol 2007;25(4):689-94.
(660) Portari GV., Mathias MGM., Almeida BB., Marchini JS., Jordao AA. Effect of the Temperature
and pH on Methanol Release in Coffee Brew Sweetened with Aspartame. Acta Alimentaria
2009;38(3):303-7.
(661) Anonymous. Formic acid Material Safety Data Sheet. Scholar Chemistry and Columbus
Chemical Industries, Inc.; 2009.
(662) Environmental Risk Management Authority of New Zealand. ERMA New Zealand makes meths
safer. New Zealand Environmental Risk Management Authority; 2007.
(663) Duester G. Families of retinoid dehydrogenases regulating vitamin A function

Production of visual pigment and retinoic acid. Eur. J. Biochem 2000;267:4315-24.
(664) Delille HK., Alves A., Schrader M. Biogenesis of peroxisomes and mitochondria: linked by
division. Histochem Cell Biol 2009;131:441-6.
(665) Tephly TR., Watkins WD, Goodman JI. The Biochemical Toxicology of Methanol. New York
and London: Acidemic Press; 1974. (Hayes JH., ed. Essays In Toxicology; vol. 5).
(666) Chao MJ., Ramagopalan SV., Herrera BM., Orton SM., Handunnetthi L., Lincoln MR., et al.
MHC transmission: Insights into gender bias in MS susceptibility. Neurology 2011;76(2).
(667) Cong R., Zhou B., Sun Q., Gu H., Tang N., Wang B. Smoking and the risk of age-related
macular degeneration: a meta-analysis. Ann Epidemiol 2008;18(8):647-56.
(668) Evans J., Wormald R. Is the incidence of registrable age-related macular degeneration
increasing? British Journal of Ophthalmology 1996;80:9-14.
(669) McKinley MG. Alcohol Withdrawal Syndrome Overlooked and Mismanaged? Critical Care
Nurse 2005;25(3):40-9.
(670) Becker CE. Acute Methanol Poisoning - The Blind Drunk. West J. Med. 1981;135:122-28.

(671) Prabhakaran V., Ettler H., Mills A. Methanol poisoning; Two cases with similar plasma
methanol concentrations but different outcomes. Can Med Assoc J 1993;148(6):981-84.
(672) Paasma R., Hovda KE., Jacobsen D. Methanol poisoning and long term sequelae - a six years
follow-up after a large methanol outbreak. BMC Clin Pharmacol 2009;27(9):1-5.
(673) Hovda KE., Hunderi OH., Tafjord AB., Dunlop O., Rudberg N., Jacobsen D. Methanol outbreak
in Norway 2002-2004: epidemiology,
Clinical features and prognostic signs. J Intern Med 2005;258(2):181-90.
(674) Jacobsen D., Jansen H., Wiik-Larsen E., Bredesen JE., Halvorsen S. Studies on methanol
poisoning. Acta Med Scand 1982;212(1-2):5-10.
(675) Cursiefen C., Bergua A. Acute bilateral blindness caused by accidental methanol intoxication
during fire “eating”. Br J Ophthalmol. 2002 Sep;86(9):1064-5 2002;86(9):1064-5.
(676) Cornblatt JA. The Water Channel of Cytochrome c Oxidase: inferences from
Inhibitor Studies. Biophys J. 1998 Dec;75(6):3127-34 1998;75(6):3127-34.
(677) Collins TFX. Memorandum: Aspartame shown to cause nural tube birth defects in the New
Zealand rabit, an animal very resistant to methanol poisoning. Freedom of information:
Department of Health Education and Welfare, Food and Drug Administration; 1978.
(678) anonymous. Seventeenth Report of the Joint FAOWHO Expert Committee on Food Additives,
Formic Acid. FAO WHO; 1973.
(679) Christie RH., Freeman M., Hyman BT. Expression of the Macrophage Scavenger Receptor, a
Multifunctional Lipoprotein Receptor, in Microglia Associated with Senile Plaques in
Alzheimer’s Disease. Amer J Path 1996;148(2):399-403.
(680) Roe O. Clinical Investigations of methyl alcohol poisoning with special references to the
pathogenesis and teatment of amblyopia. Acta Med Scand 1943;63:558-605.
(681) Fisher MA. The Toxic Effect of Formaldehyde and Formalin. J Exp Med 1905;6:487-518.
(682) Moore KJ. Freeman MW. Targeting Innate Immunity for Cardio Vascular Benefit. Drug Discov
Today Ther Strateg 2008;5(1):15-23.
(683) Holman RL., McGill HC., Strong JP., Geer JC. The Natural History of Atherosclerosis. Amer J
Path 1958;34(2):209-35.
(684) Marrugat J., Sala J., Aboal J. Epidemiology of cardiovascular disease in women. Rev Esp
Cardiol 2006;59(3):264-74.
(685) U.S. Environmental Protection Agency. Toxicoilogical Review of Methanol EPA/6.35/R-

09/013. Draft ed. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=56521#Download:

U.S. Environmental Protection Agency; 2010.
(686) Gardener H. Diet Soda Tied to Vascular Risk “Soda consumption and risk of vascular events in
the northern Mahattan Study ASA 2011 Abstract P55. American Stroke Association’s
International Stroke Conference; 2011; Los Angeles.
(687) Berneisa K., Rizzob M. LDL Size; Does it Matter? Swiss Med Wkly 2004;134:720-24.
(688) Baker JR. Principles of biological microtechnique. London, UK.: Methuen; 1958.
(689) Blomhoff R., Eskild W., Berg T. Endocytosis of formaldehyde-treated serum albumin via
scavenger pathway in liver endothelial cells. Biochem J 1984;218:81-6.
(690) Kaesberg B., Harrach B., Dieplinger H., Robenek H. In situ immunolocalization of lipoproteins
in human arteriosclerotic tissue. Arterioscler Thromb 1993;13(1):133-46.
(691) Smedsrød B., Melkko J., Araki N., Sano H., Horiuchi S. Advanced glycation end products are
eliminated by scavenger-receptormediated endocytosis in hepatic sinusoidal Kupffer and
endothelial cells. Biochem J 1997;322:567-73.
(692) Harrach B., Robenek H. Polyclonal antibodies against formaldehyde-modified apolipoprotein A-

I. An approach to circumventing fixation-induced loss of antigenicity in
immunocytochemistry. Arteriosclerosis 1990;10(4):564-76.
(693) Murthy VK., Monchesky TC., Steiner G. In vitro labeling of beta-apolipoprotein with 3H or 14C
and preliminary application to turnover studies. J Lipid Res 1975;16(1):1-6.
(694) Ciappuccini R., Ansemant T., Maillefert JF., Tavernier C., Ornetti P. Aspartame-induced
fibromyalgia, an unusual but curable cause of chronic pain. Clin Exp Rheumatol 2010;28(6
Sup 63):S131-3.
(695) Soffritti M., Belpoggi F., Manservigi M., Tibaldi E., Lauriola M., Falcioni L., et al. Aspartame
administered in feed, beginning prenatally through life span, induces cancers of the liver and
lung in male Swiss mice. Am J Ind Med 2010;53(12):1197-206.
(696) Cataldo JK., Prochaska JJ., Glantz SA. Cigarette smoking is a risk factor for Alzheimer’s
Disease: an analysis controlling for tobacco industry affiliation. J Alzheimers Dis
2010;19(2):465-80.
(697) Hashimoto M., Rockenstein E., Crews L., Masliah E. Role of protein aggregation in
mitochondrial dysfunction and neurodegeneration in Alzheimer’s and Parkinson’s diseases.
Neuromolecular Med 2003;4(1-2):21-36.
(698) Hernández F., Avila J. Tauopathies. Cell Mol Life Sci 2007;64(17):2219-33.
(699) Surdacki A., Martens-Lobenhoffer J., Wloch A., Marewicz E., Rakowski T., Wieczorek-

Surdacka E., et al. Elevated Plasma Asymmetric Dimethyl-L-Arginine Levels Are Linked to
Endothelial Progenitor Cell Depletion and Carotid Atherosclerosis in Rheumatoid Arthritis.
Arthritis Rheum 2007;56(3):809-19.
(700) Vallance P., Leiper J. Cardiovascular Biology of the Asymmetric Dimethylarginine:

Dimethylarginine Dimethylaminohydrolase Pathway. Arterioscler Thromb Vasc Biol
2004;24:1023-30.
(701) Sacks JJ., Helmick CG., Langmaid G., Sniezek JE. Trends in Deaths from Systemic Lupus
Erythematosus --- United States, 1979--1998. Morbidity and Mortality Weekly Report
2002;51(17):371-4.
(702) Nettleton J., et al. Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2
Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care 2009;32:688-
94.
(703) Mölsä PK., Marttila RJ., Rinne UK. Long-term survival and predictors of mortality in
Alzheimer’s disease and multi-infarct dementia. Acta Neurol Scand 1995;91(3):159-64.
(704) Mölsä PK., Marttila RJ., Rinne UK. Survival and cause of death in Alzheimer’s disease and
multi-infarct dementia. Acta Neurol Scand. 1986 Aug;74(2):103-7 1986;74(2):103-7.
(705) Matsumoto R., Nakano I., Shiga J., Akaoka I. Systemic lupus erythematosus with multiple
perivascular spongy changes in the cerebral deep structures, midbrain and cerebellar white
matter: a case report. J Neurol Sci 1997;145(2):147-53.
(706) Yocum AK., Chinnaiyan AM. Current affairs in quantitative targeted proteomics: multiple
reaction monitoring-mass spectrometry. Brief Funct Genomic Proteomic 2009;8(2):145-57.
(707) Adams CW., Bayliss OB., Hallpike JF, Turner DR. Histochemistry of myelin. XII. Anionic
straining of myelin basic proteins for histology, electrophoresis and electron microscopy. J
Neurochem 1971;18(3):389-94.
(708) Schultz M., et. al. Alcohol attributable burden of incidence of cancer in eight European countries
based on results from prospective cohort study. British Medical Journal 2011;342:1-10.
(709) Zhang L., Tang X., Rothman N., Vermeulen R., et. al. Occupational exposure to formaldehyde,
hematotoxicity, and leukemia-specific chromosome changes in cultured myeloid progenitor
cells. Cancer Epidemiol Biomarkers Prev 2010;19(1):80-8.
(710) Lai SM., Zhang ZX., Alter M., Sobel E. World-wide trends in multiple sclerosis mortality.
Neuroepidemiology 1989;8(2):56-67.
(711) Wills S., Rossi CC., Bennett J., Martinez-Cerdeno V., Ashwood P., Amaral DG., et al. Further
characterization of autoantibodies to GABAergic neurons in the central nervous system
produced by a subset of children with autism. Molecular Autism 2011;2(1):5.

(712) Gale AME. The rise of childhood type 1 diabetes in the 20th century. Diabetes
2002;51(12):3353-61.
(713) Karjalainen J., Martin JM., Knip M., Ilonen J., Robinson BH., Savilahti E., et al. A bovine
albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med
1992;327:302-7.
(714) Monte WC., Johnston CS., Roll LE. Bovine serum albumin detected in infant formula is a
possible trigger for insulin-dependent diabetes mellitus. J Am Diet Assoc 1994;94(3):314-16.
(715) Johnston CS., Monte WC. Infant formula ingestion is associated with the development of
diabetes in the BB/Wor rat. Life Sci 2000;66(16):1501-7.
(716) Soltesz G., Patterson CC., Dahlquist G. Worldwide childhood type 1 diabetes incidence--what
can we learn from epidemiology? Pediatr Diabetes 2007;6(Suppl):6-14.
(717) Karvonen M., Viik-Kajander M., Moltchanova E., Libman I., LaPorte R., Tuomilehto J.
Incidence of childhood type 1 diabetes worldwide. Diabetes Mondiale (DiaMond) Project
Group. Diabetes Care 2000;23(10):1516-26.
(718) Gloster HM, Brodland DG. The epidemiology of skin cancer. Dermatol Surg 1996;22(3):217-
26.
(719) Centers for Disease Control and Prevention (CDC). Spina bifida and anencephaly before and
after folic acid mandate--United States, 1995-1996 and 1999-2000. MMWR Morb Mortal
Wkly Rep 2004;53(17):352-5.
(720) Centers for Disease Control and Prevention (CDC). Recommendations for the use of folic acid
to reduce the number of cases of spina bifida and other neural tube defects. MMWR Recomm
Rep 1992;41(RR-14):1-7.
(721) Cragan JD., Roberts HE., Edmonds LD., Khoury MJ., Kirby RS., et.al. Surveillance for
anencephaly and spina bifida and the impact of prenatal diagnosis--United States, 1985-1994.
MMWR CDC Surveill Summ 1995;44(4):1-13.
(722) Choi SW., Mason JB. Folate and carcinogenesis: an integrated scheme. J Nutr 2000;130(2):129-
32.
(723) Jones JG., Bellion E. Methanol oxidation and assimilation in Hansenula polymorpha. An
analysis by 13C n.m.r. in vivo. Biochem J. 1991 Dec 1;280 ( Pt 2):475-81. 1991;280(2):475-
81.
(724) Suarez L., Felkner M., Brender JD., Canfield M., Hendricks K. Maternal exposures to cigarette
smoke, alcohol, and street drugs and neural tube defect occurrence in offspring. Matern Child
Health J. 2008 May;12(3):394-401 2008;12(3):394-401.

(725) Elwood JM., Coldman AJ. Water composition in the etiology of anencephalus. Am J Epidemiol
1981;113(6):681-90.
(726) Larsson KS. The dissemination of false data through inadequate citation. J Intern Med. 1995
Nov;238(5):445-50. 1995;238(5):445-50.
(727) Sever LV. Looking for causes of neural tube defects: where does the environment fit in? Environ
Health Perspect. 1995 Sep;103 Suppl 6:165-71. 1995;103(6):165-71.
(728) Mills JL., Rhoads GG., Simpson JL., Cunningham GC., et. al. The absence of a relation between
the periconceptional use of vitamins and neural-tube defects. National Institute of Child Health
and Human Development Neural Tube Defects Study Group. N Engl J Med. 1989 Aug
17;321(7):430-5. 1989;32(7):430-5.
(729) Heseker HB., Mason JB., Selhub J., Rosenberg IH., Jacques PF. Not all cases of neural-tube
defect can be prevented by increasing the intake of folic acid. Br J Nutr 2009;102(2):173-80.
(730) Ly A., Lee H., Chen J., Sie KK., Renlund R., et. al. Effect of maternal and postweaning folic
acid supplementation on mammary tumor risk in the offspring. Cancer Res 2011;71(3):988-97.
(731) Schmidt RJ., Hansen RL., Hartiala J., Allayee H., Schmidt LC., Tancredi DJ., et al. Prenatal
Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism. Epidemiology
2011;22(4):476-85.
(732) Oyedele OO., Kramer B. Acute ethanol administration causes malformations but does not affect
cranial morphometry in neonatal mice. Alcohol 2008;42(1):21-7.
(733) May PA., Gossage JP., Brooke LE., Snell CL., Marais AS., Hendricks LS.Croxford JA., et al.
Maternal risk factors for fetal alcohol syndrome in the Western cape province of South Africa:
a population-based study. Am J Public Health 2005;95(7):1190-9.
(734) Madsen KM., Hviid A., Vestergaard M., Schendel D., Wohlfahrt J., Thorsen P., et al. A
population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med.
2002 Nov 7;347(19):1477-82. 2002;347(19):1477-82.
(735) Ratajczak HV. Theoretical aspects of autism: biomarkers - a review. J Immunotoxicol

2011;8(1):80-94.
(736) Gillis RF., Rouleau GA. The ongoing dissection of the genetic architecture of Autistic Spectrum
Disorder. Molecular Autism 2011, 2:12 Doi:10.1186/2040-2392-2-12 2011;2(12).
(737) Thompson M. NTP Technical Report on Toxicity Studies of Formic Acid (CAS No: 64-18-6)
National Toxicology Program Toxicity Report Series Number 19. United States Department of
(738) Ratajczak HV. Theoretical aspects of autism: Causes--A Review. J Immunotoxicol

2011;8(1):68-79.
(739) Courchesne E., Carper R., Akshoomoff N. Evidence of Brain Overgrowth in the First Year of
Life in Autism. JAMA 2003;290(3):337-44.
(740) Jansen GR., Monte WC. Amino Acid Fortification of Bread Fed at Varying Levels During
Gestation and Lactation in Rats. J Nutr 1977;107(2):300-9.
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1 A Time When All the Easy Questions Have Been Answered 7

2 Methanol: Where Is It Found? How Can It Be Avoided? 20

3 Man And Methanol: A Tragic History of Mutation and Deceit 27

4 Formaldehyde Is The Real Problem 44

5 The Silent Battle That Turns Methanol Into Disease 64

6 How Methanol Kills 73

7 Atherosclerotic Cardiovascular Disease (Heart Disease) 94

8 Alzheimer's Disease and its Perivascular Nature 122

9 Multiple Sclerosis 136

10 Classic Autoimmune Diseases Lupus and Rheumatoid Arthritis 184

11 Cancers of Aspartame 194

12 Autism and other Birth Defects 216

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The Conflagration That Is Multiple Sclerosis

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Listening to Nature’s Whispers

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The Scene of the Crime

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Location, Location, Location

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Details of Plaque Formation

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The Look, Touch, Taste and Smell of Multiple Sclerosis

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The Cause of MS is within the Thickening Blood Vessels

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Learn a Little About Arginine

Myelin Basic Protein (MBP)

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Looking for the Shadow of Formaldehyde

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formaldehyde as the cause of an important disease of civilization. We parted in a state of great

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Evidence That Methanol Causes MS

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The Etiology of Multiple Sclerosis – Follow the Methanol

The History of Man’s Methanol Consumption Corresponds to the History of MS

The Early Years of the Multiple Sclerosis Timeline

An Explosion of Methanol and Disease: The Turn of the 19th Century

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A Food Scientist’s Nightmare Called Aspartame

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MS: A Disease of Colder Climates and Flush Toilets – Before Aspartame

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A World Awash in MS After Aspartame

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