Cancers of Aspartame

Abstract

Helps to explain the recent link to cancer with the consumption of the artificial sweetener Aspartame via it's conversion to formaldehyde within human cells.

Full text

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Table of Contents
Introduction 3
I A Time When All the Easy Questions Have Been Answered 7
II Methanol: Where Is It Found? How Can It Be Avoided? 20
III Man And Methanol: A Tragic History of Mutation and Deceit 27
IV Formaldehyde Is The Real Problem 44
V The Silent Battle That Turns Methanol Into Disease 64
VI How Methanol Kills 73
VII Atherosclerotic Cardiovascular Disease (Heart Disease) 94
VIII Alzheimer's Disease and its Perivascular Nature 122
IX Multiple Sclerosis 136
X Classic Autoimmune Diseases Lupus and Rheumatoid Arthritis 184
XI Cancers of Aspartame 194
XII Autism and other Birth Defects 216
Bibliography 242

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<CN>Chapter 11
<CT>Cancers of Aspartame
Aspartame's proclivity to cause cancer in humans should be a surprise to no one. The unimpeachable
biochemical pathway whereby its methanol transforms into formaldehyde at cancer prone ADH
containing tissue locations throughout the human body constitutes sufficient scientific basis for
considerable concern. Animal feeding studies of aspartame show statistically significant, dose
dependent increases of breast and kidney cancers in test animals even though these animals are known to
be more resistant to the toxicity of methanol than humans. The Center for Disease Control Seer program
which monitors the wellness of the US population has published data showing an alarming increase in
these and other important cancers that mirrors the popularity and consumption of aspartame over the last
30 years. The real question is why hasn't this overwhelming commonality of logic and fact been
sufficient evidence to remove aspartame from the marketplace?
Considerable evidence against the safety of aspartame comes directly from it's regulatory file
history stored in the vaults of the US Food and Drug Administration. Aspartame's carcinogenity (ability
to cause cancer) in laboratory animals is documented in studies done on the sweetener before its
approval.[#57] Cancerous brain tumors found in laboratory rats in a dose-dependent relationship to the
content of aspartame in their diet were among the most compelling reasons it was consistently rejected
for use in foods.[#56] It took the hiring, by the G.D. Searle company that invented the sweetener, of a
Washington insider, Donald Rumsfeld, as CEO in March of 1977 to force aspartame into the food
supply.
The exquisite and pivotal laboratory work done by Professor Marie Alemany despite the
strenuous, though unconvincing, objections of the opposition[#40] is proof conclusive that aspartame and

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therefore methanol does turn into formaldehyde within the living organism. Dr. Alemany skillfully used
radioactive tracing of the methanol component of aspartame and thus clearly and unequivocally
demonstrated methanol's evolution into the formation of formaldehyde modified proteins and DNA.[#7]
How strange it seems now that anyone would ever doubt that formaldehyde is produced from methanol
or be convinced to think otherwise. For his exquisite work Dr. Alemany had his university funding
revoked and like so many other scientists that dared go against the corruption that abounds in the
western bureaucracies was made to endure indignities designed to discourage dissension.[#222]
Laboratory animals that take our place in safety testing have catalase enzyme in sufficient
quantity within their bodies to protect them from the lion‟s share of the carcinogenetic effect of
methanol's formaldehyde. When an animal does show signs of cancer the ramifications for humans are
ominous. Therefore when it comes to making a fair determination of the carcinogenic potential of
methanol or aspartame, we are dependent on careful epidemiological observation of exposure of human
populations to either methanol or aspartame. There is nothing wrong with this approach, it brings us
back to the roots of the health sciences where observation leads to the application of logic and, in more
cases than modern practitioners of medicine would like to admit, to the development of methods to
prevent disease.
For aspartame, we have excellent data of its consumption rate during the extremely important
time its popularity was ramping up in the United States. The entire US population has been a study
group, with no knowledge or forewarning of its participation in a ghastly experiment. Using this data
may be the very best way that its cancer causing potential can be determined. Toxicologists could only
dream of such a large blind research population, which normally would make the job of the
epidemiologist quite simple. Unfortunately, many toxicologists owe their allegiances to various
industrial and pharmaceutical groups who insist they waste their skills proving how safe new chemicals

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are rather than showing the havoc that they might cause. No worries; we will see for ourselves where the
truth lies and make our own determinations by looking at the graphs of the aftermath of thirty years of
aspartame consumption. We will put ourselves in the position of the ancient Aztec, Inuit or Judean
intelligentsia whose insights guided their people away from foods that might do harm. The edge we have
over the ancients is that our culture has uncovered knowledge of the chemistry of nature, and this can
reinforce our observations with reasonable insights as to the molecular details that might lead to cancer
production.
<S1>Formaldehyde's Cancer-Causing Prowess is Enhanced When it Comes From Methanol
What exactly is the link between cancer and aspartame's methanol component? There can be no doubt
that a poison such as methanol that produces formaldehyde within cancer-prone tissue throughout the
human body will eventually cause cancer. On the very day this paragraph was begun, June 10, 2011, the
government of the United States finally caught up with the rest of the world[#451] and officially declared
formaldehyde a "known human carcinogen."[#11]
A full grown human can die from ingestion of just a "few drops" of formaldehyde with death
from acute formaldehyde poisoning often taking only minutes.[#448] Air contaminated with
formaldehyde, even at very low concentrations, is now known to cause cancer in humans.[#11] Again let
me stress that formaldehyde is one of a handful of chemicals classed as a Group I carcinogen by the
IARC, the International Agency for Research on Cancer, Lyon, France. No known safe level of
formaldehyde exposure exists; it is in all amounts a dangerous carcinogen[#11] and mutagen.[#86] Even so,
were it not for one major obstacle, formaldehyde might reach the status of one of the most perfect and
powerful of carcinogens. Its only weakness is that it is so highly reactive that its destructive power is
usually used up before it can travel all the way to the nucleus of the cell, where cancers originate. Like

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an overanxious lover, it spills its energy long before it makes its mark, prematurely squandering itself
prior to reaching the perfect site for its application. On the other hand, methanol as a source of
formaldehyde acts as a partner to its carcinogenic potential, easing it into places much closer to where it
can more successfully work its dark magic, potentially producing cancers in all the human sites of ADH
activity, including the liver.
It only takes one cell succumbing perfectly to formaldehyde‟s attack to produce a full blown
cancer. Other methanol diseases, such as multiple sclerosis, atherosclerosis and Alzheimer's, are all
slowly developing diseases that require years of collective damage caused by countless formaldehyde
interactions that eventually add up to a defect that manifests as a chronic disease. Not so with cancer. A
single cell‟s bad encounter with a carcinogen can initiate cancer progression that is virtually
unstoppable. The exact behavior of the cancer from then on depends on which type of cell is affected
and how quickly it can multiply. In some cases, individuals have been exposed to known cancer-causing
agents for years and never experienced cancer, but in others, after just one encounter with asbestos,
plutonium or formaldehyde, a cellular change was induced, turning one cell into the seed of a fatal
malignancy.
Does that mean that just one sip of diet coke could start a cancer? Regrettably, the answer is yes.
Cancer, therefore, is a purely statistical phenomenon in a game of environmental roulette. We turn the
wheel each time we take a sip of diet soda or a puff of cigarette smoke and the wheel does not stop
spinning until all the resultant formaldehyde has found its final home. If science understood the exact
details of what cancer "really" is, I would certainly spend time in its explanation. Here again, we have
put our trust to find the cure for cancer into the hands of those who have the most to lose when a remedy
is found. We know little more about the truth of cancer than we did when lone scholars worked long
hours in underfunded university laboratories out of the reach of Big Pharma.

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What we do know with certainty is that unwanted methylation[#560] and inappropriate cross-
linking of chromosomal tissue[#449] play a major part in the production of cancers. Both these phenomena
are the handywork of our crazy hawk.[#596] Formaldehyde is actually just a reactive methyl group, a
"methyl molecule" that is essentially a methylation machine. It is capable of the methylation of DNA as
long as enzymes are available, as they are in the living cell, to finish the job.[#564] Over 60 methylation
defects of DNA from human cancer cells have been identified thus far.[#567] This hyper-methylation of
DNA causes the shutdown of the expression of genes involved in preventing the production of important
proteins that have been coded into the methylated portion of DNA. These are the changes that also come
into play during the evolution of Autism and other birth defects, which we will discuss in the next
chapter.
As for cross-linking of DNA, there are few chemicals more likely to form a bridge between a
DNA molecule and protein or other DNA than formaldehyde hydrate. The indiscriminate attachment of
formaldehyde to the chromosomes in the nucleus of a living cell has been shown time and time again to
cause the inappropriate linking together (cross-linking) of these molecules in such a way as to induce
cancer.[#596], [#633] This works much the same way as the linking together of the Tau proteins, resulting in
Alzheimer's. In humans, the methanol placement of formaldehyde is the key to its ultimate perfection as
a carcinogen. Methanol is a very small and nonreactive molecule. It can go anywhere in the body with
no effort at all, as a Trojan horse delivering formaldehyde where it can cause severe damage.
You should come away from this discussion with the knowledge that the ultimate cancer-causing
agent in humans just might be a trinity of unfortunate circumstances. Methanol making contact with
ADH which converts it to formaldehyde. Show me a place where ADH can be found in the human body
and I will more than likely be able to show you a cancer that has increased in incidence since that fateful
day in 1981 when a new source of methanol was forced into the diet of the unsuspecting consumer.

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<S1>There are Thousands of Carcinogens
Thanks to a lack of genuine governmental oversight and the extraordinarily unrestrained involvement of
chemical and pharmaceutical interests into the bureaucratic decision-making process relative to the
safety of chemical substances. Along with the largely industrial leanings of the toxicological and
epidemiological professions in general. We have a number of new chemicals in our environment which,
to my way of thinking, have not undergone proper screening for carcinogenity. It is still technically
against the law of the United States to allow any chemicals (pesticides have been exempted) which are
known to cause cancers in man or animals to be an ingredient added to foods. Since we now know that
aspartame turns into a cancer-causing agent, we need to look at what the effect of adding millions of
pounds a year of that carcinogen to the food supply over the last thirty years has done to the cancer rates
in the US. We will concentrate on those cancers that originate in the known centers of ADH I
concentration in the human body where formaldehyde is the predictable outcome of aspartame
consumption.
Cancer statistics for the United States is published by the Surveillance Research Program of the
National Cancer Institute, which manages the Surveillance, Epidemiology, and End Results (SEER)
Program. The SEER program is an authoritative source of information on cancer incidence in the
United States. SEER collects and publishes these statistics from population-based registries covering
26% of the US population.[#577] Looking first at an overview of the total cancer burden for the United
States. I have plotted the CDC SEER data for incidence of "all cancer" occurrences in the United States
for the period since the introduction of aspartame (Chart 1) which clearly shows the full impact of the
sudden increase in aspartame consumption. Why does there appear to be a peak in cancer incidence in
1993?

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Insert Chart 1 here
<S1>The Sensitive, Vulnerable, and Susceptible will be Lost First
To answer the question of the apparent peak of cancers in the above chart I will need to relate a story. A
few years back, upon landing in Christchurch on one of my many flights from the States to sanctuary in
New Zealand, I was contacted by a good friend who asked if I wouldn't mind sitting for the filming of a
TV interview that might never see the light of day. The interviewer, a Kiwi with a reputation as a hard-
hitting investigative journalist, was said to have an interest in aspartame, but he didn't think he could talk
his managers into what would be an outright challenge to the cola industry, a major source of
advertizing dollars to his company. New Zealand media, once run by the government with no need to
pander for its survival, had deteriorated quickly to the US model after deregulation. I accepted and we
asked the airport hotel to let us use an unoccupied garden area as a temporary studio.
I will never forget one of his questions, obviously something that he had researched and which
had been on his mind for some time. "Professor Monte, do you think that the unexplained increase in
teen suicides in New Zealand has anything to do with allowing carbonated diet beverages into the tucker
(school lunch) programs?" I explained that I did not realize that New Zealand had experienced a similar

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problem to ours in the US. My answer was in the affirmative, and followed the lines of logic that I used
to explain the chart in chapter 9 of the teen suicide experience in the US. He quickly countered with a
question that I am sure he hoped would please his employers. “Well, how do you explain that the
consumption of diet soda has been steady over the last few years and the teen suicide rate is now in
decline?” Without hesitation, I countered with "It is obvious your advertiser has succeeded in killing off
the most sensitive kids."
The show never aired, but I relate the incident to you because it points out a common outcome of
toxicological experimentation done on large populations of test animals. The introduction of a poison
into the diet of a colony of test animals is the very most important stage of the experiment. It is at some
point after this that we expect to see the most susceptible individuals of the colony, never before stressed
at these levels, are killed off. I have done such experimentation myself and know what to expect. The
horror of this, to me personally, is that the curve I would expect to see in a laboratory study of a deadly
poison would be shaped very much like Chart 1, with a spiking of incidents followed by a slow down as
the more resistant animals remain alive and in the study. The time it takes to achieve this peaking of the
curve varies, depending on the characteristics of the poison administered. The most interesting
indication of this phenomenon is the curve never drops all the way back down to the baseline (where it
started before the experiment began) for as long as the poison is being administered to the colony. Thus
indicating a definite cumulative effect on the population as a whole. The "depletion of the weaklings" is
what we used to call it before we came to realize that in the case of aspartame each of these data points
represented a person.
<S1>Brain Cancer: The Killing Begins

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Increasing Brain Tumor Rates: Is There a Link to Aspartame?[#329] is the title of an article published in
1996 by the American Association of Neuropathologists and written by the renowned research
neuroscientist John W. Olney. John cites the results of the original aspartame animal studies I mention
above "revealing an exceedingly high incidence of malignant brain tumors in aspartame-fed rats" and
notes that "spontaneous brain tumors in laboratory rats are quite rare." He goes on to point to the
relevancy of a Public Board of Inquiry, called together by the US Food and Drug Administration in 1980
to evaluate these studies, "included prominent neuroscientists Walle Nauta and Peter Lampert." This
Board subsequently concluded that "aspartame may contribute to the development of brain tumors in the
human population." They recommended that the Food and Drug Administration withhold approval of
aspartame as a food additive. Within months of this decision, Donald Rumsfeld's team was in control of
the White House, and within days aspartame was a “food.”
Nauta points out that a sharp upward trend in deaths from brain tumors was detected in the mid
1980s in countries that approved the use of the sweetener, including the United Kingdom, France,
Germany and Italy. Nauta found during his study similar increases in brain cancers in the States, noting
that "it was not a fleeting phenomenon. Rather, it was the initial phase of an upward swing in the brain
tumor incidence which evolved into a sustained increase in both the per capita number and malignancy
of brain tumors, a phenomenon that has endured for at least 8 years."
I have taken the liberty to chart the data from figure 3 on page 1119 of Dr. Olney's article on our
standard graph of aspartame consumption (Chart 2). You can see from this chart that the brain cancer
rate in the US population more than doubled after the introduction of aspartame. Olney goes on to warn
that "Compared to other environmental factors, aspartame appears to be a promising candidate for
explaining the surge in brain tumors in the mid-1980s." In his concluding sentence he pleads for a

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"reassessment of the carcinogenic potential of aspartame which is currently being ingested widely
throughout many parts of the world."
Insert Chart 2 here
John's fine article is a professional plea from a world renowned scientist and physician who is
respected by not only his neurological peers, but by the scientific community in general. The plea is in
the form of a scientific article that had been reviewed and published in the premier journal of a leading
neurological association whose scope includes this exact type of research. Reading the article you will
see the high standard that is used to evaluate the potential of aspartame to act as a human carcinogen.
John asks three questions. Does the agent have carcinogenic potential? (This is John's weakest argument
since he cannot use the formaldehyde link.) Do experimental animals show an increased incidence of
specific types of cancer when exposed to the agent? Do humans show an increase incidence of the same
types of cancer when exposed to the agent? John claims, rightly so, that "aspartame appears to meet all
three criteria."
There is nothing more that this man could have done. He is an expert in his field and he
proceeded in the proper way, and yet absolutely nothing changed. He was ignored by the FDA and all
the other such public organizations of the world that are charged to protect their respective populations
from poisons. The argument used against John's premise was the so-called "ecological fallacy". The
meaning of the fallacy goes something like this: "The temporal coincidence of two events observed at an

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ecological level without examination of individual data can lead to faulty conclusions regarding risk
association." In other words, because two thing happen at the same time doesn't mean that they are
related. This, of course, could be true in this case except for the ignored fact that John went beyond this
and made a good case for the science behind the cause of the cancer and showed that the same cancer
was demonstrated in laboratory animals. John did all this and his premise should have won the day. His
argument should have swayed the FDA to immediate action against the use of aspartame in foods. He,
in fact, went well beyond the standard used to remove Thalidomide from the marketplace.
Breast Cancer
Something quite remarkable happened during the aspartame feeding studies done by Dr. Morando
Soffritti – something that prompted him to break with tradition, go beyond what John Olney had done
and call publicly for an "urgent reevaluation" of the current guidelines for the use and consumption of
aspartame. During a long term aspartame feeding study done by the industry independent European
Ramazzini Foundation headed by Dr. Soffritti it was shown conclusively that Sprague Dawley rats,
which have the highest resistance to methanol toxicity of any laboratory animal, developed breast
(mammary) and other cancers on a statistically significant and dose dependent basis when fed aspartame
at low levels.[#50] Results that Morando reports eloquently in his own words, "Our study has shown that
aspartame is a multipotential carcinogenic compound whose carcinogenic effects are also evident at a
daily dose of 20 milligrams per kilogram of body weight (mg/kg), notably less than the current
acceptable daily intake of aspartame for humans."[#50] The horror that Morando witnessed happening to
his test animals was a partial reflection of what the aspartame consuming world had been going through
for "the last thirty years."

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The considerable evidence linking breast cancer to methanol is very convincing. There is good
reason to believe that the epidemic of breast cancer over the last thirty years has more to do with the
introduction of aspartame into the food supply than any other proposed causes. The production of breast
cancer in laboratory animals fed aspartame, the increased rate of breast cancer in school teachers
exposed to occupational methanol (see below) and the direct implication of high ADH tissue levels in
those more prone to developing breast cancer over the course of their lifetimes goes a long way to prove
methanol as an etiologic agent of breast cancer.
<S1>Why is the Human Breast Particularly Sensitive to Methanol?
Methanol travels easily to breast tissue and has been found in human milk.[#219] The cells that produce
milk within the breast, cells prone to develop the most common of breast cancers, adenocarcinoma,[#358]
contain high concentrations of ADH enzyme,[#358] allowing methanol's conversion to formaldehyde.
Mammary epithelial cells have no way to protect themselves from formaldehyde[#216] no means to render
it harmless. They unlike other breast tissue contain no aldehyde dehydrogenase enzyme[#216] (remember
ADH III) which could transform formaldehyde into the non-carcinogenic formic acid.
Of particular interest are recent findings implicating ADH as playing a pivotal role in the
formation of breast cancer, documenting a greater incidence of the disease in women with higher levels
of ADH I activity in their breasts.[#357] These articles go on to indict acetaldehyde as the potential
culprit.[#357] Remember acetaldehyde, as stressed in previous chapters, is essentially vinegar that results
when ethanol is changed by ADH, it is a largely benign molecule with no link to cancer in humans. The
role of acetaldehyde must be questioned when the same researchers report: "Very heavy drinking has not
been associated with increased breast cancer risk relative to moderate drinking. We cannot explain why
we have not observed an increase in risk from heavy lifetime consumption of alcohol."[#501] What they

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are saying is that those who are constantly inebriated would have the cells in their breasts continuously
producing acetaldehyde, therefore increasing the chances of breast cancer if acetaldehyde was indeed the
culprit. This, of course, is not what actually occurs. Acetaldehyde is not the problem formaldehyde is
the problem. The correct answer here is that the cause of breast cancer is not the ADH metabolite of
ethanol, but rather the ADH metabolite of methanol . As you know it is ethanol in the blood that keeps
the ADH busy and prevents it from producing formaldehyde from methanol.
<S1>School Teachers Have Higher Risk of Breast Cancers
In Chapter 9 we learned of the long term exposure of school teachers to methanol vapors from ditto
machines and the increase of autoimmunity that appears to be endemic in that group.[#210] Statistically
significant evidence, developed from several different sources during large cohort studies, shows that
teachers in the United States and Canada also have been at much higher risk of developing and dying
from breast cancer than professional women in any other occupation. In a comprehensive study done of
school teachers in British Columbia from 1950 to 1984, long before aspartame was allowed into
carbonated beverages, it was shown that school teachers had a 70% greater chance of dying from breast
cancer than women in other occupations. [#217] A study done at the Yale Cancer Center of breast cancer
incidence in Connecticut women found only one occupational group of women with a statistically
increased risk of breast cancer. That group – teachers – had twice the chance of developing breast
cancer even after adjustment for major breast cancer risk-factors.[#241]
An article titled High breast cancer incidence rates among California teachers,[#213] published in
2002, found that "teachers have long been suspected to be at high risk of breast cancer." In a mortality
study done between 1979-1981, the California Department of Health Services noted a substantial excess
mortality from breast cancer in California teachers. A large cohort study of over 133,000 California

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female teachers showed these women were statistically more likely to develop invasive breast cancer,
in-situ breast cancer, and localized invasive breast cancer than other female professionals with 51%,
67% and 65% respective greater risks.[#213] The Yale study cited above points out that increased breast-
cancer risk among teachers is "consistent with most earlier studies" and "it is currently unknown,
however, what factors may explain the observed increase," however, "considering teachers represent one
of the largest single occupational groups among employed US women, further investigation of this
association is warranted."[#241]
<S1>Aspartame Causes Breast Cancer in Human Feeding Study done by Searle
Remember from the introduction that in the summer of 1983 I spent time in a cramped conference room
in Washington DC that housed the docket file and application made by the G.D. Searle company to the
US FDA to allow aspartame into carbonated beverages. A nameless FDA employee handed me one of
the files he had been reading. Staring straight into my eyes he said in a whisper "did you see this?" I
was taken aback, but before I could ask any questions he had disappeared, just as other such angels had
into the endless corridors of that bleak federal building.
The study he handed me was damning evidence of the danger aspartame posed to the public. It
was a long-term human study of diabetics who consumed 6 capsules daily containing a total of 1.8
grams of pure aspartame for 13 consecutive weeks.[#48] This dosage of aspartame is tantamount to
taking 200 milligrams of pure formaldehyde daily. This was the equivalent to the daily consumption of
the amount of aspartame to be found in between three and 5 liters of diet cola. The subject base
consisted of a total of 77 individuals, only 39 of which were aspartame consumers, the others were
controls. As a prerequisite to being accepted into the study, each participant had to pass a through
physical examination that included considerable blood work before they were allowed to join. It was a

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double blind study, so neither the subjects nor the researchers had any idea who was taking the
aspartame capsules or who was taking the placebo until the end of the experiment or until the subject
was dropped from the study or died. Yes, one of the aspartame consuming subjects died while two
others from the aspartame group developed cancer ( one breast cancer) during the study.[#48]
Three subjects had to be dropped from the study before the 13 weeks ended. The culls had three
things in common: they were female, they were dropped due to disease developed during the study, and
they were all from the group that was consuming aspartame. None were dropped from the control group.
The one death resulted from a stroke experienced after 8 weeks of aspartame consumption. The
remaining two women survived 11 weeks on aspartame before developing epithelial cell cancers, one of
the lining of her stomach, with hyperplasia reported in her lymph nodes during her pathology. The other
woman's breast cancer resulted in a mastectomy and she was diagnosed with adenocarcinoma.[#48] Both
breast adenocarcinoma and hyperplasia had been found in laboratory rats fed aspartame during the
testing of the product by Searle.[#197]
This damning animal carcinoma information tragically was kept from the pathologist who
reviewed the tissue samples from the two women who developed cancers during the study. In the final
report of the results of the feeding study it states that the reason these human cancers were ignored was
because there was no instance of carcinogenicity in animal feeding studies. To quote the report, the
cancers were considered "coincidental" "in view of information showing no evidence of such
carcinogenesis in animals who received large amounts of Aspartame over a prolonged period[#48] ."
The pathologist's report was sent directly to the G.D. Searle company. He refers to viewing
slides of breast and stomach tissue from the long term rat studies done by Searle. It is obvious that the
cancerous tissue slides were kept from him.[#48] To my most profound horror, the executive summary of
the human diabetic study concluded, "In summary, aspartame appears to be well tolerated by diabetic

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subjects as a safe sugar substitute." The rationale used to ignore the fact that fully 8% of the Aspartame
consumption subjects, developed epithelial cancer during the study was that “no such cancers were seen
in the numerous animal studies.”[#48] The Bressler Report, which resulted from an audit of all of Searle's
aspartame experimentation by a group of FDA investigators, reports that this was a lie, breast cancer
was an outcome of the animal feeding studies. [#197] The cancers found in the diabetic women should
have never been ignored. Such a high mortality and cancer rate in a human study should have raised red
flags and prevented aspartame from being rushed into the market against the clear intent of the US food
law, which prohibits cancer causing additives
<S1>The Scene of the Crime
The only reliable way that formaldehyde can reach the mammary tissue, aside from purposely injecting
formaldehyde solution,[#122] is to administer the formaldehyde as methanol.
Insert Figure 1 here
<S1>Matching Epidemics of Breast Cancer and Multiple Sclerosis: The Legacy of Aspartame
I don't always remember to bring my reading glasses with me when I go to professional offices, but only
once did I not regret the oversight. Since my only chore on this occasion was to pick up a good friend

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who had been deposing another attorney at the offices of that attorney I had no intention of spending
much time in the waiting room. As fate would have it, the deposition was taking longer than expected
and the receptionist said that I could make myself comfortable in the lounge. Without my spectacles I
had to look through the pile of surprisingly up-to-date periodicals for something that might have lots of
pictures – big pictures. I found a favorite, Time Magazine, that looked as if it would fill the bill and sat
down to make myself as comfortable as I could in what was essentially enemy territory.
I quickly came to a two page fold-out map of the world, big enough to easily make out the
countries. From the shading I was certain I was looking at a recent full color rendition of one of Dr.
Kurtzke's Multiple Sclerosis disease distribution maps that can be found in the second slide shows in the
MS chapter. It would be great news if Time Magazine was doing an article on the MS epidemic. I
returned to the receptionist and told her my story and she not only found me a pair of magnifying glasses
she gave me the magazine. I was awestruck by what I could finally see clearly. Here was a feature
article about the epidemic of breast cancer, not MS.[#190] How could I have missed this epidemic? One
look at the disease distribution throughout the World (Figure 2) and I knew I was looking at what would
turn out to be the twin sister of MS. Breast cancer was a disease of well off northern women, a disease
of "affluence"[#250] that was now spreading quickly to their poorer sisters in the warmer climates – all
coinciding with the timing of the popularity of aspartame. I shook with a strange mixture of rage and
excitement as I vowed to learn all I could about this epidemic of breast cancer.

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Insert Figure 2 here.
It turns out that breast cancer is no stranger to women suffering from multiple sclerosis. Those
afflicted with MS have over a twenty percent greater chance than women in the general population of
developing breast cancer. This increased risk is cannot be attributed to reduced parity or delayed first
child birth, and is an increased risk that the authors of the study who found the association admit it is
"consistent with previous observations and remains unexplained and warrants further attention."[#658] A
quick look at Figure 2 will bring back memories of Chapter 9 on multiple sclerosis. The darker shades of
grey in the map of Figure 2 indicate higher incidence of breast cancer, note the abundance of countries
that seem to have matching high or low incidence of both diseases, particularly in the most recent MS
distribution chart. Take note particularly of Argentina and how that little country was so quick to
become a nation committed to consuming aspartame.
<S1>Breast Cancer Increases as does Popularity of Aspartame
Chart 3 illustrates the SEER numbers for the incidence of breast cancer in the United States during the
ramp up of aspartame in the US diet.[#577] The tight relationship of the two curves is indicative of a
relatively short time period between methanol consumption and breast cancer development. However, it
is important to note that methanol began increasing in the US diet with the growth in consumption of
aseptic canned juice drinks some years before aspartame's official introduction. This was also a period
with an increase in breast cancer screening, which may account for the meandering of the incidence
curve between the years 1987 to 1994. Implementation of more accurate screening methods will only

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temporarily appear to increase incidence with a sudden rise for a period of time and then a snap back a
few years later. A good example would be a haystack that contains only so many needles, and whether
you count them by hand, which may take a long time, or use a magnet to gather them more quickly, the
end results is always the same number of needles. This improved screening effect has been used to
explain away the apparent incidence increase in breast cancer over "the last 30 years," but the truth is
that it cannot fully account for the relentless rise in the cumulative breast cancer rate since the
introduction of aspartame.
Insert Chart 3 here.
It can be shown that the incidence of breast cancer has increased over the last 30 years,[#219] and
particularly in populations exposed to aspartame.[#194] The uneven distributions of both MS and breast
cancer throughout the world show a disarming similarity,[#193] including the unexplained increases to
epidemic proportions in the same regions, such as Japan,[#192] over that short period of time.[#190] Chart 3
shows a disconcerting and abrupt rise in the incidence of breast cancer coinciding exactly with the ramp
up of aspartame consumption after it was approved for sweetening carbonated beverages in the United

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States.[#194] The breast cancer rate of the other countries throughout the world, even in countries with
normally low breast cancer rates, also appears to have risen soon after aspartame was introduced into
their diets.
<S1>Genetic Distribution of Slow ADH Verses Fast ADH Linked to Breast Cancer Risk
In Chapter 7 we discussed the discovery that there exists three different genetically defined versions of
ADH I. They vary based on the speed at which they metabolize ethanol. Our genetic makeup
determines which one of these is distributed throughout our bodies. The fast-ADH is 2.5 times faster at
removing ethanol from the bloodstream than the slow-ADH. When it comes to heart disease, individuals
who are genetically endowed with the slow-ADH that metabolizes ethanol 2.5 fold slower than the fast-
ADH have a 86% reduction in risk from developing myocardial infarction – but only if they consume
ethanol on a daily basis.[#483]
Interestingly, the role of ADH metabolism in the development of breast cancer mimics exactly
its role in the development of heart disease. Women who are genetically endowed with the slow-ADH
have less of a risk of contracting breast cancer during their lifetime than those that remove ethanol more
quickly from their blood. This remains true even when both groups consumed the same amount of
alcohol on a daily basis.[#501] Fast metabolizers who drank 15-30 grams of alcohol a day had a 2.3
greater risk of breast cancer even than non-drinkers who were slower metabolizers.[#501] The only
advantage to having an ADH that more slowly removes ethanol from the blood would be the ability of
these individuals to maintain low levels of ethanol in the body fluids for longer periods of time, thus
preventing the ADH in their breast tissue from converting methanol into the powerful carcinogen
formaldehyde.

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The U-shaped curve of ethanol's protective effect against breast cancer has not yet been
elucidated, and the present mindset of the breast cancer community may never allow for such a study to
be performed. Time will tell, but this information would be vital before we could make a
recommendation as to safe levels of ethanol consumption. The literature clearly indicates that the
beneficial effect of ethanol for women is limited to one standard alcoholic drink a day, and no more.
One issue that must temper the enthusiasm of all of us who consider low dose ethanol beneficial is the
results of one large study that claims to show an increase in breast cancer among women who drank.[#279]
Avoiding methanol consumption appears to be the best way to help prevent breast cancer (see chapter
2).
<S1>Exposure to Organic Solvents and Breast Cancer
An article published in 1997 stresses that the incidence rates for breast cancer have increased steadily in
both the US and Canada over "the last 25 years." The author points to the increasing number of women
in the workforce and the possibility that the problem may be caused by occupational exposure to
hazardous agents. No such increase was seen during the entire Second World War, when women, in
mass, replaced their solider husbands in heavy industry. That aside, the author has some insight into the
sensitivity of breast tissue to solvents such as methanol. He reminds us that solvent molecules quickly
reach the breast epithelium cells, where they cannot be detoxified effectively because of the reduced
activity of the "necessary enzymes" (aldehyde dehydrogenase) in breast cells. Second, because of the
unique physiology of mammary glands, solvents or their "metabolites" accumulate in the milk ducts
long enough to exert detrimental effects locally.[#219]
<S1>Cigarette Smoking With a U-Shaped Twist

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Women with a history of having smoked are more likely to develop breast cancer than those who never
smoked.[#574] It has been shown that a consistent dose-response enhances the plausibility of an increased
breast cancer risk due to cigarette smoking.[#191] Most intriguing of all is that women who start smoking
as teenagers and continue to smoke for at least 20 years have a statistically significant (50% greater)
chance of developing breast cancer compared with never smokers. This association, however, only
applies if the women studied were nondrinkers of alcohol. Drinkers who smoke showed no significant
increased in breast cancer incidence in the same study.[#191] This appears to be an indication of the
protective effect of ethanol against methanol's conversion to formaldehyde.
<S1>Cancer of the Kidney (Renal Cancers)
<S2>Kidney: A Target Organ of Methanol Poisoning
Early pathology of humans who die from methanol poisoning consistently show considerable gross
anatomical and histological damage to the kidneys and the lungs.[#416] These organs both have extra
hepatic stores of ADH I. The adult kidney contains ADH in measurable quantities.[#640] The exact
location of these ADH rich tissues coincides with the epithelial tissue of the kidney, which remarkably is
where the cancers in question originate.[#636]
Cigarette smoking has been the target of 24 investigations looking into its contribution directly as a
cause of renal cell carcinoma. A Meta-analysis of all 24 of these studies published in 2005 shows a
strong dose-dependent increase in risk associated with the numbers of cigarettes smoked per day and a
substantial reduction in risk for long-term former smokers. For those who smoked over one pack of
cigarettes a day the risk of developing renal cancer was about twice that of non smokers.[#652]
Spontaneous carcinomas of the kidney are extremely rare in laboratory rats. During the
Ramazzini Institute study described above, male and female rats that had been fed aspartame developed

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statistically significant and dose related increases in kidney cancers. Twenty one carcinomas of the
renal pelvis developed in their study whereas the control rats had none.[#50] The generation of cancers of
the kidney, liver and lungs by aspartame was intrusive and unexplainable except by the unpopular
formaldehyde theory. The results for all three cancers were not only highly significant but strongly dose
related, showing that stronger doses were having a greater cancer-causing impact.[#50] The real tragedy
here is that similar cancers were generated in test animals by the company that invented aspartame 30
years before the Ramazzini study. The data was kept out of sight of the FDA until the Bressler
investigation,[#197] which came too late and fell on deaf ears.[#39] This becomes remarkably important
immediately upon the visualization of the human experience with identical cancers exploding in the US
population in the years since aspartame entered the food supply. Kidney cancer incidence rates, for
instance, have inexplicitly doubled "in the last thirty years.[#646]"
I have plotted the Center for Disease Control SEER data for the US in the customary format in
Chart 4. A Journal of the American Medical Association article entitled Rising Incidence of Renal Cell
Cancer in the United States, published just months ago, unsuccessfully attempts to link the soaring rate
of these adenocarcinomas (remember this term) to increased detection techniques. Its authors admit in
their conclusion that increased detection alone "does not fully explain the upward incidence trends of
renal cell carcinoma. Other factors must be contributing to the rapid increasing incidence of renal cell
cancer in the United States, particularly among blacks".[#646]

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Insert Chart 4 here
<S2>Kidney Damage Beyond Cancer
The constant production of formaldehyde, from methanol produced as a result of consuming diet soda,
within the epithelial cells of the kidney may be responsible for other damage beyond cancer. Aspartame
has been shown to damage the kidneys of fetal rat pups who's mothers were fed it during pregnancy.[#659]
We can learn something from the autopsies and histological workups done to those who have died from
acute methanol poisoning. The tubules of the kidneys of these individuals often reveal extensive
degeneration.[#416] Formaldehyde is a fierce deactivation agent for a number of enzymes and even the
mitochondria, which plays such an important role in kidney function, is itself extremely vulnerable to its

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presence.[#582] It has been convincingly shown that heavy cigarette smoking more than doubles the risk
of Chronic Renal Failure.[#651] A recent study done at Harvard Medical School looking into the possible
association between consumption of sweetened beverages with kidney function decline showed no such
relationship, but the collected data inadvertently resulted in the conclusion of the report that more than
two servings of diet soda a day is responsible for a statistically valid two fold increased risk for kidney
function decline.[#588] One liter of diet beverage, sweetened with aspartame, contains the same amount
of methanol to be found in the average pack of unfiltered cigarettes.
<S1>Melanoma and Cancers of the Skin
<S2>"The Incidence of Skin Cancer is Increasing at an Alarming Rate"
"The incidence of skin cancer has reached epidemic proportions. Only through heroic
efforts by health care professionals and the general public to prevent the development of
progression of skin cancer will this epidemic be abated."[#718]
This quote from The Epidemiology of Skin Cancer, an article published in the Journal of Dermatological
Surgery[#718] in March of 1996, indicates that this increase in skin cancers had been going on for the
previous 25 years. What makes this particularly confounding to dermatologists is that although
nonmelanoma skin cancer is directly related to cigarette smoking,[#645] the nonmelanoma skin cancer
incidence has climbed steadily since the end of the of the late 1970s[#95] during the same period of time
in which cigarette smoking has steadily declined. The explanation tying this cancer increase to the
thinning of the ozone layer can apply well only to a sparsely populated segments of the earth that lie
close to the world‟s polar extremities. For all other areas the ozone layers have healed with no timely
response from the skin cancer curves.

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<S2>Skin Fibroblasts are an ADH I Stronghold
Dr. Nelson Novick, whose patient developed macrophage-filled deep skin lesions (Granulomatous
Panniculitis) over her lower body after consuming aspartame proved that it was indeed aspartame
consumption that caused that serious skin reaction.[#228] The skin contain numerous fibroblasts that
contain ADH I.[#221] This ADH will convert methanol to formaldehyde as easily as the ADH found in
the other tissues we have discussed.[#638] The reaction that Dr. Novick's patient had was an inflammatory
response to something produced in her skin from the aspartame that caused the attraction and eventual
activation of her body‟s macrophages.[#555] We know that macrophages respond in such a way to
formaldehyde modified protein.[#25] The truth is that it would be very difficult to propose an alternative
to the formaldehyde mechanism for such a skin reaction to occur from the consumption of aspartame, a
substance made up only of two amino acids and methanol. Fibroblasts when activated are associated
with cancer cells at all stages of cancer progression.[#656] Their functional contributions to cancer
production may emerge to have more to do with this unappreciated production of formaldehyde from
environmental methanol than anything else. In the mean time, what better mechanism to increase the
incidence of skin cancer than the production of formaldehyde directly within the skin.
<S1>Formaldehyde From Aspartame
The confirmation of aspartame's formaldehyde in human skin is important to our present discussion on
aspartame skin issues.[#7] Though methanol has been known for almost a hundred years to cause several
forms of dermatitis,[#227] the descriptions of which vary widely.[#437] Individuals who are extremely
sensitive to formaldehyde can develop contact dermatitis reactions to a minute amount of it, such as that
found in newsprint.[#438] Dermatologist have used this "exquisite sensitivity" of the human immune

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system to formaldehyde to show compellingly the connection of aspartame consumption to
formaldehyde formation within skin tissue.
Two professors of Dermatology from the University of Kansas Medical Center, in a case report
titled Systemic Contact Dermatitis of the Eyelids Caused by Formaldehyde Derived from Aspartame
published in the journal Contact Dermatitis, were the first to report eyelid dermatitis caused by
aspartame consumption in one of their formaldehyde sensitive patients.[#545] Since then, "severe
systematized dermatitis" has been confirmed to be linked directly to aspartame consumption in patients
who have tested positively for formaldehyde sensitivity.[#630] It is interesting to note that positive
reactions to formaldehyde on patch testing has now repeatedly been linked to both "systemic contact
dermatitis" and a new syndrome called "aspartame-induced migraines," often presenting in the same
patients.[328] In the most recent article confirming the positive link between formaldehyde sensitivity,
systemic dermatitis and migraines[#544] you may find the published rebuttal letter from the manufacturer
of aspartame, Ajinomoto, both enlightening and entertaining.[#543]
<S1>Young Women Take the Burden of the Epidemics of Two Skin Cancers
Dermatologists from the Mayo Clinic reported in the Journal of the American Medical Association
(JAMA) in August of 2009[#95] that they had been keeping track of the incidence of Basal Cell
Carcinoma in their home county of Olmsted in Minnesota since 1976. They documented and
histologically confirmed that since exactly 1980 the incidence of that non-melanoma cancer steadily
increased by 400% (see Chart 5). This county in which Rochester is a major city is halfway between the
North Pole and the Equator – far from any ozone hole and in an area with average daily sunshine
saturation.

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Insert Chart 5 here
The most sobering aspect of the research reported in JAMA is that women younger than 40 years
were at a significantly greater risk than their male counterparts. The exact quote is "This incidence of
skin cancer is significantly higher for women than for men. A trend toward higher incidence of basal cell
carcinoma in young women than in men has been reported by others."[#95]
By far the most deadly form of skin cancer is Melanoma, the origins of which is controversial.
In fact, it appear to be much less related to UV light exposure than traditionally thought, and in fact is
often found in areas of the body where scant exposure to the sun‟s rays would be expected. The year
before the JAMA article was published another much more ambitious study performed by investigators
from the National Cancer Institute's (NCI) Division of Cancer Epidemiology and Genetics studied the
incidence patterns of invasive cutaneous melanoma throughout the United States. Chart 6 shows the
change in incidence of melanoma for the population as a whole in the years since the introduction of
aspartame. The study done by the NCI and published in the Journal of Investigative Dermatology broke
down the original data to look for trends based on age and sex. I will let the National Cancer Institute's
results speak for themselves. "Invasive cutaneous melanoma, the deadliest form of skin cancer,

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increased among Caucasian women in the United States aged 15 to 39 by 50 percent between 1980 and
2004." Further, they make conclude, "our analysis of SEER data suggests that melanoma incidence is
increasing among young women.[#557]
The outcome again goes to our premise that methanol in food will always have a more
devastating effect on women due to their reduced ability to detoxify methanol in their guts. This is
compounded considerably by the poorly kept secret that young women are the prime target of
multimillion dollar diet soda advertisement campaigns which we can presume have been very
successful.
Insert Chart 6 here
<S1>A Short Summer Tale
A hot summer day on a lovely Mexican Pacific coast beach. A beautiful young person lying on the
white sand renewing her tan before she hits the surf just one more time before lunch. She reaches into
the cooler and pulls out an ice cold diet cola to quench her thirst. The soundtrack now switches to the
unforgettable theme from Jaws. The aspartame in the carbonated beverage starts to down to methanol
before she can empty the bottle. By the time she hits the beach again after lunch, the methanol is already
turning into formaldehyde in the fibroblasts of her skin. Fibroblasts are known to have a pivotal, yet

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little understood role in cancer formation. Her skin is already under attack from the very short UV
radiation from the equatorial sun. Does this sound to you like the makings of a perfect surfer movie or a
perfect storm?
<S1>Cancers of the Liver and Lungs
<S2>The Liver: The Ultimate Source of ADH
Alcohol dehydrogenase Class I (ADH I) is also called Human Liver Alcohol Dehydrogenase because it
was originally discovered in – and is still mistakenly thought by many to only be found in – the liver. In
fact the highest concentration of ADH I in the body is in the liver[#221] and this is what may account for
the considerable carcinogenic stress on that organ from aspartame consumption. During the aspartame
feeding studies of Swiss mice by the Ramazzini group they showed a significant dose-related increase in
both liver carcinomas and adenomas.[#657]
We have said many times that the liver contains large quantities of protective enzymes such as
aldehyde dehydrogenase that help protect it from formaldehyde. However since cancer is a statistical
disease that only requires one molecule of formaldehyde in the wrong place at the wrong time it is
probably the number of molecules of formaldehyde produced in the liver that will eventually work
against a heavy aspartame consumer. When we look at the tripling of the incidence rate of human liver
cancers in the US during the aspartame years, nothing more needs to be said.

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Insert Chart 7 here
<S2>What About the Lungs?
One can not come away from the study of methanol without having some very serious concern about the
lungs. All the autopsies in the older literature of humans killed by methanol ingestion always point to
oddly congested or hemorrhaging lung tissue. Often lungs at autopsy show marginal emphysema with
petechial hemorrhages.[#416] Again we have a significant dose-related increase of alveolar/bronchiolar
lung cancers in the aspartame feeding studies done by Dr. Soffritti. Lung tissue contains fibroblast
tissue[#221] with a heavy burden of ADH that is ready and able to turn methanol into formaldehyde.[#503]
During our experiments with pregnant rats fed methanol we often autopsied pups with lung damage as
can be seen in the slide show from Chapter 12.
Cigarette smoking has a direct and undeniable correlation and dose relationship to lung cancer.
Most scientists would find it difficult to associate lung cancer or Chronic Obstructive Pulmonary
Disease (COPD) with a food product. In the last thirty years, however, a considerable decrease in

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smoking in the United States has not been paralleled by a degree of decrease in lung cancer as was
expected. Instead, the incidence of fibroblast centered lung adenocarcinoma has increased. The
incidence of COPD has more than doubled, and in the last ten years the mortality from COPD has gone
up over 20%.[#641] Could this all be related to the methanol from aspartame? I just don't know; however,
I can say with certainty that a lung bombarded daily by methanol placed formaldehyde should be under
suspicion for such developments. There would be good reason for serious consideration of methanol's
role in these disorders.
<S1>The Strange Case of the Female Thyroid Gland
During the Bressler investigation of the hidden aspartame toxicity files, one of the tumors that were
recovered from those "lost" from Searle's animal study of aspartames safety was of the thyroid gland of
one of the experimental animals.[#197] Since that time a methanol vapor exposure study of Sprague
Dawley rats of both sexes noted in particular that "The thyroid gland in females appeared to be a target
organ for methanol."[#593] This all would have been of little import had it not been for a Swedish study
that identified, in particular, school teachers that were in the workforce between 1971 and 1989 as
having a significantly increased incidence of cancer of the thyroid.[#405] The California teachers study
that we used to point out the considerable increase risk of breast cancers does give the teachers they
studied a 16 % greater chance of developing thyroid cancer.
We cannot do much more with this limited data. I was able to procure from the CDC SEER data
thyroid incidence data that separated out the sexes, which when graphed in the usual fashion produced
the graph below which does indeed seem to indicate that the Thyroid gland may indeed be an organ
sensitive to methanol that has been overlooked by those who have searched for sites of ADH activity.

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Insert Graph 8 here
<S1>Limitation of Animal Studies
I have mentioned a number of times now that animals are not an acceptable venue for testing methanol
safety. Only humans will suffice for testing methanol. We have been very fortunate to have good
scientists, such as Morando Soffritti and his dedicated staff at the Ramazzini Institute in Italy, who are
willing to spend the extraordinary time, effort and money to do long term animal studies. We must make
the most out of it. To do that we have to understand the limitations of the species they are working with.
Rats and mice are not only between one or two hundred times less sensitive to the acute lethal effect of
methanol, but also are blessed with a powerful enzyme, catalase, that protects them in ways that we
don't understand from its many toxic and disease outcomes. To use the results of their testing we must
take seriously any disease outcome that their experimental animals exhibit in excess of the controls and
allow the experimenters to use, at the very minimum, a hundred fold greater dosage concentration of

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methanol than the equivalent dose to extrapolate to humans. Even at this level, some human diseases or
cancers will never become apparent in these poor surrogates no matter how long the study.
The only appropriate test animal for methanol's toxicity is human. The innocent that have suffered and
died to unknowingly test the safety of aspartame and thus methanol must not have given their lives in
vain.
Epilogue
Reading this book may have various outcomes, depending on your determination and perseverance.
Some of you may suffer or love someone who suffers from one of the diseases discussed here who can,
on a superficial level, glide through the text lighting easily on all the important facts and find the
evidence needed to justify and commence the simple change of diet that will begin the ending of the
damage done to the body and mind by methanol. I wrote this book with such individuals in mind and
sincerely hope this information comes in time to help.
Those who chose to read more deeply will come away with sufficient scientific knowledge to peruse
professional publications that will help them answer their many additional questions and perhaps afford
a greater respect for the breadth of the natural world.
The third level is a darker encounter requiring several readings with considerable concentration on the
meaning of every word, illustration and graph, the sounding of the full depth of every sentence. The
reader must test the references for their appropriateness and veracity and become satisfied of the entire
truth set out here. The result of all of this effort will have a different effect on each of you but it will be
disconcerting to say the least. The warriors of you will want blood, the scholars will want change, the
parents will want revenge, and the politicians will want sanctuary. At that point of clarity, you will know
what I know.
Woodrow C. Monte PhD.
Emeritus Professor of Nutrition (Arizona State University)
Pahoa - USA
The References can be found in the book Bibliography on my website whilesciencesleeps.com/

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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.

While Science Sleeps© W. Monte (Prepublication) Page | 38
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 39
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 40
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 41
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 42
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 43
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 44
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 45
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 46
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 47
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 48
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(162) Main R, Barry M. On The Toxicity of Methyl Alcohol in Extracts and Medicine. Illinois
Medical Journal 1903;69:153-58.
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 49
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 50
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 51
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 52
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 53
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 54
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 55
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 56
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 57
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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;

While Science Sleeps© W. Monte (Prepublication) Page | 58
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 59
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 60
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 61
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 62
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 63
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 64
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 65
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 66
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 67
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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

While Science Sleeps© W. Monte (Prepublication) Page | 68
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 69
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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
Medical Journal 1930;57:260-63.
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 70
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 71
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 72
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 73
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 74
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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-

While Science Sleeps© W. Monte (Prepublication) Page | 75
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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
Health and Human Services; 2003.
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 76
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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,

While Science Sleeps© W. Monte (Prepublication) Page | 77
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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
Health and Human Services; 2005.
(579) Agency for Toxic Substances and Disease Registry. Petitioned Public Health Assessment,
LaFarge Corporation - Alpena Plant, Alpena, Alpena County, Michigan. U.S. Department of
Health and Human Services; 2001.
(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

While Science Sleeps© W. Monte (Prepublication) Page | 78
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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

While Science Sleeps© W. Monte (Prepublication) Page | 79
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
& 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.

While Science Sleeps© W. Monte (Prepublication) Page | 80
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 81
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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

While Science Sleeps© W. Monte (Prepublication) Page | 82
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 83
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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

While Science Sleeps© W. Monte (Prepublication) Page | 84
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
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.

While Science Sleeps© W. Monte (Prepublication) Page | 85
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 86
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 87
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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.

While Science Sleeps© W. Monte (Prepublication) Page | 88
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
(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
Health and Human Services; 1992.
(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

While Science Sleeps© W. Monte (Prepublication) Page | 89
Reproduction with permission only - http://www.whilesciencesleeps.com/contact/
Gestation and Lactation in Rats. J Nutr 1977;107(2):300-9.