role of formaldehyde, made by body from methanol from foods and
aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition Prof.
Woodrow C. Monte, retired, Arizona State U., two reviews, 190 references
supplied, Fitness Life, New Zealand 2007 Nov, Dec: Murray 2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498
[ Rich Murray comments: Woody Monte sent me the URLs to these wonderful
reviews on Christmas Eve -- a wonderful present for this medical layman,
who has similarly reviewed many areas of mainstream medical research
since January, 1999 as a volunteer information activist on the Net for
quality, civil, balanced, detailed research on aspartame toxicity and
related issues.
His opus makes the essential, central point that aspartame toxicity
research intimately involves methanol, formaldehyde, and formic acid, as
well as co-factors like alcohol and folic acid that can mitigate the
toxicity of methanol.
Striking evidence is given to support bold claims that methanol is a
major cause of fetal alcohol syndrome, autism, multiple sclerosis,
lupus, teen suicide, and breast cancer.
It is easy to suggest: obesity, diabetes, depression, seizures,
Alzheimer's, fibromyalgia, Multiple Chemical Sensitivity, infertility,
impaired pregnancies, birth defects, ADHD, accidents, and violent crimes.
Indeed, we have here "Right To Life" issues comparable to the millions
of deaths worldwide from war, murder, suicide, modern urban diet,
vehicle accidents, air and water pollution, tobacco, alcohol, sugar,
salt, toxic metals, fluoride, and a variety of illegal addictive drugs,
including heroin, cocaine, and meth. There is much to be done, and quickly.
Despite the urgency and huge scale of these problems, the toxicity of
methanol and its products in humans is a remarkably undeveloped field of
research and therapeutic practice.
So far, most evidence is available mainly from alcohol hangover studies,
and it may still be true that these teams are largely unaware that
aspartame is an ubiquitous, potent methanol source that impinges all
medical research and practice.
Woodrow C. Monte has set a powerful precedent for effective, efficient
scientific communication in today's Internet age, by putting full texts
of over 190 references on the Net at no cost, expediting the process of
assessing his interpretations and quickly developing a working paradigm
among competent researchers, not controlled by various vested interests,
for the necessary immediate next steps in focused research, as well as
raising an urgently needed warning alert that reaches all levels of
world society.
Following the lead of all the major supermarket chains in the United
Kingdom, producers, distributors, advertisers, media, medicine,
education, service organizaions, governments at all levels, and
corporate users should act immediately to protect the public, including
their own staff and clients.
I welcome civil comments, feedback, and papers, based on reason and
evidence, to
aspartameNM@yahoogroups.com, while of course the increasing
network of concerned, competent citizens will doubtless form many such
networks of frank, rapid collaboration, both privately and publicly.
In recent years, without editing the text, I change the format to single
lines with single spaces, in order to improve the readability of dense
scientific prose, as with electronic media there is no need to conserve
paper costs. Changing the format to plain text allows texts to be easily
searched and combined on any computer in the world. ]
http://www.thetruthaboutstuff.com/listener.shtml
Listener:
While applauding the caution suggested by the Listener article on the
dangers of Aspartame, I am disappointed that it did not more fully
explain the biochemical processes by which Aspartame causes harm.
The dangerous “poison” produced by consumption of this sweetener is wood
alcohol (methanol)(1).
Methanol is a poison that cannot legally be added to food in any
civilized country in the world.
All of John’s and Abby Cormack’s symptoms were the classic symptoms of
chronic methanol poisoning...all.(12,13)
Unlike the species of lab animals employed in most studies of Aspartame
safety, humans lack enzymes which prevent methanol from metabolizing
into formaldehyde.
Consequently, when consumed by human beings, methanol enters the body’s
cells and is converted to formaldehyde (7).
This extremely dangerous chemical has been relegated to the highest
level of cancer causing agent, Group I, by the IARC the International
Agency for Research on Cancer. Lyon. France.(11)
The NZFSA is seriously challenged by the methanol issue.
Using the industry’s standard response, they indicate that some methanol
is consumed as a part of our normal diets so what harm a little more?(19)
They also cite unusually high levels of methanol in black currant and
tomato juice to support the premise that methanol is not an uncommon
component in our diets (1).
However, when asked about the amount of methanol consumed in the typical
Kiwi diet, sans Aspartame, they offer no reply.
In the absence of unbiased baseline data on consumption, how can the
NZFPA reach an informed decision or propose reasoned policy?
The rate of consumption of a poison in a large population cannot be
increased without consequence.
The toxicological concept of LD01 refers to the amount of a poison that,
when fed acutely to a population, will kill on average, one percent of
that population.
The level that causes symptoms is always much lower than the LD01.
Is the NZFPA aware that the LD01 is not known for methanol in humans nor
can it be extrapolated from animal testing since there are no animals
that are as sensitive to methanol as humans?
Aspartame is not safe enough to mandate its consumption in Schools.
Woodrow C. Monte Ph.D.
http://www.thetruthaboutstuff.com/published/Your%20Health%2033%20-2.pdf
http://www.thetruthaboutstuff.com/review1.shtml plain text
Review 1 - Published November 2007
Monte WC. 2007, Is your Diet Sweetener killing you?
Fitness Life Nov. 33: 31-33
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Abby Cormack is a young lady from Wellington who recently made headlines
because of serious adverse reactions her physician attributed to her use
of the artificial sweetener aspartame.
She sent me an email to ask for help.
I was happy to assist since I have seen hundreds of similar complaints (1).
Aspartame contains methanol(14, 48, 5). [ 50?]
Methanol is a dangerous poison that, over time, is known to remove the
insulation from nerve axons(18, 53), producing symptoms identical to
Multiple Sclerosis (MS)(2).
In fact, in the German scientific literature, Swiss physician, Dr Hugo
Henzi, argued eloquently, that naturally occurring methanol was the
cause of Multiple Sclerosis(5, 6, 8, 9, 10).
[ Med Hypotheses. 1984 Jan; 13(1): 63-75.
Chronic methanol poisoning with the clinical and pathologic-anatomical
features of multiple sclerosis.
Henzi H.
The details of two cases of chronic methanol poisoning are presented.
Both patients initially developed clinical symptoms of multiple
sclerosis: visual disturbances, intention tremor, reduced abdominal
reflexes, impaired coordination and difficulties with walking.
After the exposure to methanol had ceased the multiple sclerosis
symptoms persisted in patient 1 but disappeared gradually in patient 2
(patient 2 had a history of excessive alcohol consumption, which is a
critical fact in this discussion).
Ultimately autopsies confirmed this picture: histological examination of
patient 1 revealed plaques in the spinal cord, in the stem and in the
proximity of the lower horn of one lateral ventricle, whereas no
localized demyelination could be found in patient 2.
The results are discussed in connection with the theory ("Methanol
Hypothesis") that under certain circumstances multiple sclerosis itself
is induced by formaldehyde stemming from the metabolism of methanol.
PMID: 6708848 ]
My name is Dr. Woodrow Monte.
My 26 year career as Professor at Arizona State University was devoted
to research and teaching of the composition and safety of foods.
For 25 years I have had serious concerns about the consequences of the
consumption of Aspartame.
In 1983, I filed the first petition to the US Food and Drug
Administration seeking Aspartame’s removal from foods(39).
My 287 page petition, containing copious documentation of published
research, was denied without explanation.
In 1984, I wrote the first scientific article warning of the methanol
produced when Aspartame is consumed(1).
This issue of aspartame safety is embedded in a quagmire of politics(39).
Aspartame’s approval by the American Food and Drug Administration (FDA)
was championed, by the former US Secretary of Defense Donald Rumsfeld.
At the time of Aspartame’s FDA approval, he was president of the company
that invented it and which stood to make considerable financial gain
from its manufacture and sales(39, 56).
NZFAS Public Relations for the Beverage Industry The New Zealand Food
Safety Authority (NZFSA) has endorsed Aspartame safety in all of their
handouts, for the most part paraphrasing the claims of the sweetener
industry(39, 56).
The New Zealand government currently is considering a measure which
endorses diet sweeteners as replacement for sugar sweetened beverages in
schools.
Inexpensively produced aspartame from China is the product most likely
to be selected to replace sugar.
Fizzy drink beverage manufacturers stand to reap a substantial profit
from the money saved substituting aspartame for sugar.
But at what cost to the public health?
Despite vigorous protest, the NZFSA has maintained a pro-aspartame stance.
They have chosen not to allocate resources for study of the many
hundreds of scientific works that comprise just the methanol toxicity
literature.
I have studied this scientific literature and, in the remainder of this
article, will present to you what I have learned, and why I believe, it
is so important to reject this proposed measure.
The Science: Aspartame tastes sweet because, attached to it, is a
molecule of methanol (wood alcohol).
The methanol is very loosely bound and will fly off with the slightest
heating or when consumed(20, 51).
Because methanol’s toxicity is well known, millions of dollars were
invested by Aspartame’s inventors in an attempt to attach some other
“safer” substance, but this attempt was not successful.
With the approval of Aspartame, a new source of methanol was added to
what is a very short list of methanol containing foods.
Methanol -- Trojan Horse: Why is methanol dangerous?
Inside cells, methanol is converted to formaldehyde(30), an undetectable
toxin and recognized cancer causing agent of the highest order (Group
I)(11).
Even when formaldehyde is injected directly into a living human, it
turns into formal hydrate(4, 27), a very aggressive molecule that
instantly attaches to any protein molecule which it makes contact.
The formaldehyde molecule then completely disappears within the cover of
the much larger protein(31, 32).
No diagnostic procedures, can detect a protein molecule so changed, yet
the damaged molecule, loses function.
Damaged protein molecules are not tolerated by the immune system.
Specific detection sites for “formaldehyde modified protein” are found
on white blood cells called macrophages(23, 24).
Macrophages seek out and destroy these proteins at a rate 100 times
faster than proteins not treated with formaldehyde(25).
Upon autopsy, macrophages are found in the damaged areas of the brains
of those who have died with MS(42, 44).
Pharmaceutical companies use formaldehyde treatment of viral proteins to
greatly enhance antibody production during the manufacture of vaccines(26).
However, the effect of formaldehyde (resulting from methanol poisoning)
on human proteins, has not been examined as a cause of autoimmunity.
A Question Never Answered: In response to these concerns, spokespersons
for the soft drink beverage industry and for NZFSA claim that there is a
large amount of methanol consumed in the normal diet and that a “little”
more from aspartame will do no harm.
This is their only justification for allowing more of this toxin to be
introduced into foods.
No estimate has been publicly presented by these spokespersons regarding
the amount of methanol consumed per person, per day in the average diet.
Consistent with the data in my published research(1), I believe that the
amount of methanol in the typical diet without artificial sweeteners
would be less than 8 milligrams per day.
One can of aspartame sweetened diet cola yields 16 milligrams of
methanol(47), more than twice the amount of methanol from other sources
in a typical diet.
Fresh fruits and vegetables contain small traces of methanol(28, 29) but
their consumption is not problematic, in that, during fermentation in
the gut, they produce a natural substance that stops the conversion of
methanol to formaldehyde(35, 36).
In fact, before Aspartame, methanol in the normal human diet came
primarily from heat processed plant foods such as canned fruit and
vegetables and their juices(33).
While there are unusually high levels of methanol in black currant and
tomato juices(1, 19, 33), these foods are included only occasionally in
most diets and, thus, would have little impact on an average person’s
methanol intake(1).
Methanol is only found in natural foods that contain pectin(33), the
glue that holds certain plants together.
Fortunately, the bond that holds the methanol to pectin is so strong
that it rarely breaks(36), or breaks only under certain conditions.
These conditions include fermentation(35) or the high temperatures of
the food canning process(1, 28, 29, 34).
Even under these conditions only a small percentage of pectin’s methanol
is released(35, 36).
(It is interesting to note that MS was first documented as a disease(45)
at about the time that canning began to flourish in Europe(46).
Further, humans have no enzymes for pectin digestion (36), thus making
pectin consumption rather unlikely to yield much methanol.
In contrast, aspartame consumption yields methanol always and
readily(20, 48).
The Second Attempt to put Methanol into Foods
A hundred years ago the scientific community believed methanol was
benign and swore to its safety with disastrous consequences(21).
At the turn of the century, industry scientist wanted to use the newly
developed, inexpensive and odorless form of wood alcohol,... methanol,
to extract vanilla and other flavorings(17, 21).
Over the previous 50 years, many toxicity studies performed in reputable
laboratories showed that more methanol than ethanol is required to kill
a test animal(15, 30).
Testing of this sort was repeated with monkeys, dogs, rabbits and
laboratory rats(17, 30).
Each time with the same result.
This data was presumed to support the safety of methanol consumption.
Accordingly, food and drug industries proceeded to use methanol in
patent medicines and to produce flavorings.
Soon after the first bottles of methanol laden extracts appeared on the
market, many fell seriously ill(17).
The stories that linked suffering, blindness and death were discounted
by the scientific community as “anecdotal” and unrelated to the methanol
which “had gone through so much testing”(17).
When incidence of death(16) and vision loss(37) continued to mount,
professionals surmised that some “impurity” had found its way into
individual products.
They maintained that nothing was wrong with methanol per se(17, 30).
Thousands died before the scientific community determined that animals
and humans do not metabolize methanol in the same manner(52).
Eventually, scientists learned that a liver enzyme that metabolizes
methanol, present in animals but absent in humans accounts for
methanol’s toxicity for humans(52).
While animals consume methanol safely, as little as 2 teaspoons can be
lethal for a human(16).
Since that time methanol has been forbidden in foods and must always be
packaged with a label showing a skull and crossbones, the universal
symbol for poison(49).
Why I question the Safety of the worlds most tested food additive: The
inventors of aspartame would have the advantage of hindsight when
designing studies for determining the safety of their methanol
containing product.
Inexplicably, all of their toxicological testing was conducted on the
same selection of animals that falsely supported methanol’s safety more
than 60 years earlier(48).
Despite this bias in sample selection, long term toxicity studies of
Aspartame has shown an increased likelihood of cancer in test
animals(50), an outcome not examined in earlier methanol studies.
As a consequence, Aspartame became the first additive in the history of
the US FDA denied approval for use in foods by the scientists of a
Public Board of Inquiry (39, 57).
Ultimate approval did occur, however, and it resulted not from
additional research but rather from political intervention(39).
What was remarkable was the method used to bend science to the will of
an aggressive drug company.
When it was clear that chances of approval were waning, representatives
of the company sought out the few laboratories in the United states that
were performing methanol research.
These laboratories were, in effect, hired to help prove aspartame is
safe(39).
Participating labs were tasked to find an animal that would respond as a
human does to methanol(39), then to find a way to prove that
formaldehyde was not producing the symptoms of methanol poisoning in
that animal(39).
If formaldehyde was proved the cause of the symptoms and death from
methanol poisoning, (the opinion held by the scientific community at
that time(21, 30), formaldehyde’s inability to be detected would put a
quick end to any hope for the approval of Aspartame.
Millions of dollars bought many scientific papers, few indicating the
research therein was “contracted” by the manufacturers of the product(39).
This “research” is now forever embedded in the scientific literature.
Scientists who were on the corporate dole are now considered “experts”
in the field of methanol safety.
It should be noted that research not funded by the manufacturer of
Aspartame has led to different conclusions.
For example, 10 years ago an independent Spanish laboratory found that
Aspartame most definitely turns into formaldehyde(7, 40).
Because of differences across species in the production of enzymes that
metabolize methanol, the results of animal research with Aspartame
cannot safely be generalized to humans.
Humans have become the test subjects in a 27-year long experiment on
Aspartame safety.
Unfortunately, the damage that methanol can cause is being revealed in
populations of Aspartame consumers such as Abby Cormack.
The issue is complex but the choice is simple.
Fortunately there are several other readily available, artificial
sweeteners that do not contain dangerous toxins.
Therefore, it just makes good sense to keep Aspartame out of our schools.
Woodrow Monte Ph.D.
Professor of Food Science (retired)
Arizona USA
* please go to TheTruthAboutStuff.com to see my 1984 article for a full
discussion of this issue and references for this article.
http://www.thetruthaboutstuff.com/pdf/(1)%20Aspartame%20Methanol%20and%20the%20P\
ublic%20Health%201984.pdf
Reference List 1 - 60 are given after the 2nd review, 2007 Dec.
The abstracts and texts of all 190 references are given in pdf form at
http://www.thetruthaboutstuff.com/articles.shtml
REFERENCED
Aspartame
Multiple Sclerosis
Breast Cancer
Listener
PUBLISHED
Aspartame
Multiple Sclerosis
Breast Cancer
Listener
GRAPHS
Autism
Breast Cancer A
Breast Cancer B
Fetal Alcohol
Lupus
Multiple Sclerosis
Teen Suicide
http://www.thetruthaboutstuff.com/published/Article%202%20Methanol%20and%20MS.pd\
f
http://www.thetruthaboutstuff.com/review2.shtml plain text
TheTruthAboutStuff.com
Sweet Misery: A Poisoned World
Review 2 - Published December 2007
Monte WC. 2007, A Deadly Experiment – (Fitness Life 2007 Dec.34:38-42)
We cannot introduce a poison into the food supply without paying a
terrible price, and I am convinced that this tragic scenario has and is
playing itself out.
In an earlier article regarding the dangers of Aspartame (Fitness Life
2007 Nov 33:31-33), I explained how this artificial sweetener can
degrade into methanol and then into formaldehyde, and I touched on some
of the deleterious effects of formaldehyde on the human body.
In this article I make the case that increased methanol consumption is
implicated in the appearance and increased incidence of multiple
sclerosis (MS) and that Aspartame consumption is one of the two primary
sources of methanol in our diets.
What Price Aspartame: The Early Warnings Ignored
We have consumption data for Aspartame in the United States from
mid-1981 when a ban on its use was reversed through political
intervention (39).
The increase in production and consumption was relatively slow until a
surge occurred when approval came for its use in carbonated beverages.
Although we would wish such periods did not occur, a period in which a
substance is introduced into the diet of an unsuspecting population is a
perfect time to look for anomalies that can help us to hypothesize about
the extent to which the substance may be toxic.
I examined data on diseases and conditions that I thought might be
affected by the increased consumption of Aspartame such as depression,
autoimmunity, and birth defects (terata).
Both methanol and Aspartame are proven teratogens in animals far less
sensitive to methanol than humans (92, 96, 103-105, 124, 159, 177).
Data from the US National Center for Health Statistics regarding
morbidity numbers during those critical early years are presented here
in graphic form.
These are the original data with no modification save for those
regarding autism; these were displaced by six years because the data
presented to me were for patients diagnosed at six years of age(98).
This displacement reflects that exposure to methanol occurred in the womb.
If these data teach us anything they teach us that the first question we
should ask a depressed child is “Do you drink diet soda?"...
and that pregnancy is not the time to consume Aspartame(100).
It is interesting to note that Breast Cancer has the same worldwide
distribution and incidence characteristics as MS (190) and shares with
MS the known, methanol rich, causal agent…cigarette smoking.
I found the most striking graph to be the one showing increase in
diagnosed cases of multiple sclerosis.
It usually takes, at least, 10 years from first onset of symptoms to
reportable diagnosis of the disease(86, 167).
This early reporting was evidence, to me, of much worse to follow.
Science has been seeking the cause of multiple sclerosis for 150 years.
It has repeatedly been suggested there is evidence to implicate a small
toxic molecule(153, 185)... a solvent(74, 140).
Methanol is the smallest of solvents.
The results of 27 years of Aspartame consumption
The Worst of Timing
The 1980’s was well into the era when laboratories that had been
performing methanol toxicity research were being paid by the company who
invented Aspartame to prove the safety of its sweetener(121, 131).
Dr. Hugo Henzi, an M.D. now deceased, published a book in 1980
purporting to prove dietary methanol as the cause of multiple sclerosis(5).
His clinical logic and anatomical observations were impeccable (6,
8-10), but he made a major mistake.
He erroneously believed that the methanol that caused MS came from
“fresh” fruits and vegetables, and as a consequence, he proposed a
curative diet that we now know had little chance of success(101).
However, several lines of evidence are now converging to support Dr.
Henzi’s primary assertion.
The Secret Battle that is Autoimmunity
From an early moment in the evolution of man…from as far back as the
mutation that accounted for universality in its distribution...
a biochemical battle has quietly raged within the most intimate anatomy
of the human body.
Two alcohols competing for the attention of a serendipitously
distributed and poorly understood enzyme... an enzyme that, by accident,
has become the lonely suitor to and only benefactor of their advances.
The outcome, after years of struggle, determines who will and who will
not die with MS.
The alcohols are ethyl and methyl alcohol.
Methanol is the smallest known alcohol containing only one carbon atom;
ethanol has two carbon atoms.
The enzyme has had several names as it has been discovered and
rediscovered over the years in the physiological, neurological, and
opthalmological sciences.
However, it is most commonly referred to as ADH (alcohol dehydrogenase).
ADH is known to serve a number of functions in the healthy human body.
In the retina it is called retinal reductase and plays a major role in
vision (112), but ADH’s ability to convert alcohols to aldehydes is what
is paramount to our discussion here.
ADH is a large protein molecule and due to its unique structure it much
“prefers” coupling with ethanol, which it converts to acetaldehyde that
our body uses for many good purposes.
It is only when ADH finds no ethanol in the blood or when the methanol
concentration in the blood is 10 times greater than that for ethanol
that ADH slowly and “reluctantly” turns methanol into formaldehyde
(113, 114, 116-118, 122).
Only a small amount of ethanol in one’s blood prevents methanol from
turning into formaldehyde (141).
This is fortunate for without this inhibiting effect on formaldehyde
formation humans would have become extinct eons ago.
Another bit of good fortune for the majority of those in the human race
is something that was noticed during the development of breath analyzers
for the detection of drunk drivers and subsequently confirmed in the
scientific literature.
That is, we nearly always have ethanol, circulating in our bloodstreams
(64, 188).
The presence of ethanol is the natural outcome of digesting plant
material in the gut(134, 174), but the amounts of this endogenous
ethanol in our blood varies greatly across individuals(64, 173).
No ethanol could be found in the blood of some subjects while others
have high enough ethanol in their blood to be considered impaired (186).
Individual differences in the presence of endogenous ethanol (and the
location of tissue containing ADH) may well account for why some people
die or become blind from a teaspoon of methanol(16) and some consume it,
mixed with ethanol, as a preferred source of intoxication(110).
I also believe that these individual differences in the presence of
endogenous ethanol provides an explanation for why some people develop
autoimmune disease and others do not, no matter what they consume or smoke.
Interestingly the location of ADH in our bodily tissue seems to vary
with our genetic makeup(187).
ADH might, for reasons not fully understood, be found in the liver, gut,
brain, eye, skin and sinew.
These hereditary differences are most likely responsible for the varied
manifestations of autoimmunity.
Higher enzyme representation in the brain might predispose the
individual to develop MS while its presence in the skin would be
required for the evolution of lupus.
Autoimmunity: Teaching our Body to Produce Antibodies against our own
tissue.
During the evolution of vaccines, not long after the pioneering work of
Jennings and Pasture, the pharmaceutical industry noticed and took good
advantage of the “trick” of toxoid production(75, 114, 179).
A toxoid is a bacterial or viral protein that has been treated in the
laboratory with a low concentration of formaldehyde (26).
The concentration is just enough to attract the attention of the
macrophage but not enough to completely change the protein’s structure.
The toxoid (vaccine) is injected into humans who then produce antibodies
and thus develop immunity to the original, offending organism.
It is interesting to note that injection of the original protein without
formaldehyde treatment often causes little or no antibody production and
therefore little immunity to that bacterium or virus.
As discussed in my previous article, once methanol is changed into
formaldehyde and then, by water, to formal hydrate (4, 27, 114), all
hell breaks lose.
Unbeknownst to most researchers, formal hydrate is extremely acidic(114)
along with being a powerful esterifying agent (122).
These two characteristics make it irresistibly attractive to our body’s
protein molecules, especially to those found in the insulation of the
human brain(18, 53).
Opposites attract and the basic protein (MBP) of myelin quickly falls
prey to acidic formal hydrate.
Macrophages are large white, amoeba like blood cells for which the major
purpose in our body is to destroy attacking life forms and consume
foreign and broken protein from our bodies.
For reasons yet unknown, evolution has equipped macrophages with
chemical receptors to detect and destroy specifically and with great
vigor protein treated with formaldehyde (23, 24, 25).
Macrophages can signal the immune system to produce antibodies to the
proteins that they consume.
This is a dark side to the good work of the macrophage.
What happens when the protein in our brain comes in contact with
formaldehyde from diet soda?
An Increase in MS
There is no denying…there has been an epidemic of autoimmune disease
throughout the world over the last 30 years (79, 79a-j, 80, 80a-c, 81,
81a, 82).
Multiple sclerosis, once almost unknown in Japan( 44, 85, 168), has now
risen to menace a large portion of the population(81, 81a).
The lower latitudes and warmer climates once “mysteriously” protected
from the full brunt of this tragically debilitating disease (83, 85,
168) have seen incidence and prevalence of MS climb to as much as four
times what they were in the days before summer drinks were sweetened
with Aspartame (79, 79b, 79d, 79f,g,h, 79j, 80, 80a-c).
The United States which has long had a relatively high MS incidence has
seen at least a 50% increase (77).
Medical journals in Australia (82) and New Zealand (90) both report
unexplainable increases in their inordinately high (168) “infection” rates.
Where Does Methanol Come from Aside from Aspartame?
Cigarette Smoking
After 150 years of study of MS only cigarette smoking is universally
accepted as a causative agent(67-70, 70a-d, 71).
Smoking has also been causally linked to the progression of MS,
transforming a relapsing-remitting clinical course into a much more
serious secondary progressive course (69).
Tobacco leaves contain large amounts of pectin; and although most
scientists are unaware of this, tobacco leaves are left in barns to
ferment for weeks (61, 62, 66).
This fermentation releases much of the available methanol from the
pectin into the moisture content of the tobacco before it is sold to be
made into cigarettes (65).
Consequently, methanol is one of the most abundant toxic compounds found
in cigarette smoke (63).
Methanol is found in human breath following smoking (64) indicating a
presence in the blood.
A large case-controlled study, mostly of prevalent disease, has shown
that systemic lupus erythematosus (SLE) is also positively associated
with cigarette smoking and inversely associated with alcohol consumption
(73).
Food Processing
Although acknowledging the role played by smoking, I believe that food
processing and preserving is what first dramatically increased methanol
consumption.
At some point in our genetic history a mutation occurred that disrupted
the ability of liver catalase enzyme’s to quickly and safely clean
methanol from our blood (52).
For several million years after this mutation there was no downside to
the mutation, no autoimmunity.
We ate fresh food, and what very little methanol is in fresh fruits and
vegetables is countered by their own ethanol content (1, 28, 29) and
their ubiquitous gift for slow, steady ethanol production in the gut(64,
134, 188).
However, when the fruits and vegetables and their naturally occurring
pectin is placed in a sealed container (as in canning) that is then
sterilized, heated or even just stored at room temperature for months,
the normally unavailable, chemically bound methanol is released from the
pectin (1, 28, 29, 34).
The methanol slowly builds up, trapped in the container, to hundreds of
times more than when fresh(28, 29).
Very simply it is “canned” fruits and vegetables that were (before
aspartame) the major source of free methanol in the human diet.
The History of MS Recapitulates the History of the Canning Industry
Nicolas Appert invented canning in the 1790s, and the first canning
factory was fully operational in England by 1813 (46).
Due to the expense, early canning was undertaken primarily with meats
which have no pectin content and therefore would not have caused
methanol accumulation.
However, canning of fruits and vegetables followed.
Over time canning became more prevalent and less expensive(46), and the
consumption of canned food skyrocketed as did the incidence of multiple
sclerosis.
As the canning industry flourished so did the practice of incorporating
into recipes the “natural”, methanol-laden juices from canned fruits and
vegetables rather than throwing them away(74).
The first documented case of multiple sclerosis was reported by
Jean-Martin Charcot in a lecture in 1868(45), although it is thought
that the “first identifiable instance of MS” was that of Augustus d”Este
whose symptoms started between 1822 and 1843(45).
During the 19th century MS was recognized as a disease but considered
“quite rare” with Charcot reporting fewer than 40 cases during his long
career(45).
Increasing numbers of cases were reported in the late 19th century(45).
Although co-occurrence is not proof of causality, similarities in
initial appearance and in rate of increasing incidence are consistent
with a close linkage between MS and consumption of canned fruits and
vegetables.
Explaining the Unexplainable
MS a Disease of the Colder Countries
The differential prevalence of MS across different geographical regions
also supports this linkage.
The “latitude gradient theory” of MS is a way to explain the occurrence
of higher MS prevalence in colder regions of the world (168).
The tropics have until recently been blessed with very low incidence of
MS (83, 85, 168).
These warmer climes are, of course, regions in which the on-going supply
of fresh fruits and vegetables has obviated the need for more expensive,
canned produce, hence minimizing daily methanol consumption.
The last 30 years has seen an increase in aspartame consumption in these
areas and with it a significant attenuation of this gradient (91b, 95)
An exception to the generalization regarding temperate regions would be
expected in areas with established canning industries that are able to
offer products so economically as to make the canned product a tempting
alternative even in the summer months.
For many years both Australia and New Zealand have had such a canning
infrastructure and these countries are significant exceptions to the
latitude gradient theory.
Both have extremely high MS prevalence and incidence numbers (168).
Another exception (albeit in the opposite direction) is Japan which is
in the colder latitudes but which has had little MS incidence through
most of its recorded history(85, 168).
Note, however, that the Japanese cultural habit of eating everything in
its season did not foster the production or importation of much canned
plant material.
Although far from tropical, until recently Japan has had one of the
lowest rates of methanol consumption per person in the world.
This rate has increased with the growing popularity of diet beverages
(81, 81a).
The worlds largest manufacturer of Aspartame is a Japanese company.
Seasonally speaking, in the northern latitudes, before Aspartame,
patients with relapsing-remitting MS could expect relapses to be
experienced in the winter or Spring (72a) during periods of peak
methanol consumption.
With increased consumption of diet beverages, Japan and the warmer
countries are now reporting their worst relapse period to be the summer
(72, 72a-b).
The difference between warm and cool regions in remission-relapse cycles
appears to parallel periods during which toxic canned vegetables and
toxic thirst quenchers are most frequently consumed.
Epidemics of MS
There have also been bizarre epidemics or clusters of MS on the Faroe
Islands, Orkney and Shetland Islands, and Iceland (84).
All of these have been studied in great detail and all involve the
influx of massive numbers of British or Allied troops (84, 168).
One researcher concluded that those individuals most affected were those
who had been in direct contact with these troops(168).
Another article goes so far as to accuse MS of being a “sexually
transmitted infection”(184).
An alternative explanation is that these islands had a very low
incidence of MS to begin with due the lack of an established canning
industry.
Troops brought with them items such as canned foods, fruit preserves,
marmalades and rations along with the ubiquitous cigarette, all of which
would be very desirable to the island people, especially during war time.
Methanol consumption was overlooked as a factor in all these studies.
The Scandinavian countries and portions of the Slavic nations have some
of the highest incidence of MS of any populations in the world (95a, 168).
In these countries consumption of canned and home-canned fruits and
vegetables is high, as is consumption of smoked-food products and
traditional liquors made from rotted culled fruit.
Some of these liquors have high enough methanol content to exclude them
from international commerce.
The alternate name for methanol is “wood alcohol” due to its original
source as a condensate product made from wood smoke.
Smoked meats and fish are the exception to the rule that animal products
do not contain methanol.
The White Man’s Burden
MS was once considered to be a “rich man’s disease” in that its
prevalence was positively correlated with the trappings of civilization
including modern sanitation practices (85).
It now appears that consumption of canned produce provides a better
explanation for the relative dearth of MS in many economically depressed
regions.
To this day the very poorest people of the world are free from
autoimmune diseases such as MS (168), lack proper sanitation, and cannot
afford canned fruits and vegetables or diet soda.
Identical Symptoms of MS, Methanol Poisoning and Aspartame Toxicity
The symptoms of multiple sclerosis (44, 83, 85, 169), chronic and acute
methanol poisoning (13, 144, 189), and Aspartame toxicity (54, 58, 93,
181), are in all ways identical.
There is nothing that happens to the human body from the toxic effect of
methanol that has not been expressed during the course of MS... nothing
(143, 144).
This generalization extends even to the remarkable opthomological
conditions common to both: transitory optic neuritis and retrolaminar
demyelinating optic neuropathy with scotoma of the central visual field
(which occasionally manifests as unilateral temporary blindness (85,
138, 163).
In fact, these opthomological symptoms have been thought of for years in
their respective literatures to be “tell tale” indications for the
differential diagnosis for each of these maladies independently (85,
138, 148, 163, 169).
The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet again by
complaints from aspartame poisoning (54, 58, 93, 181).
I take these strikingly similar symptom patterns as evidence that these
disorders act on identical components of the central nervous system and
in the same way.
The “Miracle” that MS shares with Methanol poisoning In the early stages
of MS, or when a non-lethal dose of methanol has been administered,
complete recovery is a possibility.
The only two afflictions for which such dramatic “remissions” are
reported from identical neuromuscular and opthomological damage, even
“blindness” is relapsing-remitting multiple sclerosis (85) and methyl
alcohol poisoning (138, 163).
The pathology of the two maladies is in may ways identical, particularly
when it comes to destruction of the myelin sheath with no harm to the
axon itself (18, 148, 176).
Sex Ratios for MS and Aspartame Reactions Women bear the brunt of
multiple sclerosis (91a-c) and lupus (SLE)(73) with fully three-fold
representations in infliction numbers over men for both diseases.
This is exactly the proportion represented by adverse reactors to
Aspartame reported by the US Center for Disease Control in their study
of 1984(58).
The Center found three women to every man whose Aspartame consumption
complaints were serious enough to warrant investigation (93).
Although the female/male ratio for those stricken with MS has always
been high recent estimates place it at over 3 to 1(91, 91a, 91c).
What might account for the difference across sexes in incidence?
A study published in the New England Journal of Medicine (94) reports
biopsies of the gastric lining of men and women.
A result was that the concentration of ADH in the gastric lining of men
was much higher than for woman.
Men have the advantage of removing methanol from the bloodstream four
times faster on an equal-body-size basis than women.
Thus, for men, methanol is more likely to be removed from the blood
before it reaches the brain.
The brain is spared but the methanol removed would still be metabolized
to formaldehyde in the gut where it would reap its havoc on a more
forgiving organ.
This may help explain why men have more gastrointestinal complaints from
both methanol and Aspartame consumption (93, 99).
On the other hand, women’s complaints from both more frequently involve
serious neurological complications.
MS Cures and treatments
There are no known cures for MS and after reading about all of the many,
many treatments, I conclude that the only one that shows statistically
valid improvement in double-blind studies, albeit for a relatively short
period of time, is plasmapheresis (186).
Plasmapheresis involves removing the liquid portion (plasma) of a
patient’s blood, then returning the red and white blood cells to the
patient without the plasma.
Although not done for this reason, the process would be expected to
remove much of the methanol from the bloodstream reducing its
concentration substantially in the tissues.
Transfusions (43) seem also to have similar effect.
Viewing methanol toxicity as the ethnologic cause of MS seems to answer
all of the nagging question and unexplained anomalies that have stalled
the cure for this increasingly persistent disease.
Consumption of aspartame always results in methanol consumption (14, 48,
51).
Methanol will always convert to formaldehyde where it finds an idle ADH
(30).
When this happens in the brain any protein changed by the formaldehyde
will be destroyed by white blood cells (20, 23, 24, 25).
The protein most likely destroyed would be myelin basic protein MBP
found in the axons.
Over a long enough period of time, even without concomitant antibody
production, there are those who would call this MS(44).
This ends my case for considering methanol to be the cause for multiple
sclerosis.
Call all this hypothesis and circumstantial evidence if you like.
The best experiment to confirm it would never have been allowed by any
human subjects committee even though it has been going on for 27 years;
and as far as I am concerned it is time to call the experiment complete
and to count the bodies.
Woodrow C. Monte Ph.D. Professor of Food Science (retired) Page, Arizona
Note 1: It has been over 25 years since I heard my first unsolicited
plea for help from an Aspartame consumer who had linked consumption of
the product to her suffering.
My first thought after an hour’s listening was that this courageous
young woman would soon be diagnosed with Multiple Sclerosis.
It is in her honor that I seek to explain the compelling link between
Aspartame, methanol and autoimmunity.
Note 2: A fully referenced version of this article will be available at
TheTruthAboutStuff.com.
The abstracts and texts of all 190 references are given in pdf form at
http://www.thetruthaboutstuff.com/articles.shtml
Many full original texts are provided, annotated by Monte by hand, and
often collected together as brief reviews of specific topics.
In Mozilla ThunderBird email client, you can click on the pdf text, use
Ctr A to highlight the text, and then Ctr C to copy it to the Note Pad,
and then left click on an email and use Ctr V to paste the full text
into the email as plain text.
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REFERENCED
Aspartame
Multiple Sclerosis
Breast Cancer
Listener
PUBLISHED
Aspartame
Multiple Sclerosis
Breast Cancer
Listener
GRAPHS
Autism USA cases vs aspartame consumption 1978-1996
1985 ---- 16,000 cases (adjusted by age)
1996 --- 142,000
http://www.thetruthaboutstuff.com/charts/Autism%20USA.pdf
Breast Cancer A North and South America incidence, cases per 100,000
USA -------- 1975-2005 --- 75 --> 83.3
England ---- 1975-2005 --- 55 --> 88.0
also USA rates compared with aspartame 1978-1996,
http://www.thetruthaboutstuff.com/charts/Breast%20Cancer%20USA%20A.pdf
Breast Cancer B rest of World, cases per 100,000
Denmark ----- 1975-2003 --- 60 --> 85.3
Slovakia ---- 1975-2003 --- 30 --> 47.4
Finland ----- 1975-2005 --- 38 --> 82.1
Singapore --- 1975-2005 --- 23 --> 58.8
http://www.thetruthaboutstuff.com/charts/Breast%20Cancer%20USA%20B.pdf
TIME Graphic by Joe Lertola
USA Fetal Alcohol Syndrome rates per 10,000 births and aspartame
consumption 1980-1995
1984 --- 1.8 cases per 10,000 births
1993 --- 6.8
http://www.thetruthaboutstuff.com/charts/FAS%20USA.pdf
USA Lupus cases and aspartame 1978-1993
Lupus-ALD (females)---- Lupus-ALD 710.0
1983 --- 31 ----------- 56 cases diagnosed
1993 --- 42 ----------- 65
http://www.thetruthaboutstuff.com/charts/Lupus%20USA.pdf
USA Multiple Sclerosis cases and aspartame 1978-1996
MS-ALD 340 cases diagnosed
1983 --- 10
1996 --- 77
http://www.thetruthaboutstuff.com/charts/MS%20USA.pdf
USA Teen Suicide deaths and aspartame 1978-1991
1983 1860 deaths
1991 2230
http://www.thetruthaboutstuff.com/charts/Teen%20Suicide%20USA.pdf
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http://www.thetruthaboutstuff.com/pdf/(2)%20FASEB%20Meeting%201990%20Abstract%20\
and%20paper.pdf
ABSTRACT MUST BE RECEIVED AT SOCIETY OFFICE BY MONDAY, DECEMBER 4, 1989.
9650 Rockville Pike, Bethesda, MD 20814
Mail to your Society of membership (APS, ASPET, AAP, AIN)
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is at the discretion of the programing society.
MAILING ADDRESS OF FIRST AUTHOR
(Please print in black ink or type. Provide full
name rather than initials.)
Woodrow C. Monte, Dept. of Family Resources & Human Development
Arizona State University, Tempe AZ 85287-2502
Phone: 602-935-6938
SELECT CATEGORY NUMBERS & TITLES
(See Minisympgsium and Topic Category Ljsts)
Auto immunity and
1 408-4 Immuno deficiency
2. 795-3 Immunoparm & Toxic
g . 785-4 Autoimmune Disease
Is first author graduate student? q Yes ***No
METHYL ALCOHOL INGESTION AS A MODEL ETIOLGIC AGENT IN
MULTIPLE SCLEROSIS.
W. Monte, D. Glanzman, and C. Johnston
(SPON: S. Hoffman).
Arizona State University, Tempe, AZ 85287
Human catalase, unlike that of all other species, does not
metabolize methyl alcohol (methanol).
This unfortunate evolutionary deficiency makes_methanol a poison only to
humans.
Methanol is known to be a demyelinating toxin in humans, producing
symptoms markedly similar to those in multiple sclerosis,
including bizarre and inconsistent visual field disruptions.
Human alcohol dehydrogenase metabolizes methanol directly to
formaldehyde, which actively cross-links native proteins in-situ.
Such formaldehyde-modified proteins have been shown to induce macrophage
scaveging at a rate 100 times that of unmodified protein.
What better method to elicit an autoimmune response than to react
endogenous proteins with formaldehyde consistently and intermittently
over a long period of time?
In our model, the neurotoxic effect of orally-administered methanol was
visualized in the rat central nervous system using reduced silver
degeneration staining techniques.
Following chronic administration for 18-33 days, all experimental
animals demonstrated massive cellular, axonal and terminal degeneration
in numerous regions of brain, including cerebellum, hippocampus,
brainstem nuclei, internal capsule and optic chiasm.
These results show for the first time that by using sufficiently
sensitive histological techniques, the neurotoxicity of methanol is
revealed in the mammalian central nervous system.
MEMBER'S AFFILIATION (Check one only): j
q APS q ASBMB q ASPET q AAP q AIN Ifd'AA) q ASCB q BMES q SEBM q ISB
Submission of signed form indicates acceptance of rules including final
withdrawal data of December 27, 1989.
No exception will be made.
Steven A. Hoffman Member's Name
Member's Signature
602-965-7024 Member's Phone
Dietary Methanol as a Cause of Multiple Sclerosis
Human Catalase, unlike that of all other species, cannot detoxify
methanol.
This unfortunate evolutionary deficiency makes methanol
a "poison" only to humans, contradicting Richardson's Rule
which successfully predicts ethanol as consistently more toxic
than Methanol in all other species.
Methanol is known to be a demyelinating toxin in humans.
The symptoms of chronic methanol poisoning in humans are identical to
the symptoms of Multiple Sclerosis.
Even to the bizarre nature and inconsistency of the visual field
disruptions, thought to be the toxicological marker that sets methanol
poisoning apart from all other intoxications.
Human alcohol dehydrogenase metabolizes methanol directly to
Formaldehyde.
Location of Alcohol dehydrogenase activity in the human brain, though
individually variable, is generally consistent with MS Plaque distribution.
The Liver also has ADH activity with concomitant high aldehyde
dehydrogenase activity.
Aldehyde dehydrogenase facilitates detoxification of Formaldehyde via
1-carbon metabolism to CO2.
Without ready availability of Aldehyde Dehydrogenase, Formaldehyde will
"immediately" complex with any available protein.
Formaldehyde treatment of antigens is known to stimulate the immune
response and is, in fact, the requisite proprietary mechanism normally
utilized by pharmaceutical companies in the preparation of virus
proteins for vaccine production.
Recently sites on macrophages specific to "Formaldehyde Modified
Protein" have been elucidated.
Protein modified by formaldehyde are scavenged by macrophages at a rate
100 times that of unmodified protein.
What better method to elicit an auto-immune response than to react
endogenous proteins with Formaldehyde consistently and intermittently
over a long period of time.
Although differences in distribution and density of alcohol
dehydrogenase sites in the brain may account for the great individual
variability in symptoms and severity of MS and methanol poisoning, it is
more likely that variability of ethanol levels in the blood may be an
even more important factor.
Alcohol Dehydrogenase(ADH) metabolizes ethanol preferentially to
Methanol by a ratio greater than 9.
For this reason ethanol is the only known antidote to methanol
poisoning, its ingestion prevents the conversion to formaldehyde and
allows methanol to be removed by the kidneys and the lungs.
There is some indication that endogenous ethanol produced by gut
fermentation, can be found in the human bloodstream.
Sobriety testing indicates that there is great variability in these
residual levels of ethanol, perhaps due to the variation of the
population of gut flora.
page 1
Small amounts of methanol are produced as a result of gut fermentation.
There are sources of dietary methanol that are substantial enough to
cause concern.
Canned fruits and vegetables have been exposed to enough heat to
liberate methanol from the pectin in the plant cell walls.
This methanol would normally not be available to the digestive process
of humans.
Certain alcoholic beverages are so high in methanol as to not be
exportable to the United States.
It is worth noting that countries in which they are produced have the
highest, per capita incidence of MS.
Although MS occurrence in populations varies with geographical and
climatological consistency, a very believable case can be made for
direct correlation to preformed dietary methanol.
page 2
METHANOL INDUCED NEUROPATHOLOGY IN THE MAMMALIAN CENTRAL NERVOUS SYSTEM
WOODROW C. MONTE Ph.D
RENEE ANN ZEISING
Department of Family Resources and Human Development
Arizona State University, Tempe, AZ 85287 (U.S.A.)
Key words: Methanol--Degeneration--Axon--Rat--
Brain--Central Nervous System--Neuropathology
Please address correspondence to:
Woodrow C. Monte
Department of Family Resources and Human Development
Arizona State University, Tempe, Az. 85287
SUMMARY
The neurotoxic effect of methyl alcohol (methanol) was visualized in the
rat central nervous system using reduced silver staining techniques.
Following chronic administration of methanol (intubation with 0.95 gm/kg
for 18, 25 or 33 days) all experimental animals showed massive axonal
degeneration in multiple regions of brain, regardless of the duration of
exposure.
Histological processing yielded degeneration by-products of fibers with
cells of origin lying in cerebellar cortex, deep cerebellar nuclei,
cranial nerve nuclei and the red nucleus.
Additional regions of axonal degeneration were found in the hippocampus,
the flocculus, dorsal raphe nucleus, ventral cochlear nuclei,
retrosplenium, the internal capsule of the corpus striatum and the optic
chiasm.
These results show that by using sufficiently sensitive
neurohistological techniques, the neurotoxicity of methyl alcohol is
revealed in the vertebrate central nervous system.
INTRODUCTION
Methanol has been widely suggested as a neurotoxin in humans (9, 7), yet
the demonstration of such purported toxicity has been difficult to
achieve with consistency.
"Surprisingly low levels" of methanol (14) are known to cause various
and nonspecific neurological complaints, including headache, vertigo,
chills, gastric pain, insomnia (23), tinnitus (4), shooting pains in
the lower extremities, and a form of multiple neuritis characterized by
paresthesia, numbness, prickling and shooting pain in the back of the
hands and forearms as well as edema of the arms.
Bilateral blindness, nystagmus (20, 10), bladder paresis (7) and
permanent motor dysfunction (9) are long term neurotoxic sequelae
following acute poisonings (18).
The most characteristic signs and symptoms of chronic methyl alcohol
exposure in humans are diverse visual disturbances with progressive
contraction of visual fields (23).
Acute exposure to methanol can also lead to blindness.
These data are inconsistent on two grounds:
Reports of both transient and permanent blindness, as well as unilateral
and bilateral disturbances, have appeared in the clinical literature
(20, 25).
Methanol is generally considered to be a cumulative toxin, both due
to its unusually long half life (estimated to be over thirty five hours
in humans;(2),
and to the progressive damage reported in test animals chronically
exposed to methanol in early studies (10).
Methanol poisoning of humans is the only known exception to
"Richardsons' Rule," by which the toxicity of alcohols increases
directly with the length of the carbon chain (18).
Unfortunately, little is yet known of the mechanism by which methanol
exerts its apparently selective cellular toxicity (22).
There are considerable differences methanol toxicity across species (19).
For example, the minimum acute lethal dose (MLD) in rat is 9.5 g/kg,
rabbit 7.0 g/kg and dog is 8 g/kg (19).
Primates also vary considerably across species and strains, with
lethality reported to occur in the range of 3-9 g/kg (24).
Humans have succumbed to doses as low as 100 mg/kg (1);
blood levels above 115 mg/dl (milligram percent) are generally
considered lethal (3). {{See footnote 1}}
Several early studies of chronic methanol exposure have reported,
although with little substantiation, the occurrence of extensive
peripheral "nerve damage" (12, 21) and "destruction of the parenchyma
[sic] cells of the cerebrum" (6) with long term inhalation of methanol
both in monkeys and in dogs.
Both the ingestion and the inhalation of methanol have been reported to
induce behavioral abnormalities (11) and gross neurological teratology
in rat pups whose dams had been exposed to methanol during gestation (15).
Similarly, rabbits acutely exposed to methanol showed "thinning and
focal loss" of myelin, though the nature and extent of the damage was
not fully described (20).
Heretofore laboratory animals have not been considered as appropriate
model systems for the study of methanol toxicity in humans, due to the
increased methanol tolerance among all lower species thus far examined
(19).
The present experiments addressed the question of whether an adequate
dose and treatment regimen could provide a reliable animal model of
methanol neurotoxicity.
METHOD
Eight adult male and female Long Evans derived rats weighing between
200-250 grams were intubated once a day with 20 percent (v/v) spectral
grade methanol (Sigma Chemical Company, M3641) in glass distilled water
sufficient to provide 0.95 g/kg body weight (10 percent of the MLD).
Six control animals received intubation with an equivalent volume of
glass distilled water.
Animals were randomly selected for histological examination on day 18,
25 or 33 of treatment.
For histology, animals were deeply anesthetized with sodium
pentobarbital (100 mg/kg), and perfused transcardially with normal
saline followed by 4% paraformaldehyde, pH adjusted to 7.4.
Brains were removed from the calvaria and postfixed in the perfusate for
7-48 days awaiting further analysis.
On the day before sectioning brains were transferred to 10% sucrose to
facilitate sectioning.
Frozen sections were cut at 40 microns and processed for degenerating
neuronal byproducts using the reduced silver method of Giolli and Pope (8).
Sections were then mounted on gelatin coated slides, counter stained
with thionin, cleared and cover slipped.
Tissue was analyzed and regions of degenerating neuronal byproducts were
photographed using conventional bright field light microscopic techniques.
RESULTS
Analyses of degenerating neuronal tissue were performed by three
investigators.
All experimental animals showed massive axonal degeneration in numerous
and widely distributed regions.
Microscopic analyses indicated degeneration of fibers whose cells of
origin lay in cerebellar cortex, deep cerebellar nuclei, several cranial
nerve nuclei and in the red nucleus.
Of particular interest was the surprising absence of neuronal cell body
involvement:
All observable damage was restricted to axons and axon terminals.
All experimental animals showed massive degeneration throughout the
medullary layer of the cerebellum.
The spinocerebellar tracts were so heavily stained with degeneration
byproducts as to preclude tracing the course of individual fibers.
The corticospinal tract, rubrospinal tract, the trapezoid body, the
trigeminal nerve, trigeminal nucleus and particularly the NTST nerve)
were virtually filled with degenerating fibers.
Exceptionally heavy degeneration was observed in the flocculus and in
the ventral-most aspect of the periventricular gray (dorsal raphe nucleus).
There was also extensive damage to the dorsal and ventral cochlear nuclei.
The optic chiasm showed patchy areas of degeneration.
The neocortex was mostly free of degeneration except for the retrosplenium.
The corpus striatum showed damage only in the isolated fibers of the
internal capsule.
The hippocampus exhibited degeneration scattered throughout regions CA 1
thru CA 4, with some involvement of the dentate leaf.
The locus and extent of the axonal damage was independent of the
duration of methanol exposure and of the sex of the experimental animals.
The thalamus, hypothalamus, cingulate cortex, substantia nigra and the
reticular formation showed no signs of degeneration in any animal.
DISCUSSION
Our present findings indicate that chronic high doses of methanol are
capable of inducing severe axonal damage in many brain loci of the rat.
There are surprisingly few published reports of the effect of long term
methanol exposure in any species, due, in part, to the relatively high
resistance to methanol found in virtually all lower animals.
Many of the symptoms of acute and chronic methanol toxicity in humans
are indicative of neurological damage (perhaps via demyelination).
There is virtually no literature addressing the long term exposure of
humans to this ever-increasing environmental contaminant (16) and food
toxicant (13) which has a particularly high, and as yet unexplained,
potency toward man.
It is highly unlikely that this neurological damage is caused by the
direct effect of methanol itself, but rather by one or more of its
metabolic products.
Both formaldehyde and formic acid are far more potent neurotoxins.
LITERATURE CITED
(1) Bennett, I.L., Cary , F.H., Michell , G.L. and Cooper, M.N. (1953)
Acute Methyl Alcohol Poisoning: A Review Based on Experience in an
Outbreak of 323 Cases.
Medicine 35, 431-463.
(2) Bergeron, R., Cardinal, J. and Geadah, D. (1982)
Prevention of Methanol Toxicity by Ethanol Therapy.
N Engl J Med 304(24), 1528.
(3) Berkow, R. (1982)
Merck Manual. p. 2186 vol. 14.
Merck and Co Inc., New Jersey.
(4) Browing, E. (115) Methanol Toxicology:
In Toxicity and Metabolism of Industrial Solvents.
p. 315-323. Elsevier Publishing Co., Amsterdam.
(5) Clay, K.L., Murphy, W.C. and Watkins, W.D. (1975)
Experimental Methanol Toxicity in the Primate: Analysis of Metabolic
Acidosis.
Toxicology and Applied Pharmacology 34, 49-61.
(6) Eisenberg, A.A. (1917)
Visceral Changes in Wood Alcohol Poisoning by Inhalation.
American Journal of Public Health 7, 765.
(7) Erlanson, P., Fritz, H., Hagstam, K. E., Liljenberg, B. (115)
Tryding, N., Voigt, G.,
Severe Methanol Intoxication.
Acta Medica Scand. 177(4), 393-408.
(8) Giolli, R.A. and Pope, J.E. (1973)
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. 147, 129-144.
(9) Guggenheim, M.A., Couch, R. and Weinberg, W. (1971)
Motor Dysfunction as a Permanent Complication of Methanol Ingestion.
Archives of Neurology 24, 550-554.
(10) Hunt, R. (1902)
The Toxicity of Methyl Alcohol.
John Hopkins Hospital Bulletin. 13, 213-225.
(11) Infurna, R., Schubin, W. and Weiss, B. (1981)
Developmental Toxicology of Methanol,
Toxicologist 1, 32.
(12) McCord, C.P. (1931)
Toxicity of Methyl Alcohol (Methanol) Following Skin Absorption
and Inhalation.
Industrial and Engineering Chemistry 23, 931-936.
(13) Monte, W.C. (1984)
Aspartame: Methanol and the Public Health.
Journal of Applied Nutrition. 36(1), 42-54.
(14) National Institute for Occupational Safety and Health.
Health Hazard Evaluation Report No HETA-81-177,178-988:
NTIS Order No. 1982; PB82-194648: 1-14.
(15) Nelson, B.K., Brightwell, W.S., MacKenzie, D.R, Khan, A., Burg,
J.R., Weigel, W.W. and Goad, P.T. (1985)
Teratological Assessment of Methanol and Ethanol at High Inhalation
Levels in Rats.
Fundam Appl Toxicol 5, 727-736.
(16) Posner, H.S. (1975)
Biohazards of Methanol in Proposed New Uses.
Journal of Toxicology and Environmental Health 1, 153-171.
(17) Rao, K.R., Aurora, A.L., Muthaiyan, S. and Ramalrishnan, S. (1977)
Methanol toxicity -- an experimental study.
Jawaharlal Inst. Post-Grad. Med. Educ. Res 2, 1-11.
(18) Roe, O. (1955)
The Metabolism and Toxicity of Methanol.
Parmacological Review 7, 399-412.
(19) Roe, O. (1982)
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, 275-286.
(20) Roe, O.(1946)
Methanol Poisoning: Its clinical course, pathogenesis and treatment.
Acta Medica Scandinavica 126(supplement 182), 1-253.
(21) Scott, E., Helz, M.K. and McCord, C.P. (1933)
The Histopathology of Methyl Alcohol Poisoning.
American Journal of Clinical Pathology 3, 311-319.
(22) Smith, E.N. and Taylor, R.T. (1982)
Acute Toxicity of Methanol in the Folate-Deficient Acatalasemic Mouse.
Toxicology 25, 271-287.
(23) U. S. Department of Health, Education, and Welfare.
Occupational Exposure to Methyl Alcohol:
HEW Pub. No. (NIOSH) 76-148, March 1976.
(24) Wimer, W.W., Russell, J.A. and Kaplan, H.L. (1983)
Alcohols Toxicology: Alcohols Toxicology. p. 1-277.
Noyes Data Corporation.
(25) Wood, C.A. and Buller, F. (1904)
Poisoning by Wood Alcohol.
Journal of the American Medical Association 43, 972-977, 1058-1062,
1117-1123, 1213-91, 1289-1301.
////////////////////////////////////////////////////////////
"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act upon
evidence about healthy and safe food, drink, and environment."
Rich Murray, MA Room For All
rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 116 members, 1,498 posts in a public archive
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.27
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
http://groups.yahoo.com/group/aspartameNM/message/1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31
http://groups.yahoo.com/group/aspartameNMmessage/1488
Coca-Cola, Cargill Inc., PureCircle global operations market stevia for
foods and drinks: Murray 2007.11.12
http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation
cancer studies 2007.06.25: Murray 2007.07.18
http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring
agents will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12
http://groups.yahoo.com/group/aspartameNM/message/1487
Sainsbury's supermarket chain in UK details its bans of aspartame,
sodium benzoate, and artificial flavourings and colours: Carol Key,
Customer Manager: Murray 2007.11.09
http://groups.yahoo.com/group/aspartameNM/message/1427
more from The Independent, UK, Martin Hickman, re ASDA
(unit of Wal-Mart Stores) and Marks & Spencer ban of
aspartame, MSG, artificial chemical additives and dyes
to prevent ADHD in kids: Murray 2007.05.16
http://news.independent.co.uk/uk/health_medical/article2548747.ece
http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit
aspartame, MSG, artificial flavors dyes preservatives additives,
trans fats, salt "nasties" to protect kids from ADHD:
leading UK media: Murray 2007.05.15
http://en.wikipedia.org/wiki/Aspartame_controversy
http://en.citizendium.org/wiki/Aspartame
////////////////////////////////////////////////////////////
folic acid prevents neurotoxicity from formic acid, made by body from
methanol impurity in alcohol drinks [ also 11 % of aspartame ], BM
Kapur, PL Carlen, DC Lehotay, AC Vandenbroucke, Y Adamchik, U. of
Toronto, 2007 Dec., Alcoholism Cl. Exp. Res.: Murray 2007.11.27
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 27, 2007
http://groups.yahoo.com/group/aspartameNM/message/1495
[ See also:
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 28, 2007
http://groups.yahoo.com/group/aspartameNM/message/1496
explosion in numbers of children with serious food allergies has
bewildered experts and parents, Helen Francombe, The Australian
2007.11.17: role of formic acid from methanol in liquors and aspartame,
Murray 2007.11.28 ]
http://www.faslink.org/Formic%20Acid%20Kapur.htm
Brief Summary:
Methanol in small amounts is present along with ethanol in beverage
alcohol. [Murray: and about the same amounts from aspartame diet sodas]
The body's natural enzymes preferentially metabolize ethanol while
methanol breaks down into highly neurotoxic Formic Acid.
Use of high levels of Folic Acid was found to inhibit brain damage
caused by the methanol.
The use of Folic Acid during pregnancy has been recommended for several
years to prevent neural tube defects.
However, this study indicates that even higher levels of Folic Acid can
be very beneficial to the developing baby, particularly where alcohol
exposure is a factor.
Folic Acid is mandated as an additive to all flour sold in Canada.
The debate has begun on its required addition to all beverage alcohol to
help mitigate damage caused to both infants and adults.
Formic Acid in the Drinking patient and the expectant mother
Dr. Bhushan M. Kapur
Departments of Laboratory Medicine,
St. Michael's Hospital , Toronto, Ontario, Canada
Abstract
Methanol is produced endogenously in the pituitary glands of humans and
is present as a congener in almost all alcoholic beverages.
Ethanol and methanol are both bio-transformed by alcohol dehydrogenase;
however, ethanol has greater affinity for the enzyme.
Since ethanol is preferentially metabolized by the enzyme, it is not
surprising that trace amounts of methanol, most likely originating from
both sources, have been reported in the blood of people who drink alcohol.
Toxicity resulting from methanol is very well documented in both humans
and animals and is attributed to its toxic metabolite formic acid.
To understand ethanol toxicity and Fetal Alcohol Spectrum Disorders, it
is important to consider methanol and its metabolite, formic acid, as
potential contributors to the toxic effects of alcohol.
Accumulation of methanol suggests that alcohol-drinking population
should have higher than baseline levels of formic acid.
Our preliminary studies do indeed show this.
Chronic low-level exposure to methanol has been suggested to impair
human visual functions.
Formic acid is known to be toxic to the optic nerve.
Ophthalmological abnormalities are a common finding in children whose
mothers used alcohol during pregnancy.
Formic acid, a low molecular weight substance, either crosses the
placenta or may be formed in-situ from the water soluble methanol that
crosses the placenta.
Embryo toxicity from formic acid has been reported in an animal model.
To assess neurotoxicity we applied low doses of formic acid to rat brain
hippocampal slice cultures.
We observed neuronal death with a time and dose response.
Formic acid requires folic acid as a cofactor for its elimination.
Animal studies have shown that when folate levels are low, the
elimination of formic acid is slower and formate levels are elevated.
When folic acid was added along with the formic acid to the brain slice
cultures, neuronal death was prevented.
Therefore, folate deficient chronic drinkers may be at higher risk of
organ damage.
Women who are folic acid deficient and consume alcohol may have higher
levels of formic acid and should they become pregnant, their fetus may
be at risk.
To our knowledge low level chronic exposure to formic acid and its
relationship to folic acid in men or women who drink alcohol has never
been studied.
Our hypothesis is that the continuous exposure to low levels of formic
acid is toxic to the fetus and may be part of the etiology of Fetal
Alcohol Spectrum Disorders.
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1530-0277.2007.00541.x
Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007
Bhushan M. Kapur,
b.kapur@...,
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay,
dlehotay@...,
Peter L. Carlen
carlen@...,
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol Abuse, Causes
Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114–2120.
doi:10.1111/j.1530-0277.2007.00541.x
From:
the Department of Clinical Pathology (BMK),
Sunnybrook Health Science Centre, Division of Clinical Pharmacology and
Toxicology, The Hospital for Sick Children, Toronto, Ontario, Canada;
St. Michael’s Hospital (ACV), Toronto, Canada; Department of Laboratory
Medicine and Pathobiology (BMK, ACV),
Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada;
Departments of Medicine (Neurology) and Physiology (YA, PLC),
Toronto Western Research Institute, University of Toronto,
Toronto, Ontario, Canada;
and University of Saskatchewan (DLC), Saskatchewan, Canada.
Reprint requests: Dr. Bhushan M. Kapur, Department of Clinical
Pathology, Sunnybrook Health Science Centre, 2075 Bayview Ave,
Toronto, Ontario, M4N 3M5, Canada; Fax: 416-813-7562; E-Mail:
k.kapur@...,
Abstract
Background: Methanol is endogenously formed in the brain and is present
as a congener in most alcoholic beverages.
Because ethanol is preferentially metabolized over methanol (MeOH) by
alcohol dehydrogenase, it is not surprising that MeOH accumulates in the
alcohol-abusing population.
This suggests that the alcohol-drinking population will have higher
levels of MeOH’s neurotoxic metabolite, formic acid (FA).
FA elimination is mediated by folic acid.
Neurotoxicity is a common result of chronic alcoholism.
This study shows for the first time that FA, found in chronic
alcoholics, is neurotoxic
and this toxicity can be mitigated by folic acid administration.
Objective:
To determine if FA levels are higher in the alcohol-drinking population
and to assess its neurotoxicity in organotypic hippocampal rat brain
slice cultures.
Methods:
Serum and CSF FA was measured in samples from both ethanol abusing and
control patients, who presented to a hospital emergency department.
FA’s neurotoxicity and its reversibility by folic acid were assessed
using organotypic rat brain hippocampal slice cultures using clinically
relevant concentrations.
Results:
Serum FA levels in the alcoholics
(mean ± SE: 0.416 ± 0.093 mmol/l, n = 23) were significantly higher than
in controls (mean ± SE: 0.154 ± 0.009 mmol/l, n = 82) (p < 0.0002).
FA was not detected in the controls’ CSF (n = 20),
whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.
Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the
rat brain slice cultures caused neuronal death as measured by propidium
iodide staining.
When folic acid (1 ?mol/l) was added with the FA, neuronal death was
prevented.
Conclusions:
Formic acid may be a significant factor in the neurotoxicity of ethanol
abuse.
This neurotoxicity can be mitigated by folic acid administration at a
clinically relevant dose.
http://www.uhnresearch.ca/researchers/profile.php?lookup=801
Peter L Carlen, FRCPC, MD
Head, Division of Fundamental Neurobiology
Toronto Western Research Institute (TWRI)
Senior Scientist, Division of Fundamental Neurobiology
Toronto Western Research Institute (TWRI)
Keywords: stroke, gap junctions, synaptic transmission, mitochondria,
calcium chelators, whole cell patch clamp recordings, fluorescence
imaging, epilepsy, dementia, fetal alcohol syndrome, brain state
classification
Research Interests:
Mechanisms of neural synchrony and entrainment (epilepsy), and
neurodegenerative processes
* We have several projects on cellular mechanisms of epilepsy,
particularly the synchronizing role of electrotonic coupling via gap
junctions.
Molecular biological and cellular electrophysiological recording
techniques are being used to measure the upregulation of gap junctional
function in several in vitro seizure models, including the use of the
intact mouse hippocampus preparation.
Also a project on the pathogenesis of hypoglycemic seizures is in progress.
* In collaboration with Drs. Berj Bardakjian and Frances Skinner,
the linear and nonlinear electrical and network properties of central
mammalian neurons in physiological and pathophysiological conditions
(e.g., epilepsy) are being described by neural modelling techniques.
We are developing nonlinear techniques for the identification different
brain states including those associated with anesthesia and epilepsy.
* In models of stroke and Alzheimer's disease, calcium homeostasis
and free radical production are under investigation, focusing on the
role of degenerating mitochondrial function in presynaptic terminals.
Fluorescence and confocal microscopic imaging of intracellular calcium
and mitochondrial function coupled with whole cell and field
electrophysiological recordings are being used.
* In collaboration with Drs. Bhushan Kapur, James Reynolds and
James Brien, we are examining the role of formic acid in the causation
of the brain damage in the fetal alcohol spectrum disorder and its
rescue by folate.
Peter L Carlen
Mailing Address
Primary Office
Toronto Western Hospital, McLaughlin Pavilion, 12th Floor Rm. 413
399 Bathurst St., Toronto, Ontario Canada M5T 2S8
Email
carlen@...,
Phone Numbers 416.603.5800 x5044
Staff and Trainees:
Yana Adamchik
Marija Cotic
Youssef El-Hayek
S Sabet Jahromi
Eunji (Ellen) Kang
Borna Kavousi
Philip Liang
Shanthi Mylvaganam
Marina Samoilova
Evan Sheppy
Damian Shim
Alexandre Tonkikh
Hui Ye
Wilson Yu
Zhang (Jane) Zhang
http://www.clinpharmtox.utoronto.ca/Page60.aspx
Dr. Bhushan Kapur
Selected Publications
Kapur BM. Drug Testing Methods and Clinical Interpretation of Test
Results. In: Carson-Dewitt R, ed. Encyclopedia of Drugs, Alcohol and
Addictive Behaviour. Vol 1. Macmillian Press; 2001, p. 450-461.
Kapur B, Hackman R, Selby P, Klein J, Koren G.
A randomized, double-blind placebo control trial of nicotine replacement
therapy in pregnancy. Current Therapeutic Research 2001; 62(4): 274-278.
Bailey B, Lalkin A, Kapur B, Koren G. Is chronic poisoning with
acetaminophen in children a frequent occurrence in Toronto?
Can J Clin Pharmacol 2001; 8(2): 96-101. [Read More]
Ho E, Collantes A, Kapur B, Moretti M, Koren G. Alcohol and breast
feeding: Calculation of time to reach zero-level in milk.
Biol Neonate 2001; 80(3): 219-222. [Read More]
[ Dr. Gideon Koren
Division of Clinical Pharmacology and Toxicology, Hospital for Sick
Children, 555 University Ave., Toronto, Ont. M5G 1X8 (Canada)
Tel. +1 416 813 5781, Fax +1 416 813 7562
E-Mail
gkoren@...,
pharmtox@..., ]
Kapur B, Koren G. Folic acid fortification of flour: three years later.
Can J Clin Pharmacol 2001; 8(2): 91-92. [Read More]
Ahn E, Kapur B, Koren G. Iron bioavailability in prenatal multivitamin
supplements with separated and combined iron and calcium.
J Obstet Gynaecol Can 2004; 26(9):809-14. [Read More]
Railton CJ, Kapur B, Koren G. Subtherapeutic risperidone serum
concentrations in an adolescent during hemodialysis: A pharmacological
puzzle.
Ther Drug Monit 2005; 27(5):558-561. [Read More]
Lehotay DC, George S, Etter ML, Graybiel K, Eichhorst JC, Fern B,
Wildenboer W, Selby P, Kapur B.
Free and bound enantiomers of methadone and its metabolite, EDDP in
methadone maintenance treatment: Relationship to dosage?
Clin Biochem 2005; 38(12): 1088-1094. [Read More]
Langman L, Kapur B. Toxicology-then and now.
Clin Biochem 2006; 39(5):498-510.
Kapur BM, Vandenbroucke A, Adamchik Y, Lehotay DC, Carlen PL.
Formic acid, a novel metabolite of chronic ethanol abuse: neurotoxicity
and its prevention by folic acid.
Submitted to Alcohol Clin Exp Res, April 30, 2007.
http://www.medicalnewstoday.com/articles/45698.php
Queen's-led Network Looks At FAS Aiming To Minimize Life-long Learning
Problems
Main Category: Pregnancy / Obstetrics News
Article Date: 24 Jun 2006 - 12:00 PDT
For the first time researchers are testing to see whether fetal exposure
to methanol, a contaminant found in many alcoholic beverages, plays an
important role in causing the life-long learning and behavioural
problems associated with Fetal Alcohol Spectrum Disorders (FASD).
By understanding fetal brain injury caused by exposure to methanol and
related toxins, an emerging team of researchers is laying the groundwork
for potential new therapeutic interventions to protect fetuses at risk
for FASD.
"The main goal will always be prevention of FASD," says lead researcher
James Reynolds, Queen's University professor of Toxicology and
Pharmacology, "but we also have to develop strategies to minimize injury
to the developing fetus and individualize earlier therapeutic
interventions for children with pre-natal exposure to alcohol."
The interdisciplinary research team, which also includes
James Brien and Doug Munoz from Queen's,
Peter Carlen (University Health Network),
Bhushan Kapur (Sunnybrook Hospital)
and Brenda Stade (St. Michael's Hospital) from Toronto,
received just under $1.5 million dollars in funding
from the Canadian Institutes of Health Research.
The Queen's researchers have found that simple eye movement tasks can be
used to assess brain function in children with FASD. Since this
technology is portable, the researchers plan to travel across the
country to bring the research program into affected communities. "It's
estimated that the incidence of FASD is about one per cent in the
general population," Dr. Reynolds says, "but there are regions and
communities in this country where the population affected by FASD
increases dramatically."
Using blood samples from at risk mother-baby pairs, the Toronto team
members hope to identify biological markers that may predict brain
injury in the child. At risk babies will be tracked for 24 months
following birth so researchers can identify early signs of FASD and
develop aggressive therapeutic interventions at earlier stages to
minimize the effects on a child's development.
To understand the underlying mechanisms of this novel hypothesis of
FASD, the Toronto team members are studying the effects of formic acid
and folic acid on the biological functions and survival of neurons in
isolated brain tissue. In parallel studies, the Kingston team will
assess the efficacy of folic acid supplementation as a potential
therapeutic intervention in preventing FASD.
For these researchers, an exciting opportunity has been created by
linking this study with Queen's University's state-of-the-art Magnetic
Resonance Imaging (MRI) facility. New experimental procedures being
developed at Queen's will link eye movement tasks to MRI images of the
brain, creating an objective and much more specific way to evaluate
brain function. By isolating individual brain responses, FASD
researchers hope to gain greater insight into the underlying brain
injury caused by prenatal exposure to alcohol, leading to more specific
intervention therapies designed to minimize the affects of FASD.
"Not all children exposed to alcohol during prenatal life develop FASD,"
adds Dr. Reynolds. "There are other contributing factors including
genetic predisposition and nutrition during gestation that make
important contributions to the ultimate outcome. We need a way to
identify the different sub-groups within the FASD spectrum. This
research will help us develop the standardized tools we need to evaluate
and treat children with FASD."
----------------------------
Article adapted by Medical News Today from original press release.
----------------------------
Contacts:
Lorinda Peterson, 613-533-3234,
lorinda.peterson@...,
Nancy Dorrance, 613-533-2869,
dorrance@...,
Contact: Lorinda Peterson
name: James N Reynolds
email:
jnr@...,
phone: 613 533 6946
campus_extension: 36946
department: Pharmacology and Toxicology
type: Faculty
name: James F Brien
email:
brienj@...,
phone: 613 533 6114
campus_extension: 36114
department: Pharmacology and Toxicology, School of Medicine, Psychiatry
type: Faculty
Dr. Douglas P. Munoz
doug@...,
Canada Research Chair in Neuroscience
Director, Centre for Neuroscience Studies
Professor of Physiology and Psychology
Member, CIHR Group in Sensory-Motor Systems
Queen's University, Kingston, Ontario, Canada K7L 3N6
Phone: (613) 533-2111 Fax: (613) 533-6840
Dr. Brenda Stade St. Michael’s Hospital Fetal Alcohol Spectrum Disorder
Diagnostic Clinic 61 Queen Street Toronto, Ontario M5B 1W8
Tel: (416) 867- 3655
stadeb@...,
http://www.faslink.org/toc2.htm
FASlink
2448 Hamilton Road, Bright's Grove, Ontario, Canada N0N 1C0
Phone: (519) 869-8026 E-mail:
info@...,
Fetal Alcohol Spectrum Disorders (FASD),
Fetal Alcohol Syndrome (FAS),
Fetal Alcohol Effects (FAE),
Partial Fetal Alcohol Syndrome (pFAS),
Alcohol Related Neurodevelopmental Disorders (ARND),
Static Encephalopathy (alcohol exposed) (SE)
and Alcohol Related Birth Defects (ARBD)
are all names for a spectrum of disorders
caused when a pregnant woman consumes alcohol
FASlink CD -- more than 170 MB of information.
While "officially" FASD is not a diagnosis but describes the broad range
of disorders caused by prenatal alcohol exposure, the reality is that
FASD IS the diagnosis and the other terms are sub-diagnoses describing
the specific effects on a specific patient.
"St. Michael's Hospital, Fetal Alcohol Spectrum Disorder Clinic is
pleased to support the work of FASlink.
St. Michael's FASD Clinic views FASlink as an essential service for our
clients.
We are fortunate to partner with FASlink in our attempt to improve the
lives of individuals and their families with FASD.
Dr. Brenda Stade, St. Michael's FASD Clinic" St. Michael's Hospital is a
teaching hospital affiliated with The University of Toronto.
FASD Overview
Invisible Disabilities -- An individual’s place, and success, in society
is almost entirely determined by neurological functioning.
A child with a brain injury is unable to meet the expectations of
parents, family, peers, school, career and can endure a lifetime of
failures.
The largest cause of brain injury in children is prenatal exposure to
alcohol.
Often the neurological damage goes undiagnosed, but not unpunished.
There are strategies that can work to help the child with an FASD
compensate for some difficulties.
Early diagnosis and intensive intervention and tutoring can do wonders,
but the need for a supportive structure is permanent.
Report on FASD -- Exposure Rates, Results of Prenatal Exposure to
Alcohol, and Incidence Markers -- Bruce Ritchie - February 2, 2007
(PDF download 1.2 MB)
37% of babies have been exposed to multiple episodes of binge drinking
(5+ drinks per session) during pregnancy.
An additional 42% have been multiply exposed to 1 to 4 drinks per
session during pregnancy.
Prenatal alcohol exposure has been linked to more than 60 disease
conditions, birth defects and disabilities.
Damage is a diverse continuum from mild intellectual and behavioural
issues to profound disabilities or premature death.
Prenatal alcohol damage varies due to volume ingested, timing during
pregnancy, peak blood alcohol levels, genetics and environmental factors.
For example, ethanol was found to interact with over 1000 genes and cell
events, including cell signalling, transport and proliferation.
Serotonin suppression causes loss of neurons and glia, inducing
excessive cell death during normal programmed death (apoptosis) or
triggering apoptosis at inappropriate times leading to smaller or
abnormal brain structures with fewer connections between brain cells,
leading to fewer cells for dopamine production, leading to problems with
addiction, memory, attention and problem solving, and more pronounced
conditions such as schizophrenia.
Approximately 20% of Canadian school age children are receiving special
education services, most for conditions of the types known to be caused
by prenatal alcohol exposure.
As FASD is a diverse continuum, issues range from almost imperceptible
to profound.
It is somewhere in the middle that the issues attract the attention of
parents, educators, medical and social work professionals, and
eventually the justice system.
Most of the issues that attract sufficient attention are behavioural and
performance issues.
It is probable that about 15% of children are significantly enough
affected by prenatal alcohol exposure to require special education.
As they become adults, FASD does not disappear but the issues of youth
translate into ongoing problems in family relationships, employment,
mental health and justice conflicts.
The cost to the individuals affected, their families and society are
enormous and as a society, we cannot afford to ignore them.
To ignore the facts does not change the facts.
Most girls are 2 to 3 months pregnant before they find out.
Maternal prenatal alcohol consumption even at low levels is adversely
related to child behavior.
The effect was observed at average exposure levels as low as 1 drink per
week.
FASD Prevention
Folic acid should be added to all beverage alcohol.
Break the cycle. Properly fund addiction intervention and rehabilitation
programs.
Identify women at risk of having children with FASD and intervene.
Meconium testing for Fatty Acid Ethyl Esters should be mandatory for
every birth.
Intensive family and social service supports for FASD and recovering
alcoholics.
Poverty is a result of, and breeds, substance abuse. Deal with it.
Alcohol Vendors
The beverage alcohol industry pays less than 1% of the total damages
caused by their products. Increase taxes on beverage alcohol.
All tax revenue to be returned to support rehabilitation programs and
victims of alcohol.
Remove all incentives for governments to promote alcohol.
End all government supports for beverage alcohol industry, including
"wine and beer tourism".
End all alcohol advertising
Alcohol must be served with food.
Breathalyzers in all alcohol establishments
Ban alcohol sales incentives, contests, games.
Ban "Happy Hour" discounted promotions. They encourage binge drinking.
Public Education
Educate the public that addiction is a medical issue not a moral failure.
Educate children from a very young age about dangers of alcohol.
Have youth design anti-alcohol programs targeting youth.
The ONLY purpose of beverage alcohol is to make your brain take a hike.
Research
Better diagnostic tools for the full range of FASD damage.
True incidence and scaling of FASD damage.
Chemically turn-off addiction center in brain.
FASlink began online in 1995.
FASlink's website contains more than 110,000 searchable FASD related
documents and serves more than 400,000 visitors annually.
The FASlink Discussion Forum shares 50 to 100 letters daily and compiles
the papers and discussions into the FASlink Archives.
Our membership is worldwide but most are in Canada and the USA, from the
most remote locations to urban centers.
http://www.faslink.org/faslink.htm
The FASlink Discussion Forum is a free Internet maillist for
individuals, families and professionals who deal with Fetal Alcohol
Spectrum Disorders.
FASlink provides support and information 24/7.
FASlink has the largest archive of FASD information in the world.
FASlink serves parents (birth, foster and adoptive), caregivers, adults
with FASD, doctors, teachers, social workers, lawyers, students and
government policy makers, etc.
Bruce Ritchie is the Moderator.
To join FASlink, go to
http://listserv.rivernet.net/mailman/listinfo/fas-link
Once you have subscribed, to send mail to the FASlink members, send it
to:
fas-link@...
info@... sends email directly to the Moderator, Bruce Ritchie
////////////////////////////////////////////////////////////
The aspartame content of two liters diet soda, 5.6 12-oz cans, is 1,120
mg, releasing 11 % as 123 mg methanol.
Usually, there is not a concurrent larger amount of ethanol taken, which
would prevent the production of formaldehyde.
So, the methanol from any aspartame is quickly turned into formaldehyde.
An expert review by a competent, unbiased team led by M. Bouchard, 2001,
cites references, many from aspartame industry funded studies, states
that about 30 - 40 % of the methanol remains in the body as unknown,
durable reaction products.
J. Nutrition 1973 Oct; 103(10): 1454-1459. Metabolism of aspartame in
monkeys. Oppermann JA, Muldoon E, Ranney RE. Dept. of Biochemistry,
Searle Laboratories, Division of G.D. Searle and Co. Box 5110, Chicago,
IL 60680
They found that about 70 % of the radioactive methanol in aspartame put
into the stomachs of 3 to 7 kg monkeys was eliminated within 8 hours,
with little additional elimination, as carbon dioxide in exhaled air and
as water in the urine
They did not report any studies on the distribution of radioactivity in
body tissues, except that blood plasma proteins after 4 days held 4 % of
the initial methanol.
The low oral dose of aspartame and for methanol was 0.068 mmol/kg, about
1 part per million [ppm] of the acute toxicity level of 2,000 mg/kg,
67,000 mmol/kg, used by McMartin (1979).
Two L daily use of diet soda provides 123 mg methanol, 2 mg/kg for a 60
kg person, a dose of 67 mmole/kg, a thousand times more than the dose in
this study.
By eight hours excretion of the dose in air and urine had leveled off at
67.1 +-2.1 % as CO2 in the exhaled air and 1.57+-0.32 % in the urine, so
68.7 % was excreted, and 31.3 % was retained.
This data is the average of 4 monkeys. "...the 14C in the feces was
negligible."
"That fraction not so excreted (about 31%) was converted to body
constituents through the one-carbon metabolic pool." "All radioactivity
measurements were counted to +-1 % accuracy..."
The abstract ends, "It was concluded that aspartame was digested to its
three constituents that were then absorbed as natural constituents of
the diet."
http://health.groups.yahoo.com/group/aspartameNM/message/1143
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988)."
"Experimental studies on the detailed time profiles following controlled
repeated exposures to methanol are lacking."
"Thus, in monkeys and plausibly humans, a much larger fraction of body
formaldehyde is rapidly converted to unobserved forms rather than passed
on to formate and eventually CO2."
"However, the volume of distribution of formate was larger than that of
methanol, which strongly suggests that formate distributes in body
constituents other than water, such as proteins."
http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition: Bouchard M et al, full
plain text, 2001: substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.04.02
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
Toxicological Sciences 64, 169-184 (2001) Copyright © 2001 by the
Society of Toxicology BIOTRANSFORMATION AND TOXICOKINETIC A Biologically
Based Dynamic Model for Predicting the Disposition of Methanol and Its
Metabolites in Animals and Humans
Michèle Bouchard *, ^,1,
bouchmic@...,
Robert C. Brunet, ^^
brunet@...,
Pierre-Olivier Droz, ^
and Gaétan Carrier *
gaetan.carrier@...,
* Department of Environmental and Occupational Health, Faculty of
Medicine,
Université de Montréal, P.O. Box 6128, Main Station, Montréal, Québec,
Canada, H3C 3J7;
^ Institut Universitaire romand de Santé au Travail, rue du Bugnon 19,
CH-1005, Lausanne, Switzerland, and
^^ Département de Mathématiques et de Statistique and Centre de
Recherches Mathématiques, Faculté des arts et des sciences, Université
de Montréal, P.O. Box 6128, Main Station, Montréal, Québec, Canada, H3C 3J7
1 To whom correspondence should be addressed at Département de santé
environnementale et santé au travail, Université de Montréal, P.O. Box
6128, Main Station, Montréal, Québec, H3C 3J7, Canada. Fax: (514) 343-2200.
Received May 10, 2001; accepted August 28, 2001
"However, the severe toxic effects are usually associated with the
production and accumulation of formic acid, which causes metabolic
acidosis and visual impairment that can lead to blindness and death at
blood concentrations
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