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Monday, February 11, 2008

Maybe Its Pink, Maybe Its Not Breast Healthy

Currently the legislature in Hawaii is contemplating a ban on aspartame. I have spoken out about this toxin for decades. I speak out as well about the risk of its heir, sucralose. Both should be avoided without question.

A pharmacist comments: I have practiced pharmacy for 50 years during which time several products including thalidomide, MER 29 and Vioxx, have been marketed with FDA approval, which have resulted in disfigurement and death.

In the sheer numbers, nothing has ever come close to aspartame in causing harm to people. I deal extensively with diabetics and I have seen close to miraculous improvements in insulin response once they stop using aspartame. I have seen similar results in patients with Lupus, headaches and joint pain.

To The Honorable Rep. Josh Green, M.D., Chair:

Aspartame consumption as a causative agent of Breast Cancer

Woodrow C. Monte Ph.D.
Professor of Food Science, Arizona State University (Retired), Page, Arizona

It is a pleasure to be writing to a physician. The mechanism of Aspartame poisoning is so much easier to explain to someone with a medical background.

I am a retired Professor of Food Science from Arizona State University. I have studied, researched and written about Aspartame since 1983, shortly after its manufacturer applied to the FDA to expand its use as an additive to soft drink beverages. In 1984 I published a scientific paper warning of the potential harm that
Aspartame might cause by increasing the methanol consumption of the unwary consumer(1).

I have within the last 3 months published 3 additional articles chronicling, in detail, the aftermath of 27 years of Aspartame poisoning of the general public(78,194,202). These articles and all of the reference material that they draw on are freely available on my website.
Article 1
Article 2
Article 3

Every molecule of Aspartame converts to methanol within minutes of being consumed. The first step in methanol metabolism is production of formaldehyde. Next to the liver the greatest concentration of Alcohol Dehydrogenase Enzyme(ADH) in the human body is located in the endothelial tissue of the human breast(190b). It is human ADH that converts methanol into formaldehyde, a powerful carcinogen.

The chart below shows the relationship between Aspartame consumption and the increase of breast cancer in the United States. Similar increases in breast cancer(190) have occurred in other aspartame consuming countries of the world.[]

Formaldehyde is a powerful cancer causing agent, one of the handful of chemicals classed as a Group I carcinogen by the IARC, the International Agency for Research on Cancer, Lyon, France(11), because of this there is no known safe level of formaldehyde exposure. Formaldehyde from contaminated air, at very low
concentrations(11), causes cancer in humans. Gaseous environmental formaldehyde causes nasopharyngeal cancer, however, it is not known, in the gaseous form, to cause breast cancer. The probable reason for this is that formaldehyde has an extremely high reactivity(201) it reacts with and does its damage to the first human tissue with which it makes contact. Formaldehyde does not travel well in protein rich
blood supply(122) and because of this it is blocked from reaching the breast and other internal organs. The only way that formaldehyde can reach the mammary tissue, aside from purposely injecting formaldehyde solution(122) (as in embalming) is to disguise the formaldehyde as methanol. The methanol from Aspartame can reach a woman's breast and will there is readily converted into formaldehyde by ADH(190b).

It is not possible to prevent Aspartame from producing the cancer causing compound formaldehyde in a woman's breast(78). All of the methanol in diet soda must be transformed into formaldehyde before the body can metabolize it. The scientifically acclaimed Ramazzini Institute recently found consumption of Aspartame over time caused Breast Cancer in Rats(50). The methanol that is responsible for producing this formaldehyde is also found in our processed food supply, the average modern woman not exposed to diet products consumes, conservatively, less than 8 milligrams of it a day(1). One can of diet soda contains over 4 times this amount, one liter almost 20 times what would be average. Primitive and or impoverished woman
consume little methanol and are protected, to a very great extent, from breast cancer. Conversely increased consumption of Aspartame has caused breast cancer rates to increase dramatically(194).

It can be shown that the incidence of breast cancer has increased dramatically in populations exposed to Aspartame(194).

The breast is an organ with no way to protect itself from formaldehyde with no means to render it harmless. The methanol, always produced when Aspartame is consumed (20,51),will convert directly into formaldehyde, there is no intermediate compound or
alternate path(7,30). Alcohol dehydrogenase ADH is required for the conversion of methanol to formaldehyde(112). ADH is not a common enzyme in the human body, not many cells in the human body contains this enzyme. The human breast is one of the few organs in the body with a high concentration of ADH(190b) and it is found there
exclusively in the mammary epithelial cells, the very cells known to transform into adenocarcinoma(190c) (breast cancer). The most recent breast cancer scientific literature implicates ADH as perhaps having a pivotal role in the formation of breast cancer, indicating a greater incidence of the disease in those with higher levels of ADH activity in their breasts(190a). One article went so far as to implicate acetaldehyde as a potential culprit(190a). Acetaldehyde is the molecule that ethanol is metabolized into by ADH, the first step in the manufacture of vinegar, a beneficial molecule with no link to carcinogenicity, what so ever. Recent scientific literature is a desert when it comes to methanol. It is as if there were no such thing as methanol in the environment as if methanol did not exist, as if all the laboratories doing work in methanol toxicity had vanished from the face of the
earth 40 years ago and with them the science of methanol poisoning(39).

The truth is that methanol acts as a golden bullet, wasting none of its destructive power but administering a carcinogen directly inside those breast cells most vulnerable to cancer.

All of the hundreds of test that were done to prove Aspartame safe were done on animals insensitive to methanol poisoning(78). This was well known to the company who invented Aspartame, why else would they have hired the worlds methanol research laboratories to help them prove aspartame was safe(39) These animals have a specialized catalase enzyme in their livers that humans do not(55). Catalase
keeps methanol out of their general circulation and therefore they are mostly immune to methanol as a poison. Many thousands of people lost their lives in the early nineteen hundreds when methanol was allowed in foods and medications after it was proven falsely safe by trusting methanol safety testing done on an identical array of

Twenty six years ago I traveled from my laboratory at Arizona State University to Washington DC to view the results of the testing done by the company who invented Aspartame and were seeking it's approval for use in carbonated beverages. I will never forget viewing the data from the only high dosage human consumption study done on diabetics. This study was never to be repeated. Before the test began the subjects were screened for all manner of illnesses and certified disease free (save from diabetes) as a prerequisite to being accepted into the study. During that study, after 11 weeks of high dose aspartame consumption two of the women developed
epithelial cancer. Both were removed from the study, one had a mastectomy, subsequent pathology tested conclusively for adenocarcinoma. To my most profound horror, the executive summary of that study concluded that Aspartame was safe! The
rational used to ignore the fact that none of the placebo group but fully 8% of the Aspartame consumption subjects developed epithelial cancer during the high dosage consumption study was that "no such cancers were seen in the numerous animal studies"(48). The Bressler Report exposed that this was a lie (197), These cancers should have never been ignored.

I can not say that methanol is the only cause of breast cancer, there are so many other poisons in our modern environment. I will say that it is intuitively obvious that there would be no good done producing one more cancer causing agent inside a sensitive breast cell already exposed to other cancer causing agents.


Rich Murray said...

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 [ actually, a fairly complete
review of recent developments... ]
Wednesday, November 27, 2007

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.

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


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.

Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007

Bhushan M. Kapur,,
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay,,
Peter L. 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.

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:,


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.

To determine if FA levels are higher in the alcohol-drinking population
and to assess its neurotoxicity in organotypic hippocampal rat brain
slice cultures.

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.

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 micromol/l) was added with the FA, neuronal death was

Formic acid may be a significant factor in the neurotoxicity of ethanol
This neurotoxicity can be mitigated by folic acid administration at a
clinically relevant dose.

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

Research Interests:
Mechanisms of neural synchrony and entrainment (epilepsy), and
neurodegenerative processes

* 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
Phone Numbers 416.603.5800 x5044

Queen's-led Network Looks At FAS Aiming To Minimize Life-long Learning
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.

Lorinda Peterson, 613-533-3234,,
Nancy Dorrance, 613-533-2869,,

Contact: Lorinda Peterson

name: James N Reynolds
phone: 613 533 6946
campus_extension: 36946
department: Pharmacology and Toxicology
type: Faculty

name: James F Brien
phone: 613 533 6114
campus_extension: 36114
department: Pharmacology and Toxicology, School of Medicine, Psychiatry
type: Faculty

Dr. Douglas P. Munoz,
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,

SolidInfo said...

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