old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517
__________________________________________________ __
"Every molecule of Aspartame releases a molecule of methanol within
minutes of being consumed. The first step in methanol metabolism is
production of formaldehyde. After the liver, the next 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 charts 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."
"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).
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
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 contain 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)."
Josh Green, M.D., Chair, House Health Committee
6th Representative District
Hawaii State Capitol, Room 327
415 South Beretania Street
Honolulu, HI 96813
phone 808-586-9605; fax 808-586-9608
From the Big Island, toll free 974-4000 + 69605
E-mail
repgreen@Capitol.hawaii.gov;
John Mizuno, Vice-Chair
30th Representative District
Hawaii State Capitol, Room 436
415 South Beretania Street
Honolulu, HI 96813
phone 808-586-6050; fax 808-586-6051
E-mail
repmizuno@Capitol.hawaii.gov;
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
woodymonte@canyoncountry.net;
202. Monte WC. Bittersweet: Aspartame Breast Cancer Link.
http://www.thetruthaboutstuff.com/review3.shtml
[ not online 2008.02.09 -- Rich Murray has corrected minor typos
and added spacing to increase readability of this seminal research. ]
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:
http://www.thetruthaboutstuff.com/
Article 1
http://www.thetruthaboutstuff.com/review1.shtml
Article 2
http://www.thetruthaboutstuff.com/review2.shtml
Article 3
http://www.thetruthaboutstuff.com/review3.shtml
[ the third not active as of 2008.02.11 ]
Every molecule of Aspartame releases a molecule of methanol
within minutes of being consumed. The first step in methanol
metabolism is production of formaldehyde. After 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 charts 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.
[ Breast Cancer A
http://www.thetruthaboutstuff.com/charts/
Breast%20Cancer%20USA%20A.pdf
Breast Cancer B
http://www.thetruthaboutstuff.com/charts/
Breast%20Cancer%20USA%20B.pdf ]
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 be readily converted into formaldehyde by ADH (190b).
[ 190a. Coutelle C. et al. 2004.
Risk Factors in Alcohol Associated Breast Cancer:
Alcohol Dehydrogenase Polymorphism and Estrogens.
International Journal of Oncology 25: 1127-1132
190b. Triano E. A. et al. 2003.
Class I Alcohol Dehydrogenase Is Highly Expressed in Normal
Human Mammary Epithelium but not in Invasive Breast Cancer:
Implications for Breast Carcinogenesis.
Cancer Research Arch. 63: 3092-3100
190c. Poschl G. and Seitz H. K. 2004.
Alcohol and Cancer (Review).
Alcohol & Alcoholism. 39(3): 155-165 ]
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 about 4 times this amount,
one liter [ almost 6 cans ] 20 times the average.
Primitive and or impoverished women consume little methanol,
and so are protected, to a very great extent, from breast cancer.
Conversely, increased consumption of Aspartame has caused
breast cancer rates to increase dramatically (194).
[ Methanol and formaldehyde sources include dark wines and
liquors, tobacco and wood smoke, vehicle exhaust, medical
facilities, dental materials, embalming, common cleaners and
personal care products, new carpet, drapes, furniture,
particleboard, new mobile homes and buildings, new cars,
some foreign fish and foods, and leather. ]
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 and 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 contain 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,
whatsoever.
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,
or 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 world's 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 animals (17, 30).
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 its 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).
[ 48. Anonymous1994.
Aspartame for use as a Sweetener in Carbonated Beverages.
Searle Research and Development.
Petition submitted to the United States Food and Drug
Administration -- FAP 2A3661 ]
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, as
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.
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http://www.thetruthaboutstuff.com/#
TheTruthAboutStuff.com
Sweet Misery: A Poisoned World video
"A great deal of intelligence can be invested in ignorance
when the need for illusion is deep." Saul Bellow
Dangers of Aspartame
My name is Woodrow Monte. By interest and training,
I am a scientist. Until retirement as Professor at Arizona State
University and, for a short while, at the Marine Science Center
of Oregon State University, my career 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 Aspartame / methanol consumption.
I fully realize that it is not common for a scientist to take
his
concerns directly to the public. There are time honored channels
within the scientific community to redress, filter and disseminate
science to guard against misinformation and error.
This process is particularly important when dealing with issues
concerning the public health and chronic disease.
This system has developed over hundreds of years, fostered
by various societies of intellectuals whose primary goal was to
further truth for the sake of humanity and health.
As you would expect, there have always been charlatans in
the mix; snake oil peddlers whose quest for a personal gain directly
conflicted with the goals of the scientific community.
It has not been until recent times, however, that merchants and
masters of commerce have wielded serious detrimental influence
in what had been the realm of the scholar.
Scientific data I offer for your consideration here on this
public forum directly conflicts with information advanced by
several powerful factions of these conspirators. Because of their
influence, important data directly relevant to public health has
little
or no chance of a fair hearing in the toxicological arena
Denied access to due process and fair consideration, I had to
choose between silent knowing and open public disclosure.
The choice was difficult because, in doing this, I know I will
weaken my case in the eyes of many of my peers,
but I have made it, and there is no turning back.
"Inter arma silent leges" **
I direct this discourse to scholars who like to read out of
their
field and taste the thrill of uncovering data that can be fairly
interpreted only from a naive view.
Perhaps in the future, this thesis will be deemed an example
of simple logic gone awry.
If so, I will take full blame, and offer as my only defense that
I think it cowardly to keep this compelling story to myself until
the world was safe for it, until all the demons were dead.
I urge my colleagues around the world to take these
observations I will present to heart.
Methanol may be natural, common and chemically placid.
It may have many convenient friends and protectors,
but this belies its true nature.
Methanol is a Trojan Horse which harbors the cause of some
of our most tortuous maladies.
Methanol begets formaldehyde which morphs to formal hydrate,
a two headed monster capable of altering, in degrees
imperceptible to our healing arts, the very stuff of which we are
made, a change that only nature can know.
* Now hear from the other side
** In war laws are silent
MY WRITING
Referenced [ key full texts ]
http://www.thetruthaboutstuff.com/articles.shtml
"*FAIR USE NOTICE: This posting may contain some
copyrighted ((c)) material the use of which has not always been
specifically authorized by the copyright owner. Such material is
made available for educational purposes, to advance recipient's
understanding of scientific and other issues. It is believed that
this posting is a 'fair use' of any such copyrighted material
as provided for in Title 17 U.S.C. section 107 of the US
intellectual property law.
This material is being distributed without profit."
Aspartame
Monte WC. 2007.
Is your Diet Sweetener killing you?
Fitness Life. Nov.; 33: 31-33
http://www.thetruthaboutstuff.com/review1.shtml
Multiple Sclerosis
Monte WC. 2007.
A Deadly Experiment.
Fitness Life. Dec.; 34: 38-42
http://www.thetruthaboutstuff.com/review2.shtml
Breast Cancer
Monte WC. Bittersweet: Aspartame Breast Cancer Link. 2008.
Fitness Life. 2008 Feb.; 34: 21-22
http://www.thetruthaboutstuff.com/review3.shtml
[ not online 2008.02.09 ]
Listener
http://www.thetruthaboutstuff.com/listener.shtml
Published
Aspartame
http://www.thetruthaboutstuff.com/published/
Your%20Health%2033%20-2.pdf
Multiple Sclerosis
http://www.thetruthaboutstuff.com/published/
Article%202%20Methanol%20and%20MS.pdf
Graphs
Autism
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Int J Oncol. 2004 Oct; 25(4): 1127-32.
Risk factors in alcohol associated breast cancer: alcohol
dehydrogenase polymorphism and estrogens.
Coutelle C, Höhn B, Benesova M, Oneta CM, Quattrochi P,
Roth HJ, Schmidt-Gayk H, Schneeweiss A, Bastert G, Seitz HK.
Department of Medicine and Laboratory of Alcohol Research,
Liver Disease and Nutrition, Salem Medical Centre,
Heidelberg, Germany.
Chronic alcohol consumption is associated with an increased risk
for breast cancer, even if consumed in moderate doses.
Since acetaldehyde is a carcinogenic factor associated with
chronic alcohol consumption, individuals with the alcohol
dehydrogenase 1C*1 allele (ADH1C*1 allele) seem to
be at particular risk, since this allele encodes for a rapidly ethanol
metabolizing enzyme leading to increased acetaldehyde levels.
Since recent epidemiological studies demonstrated an increased
risk for breast cancer for individuals with the ADH1C*1 allele,
we have investigated here ADH1C genotypes
in moderate alcohol consumers.
Furthermore,
estradiols are also known risk factors for breast
cancer and acute alcohol ingestion in high doses results
in increased serum estradiol concentrations.
Thus, in the present study, we tested the effect of low ethanol
doses on estrogen serum concentrations.
We analyzed the ADH1C genotype in 117 moderate alcohol
consumers with breast cancer and in 111 age-matched women
with alcohol associated diseases without cancer
(74 cirrhotics, 22 patients with pancreatitis
and 15 alcohol dependent patients).
In addition, 107 healthy controls were studied.
Genotyping of the ADH1C-locus was performed using polymerase
chain reaction-based restriction fragment length polymorphism
methods on leukocyte DNA.
To study the effects of ethanol on estradiol levels, ethanol in a dose
of 0.225 g/kg body weight was given orally to 8 premenopausal
women at various time points of their menstrual cycle.
Thereafter estradiol serum concentrations were measured over time.
The allele frequency of the ADH1C*1 allele was found to be
significantly increased in moderate alcohol consumers with breast
cancer as compared to age-matched alcoholic controls
without cancer (62% vs. 41.9%, p = 0.0035).
Women with the ADH1C*1,1 genotype were found to be
1.8 times more at risk for breast cancer than those with another
genotype (95% CI 1.431-2.330, p<0.001).
Oral ethanol increased serum estradiol levels significantly
by 27-38%.
The data demonstrate that moderate alcohol consumers with the
ADH1C*1 allele have an increased risk to develop breast cancer
and even small amounts of alcohol increase serum estradiol levels
significantly in premenopausal women especially in the midphase
of the menstrual cycle. PMID: 15375565
__________________________________________________ __
Triano E. A. et al. 2003.
Class I Alcohol Dehydrogenase Is Highly Expressed in Normal
Human Mammary Epithelium but not in Invasive Breast Cancer:
Implications for Breast Carcinogenesis.
Cancer Research Arch 63: 3092-3100
http://cancerres.aacrjournals.org/cg...ull/63/12/3092
free full text
Triano EA, Slusher LB, Atkins TA, Beneski JT, Gestl SA,
Zolfaghari R, Polavarapu R, Frauenhoffer E, Weisz J.
Department of Biology, West Chester University,
West Chester, Pennsylvania 19383, USA.
Detoxification of ethanol can contribute to oxidative cellular and
DNA damage and, thereby, to carcinogenesis.
The potential relevance of this to breast carcinogenesis is
suggested by evidence that alcohol consumption
is a risk factor for breast cancer.
It is, however, not known whether ethanol can be metabolized
in breast parenchyma.
The goal of this study was to determine whether class I and/or IV
alcohol dehydrogenase (ADH), medium chain ADHs that can
catalyze oxidation of ethanol, are expressed in human breast
parenchyma.
Normal and neoplastic human breast tissue specimens were
examined for class I and IV ADH mRNA by reverse
transcription-PCR, for protein by immunocytochemistry
and Western analysis, and for their potential to catalyze
NAD(+)-dependent oxidation of ethanol.
Together, the findings provide evidence that:
(a) class I ADH is the medium-chain ADH that is expressed in
human breast parenchyma, specifically in the mammary epithelium;
(b) human breast parenchyma can support ADH-mediated
oxidation of ethanol;
and (c) the expression of class I ADH is dramatically reduced
or abrogated in invasive breast cancers.
Expression of class I ADH in normal human breast parenchyma
was confirmed by probing a multiple human tissue polyA(+)RNA.
The unexpected finding of virtual abrogation of expression of
class I ADH in invasive breast cancer suggests that the enzyme
has some "tumor suppressor" function in the mammary epithelium.
The one property of class I ADH fitting this designation is its
potential to catalyze the oxidation of the micronutrient/prohormone
retinol to retinal, the first step in the biosynthesis of retinoic
acid,
the principal known mediator of the actions of retinoids important
for maintaining epithelia in a differentiated state. PMID: 12810634
Elise A. Triano, [ deceased by breast cancer ]
Leslie B. Slusher,
Trudy A. Atkins,
John T. Beneski,
Shelley A. Gestl,
Reza Zolfaghari,
Rathnagiri Polavarapu,
Elizabeth Frauenhoffer
and Judith Weisz 2
jxw7@psu.edu;
2 To whom requests for reprints should be addressed, at
Department of Obstetrics and Gynecology,
The Milton S. Hershey Medical Center,
The Pennsylvania State University College of Medicine,
Hershey PA 17033.
Phone: (717) 531-6213; Fax: (717) 531-0117;
E-mail:
jxw7@psu.edu;
1 Supported by NIH Grant CA65532 (to J. W.)
and a Pennsylvania System of Higher Education
Faculty Development Award (to L. B. S. and E. A. T.).
Department of Biology, West Chester University,
West Chester, Pennsylvania 19383
[E. A. T., L. B. S., T. A. A., J. T. B.];
Departments of Obstetrics and Gynecology [S. A. G., J. W.],
Pharmacology [R. P.],
and Pathology [E. F.],
Milton S. Hershey Medical Center,
Pennsylvania State University College of Medicine,
Hershey, Pennsylvania 17033;
and Department of Nutrition, Pennsylvania State University,
University Park, Pennsylvania 16802 [R. Z.]
"Dr. Elise A. Triano succumbed to metastatic breast cancer while
the manuscript was under review. The remaining authors dedicate
this article to her memory." ]
__________________________________________________ __
http://alcalc.oxfordjournals.org/cgi.../full/39/3/155
free full text
Alcohol & Alcoholism Vol. 39, No. 3, pp. 155-165, 2004
Alcohol & Alcoholism Vol. 39, No. 3
(c) Medical Council on Alcohol 2004; all rights reserved
REVIEW
ALCOHOL AND CANCER
G. Pöschl and H. K. Seitz*
Department of Medicine, Salem Medical Centre, Heidelberg
and Laboratory of Alcohol Research, Liver Disease and Nutrition,
Heidelberg, Germany
* Author to whom correspondence should be addressed at:
Helmut K. Seitz MD, Department of Medicine,
Salem Medical Centre, Zeppelinstrasse 11-33,
D-69121 Heidelberg, Germany.
Fax: +00 49 (0) 6221 483494;
E-mail:
helmut_karl.seitz@urz.uni-heidelberg.de;
(Received 9 January 2004; first review notified 29 January 2004;
in revised form 18 February 2004; accepted 18 February 2004)
ABSTRACT
Epidemiological data have identified chronic alcohol consumption
as a significant risk factor for upper alimentary tract cancer,
including cancer of the oropharynx, larynx and the oesophagus and
of the liver.
The increased risk attributable to alcohol consumption of cancer in
the large intestine and in the breast is much smaller.
However, although the risk is lower, carcinogenesis can be
enhanced with relatively low daily doses of ethanol.
Considering the high prevalence of these tumours, even a small
increase in cancer risk is of great importance, especially in those
individuals who exhibit a higher risk for other reasons.
The epidemiological data on alcohol and other organ cancers is
controversial and there is at present not enough evidence for a
significant association.
Although the exact mechanisms by which chronic alcohol ingestion
stimulates carcinogenesis are not known, experimental studies in
animals support the concept that ethanol is not a carcinogen but
under certain experimental conditions is a cocarcinogen and/or
tumour promoter.
The metabolism of ethanol leads to the generation of acetaldehyde
(AA) and free radicals.
Evidence has accumulated that acetaldehyde is predominantly
responsible for alcohol associated carcinogenesis.
Acetaldehyde is carcinogenic and mutagenic, binds to DNA and
proteins, destructs folate
and results in secondary hyperproliferation.
Acetaldehyde is produced by tissue alcohol hydrogenases,
cytochrome P 4502E1 and through bacterial oxidative metabolism
in the upper and lower gastrointestinal tract.
Its generation or its degradation is modulated due to
functional polymorphisms of the genes coding for the enzymes.
Acetaldehyde can also be produced by oral and faecal bacteria.
Smoking, which changes the oral bacterial flora, and poor oral
hygiene also increase acetaldehyde.
In addition, cigarette smoking and some alcoholic beverages
such as calvados contain acetaldehyde. [ apple brandy ]
Other mechanisms by which alcohol stimulates carcinogenesis
include the induction of cytochrome P-4502E1, which is associated
with an enhanced production of free radicals and enhanced
activation of various procarcinogens present in alcoholic beverages;
in association with tobacco smoke and in diets, a change in the
metabolism and distribution of carcinogens;
alterations in cell cycle behaviour such as cell cycle duration
leading to hyperproliferation;
nutritional deficiencies, such as methyl-,
vitamin E-, folate-,
pyridoxal phosphate-, zinc- and selenium deficiencies;
and alterations of the immune system, eventually resulting in an
increased susceptibility to certain virus infections
such as hepatitis B virus and hepatitis C virus.
In addition, local mechanisms may be of particular importance.
Such mechanisms lead to tissue injury such as cirrhosis of the liver,
a major prerequisite for hepatocellular carcinoma.
Also, an alcohol-mediated increase in oestradiols may be at least in
part responsible for breast cancer risk.
Thus, all these mechanisms functioning in concert actively modulate
carcinogenesis leading to its stimulation. PMID: 15082451
__________________________________________________ __
aspartame rat brain toxicity re cytochrome P450 enzymes, expecially
CYP2E1, Vences-Mejia A, Espinosa-Aguirre JJ et al, 2006 Aug,
Hum Exp Toxicol: relevant abstracts re formaldehyde from methanol
in alcohol drinks: Murray 2006.09.29
http://groups.yahoo.com/group/aspartameNM/message/1373
[Rich Murray notes:
As a medical layman, noting that all readers are laymen
for any topic outside the bounds of their specific expertise,
I found related abstracts that illucidate the role of cytochrome
P450 enzymes, especially the one most affected by aspartame,
CYP2E1,
in brain toxicity processes involving ethanol and methanol,
suggesting avenues of research for alcohol addiction and hangover,
and the possibilies of aspartame liver and brain toxicity
from its 11% methanol component.]
"A major finding in this study was that the daily
consumption of ASP at the two doses considered
leads to an increment in the concentration and activity
of CYP2B1/2, CYP2E1 and CYP3A2
in rat cerebral and cerebellar microsomes....
The highest increment (up to 25-fold over controls)
in a CYP-associated activity induced by ASP in brain
was that of 4-NPH corresponding to CYP2E1.
The results mentioned above must be reproduced
using a broad range of ASP concentrations in order
to define the existence of a dose-related effect.
As far as we know, this is the first report regarding
modulation of brain CYPs by the widely used
sweetener ASP.
Specific induction of brain CYPs could constitute
a local regulatory mechanism of enzyme activity,
thus influencing drug response;
for tissues exhibiting low regenerative capacity,
such as the brain,
such modulation would probably be
of major toxicological significance....
It has already been said that once ASP enters the
organism, it is rapidly metabolized by intestinal
esterases and dipeptidases to
aspartic acid,
phenylalanine
and methanol,
substances normally found in the diet and body. 37
One hour after ASP intake at a dose of 200 mg/kg
body weight by rats,
corresponding to the acceptable FDA daily intake for the
sweetener after species correction,
increased plasma and brain phenylalanine levels by 62% and 192%
respectively. 6
With regard to methanol,
it accounts for about 10% of the ASP weight administered. 38
We can hypothesize that the exposure to methanol at
the two regimens used in this study
about 7.5 and 12.5 mg/kg from the doses of 75 and 125 mg/kg)
could induce xenobiotic-metabolizing enzymes in a
similar way to that of the chronic administration of
ethanol. 39....
If methanol is the metabolite
responsible for the induction of brain CYP2E1 seen in this work,
the question of why the hepatic CYP2E1 was not altered remains.
Experiments with the three metabolites resulting from ASP
metabolism are currently being undertaken in our
laboratory in order to address this question.
In conclusion, data obtained demonstrated that a
daily consumption of ASP at doses of 75 and 125 mg/kg
body weight over 30 days provokes
a substantial increment in CYP enzymes
involved in endogenous and exogenous molecules metabolism
in the CNS of the rat.
Biological consequences of this
phenomenon should be investigated in view of
the high number of humans exposed to this artificial
sweetener and because of the recent data
indicating the potential carcinogenic effects of this
compound. 41"
Hum Exp Toxicol. 2006 Aug; 25(8): 453-9.
The effect of aspartame on rat brain xenobiotic-metabolizing
enzymes.
Vences-Mejia A 1,
Labra-Ruiz N 1,
Hernandez-Martinez N 1,
Dorado-Gonzalez V 1,
Gomez-Garduno J 1,
Perez-Lopez I 1,
Nosti-Palacios R 1,
Camacho Carranza R 2,
Espinosa-Aguirre JJ 2.
Laboratorio de Toxicologia Genetica,
1: Instituto Nacional de Pediatria, Insurgentes Sur, 3700-C,
04530 Mexico, DF Mexico.
2: Instituto de Investigaciones Biomédicas, UNAM,
Apartado postal 70228,
Ciudad Universitaria 04510 México, D.F., México
http://www.biomedicas.unam.mx/index.asp
*Correspondence: JJ Espinosa-Aguirre,
Instituto de Investigaciones Biome´dicas, UNAM,
Apartado postal 70228, Ciudad Universitaria 04510
Me´xico, D.F., Me´xico
Human & Experimental Toxicology (2006) 25(8): 453 - 459.
www.sagepublications.com
c 2006 SAGE Publications 10.1191/0960327106het646oa
[ Dra. Araceli Vences M
Jefa de Laboratorio de Toxicologia Genetica
6° P de Hospital Laboratorios
10 84 09 00 Ext.1410 -1448
aritaven@yahoo.com.mx;
ISRAEL PÉREZ LÓPEZ,
JAVIER J. ESPINOSA AGUIRRE,
jjea@servidor.unam.mx;
http://www.biomedicas.unam.mx/invest...rame.asp?ID=MG ]
Abstract
This study demonstrates that chronic aspartame (ASP)
consumption leads to an increase of phase I metabolizing enzymes
(cytochrome P450 (CYP)) in rat brain.
Wistar rats were treated by gavage with ASP
at daily doses of 75 and 125 mg/kg body weight for 30 days.
Cerebrum and cerebellum were used to obtain microsomal
fractions to analyse activity and protein levels of seven
cytochrome P450 enzymes.
Increases in activity were consistently found with the 75 mg/kg
dose both in cerebrum and cerebellum for all seven enzymes,
although not at the same levels:
CYP2E1-associated 4-nitrophenol hydroxylase (4-NPH) activity
was increased 1.5-fold in cerebrum and 25-fold in cerebellum;
likewise, CYP2B1-associated penthoxyresorufin O-dealkylase
(PROD) activity increased 2.9- and 1.7-fold respectively,
CYP2B2-associated benzyloxyresorufin O-dealkylase (BROD)
4.5- and 1.1-fold,
CYP3A-associated
erythromycin N-demethylase (END)
1.4- and 3.3-fold,
CYP1A1-associated ethoxyresorufin O-deethylase (EROD)
5.5- and 2.8-fold,
and CYP1A2-associated methoxyresorufin O-demethylase
(MROD) 3.7- and 1.3-fold.
Furthermore, the pattern of induction of CYP
immunoreactive proteins by ASP paralleled that of
4-NHP-, PROD-, BROD-, END-, EROD- and
MROD-related activities only in the cerebellum.
Conversely, no differences in CYP concentration and activity
were detected in hepatic microsomes of treated animals
with respect to the controls,
suggesting a brain-specific response to ASP treatment.
PMID: 16937917
Aug 14 2006 08:07:58
Key words: aspartame; brain; cytochrome P450; enzyme induction
Introduction
Sweeteners are paid special attention among food additives,
as their use enables a sharp reduction in sugar consumption
and a significant decrease in caloric intake
while maintaining the desirable palatability
of foods and soft drinks.
Sweeteners are also of primary importance
as part of nutritional guidance for diabetes,
a disease with increasing incidence in developed countries. 1-3
Aspartame (L-asparthyl-L-phenylalanine methyl ester, ASP)
is one of the most widely used artificial sweeteners;
it is a high-intensity sweetener added to
a large variety of foods, most commonly found in
low-calorie beverages, desserts and tabletop sweeteners
added to tea or coffee.
It does not enter into the bloodstream intact,
but is hydrolyzed in the intestine
to form aspartate,
phenylalanine
and methanol,
which are then absorbed into the circulation,
elevating their levels in plasma and in brain phenylalanine
and tyrosine levels as well. 4-6
Aspartate is a highly excitatory neurotransmitter 7
and phenylalanine is a precursor of catecholamines in the brain; 8
increased levels of these molecules could change the
basic activity level of the brain to an unhealthy,
constantly stimulated state.
Short-term studies on ASP consumption and
memory loss have been conducted in humans and rodents
and no relationship was found. 9-11
On the other hand, chronic studies have implicated ASP
consumption in learning and memory.
Consumption of 9% ASP in the diet for 13 weeks affected learning
behaviour in male rats, 12
while ASP exposure of guinea pigs to 500 mg/kg during gestation
disrupted odour-associative learning in pups. 13
Recently, Christian et al. reported that chronic ASP consumption
lengthened the time it took rats to find the reward in a T-maze
and increased the number of muscarinic receptors
in specific brain areas. 14
Despite numerous toxicological studies of ASP and its components,
its effects on metabolic and detoxification enzyme systems
have received little attention.
Metabolic enzymes are of special interest
as changes in their function could lead to an
increased susceptibility of the organisms to the
harmful effects of a variety of contaminants found
in the environment and in food products. 15,16
The presence of cytochrome P450 (CYP) in the
central nervous system (CNS) opens the question of
whether metabolism in endothelial cells may regulate
the penetration of the xenobiotics into the
brain compartment. 17,18
The role of CYP in brain includes such diverse functions as
aromatization of androgens to oestrogens,
formation of catechols,
and it may also participate in the metabolism of
neurotransmitters and of xenobiotics. 17,19
Moreover, lipophilic xenobiotics can diffuse
through the endothelial cells of the brain capillaries
and enter the neuronal cells.
Thus, in situ activation in the neuronal cell
could have far-reaching consequences
by causing irreversible disruption of the neuronal function.
The brain is the target not only for a number of toxic compounds
but also for several psychoactive drugs.
The metabolism of drugs in the brain can lead
to local pharmacological modulation at the site of action
and can result in variable drug response. 17
The purpose of this work is to study the effect of
orally administered ASP on the activity of CYP in
the CNS of the rat.
The characterization of brain specific CYP
and its regulation and localization within the CNS
is gaining importance for the understanding
of the potential role of these enzymes in the
pathogenesis of neurodegenerative disorders and in
the psychopharmacological modulation of drugs
acting on the CNS. 17
__________________________________________________ __
brief aspartame research review: Rich Murray 2008.02.10
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1516
__________________________________________________ __
http://groups.yahoo.com/group/aspartameNM/message/1513
metabolic syndrome is tied to diet soda, PL Lutsey, LM Steffen,
J Stevens, Circulation 2008.01.22: role of formaldehyde and
formic acid from methanol in wines, liquors, or aspartame?:
Murray 2008.02.07
"But the one-third who ate the most fried food increased their risk
by 25 percent, compared with the one-third who ate the least, and
surprisingly, the risk of developing metabolic syndrome was 34
percent higher among those who drank one can of diet soda a day
compared with those who drank none.
"This is interesting," said Lyn M. Steffen, an associate professor of
epidemiology at the University of Minnesota and a co-author of the
paper, which was posted online in the journal Circulation on Jan. 22.
"Why is it happening? Is it some kind of chemical in the diet soda,
or something about the behavior of diet soda drinkers?""
"The diet soda association was not hypothesized
and deserves further study."
http://groups.yahoo.com/group/aspartameNM/message/1511
vinyl acetate, ethyl alcohol, or aspartame in womb increases later
cancers in adults with lifetime exposure in many studies, M Soffritti
et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.:
Rich Murray 2008.02.07
http://groups.yahoo.com/group/aspartameNM/message/1495 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://groups.yahoo.com/group/aspartameNM/message/1490
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://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11
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/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://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/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31
http://groups.yahoo.com/group/aspartameNM/message/1455
FEMA slow to safety test Katrina toxic trailers, Charles Babington,
Associated Press -- 1 ppm formaldehyde in air is about half the
daily dose from 3 cans aspartame diet soda and ten times the
1999 EPA alarm level for drinking water: Murray 2007.07.23
"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@comcast.net
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 120 members, 1,517 posts in a public archive
http://groups.yahoo.com/group/aspartameNM/message/1510
how to send aspartame info to
Hawaii House of Representatives Health Committee
for 8 AM Friday Feb. 8 session: Rich Murray 2008.02.06
http://rmforall.blogspot.com/2008_02_01_archive.htm
Wednesday, February 6, 2008
bias, omissions, incuriosity = opportunity, aspartame safety
evaluation, Magnuson BA, Burdock GA, Williams GM, 7 more,
2007 Sept, Ajinomoto funded 98 pages html [ $ 32 pdf ]:
Murray 2007.09.15
http://rmforall.blogspot.com/2007_09_01_archive.htm
Saturday, September 15, 2007
__________________________________________________ __
old tiger roars -- Woodrow C Monte, PhD -- aspartame causes manybreast cancers, as ADH enzyme in breasts makes methanol from diet soda intocarcinogenic formaldehyde -- same in dark wines and liquors, Fitness Life 2008 
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