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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

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  • Rich Murray
    old tiger roars -- Woodrow C Monte, PhD -- aspartame causes many breast cancers, as ADH enzyme in breasts makes methanol from diet soda into carcinogenic
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      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@...;

      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@...;


      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@...;
      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.

      Reference List For All Three Recent Articles

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      http://www.thetruthaboutstuff.com/#
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      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

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      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 ]

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      http://www.thetruthaboutstuff.com/published/
      Your%20Health%2033%20-2.pdf

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      http://www.thetruthaboutstuff.com/charts/
      Autism%20USA.pdf

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      Breast%20Cancer%20USA%20A.pdf

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      http://www.thetruthaboutstuff.com/charts/
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      http://www.thetruthaboutstuff.com/charts/
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      http://www.thetruthaboutstuff.com/review2-german.shtml

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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/cgi/content/full/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@...;

      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@...;

      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/content/full/39/3/155
      free full text

      Alcohol & Alcoholism Vol. 39, No. 3, pp. 155-165, 2004
      Alcohol & Alcoholism Vol. 39, No. 3
      © 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@...-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.

      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,
      <br/><br/>(Message over 64 KB, truncated)
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