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1825check out methanol as multiple sclerosis toxin -- in humans only, ADH1 enzyme turns it into rampant formaldehyde right inside cells in 20 tissues, the WC Monte paradigm: Rich Murray 2014.06.18

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  • Rich Murray
    Jun 18, 2014
      check out methanol as multiple sclerosis toxin -- in humans only, ADH1 enzyme turns it into rampant formaldehyde right inside cells in 20 tissues, the WC Monte paradigm: Rich Murray 2014.06.18


      WC Monte text "While Science Sleeps" January 2012 -- a summary point:

      "13. The Faroe Islands are surrounded by countries with very high incidence of MS, yet the country traditionally did not have the disease represented in its population until after the occupation of large numbers of British Troops during the Second World War.
      Faroes have no trees or peat deposits and, therefore, developed methods to salt and air dry fish and other meats for preservation, unlike its neighbors, who dine on smoked foods at each meal.
      The indigenous diet of the Faroans contains no methanol."

      [ Rich Murray:
      Foods smoked over peat fires have 3 times more methanol than for wood fires.
      The northern end of Norway probably has less firewood and peat for heating and for cooking and smoking over open fires.
      A more rural lifestyle may result in lower use of aspartame and cigarettes, both major sources of methanol.
      Also far less common might be quart and gallon size jugs of unfresh tomato and fruit juices, sealed for weeks at room temperatures, in which copious methanol builds up from their pectins.
      Some homes may have methanol stoves and heaters.   ]


      top MS incidence in Shetland Islands re methanol from smoked foods via wood and peat fires, Prof. WC Monte, While Science Sleeps text 2012 Jan -- methanol and formaldehyde in particleboard, plywood, paper factories: Rich Murray 2012.05.15


      smoke from pack cigarettes gives 40 mg methanol for 20 gr tobacco, 6 tobacco methanol papers, Carl Neuberg 1926-1939, Berlin -- so methanol formaldehyde toxicity paradigm is co-factor in 18 tobacco diseases -- WC Monte gives 23 references: Rich Murray 2013.03.29


      C O'Gorman and SA Broadley, cigarettes cause MS -- give as much methanol as aspartame and unfresh juices, has blood half-life 3 hours, made into rampant formaldehyde inside human cells by ADH1 enzyme -- Prof. WC Monte paradigm: Rich Murray 2014.06.17



      Gavin Giovannoni 2014.03.22:

      "Mouse Doctor posted on the observation that the latitudinal gradient of MS incidence and prevalence has disappeared in Norway.
      Why is this Important?
      Norway was the one country that was the exception to the rule.
      Exceptions to the rule are very important they can slay hypotheses unless they can be explained.
      A previous meta-analysis showed that MS prevalence actually decreased as you went further north in Norway."
      [ map adapted from Kampman et al, 2007, showing MS prevalence about half as much in north end of Norway ]

      "Why the latitude reversal?
      The reversal in MS prevalence in Norway has been explained on dietary factors. Norwegians in the north of the country eat more fish, in particular fatty fish, and have higher vitamin D levels (see figure below).
      This observation has been used by me and others to support the vD MS hypothesis; i.e. higher levels vD protect you from getting MS."



      Lancet Neurol. 2010 May;9(5):520-32.
      doi: 10.1016/S1474-4422(10)70064-8.
      The changing demographic pattern of multiple sclerosis epidemiology.
      Koch-Henriksen N 1,
      Sørensen PS.

      Nils Koch-Henriksen MD a b Corresponding Author,
      Per Soelberg Sørensen MD c  pss@..., pss@...

      1 Department of Neurology, Aarhus University Hospital in Aalborg, Aalborg, Denmark. koch-henriksen@...

      a Department of Neurology, Aarhus University Hospital in Aalborg, Aalborg, Denmark

      b Danish Multiple Sclerosis Registry, Copenhagen, Denmark

      c Danish Multiple Sclerosis Research Centre, Department of Neurology, Neuroscience Centre, Copenhagen University Hospital, Copenhagen, Denmark


      Melinda Magyari

      Correspondence to: Nils Koch-Henriksen, Department of Neurology, Aarhus University Hospital in Aalborg, DK-9000 Aalborg, Denmark

      Abstract

      The uneven distribution of multiple sclerosis (MS) across populations can be attributed to differences in genes and the environment and their interaction.

      Prevalence and incidence surveys could be affected by inaccuracy of diagnosis and ascertainment, and prevalence also depends on survival.

      These sources of error might play a part in the geographical and temporal variations.

      Our literature search and meta-regression analyses indicated an almost universal increase in prevalence and incidence of MS over time;

      they challenge the well accepted theory of a latitudinal gradient of incidence of MS in Europe and North America,

      while this gradient is still apparent for Australia and New Zealand;

      and suggest a general, although not ubiquitous, increase in incidence of MS in females.

      The latter observation should prompt epidemiological studies to focus on changes in lifestyle in females.

      New insights into gene-environment and gene-gene interactions complicate interpretations of demographic epidemiology and have made obsolete the idea of simple causative associations between genes or the environment and MS.

      Copyright 2010 Elsevier Ltd. All rights reserved.

      PMID: 20398859


      methanol/formaldehyde paradigm for multiple sclerosis,  free full 56 page chapter 9 pdf, While Science Sleeps, 146 full text references online, Prof. Woodrow C. Monte: Rich Murray 2012.03.20



      Multiple Sclerosis: The Cause and the Solution Uncovered -- at Last!

      An exhaustive analysis of the medical and scientific literature, authored by a uniquely qualified food scientist, persuasively reveals the cause of MS and describes a path to recovery and prevention.

      The symptoms of Multiple Sclerosis are identical to those of an uncommon form of poisoning -- methanol poisoning.
      Individuals who have been exposed to this poison over a long period of time, in fact, develop MS.
      This poison -- methanol -- is a major component of cigarette smoke, which, until now, has been the only known cause of Multiple Sclerosis.

      Dr. Monte's compelling work reveals that this poison is also contained in certain foods that are canned and smoked or have had the insidious sweetener, aspartame, added to them.
      Unfortunately, the truth has been obscured due to the fact that methanol is a poison only to humans and not to (laboratory) animals.

      If you have MS, or love someone who does, you and your physician should read what Dr. Monte has to say about methanol and its link to MS.
      To expedite the free exchange of what might be lifesaving information about this disease, there is a file attached below to his website that contains a full copy of Chapter 9 of his book, While Science Sleeps.
      This chapter examines the cause of MS and posits the simple dietary changes that can save your life.

      Download a free copy of Chapter 9 and have a read
      [ 99 pages, including list of all 740 full text online references for book -- Chapter 9 has 146 references ]:


      The references are located on his website:


      as are the simple dietary changes that you must follow because your life may depend on it:


      Everything you need to know about MS is in Chapter 9.

      25 page slide show of 18 research studies showing huge increases in MS in women in warm countries since aspartame drinks became legal in the USA in July, 1983 --
      especially in the hottest months of summer.

      If you are interested in knowing more about methanol poisoning and its link to other diseases of civilization, you will want to read the entire book, While Science Sleeps, by Woodrow C. Monte PHD, Emeritus Professor of Nutrition and Food Science, Arizona State University.

      Chapter 9:
      Multiple Sclerosis

      The Conflagration that is Multiple Sclerosis;
      Listening to Nature’s Whispers;
      The Scene of the Crime;
      Location, Location, Location;
      Details of Plaque Formation;
      The Look, Touch, Taste and Smell of Multiple Sclerosis;
      The Kitchen Autopsy;
      The Cause of MS is within the Thickening Blood Vessels;
      Symptoms Mean Little Unless They Are Identical in All Ways…Then They Mean Everything!;
      Learn a Little About Arginine;
      Myelin Basic Protein (MBP);
      Looking for the Shadow of Formaldehyde;
      “Woody… They Have Done Our Experiment for Us.… But They Just Don’t Get It!”;
      Finding the Shadow of Formaldehyde in the MS Brain: The Smoking Gun (a Triple Blind Study);
      Evidence That Methanol Causes MS;
      The Etiology of Multiple Sclerosis -- Follow the Methanol;
      A Food Scientist’s Nightmare Called Aspartame;
      MS: a Disease of Colder Climates and Flush Toilets -- Before Aspartame;
      A World Awash in MS after Aspartame;
      Change in Frequency of MS by Sex:
      the Methanol Source -- Food or Smoke -- Makes All the Difference;
      Can Methanol Really Cause MS?;
      MS Can Be Found in Some Places, but Cannot be Found in Others;
      Industrial Exposure to Methanol -- Jobs that Can Last for an Eternity;
      Teachers’ Paradigm;
      MS Treatment -- Pharmaceutical Placebos or Perhaps Worse;
      Conclusion and Review;

      Conclusion and Review

      You can see for yourself now that the daily administration of methanol to the human organism does not go unnoticed by the immune system.
      The evidence is simply far too overwhelming for the pharmaceutical industries to credibly justify ignoring it any longer.
      As a scientist I can do little more than present a coherent molecular theory, and then prove the hypothesis using three paradigms with two distinct methods of methanol administration.
      Viewing methanol toxicity as the etiologic cause of MS answers all of the nagging questions and unexplained anomalies that have stalled the search for the cause of this disease.
      I realize that absolutely nothing can convince the pharmaceutical giants, who are now heavily invested in developing their own useless palliatives for MS, to give them up and rally around the methanol hypothesis.
      In the end, however, I believe that the truth will win out.
      Henry Miller prophesied over 50 years ago:
      It is possible that the cause of multiple sclerosis lies buried somewhere in these lengthy protocols waiting to be found by someone ingenious enough to unearth it.[#306]

      Review

      1. MS is a disease that begins around brain blood vessels, adjacent to the exact locations where methanol converts to formaldehyde, very much like Alzheimer’s Disease.

      2. MS was first discovered long before formaldehyde, making the determination of its cause impossible.

      3. The vast majority of early researchers believed that the cause of MS was a “toxic substance” that forms in and is distributed via the blood vessels of the brain. “Whatever is being produced within the vessel walls is the cause of the disease.”

      4. All symptoms of MS can be found during the course of methanol poisoning if the patient lives long enough.

      5. Myelin Basic Protein (MBP) is the protein of the myelin sheath that is removed during MS plaque development.
      MBP contains a high percentage of arginine, which acts as a trap for formaldehyde.
      The MBP of MS patients has been shown to have reacted with formaldehyde and cause a marked increase of the methylation of its arginine.

      6. The MBP of MS brain tissue has been shown to be severely deficient in phosphorylation, which we know can be caused by formaldehyde.

      7. The Smoking Paradigm: Cigarette smoke is high in methanol and is the only etiological cause of MS that is generally accepted by the scientific community.

      8. Consistent circumstantial evidence links increases in methanol-containing food consumption and in industrial use of methanol to corresponding increases in MS incidence during the transition from the 19th century into the 20th century.

      9. The advent of aspartame, a methanol carrier, has introduced an opportunity to quantify additional methanol in the food supply since 1981.

      10. The Aspartame Paradigm: statistics show convincingly that as more and more aspartame is consumed by the US population the incidence of -- and perhaps more importantly the death rate from -- MS has also increased dramatically.

      11. The higher incidence of MS in colder climates was due to the higher consumption levels of canned fruits and vegetables in temperate climates.
      This began reversing shortly after methanol-containing diet sodas and other thirst quenching products became popular and inexpensive in the tropics.

      12. MS was at one time a disease of men when it was caused by industrial contact.
      It is increasingly more of a women’s disease.
      When methanol is inhaled as a gas during cigarette smoking or industrial contamination the distribution tends to be equal between the sexes.
      The stomach of the man, however, has 4 or 5 times more ADH in its lining than that of a woman.
      When methanol is consumed via diet soda, the ADH removes methanol before it can get to the brain, so less of it reaches men’s brains than women’s brains.
      As more and more methanol has become a dietary poison, the shift from male to female disease has followed.

      13. The Faroe Islands are surrounded by countries with very high incidence of MS, yet the country traditionally did not have the disease represented in its population until after the occupation of large numbers of British Troops during the Second World War.
      Faroes have no trees or peat deposits and, therefore, developed methods to salt and air dry fish and other meats for preservation, unlike its neighbors, who dine on smoked foods at each meal.
      The indigenous diet of the Faroans contains no methanol.

      14. The Village of Wellington, Ohio experienced an epidemic of MS that should have been traced to the escape of methanol fumes from a foundry, affecting the populace located downwind of it.

      15. Professions such as shoemaking and papermaking that have been shown to have high incidence of MS can also be shown to have exposed their workers to levels of methanol.

      16. The Teaching Paradigm:
      The US teaching profession might just be the best profession to use to link methanol exposure to increased incidence of MS.
      Secondary school teachers suffer an incidence of MS almost twice as high as their professional counterparts.
      They also can be shown to have had consistent workday exposure to methanol fumes by the ubiquitous use of Ditto machines that use high concentrations of methanol as a print transfer agent.

      It has been over 30 years since I heard my first unsolicited plea for help from an aspartame consumer who had linked consumption of the product to her suffering. My first thought after an hour’s listening was that this courageous young woman would soon be diagnosed with Multiple Sclerosis.
      It is in her honor and in the memory of my friend from Wellington, Colorado that I seek to explain the compelling link between methanol and MS.
      [ much more ]


      welcome to the WC Monte methanol formaldehyde toxicity paradigm via this treasury of studies --  depression, diabetes, retina harm, multiple sclerosis, cancer -- crisp Michele Bouchard 2001 review -- hangovers: Rich Murray 2013.02.21


      [ in this amiable tour, repetition is deliberate... ]



      The many ill effects of diet soda

      By Ed Biado | Posted on Feb. 17, 2013 at 6:01pm | 1,244 views

      "Meanwhile, another study claims that soda may cause depression; and
      that diet soda poses a higher risk. The paper, which will be presented
      at the American Academy of Neurology meeting in March, tracked the
      beverage (soft drinks, tea, coffee, etc.) consumption of 263,925
      individuals aged 50 to 71 for two years and looked for links between
      that and depression 10 years later.

      Based on the data collected, which included more than 11,300
      participants diagnosed with depression within the period, the
      researchers found that the risk of depression was slightly higher
      among consumers of low-calorie (artificially sweetened) drinks than
      among consumers of high-calorie (naturally sweetened) drinks.

      Aspartame, again, is suggested to be the culprit."


      NIH Study Links Diet Drinks to Depression
      6 Comments
      By Lisa Garber
      Natural Society
      January 17, 2013

      A new study by the National Institutes of Health has linked diet beverages with heightened risk of depression in older adults.

      Researchers surveyed over 260,000 adults aged 50 to 71 in the United States on their beverage habits.

      Ten years later, survey responders were asked if they had been diagnosed with depression.

      Of those who reported consuming four or more daily servings of artificially sweetened soda, iced tea, or fruit drinks, 31 percent had been diagnosed.

      Twenty-two percent of regular soda drinkers reported depression diagnoses.

      Coffee drinkers (four or more cups a day), on the other hand, were 10 percent less likely to suffer depression than non-coffee drinkers.

      “Our research suggests that cutting out or down on sweetened diet drinks or replacing them with unsweetened coffee may naturally help lower your depression risk,” researcher Honglei Chen said. “More research is needed to confirm these findings.”

      Dr. Honglei Chen, a US National Institute of Environmental Health Sciences investigator, agrees with many in the scientific community that “research is preliminary and more investigation into the topic is needed.”

      Eva Redei, a psychiatry professor at the Northwestern University Feinberg School of Medicine in Chicago noted that diet beverages’ correlation to depression may have many prongs, like diabetes and obesity, both of which come with greater incidences of depression.

      Consumers with diabetes or who are obese may drink diet beverages with the intent of helping their weight or blood sugar.

      Findings will be presented at the American Academy of Neurology’s annual meeting in March. The study is also preliminary and has yet to be published in a peer-reviewed journal.

      The Beverage Industry Weighs In

      Predictably, the American Beverage Association turned up its nose at the study’s findings.

      “Neither this [study] nor the body of scientific evidence supports that drinking soda or other sweetened beverages causes depression.
      Thus, promoting any alleged findings without supporting evidence is not only premature, but irresponsible.”

      Diet Drinks and Other Health Conditions

      Admittedly, there’s a different between causation and correlation, and the NIH study shows the latter rather than the former.

      Still, let’s talk about responsibility.

      In the past decade, numerous studies have correlated diet drinks with nasty health conditions, including:

      Kidney failure -- In an 11-year study, there was a strong positive correlation found between degeneration of kidney function and consumption of aspartame-containing diet soda.

      Heart attack and stroke -- Researchers found that diet soda consumption was linked to a 44 percent higher chance of heart attack or stroke, up from the 22 percent non-soda drinkers have.

      Obesity -- Research from Texas involving 474 individuals shows found that consuming two or more diet sodas a day prompts an increase in waist size.
      In fact, the increase was a shocking six times greater than those who did not drink diet soda.

      Cell damage -- Peter Piper of the University of Sheffield says these chemicals “have the ability to cause severe damage to DNA in the mitochondria to the point that they totally inactivate it.

      While correlation is not causation, perhaps the ABA should be taking these concerns into consideration while driving their huge paychecks to the bank.



      American Academy of Neurology Meeting, March 16-23 2013, San Diego
      San Diego Convention Center

      2,300 scientific abstracts that will be presented at the 65th Annual Meeting

      more than 12,000 attendees at last year's meeting in New Orleans, including:
      2012 US attendees: 5,678
      2012 international attendees: 3,588

      (800) 879-1960
      (612) 928-6000

      [P05.122]
      Sweetened-Beverages, Coffee, and Tea in Relation to Depression among Older US Adults
      Authors:
      Honglei Chen, Research Triangle Park, NC,

      Aging & Neuroepidemiology Group
      Etiology of Parkinson's Disease
      Honglei Chen, M.D., Ph.D.
      Tenure-Track Investigator
      Tel (919) 541-3782
      Fax (919) 541-2511
      Curriculum Vitae  (178KB)
      P.O. Box 12233
      Mail Drop A3-05
      Research Triangle Park, North Carolina 27709

      Xuguang Guo, Durham,
      Yikyung Park, Rockville, MD,
      Neal D. Freedman, Rockville,
      Rashmi Shinha, Rockville,
      Albert Hollenbeck, Washington, DC,
      Aaron Blair, Rockville, MD

      Date/Time:
      Wednesday, March 20, 2013 - 2:00 PM

      Session Info:
      Session P05:
      Behavioral Neurology: Neuropsychiatry, Emotions, and Behavior
      (2:00 PM-7:00 PM)


      1 quart aspartame diet soda gives 60 mg methanol (wood alcohol), same
      dose as from smoke from a pack cigarettes -- becomes formaldehyde
      right inside cells of 19 specific tissues: Prof. Woodrow C. Monte
      breakthrough paradigm: Rich Murray 2013.02.20


      Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State
      University, retired 2004, has given detailed articles since fall 2007,
      WhileScienceSleeps.com , backed by a free online archive of 745 full
      text medical research references.


      The WC Monte January 2012 text is available at Amazon.com, "While
      Science Sleeps", low cost ebook,  backed by his online archive of 745
      free full text medical research references at WhileScienceSleeps.com ,
      while two full chapters are free: Chapter 9, "Multiple Sclerosis" and
      12, "Autism and Other Birth Defects."



      #6 diabetes 2 risk high for 2 cans aspartame diet drink weekly 14
      years 66K women study, Guy Fagherazzi et al AJCN 2013 Jan -- methanol
      (cigarettes, aspartame) formed into formaldehyde inside cells in
      pancreas by ADH1 enzyme, WC Monte paradigm: Rich Murray 2013.02.13

      The removal of methanol from the bloodstream is slow, with a half-life
      of 3 hours, while the half-life of ethanol is 1/3 hour.

      The blood carries methanol to every part of the body and fetus every minute.

      ADH1 enzyme is at high levels in 19 specific human tissues, including
      the inner walls of blood vessels (especially at the base of the brain,
      the "blood brain barrier" itself, the "perivascular loci" of both
      multiple sclerosis and Alzheimer's), purkinje brain cells in the
      vermis in the cerebullum 637, the rods and cones of the retina, the GI
      tract (especially in men), and skin and bone marrow fibroblasts.


      Bühler R., Pestalozzi D., Hess M., Von Wartburg JP.
      Immunohistochemical localization of alcohol dehydrogenase in human
      kidney, endocrine organs and brain.
      Pharmacol Biochem Behav. 1983;
      18 Suppl 1:55-9 1983;18(Suppl 1):55-9.

      Ethanol at 16 times less molar concentration than methanol will
      preoccupy ADH1, becoming mildly toxic acetaldehyde -- when blood
      ethanol falls, methanol is made into free floating, highly reactive
      acidic hydrated formaldehyde, which binds on both sides to the nearest
      DNA, RNA, and basic proteins, such as Myelin Basic Protein, which when
      formaldehyde modified, strongly attract white blood cells, monotypes,
      microglia, and macrophages, leading to pussy lesions, that grow or
      subside erratically along with dietary exposures to methanol and the
      antidote ethanol.

      Formaldehyde quickly and firmly methylates DNA, leading to cell
      malfunction and apoptosis, later cancers, and birth defects spina
      bidifa, autism, preterm birth and Fetal Alcohol Syndrome.

      Formaldehyde strongly impairs two enzymes in the mitochrondria,
      shutting down the aerobic ATP energy cycle, impairing critical
      biochemistry, including vision in the retina, and leading to anaerobic
      metabolism, with resulting blood acidosis from lactic acid.

      The smoke from a pack of cigarettes (also wood and peat smoke) gives
      60 mg methanol, as much as from a litre aspartame diet drink, while
      methanol also comes from dark wines and liquors, fresh tomatoes,
      unfresh fruits juices vegetables cut and preserved wet at room
      temperature in sealed cans jars plastic containers, smoked fermented
      spoiled foods, jams jellies marmalades, some fresh coffees, medical
      and mortuary labs and schools, the wood, paper, and solvent industries
      -- so the epidemiology is extremely complex and so far not inclusive
      of the many factors.

      Probably, cigarette diseases are to a large degree chronic
      methanol-formaldehyde toxicity disorders.

      All these diseases give twice the harm for those who never drink
      ethanol as those who have only 1 standard drink daily, due to the
      ethanol blocking formaldehyde formation from methanol by ADH1 enzyme.

      Men, who have several times more ADH1 in the GI tract, have less
      methanol reaching the brain, so far more women have eye and brain
      diseases, such as multiple sclerosis.


      comment #6 to ESFA draft aspartame safety report, due for public
      release May 2013

      [ [ Rich Murray comments in square brackets ] 3797 characters

      line 3202
      risk of lymphatic and haematopoietic cancers in relation to diet soda
      and aspartame sweeteners [ was shown ] E Schernhammer et al., 2012

      [ This study just found strong disease risks with same size cohort for
      > 14 y low diet soda, only 1-2 cans weekly ]


      Fagherazzi G et al, Am J Clin Nutr 2013 Jan 30
      Institut National de la Santé et de la Recherche Médicale U1018,
      Center for Research in Epidemiology and Population Health,
      Villejuif, France.

      Abstract

      sugar-sweetened beverages (SSBs) --
      risk of type 2 diabetes (T2D) --
      artificially sweetened beverages (ASBs) ?

      66,118 women 1993 -- 2007, 1369 incident cases T2D

      Compared with nonconsumers,
      women in the highest quartiles of SSB and ASB consumers
      were at increased risk of T2D with
      HRs (95% CIs) of 1.34 (1.05, 1.71)
      and 2.21 (1.56, 3.14) for women who consumed
      >359 and >603 mL/wk of SSBs and ASBs, respectively

      [ Ethanol is an antidote that prevents ADH1 enzyme from making
      methanol into formaldehyde right inside cells in 19 specific human
      tissues, including pancreas -- major cause of hangovers, probable
      diabetes 2 co-factor -- hangovers and other formaldehyde toxicity
      disorders start only when blood ethanol levels fall to 16 times less
      molar concentration than blood methanol, "the morning after the night
      before", as blood ethanol half life is 1/3 hour, while blood methanol
      half life is 3 hours, reaching all parts of the body and the fetus
      every minute with the blood circulation.

      Human ADH1 enzyme is high within the cells of 19 specific tissues:
      inner walls of blood vessels, retina rods and cones, skin and bone
      marrow fibroblasts, and the islands of Langerhans in the pancreas.

      Also, the smoke from a pack of cigarettes gives as much methanol, 60
      mg, as from a liter aspartame diet soda -- so this may be the actual
      toxin that causes the correlation of cigarettes with Alzheimer's and
      multiple sclerosis, atherosclerosis, diabetes 2, many chronic
      diseases, many cancers, and birth defects spina bifida, autism,
      preterm birth.

      ADH1 is "unusually highly concentrated" in the million tiny "islands
      of Langerhans" in the pancreas, where the beta cells make insulin --
      cigarette use pairs with diabetes 2 risk, with a doubling of risk for
      smoking over a pack daily.
      [ page 172, "While Science Sleeps", 2012 January, Prof. Woodrow C.
      Monte, Food Science and Nutrition, Arizona State University, retired
      2004
      www.WhileScienceSleeps.com includes free online archive of 745 full
      text medical research references:



      Bühler R., Pestalozzi D., Hess M., Von Wartburg JP.
      Immunohistochemical localization of alcohol dehydrogenase in human
      kidney, endocrine organs and brain.
      Pharmacol Biochem Behav. 1983;
      18 Suppl 1:55-9 1983;18(Suppl 1):55-9.


      Willi C., Bodenmann P., Ghali WA., Faris PD., Cornuz J.
      Active smoking and the risk of type 2 diabetes: a systematic review
      and meta-analysis.
      JAMA 2007;298(22):2654-64.


      Wei M, Gibbons L, Mitchell T, Kampert J, Blair S.
      Alcohol intake and incidence of type 2 diabetes in men.
      Diabetes Care 2000;23(1):16-21. Ming Wei mwei@... ]

      All these diseases, including diabetes 2, are twice as harmful for
      those who never drink ethanol, compared to those who have just one
      standard drink a day, due to the inhibition of formation of
      formaldehyde from methanol by ADH1.

      Ethanol is also made by fermentation by bacteria in the colon.


      #3, methanol leaves retained formaldehyde, with similar symptoms as
      multiple sclerosis for eye and brain, comment re EFSA aspartame
      review: Rich Murray 2013.01.17

      Prof. Woodrow C. Monte,
      page 17, Chapter 3, "While Science Sleeps" textbook 2012 January
      (Kindle Locations 806-812)

      "The ADH enzyme is found dissolved in the cell’s fluid, or cytosol. 531
      This makes ADH a free agent that can float around the cell
      unencumbered, releasing formaldehyde from methanol wherever it happens
      to be within the cell at the time.
      Nothing can then restrain the reactive formaldehyde;
      it is free to leave the cell or travel to the nucleus or other
      sensitive areas within the cell, where serious damage (such as
      methylation [ of DNA and RNA]) can be done.
      Whether within the cell or outside it, the necessary enzyme that would
      [ safely] convert formaldehyde to the next metabolite, formic acid,
      is, at the very least, a considerable distance away...

      Vision is the one major responsibility of ADH that is well understood,
      and the retina is one of the sites where ADH is located.
      In fact, ADH is the enzyme that makes vision possible 663 by
      metabolizing the alcohol form of Vitamin A, which begins the process
      that initiates the eye’s signal to the brain.
      This connection of ADH to vision can account for the phenomenon of
      blindness, both temporary and permanent, and other strange visual
      signs and symptoms associated with both methanol toxicity and multiple
      sclerosis."


      663. free full text pdf 10 pages [ total 745 free references available ]
      Eur. J. Biochem. 267, 4315-4324 (2000) c FEBS 2000
      Families of retinoid dehydrogenases regulating vitamin A function
      Production of visual pigment and retinoic acid
      Gregg Duester

      WSS text, pages 35, Chapter 4.2  (Kindle Locations 1300-1306):

      "Formaldehyde is slowly being produced within the lining of the
      circulatory system of the brain and diffusing outward into the tissue,
      and attaching itself to the MBP.
      The macrophages are then called in to remove all the
      formaldehyde-damaged MBP that is in its wake. [ Myelin Basic Protein ]

      It is the intermittent production of formaldehyde in the lining of the
      circulatory system of the brain, beyond the blood brain barrier, that
      turns on when methanol from the diet is high and ethanol [which
      prevents formaldehyde formation] from [fermentation by bacteria in]
      the colon is low, that [then] is more likely to lead to the slow
      progression of the perivascular plaque, which is the discerning
      feature of multiple sclerosis."
      [ end of comment 3 ]



      "Methanol travels easily to breast tissue and has been found in human milk. 219

      The cells that produce milk within the breast, cells prone to develop
      the most common of breast cancers, adenocarcinoma 358, contain high
      levels of ADH1 enzyme, 358 allowing methanol's conversion to
      formaldehyde [ inside the cells as free floating highly reactive
      acidic hydrated formaldehyde ].

      Mammary epithelial cells have no way to protect themselves from
      formaldehyde 216 -- no means to render it harmless.

      They, unlike other breast tissue, contain no aldehyde dehydrogenase
      enzyme 216 (ADH 3) that could transform formaldehyde into the
      non-carcinogenic formic acid.

      Of particular interest are recent findings implicating ADH as playing
      a pivotal role in the formation of breast cancer, documenting a
      greater incidence of the disease in women with higher levels of ADH1
      activity in their breasts. 357"



      Labreche F, Goldberg M.
      Exposure to Organic Solvents and Breast Cancer in Women: A Hypothesis.
      American Journal of Industrial Medicine 1997;32:1-14.


      Triano E, Slusher L, Atkins T, Beneski J, Gestl S.
      Class I Alcohol Dehydrogenase Is Highly Expressed in Normal Human
      Mammary Epithelium but not in Invasive Breast Cancer: Implications for
      Breast Carcinogenesis.
      Cancer Research Arch 2003;63:3092-100.

      Crabb D, Matsumoto M, Chang D, You M.
      Overview of the role of alcohol dehydrogenase and aldehyde
      dehydrogenase and their variants in the genesis of alcohol-related
      pathology.
      Proceedings of the Nutrition Society 2004;63:49-63.

      Coutelle C.
      Risk Factors in Alcohol Associated Breast Cancer: Alcohol
      Dehydrogenase Polymorphism and Estrogens.
      International Journal of Oncology 2004;25:1127-32.


      similar macular harm in multiple sclerosis as from formaldehyde made
      by ADH enzyme inside retina capillary walls from methanol, Prof.
      Woodrow C. Monte text "While Science Sleeps" 2012 Jan -- some quotes
      re retina harm: Rich Murray 2012.05.10

      WSS text, pages 35, Chapter 4.2  (Kindle Locations 1300-1306):

      "Imagine, for instance, what would be the outcome if the body’s immune system decided that the major protein that makes up the myelin sheath of the brain, myelin basic protein (MBP), was marked for destruction.
      This appears to be exactly what happens during the DOC multiple sclerosis.
      [ novel modern Diseases Of Civilization ]
      The problem with the theory -- that multiple sclerosis is an autoimmune disease -- is that not all the MBP is attacked simultaneously.
      There is a selectivity to the attacks.
      The MBP closest to the lining of the veins and arteries is attacked first, with a slow progression further and further away from the veins, taking, in some cases, years to travel a centimeter.
      If the immune system had sent out a message to attack MBP, it would disappear simultaneously and rapidly over the entire brain.
      Such a message would be an antibody against MBP, but this is only occasionally found in MS, and when it is, it is not particularly effective. 475

      This phenomenon can have only one explanation.
      Formaldehyde is slowly being produced within the lining of the circulatory system of the brain and diffusing outward into the tissue, and attaching itself to the MBP.
      The macrophages are then called in to remove all the formaldehyde-damaged MBP that is in its wake.

      It is the intermittent production of formaldehyde in the lining of the circulatory system of the brain, beyond the blood brain barrier,
      that turns on when methanol from the diet is high
      and ethanol [which prevents formaldehyde formation] from the colon is low,
      and that is more likely to lead to the slow progression of the perivascular plaque,
      which is the discerning feature of multiple sclerosis."


      WSS text, pages 73-4 Chaper 6 (Kindle Locations 2218-2223)

      "The formaldehyde produced at ADH sites throughout the body has the ability to turn off oxidative respiration within any cells that it penetrates.
      If this occurs in the liver, muscle cells, brain, or any other high-energy cell type, the affected cells will immediately begin the change over to anaerobic respiration and lactic acid levels will surge in the blood, eventually overpowering the body’s ability to neutralize the acid -- and ultimately resulting in full blown acidosis.

      Formaldehyde will also react directly proteins in the blood, making them more acidic, which will compound the acidity.
      Acidosis itself is never deadly, but it is symptomatic of insufficient respiration.

      How does this type of reaction affect one’s vision?
      Visual symptoms of methanol poisoning and acidosis are related in a very interesting way.
      One of the most energy intensive organs of the body is the retina, which requires a very large amount of ATP to make vision work.
      The rod and cone cells of the retina, which respectively are responsible for black and white and color vision, contain large numbers of mitochondria.
      The cone cells have higher mitochondria counts than the rods, indicating that color vision is a higher energy process.
      Cone cells come in three types: red, green and blue, each with a different energy requirement.

      The retina is an ADH site that, during methanol poisoning, acts as a formaldehyde generator.
      Imagine the ADH of the retina generating formaldehyde molecules that disperse throughout the retina.
      Those that make it to the mitochondria will act to turn off the flow of vital ATP to support vision.
      The effect is different for each type of cell, thus explaining the sequencing of color changes and some of the other bizarre color vision distortions, reported by those poisoned by methanol.
      The highest concentration of cones occurs in the macula of the retina, which is responsible for the sharpest vision.
      The high density of ADH explains the blurring of vision and, eventually, when the formaldehyde levels rise to a high enough level, the death of the rod and cone cells, resulting in permanent blindness.
      Even if the cells were not killed outright, enough mitochondria could be disabled to require their replacement -- a very time consuming process."


      WSS text, pages 129-30 Chapter 9, Multiple Sclerosis,  (Kindle Locations 3712-3723)
      free full text

      [ Download a free copy of Chapter 9 and have a read
      [ 99 pages, including list of all 740 full text online references for
      book -- Chapter 9 has 146 references ]:

      09%20(Prepublication%20copy)%20Website%203-15-2012.pdf


      autism as a birth defect from epigenetic methylation by formaldehyde made from methanol by ADH1 enzyme inside Purkinje cells in vermis in cerebellum and in inner walls of brain blood vessels -- Prof. WC Monte paradigm:  Rich Murray 2013.04.26


      Other resulting modern chronic brain diseases include Alzheimer's, multiple sclerosis, ALS, depression, Fetal Alcohol Syndrome, and many cancers.

      The major sources of methanol are the smoke from a pack of cigarettes, 40 mg, the same as from 2 cans aspartame diet drink.  In all likelihood, methanol is the actual toxin that causes most cigarette diseases, making it relevant that most of these diseases clearly originate in tissues high in ADH1.


      May I venture to introduce a new candidate for a toxic cause of autism -- briefly, methanol (wood alcohol) (about the same doses from cigarette smoke, aspartame, and unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers) quickly enters the blood and travels with the blood, with half-life 3 hours, to the whole body and the fetus every minute -- only in 20 specific human tissues with high levels of ADH1 enzyme, is the methanol rapidly made into free floating formaldehyde right within these cells, which include the inner walls of brain blood vessels at the base of the brain, and also the Purkinje cells in the vermis of the cerebellum:

      Chapter 12 "Autism and Other Birth Defects, free at www.WhileScienceSleeps, Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, with 745 free online full text medical research references:

      " ... our methanol poisoned rat pups lost Purkinje cells preferentially from a very specific area of the cerebellum called the vermis.  This meant little to me at the time but it has now been discovered the cerebellum is known to be preferentially damaged in human autism, 622   and the vermis 570 and hippocampus are the particular areas of the cerebellum most damaged and reduced in volume by the disease. 571 ..."


      622.  Allen G., Courchesne E.
      Differential effects of developmental cerebellar abnormality on cognitive and motor functions in the cerebellum: an fMRI study of autism.
      Am J Psychiatry 2003;160(2):262-73.
      Eric Courchesne ,


      570. Mitchell S, Reiss A, Tatusko D, Ikuta I, Kazmerski D, Botti J, et al.
      Neuroanatomic alterations and social and communication deficits in monozygotic twins discordant for autism disorder.
      Am J Psychiatry 2009;166(8):917-25.
      Wendy R Kates ,
      "...our study replicates previous findings of an enlarged dorsolateral prefrontal cortex, reduced areas of the corpus callosum, and decreased posterior cerebellar vermis in autism and demonstrates that neuroanatomic alterations are closely associated with phenotypic features of autism in children who are severely affected."

      571.  Webb S, Sparks B, Friedman S, Shaw D, Giedd J, Dawson G, et al.
      Cerebellar vermal volumes and behavioral correlates in children with autism spectrum disorder.
      Psychiatry Res 2009;172(1):61-7.
      Sara Jane Webb ,


      WC Monte provides similar robust lines of evidence to apply his paradigm to Alzheimer's, depression, multiple sclerosis, ALS, lupus, atherosclerosis, diabetes 2, arthritis, many cancers, and birth defects, spina bifida, preterm birth, and Fetal Alcohol Syndrome.


      The major sources of methanol are the smoke from a pack of cigarettes, 40 mg, the same as from 2 cans aspartame diet drink.  In all likelihood, methanol is the actual toxin that causes most cigarette diseases, making it relevant that most of these diseases clearly originate in tissues high in ADH1.


      Here are a few early reviews and studies that hint at the level of
      methanol in the blood that causes painful alcohol hangover symptoms:

      methanol (formaldehyde, formic acid) disposition: Bouchard M et al,
      full plain text, 2001: substantial sources are degradation of fruit
      pectins, liquors, aspartame, smoke: Murray 2005.04.02

      "Exposure to methanol also results from the consumption of certain
      foodstuffs (fruits, fruit juices, certain vegetables, aspartame
      sweetener, roasted coffee, honey) and alcoholic beverages (Health
      Effects Institute, 1987; Jacobsen et al., 1988)."

      "Experimental studies on the detailed time profiles following
      controlled repeated exposures to methanol are lacking."

      "Thus, in monkeys and plausibly humans, a much larger fraction of body
      formaldehyde is rapidly converted to unobserved forms rather than
      passed on to formate and eventually CO2."

      "However, the volume of distribution of formate was larger than that
      of methanol, which strongly suggests that formate distributes in body
      constituents other than water, such as proteins."

      Toxicological Sciences 64, 169-184 (2001)
      Copyright © 2001 by the Society of Toxicology
      BIOTRANSFORMATION AND TOXICOKINETIC
      A Biologically Based Dynamic Model for Predicting the Disposition of
      Methanol and Its Metabolites in Animals and Humans.

      Michèle Bouchard *, ^,1, michele.bouchard@...,
      Robert C. Brunet, ^^ brunet@...,
      Pierre-Olivier Droz, ^
      and Gaétan Carrier * gaetan.carrier@...,

      * Department of Environmental and Occupational Health, Faculty of Medicine,
      Université de Montréal, P.O. Box 6128, Main Station, Montréal, Québec,
      Canada, H3C 3J7;

      ^ Institut Universitaire romand de Santé au Travail, rue du Bugnon 19,
      CH-1005, Lausanne, Switzerland, and

      ^^ Département de Mathématiques et de Statistique and Centre de
      Recherches Mathématiques, Faculté des arts et des sciences, Université
      de Montréal, P.O. Box 6128, Main Station, Montréal, Québec, Canada,
      H3C 3J7

      1 To whom correspondence should be addressed at Département de santé
      environnementale et santé au travail, Université de Montréal, P.O. Box
      6128, Main Station, Montréal, Québec, H3C 3J7, Canada. Fax: (514)
      343-2200.

      Received May 10, 2001; accepted August 28, 2001

      "However, the severe toxic effects are usually associated with the
      production and accumulation of formic acid, which causes metabolic
      acidosis and visual impairment that can lead to blindness and death at
      blood concentrations of methanol above 31 mmol/l (Røe, 1982; Tephly
      and McMartin, 1984; U.S. DHHS, 1993).

      Although the acute toxic effects of methanol in humans are well
      documented, little is known about the chronic effects of low exposure
      doses, which are of interest in view of the potential use of methanol
      as an engine fuel and current use as a solvent and chemical
      intermediate.

      Gestational exposure studies in pregnant rodents (mice and rats) have
      also shown that high methanol inhalation exposures (5000 or 10,000 ppm
      and more, 7 h/day during days 6 or 7 to 15 of gestation) can induce
      birth defects (Bolon et al., 1993; IPCS, 1997; Nelson et al., 1985)."

      "The corresponding average elimination half-life of absorbed methanol
      through metabolism to formaldehyde was estimated to be 1.3, 0.7-3.2,
      and 1.7 h."

      "Inversely, in monkeys and in humans, a larger fraction of body burden
      of formaldehyde is rapidly transferred to a long-term component.

      The latter represents the formaldehyde that (directly or after
      oxidation to formate) binds to various endogenous molecules..."

      "Animal studies have reported that systemic methanol is eliminated
      mainly by metabolism (70 to 97% of absorbed dose) and only a small
      fraction is eliminated as unchanged methanol in urine and in the
      expired air ( 3-4%) (Dorman et al., 1994; Horton et al., 1992).

      Systemic methanol is extensively metabolized by liver alcohol
      dehydrogenase and catalase-peroxidase enzymes to formaldehyde, which
      is in turn rapidly oxidized to formic acid by formaldehyde
      dehydrogenase enzymes (Goodman and Tephly, 1968; Heck et al., 1983;
      Røe, 1982; Tephly and McMartin, 1984).

      Under physiological conditions, formic acid dissociates to formate and
      hydrogen ions.

      Current evidence indicates that, in rodents, methanol is converted
      mainly by the catalase-peroxidase system whereas monkeys and humans
      metabolize methanol mainly through the alcohol dehydrogenase system
      (Goodman and Tephly, 1968; Tephly and McMartin, 1984).

      Formaldehyde, as it is highly reactive, forms relatively stable
      adducts with cellular constituents (Heck et al., 1983; Røe, 1982)."

      "The whole body loads of methanol, formaldehyde, formate, and
      unobserved by-products of formaldehyde metabolism were followed.

      Since methanol distributes quite evenly in the total body water,
      detailed compartmental representation of body tissue loads was not
      deemed necessary."

      "According to model predictions, congruent with the data in the
      literature (Dorman et al., 1994; Horton et al., 1992), a certain
      fraction of formaldehyde is readily oxidized to formate, a major
      fraction of which is rapidly converted to CO2 and exhaled, whereas a
      small fraction is excreted as formic acid in urine.

      However, fits to the available data in rats and monkeys of Horton et
      al. (1992) and Dorman et al. (1994) show that, once formed, a
      substantial fraction of formaldehyde is converted to unobserved forms.

      This pathway contributes to a long-term unobserved compartment.

      The latter, most plausibly, represents either the formaldehyde that
      (directly or after oxidation to formate) binds to various endogenous
      molecules (Heck et al., 1983; Røe, 1982) or is incorporated in the
      tetrahydrofolic-acid-dependent one-carbon pathway to become the
      building block of a number of synthetic pathways (Røe, 1982; Tephly
      and McMartin, 1984).

      That substantial amounts of methanol metabolites or by-products are
      retained for a long time is verified by Horton et al. (1992) who
      estimated that 18 h following an iv injection of 100 mg/kg of
      14C-methanol in male Fischer-344 rats, only 57% of the dose was
      eliminated from the body.

      From the data of Dorman et al. (1994) and Medinsky et al. (1997), it
      can further be calculated that 48 h following the start of a 2-h
      inhalation exposure to 900 ppm of 14C-methanol vapors in female
      cynomolgus monkeys, only 23 % of the absorbed 14C-methanol was
      eliminated from the body.

      These findings are corroborated by the data of Heck et al. (1983)
      showing that 40 % of a 14C-formaldehyde inhalation dose remained in
      the body 70 h postexposure.

      In the present study, the model proposed rests on acute exposure data,
      where the time profiles of methanol and its metabolites were
      determined only over short time periods (a maximum of 6 h of exposure
      and a maximum of 48 h postexposure).

      This does not allow observation of the slow release from the long-term
      components.

      It is to be noted that most of the published studies on the detailed
      disposition kinetics of methanol regard controlled short-term (iv
      injection or continuous inhalation exposure over a few hours) methanol
      exposures in rats, primates, and humans (Batterman et al., 1998;
      Damian and Raabe, 1996; Dorman et al., 1994; Ferry et al., 1980;
      Fisher et al., 2000; Franzblau et al., 1995; Horton et al., 1992;
      Jacobsen et al., 1988; Osterloh et al., 1996; Pollack et al., 1993;
      Sedivec et al., 1981; Ward et al., 1995; Ward and Pollack, 1996).

      Experimental studies on the detailed time profiles following
      controlled repeated exposures to methanol are lacking."

      "Thus, in monkeys and plausibly humans, a much larger fraction of body
      formaldehyde is rapidly converted to unobserved forms

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