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re GC Ebers study, females harmed more by body making methanol into formaldehyde in brain via ADH enzyme: 589 references, WC Monte, retired Prof. Nutrition: Rich Murray 2011.01.08

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  • Rich Murray
    re GC Ebers study, females harmed more by body making methanol into formaldehyde in brain via ADH enzyme: 589 references, WC Monte, retired Prof. Nutrition:
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      re GC Ebers study, females harmed more by body making methanol into
      formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
      retired Prof. Nutrition: Rich Murray 2011.01.08
      http://rmforall.blogspot.com/2011_01_01_archive.htm
      Saturday, January 8, 2011
      [ at end of each long page, click on Older Posts ]
      http://groups.yahoo.com/group/aspartameNM/message/1614
      [you may have to Copy and Paste URLs into your browser]
      _______________________________________________


      Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
      reseach -- methanol (11% of aspartame) puts formaldehyde into brain
      and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
      headaches: Rich Murray 2010.05.13
      http://rmforall.blogspot.com/2010_05_01_archive.htm
      Thursday, May 13, 2010
      http://groups.yahoo.com/group/aspartameNM/message/1601

      [ Other formaldehyde sources include alcohol drinks and
      tobacco and wood smoke,
      while adequate folic acid levels protect most people. ]

      http://whilesciencesleeps.com/about

      589 references, many abstracts and full texts

      Methanol: Where Is It Found? How Can It Be Avoided?

      AVOID the following, ranked in order of greatest danger:

      1. Cigarettes.
      2. Diet foods and drinks with aspartame.
      3. Fruit and vegetable products and their juices in bottles,
      cans, or pouches.
      4. Jellies, jams, and marmalades not made fresh and kept
      refrigerated.
      5. Black currant and tomato juice products, fresh or
      processed.
      6. Tomato sauces, unless first simmered at least 3 hours
      with an open lid.
      7. Smoked food of any kind, particularly fish and meat.
      8. Sugar-free chewing gum.
      9. Slivovitz: You can consume one alcoholic drink a day
      on this diet -- no more! [ no fruit brandies ]
      10. Overly ripe or near rotting fruits or vegetables.

      Selection from Article 2, Fitness Life, December 2007, and
      well discussed in the DVD video:

      "Identical Symptoms of MS, Methanol Poisoning
      and Aspartame Toxicity

      The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
      and acute methanol poisoning (13, 144, 189), and Aspartame
      toxicity (54, 58, 93, 181), are in all ways identical.

      There is nothing that happens to the human body from the
      toxic effect of methanol that has not been expressed during
      the course of MS... nothing (143, 144).

      This generalization extends even to the remarkable
      opthomological conditions common to both: transitory optic
      neuritis and retrolaminar demyelinating optic neuropathy with
      scotoma of the central visual field (which occasionally
      manifests as unilateral temporary blindness (85, 138, 163).

      In fact, these opthomological symptoms have been thought of
      for years in their respective literatures to be "tell tale"
      indications for the differential diagnosis for each of these
      maladies independently (85, 138, 148, 163, 169).

      The common symptoms of
      headache (13, 83, 181, 189),
      nervousness (13, 83, 181),
      depression (58, 83, 189, 181),
      memory loss (18, 147, 85, 169, 181),
      tingling sensations (13, 85, 168, 138, 169),
      pain in the extremities (13, 85, 169),
      optic neuritis (85, 138, 148, 163, 169),
      bright lights in the visual field (139, 83),
      seizures (21, 83, 160),
      inability to urinate or to keep from urinating (139, 146, 167)
      are all shared by each of these conditions and shared yet
      again by complaints from aspartame poisoning
      (54, 58, 93, 181).

      I take these strikingly similar symptom patterns as evidence
      that these disorders act on identical components of the
      central nervous system and in the same way.

      The "Miracle" that MS shares with Methanol poisoning

      In the early stages of MS, or when a non-lethal dose of
      methanol has been administered, complete recovery is a
      possibility.

      The only two afflictions for which such dramatic "remissions"
      are reported from identical neuromuscular and opthomological
      damage, even "blindness" is relapsing-remitting multiple
      sclerosis (85) and methyl alcohol poisoning (138, 163).

      The pathology of the two maladies is in may ways identical,
      particularly when it comes to destruction of the myelin
      sheath with no harm to the axon itself (18, 148, 176).

      Sex Ratios for MS and Aspartame Reactions

      Women bear the brunt of multiple sclerosis (91a-c) and lupus
      (SLE)(73) with fully three-fold representations in infliction
      numbers over men for both diseases.

      This is exactly the proportion represented by adverse
      reactors to Aspartame reported by the US Center for
      Disease Control in their study of 1984 (58).

      The Center found three women to every man whose
      Aspartame consumption complaints were serious enough
      to warrant investigation (93).

      Although the female/male ratio for those stricken with MS has
      always been high, recent estimates place it at over 3 to 1
      (91, 91a, 91c).

      What might account for the difference across sexes in
      incidence?

      A study published in the New England Journal of Medicine
      (94) reports biopsies of the gastric lining of men and women.

      A result was that the concentration of ADH in the
      gastric lining of men was much higher than for woman.

      Men have the advantage of removing methanol from the
      bloodstream four times faster on an equal-body-size basis
      than women.

      Thus, for men, methanol is more likely to be removed from the
      blood before it reaches the brain.

      The brain is spared but the methanol removed would still be
      metabolized to formaldehyde in the gut where it would reap
      its havoc on a more forgiving organ.

      This may help explain why men have more gastrointestinal
      complaints from both methanol and Aspartame consumption
      (93, 99).

      On the other hand, women's complaints from both more
      frequently involve serious neurological complications."...

      methanol (11% of aspartame), made by body into
      formaldehyde in many vulnerable tissues, causes modern
      diseases of civilization, summary of a century of research,
      Woodrow C Monte PhD, Medical Hypotheses journal:
      Rich Murray 2009.11.15
      http://rmforall.blogspot.com/2009_11_01_archive.htm
      Sunday, November 15, 2009
      http://groups.yahoo.com/group/aspartameNM/message/1589

      formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
      (montelukast) chewable asthma medicine causes severe allergic dermatitis in
      boy, SE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.09.27
      http://rmforall.blogspot.com/2010_09_01_archive.htm
      Monday, September 27, 2010
      [ at end of each long page, click on Older Posts ]
      http://groups.yahoo.com/group/aspartameNM/message/1613
      [you may have to Copy and Paste URLs into your browser]


      http://www.medpagetoday.com/clinical-context/MultipleSclerosis/24207

      Gene Study Suggests Why MS Is Women's Disease

      This report is part of a 12-month Clinical Context series.
      By John Gever, Senior Editor, MedPage Today
      Published: January 06, 2011
      Reviewed by Michael J. Olek, DO; Director, Newport Doctors Multiple
      Sclerosis Clinic and
      Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
      Earn CME/CE credit for reading medical news

      Action Points
      Explain to interested patients that this study shows there may be a
      genetic cause for female predominance in multiple sclerosis.
      The mystery of why multiple sclerosis predominantly strikes women may
      have been unraveled a bit, thanks to a new genetic study.
      Polymorphisms in major histocompatibility complex (MHC) genes and
      their associated DNA methylation patterns may combine with
      environmental influences in ways that promote greater susceptibility
      to the disease in women than in men, according to George C. Ebers, MD,
      FMedSci, of John Radcliffe Hospital in Oxford, England, and
      colleagues.

      Published online in Neurology, their findings were based on genomic
      analyses of more than 7,000 members of 1,055 families affected by MS.

      Ebers and colleagues noted that, 100 years ago, MS was reported to
      affect men and women about equally.

      However, in their sample, of the more than 2,100 individuals who had
      MS, 73% were female.
      They noted that published reports from around the world point to an
      approximate 2:1 ratio of female versus male MS patients.

      MS risk is believed to have a strong heritable component centered on
      MHC genes, but the reason for the female predominance has been
      unclear.
      Previous studies have ruled out genes carried on the X chromosome as
      contributing significantly to MS.

      Consequently, Ebers and colleagues sought to identify genetic or
      epigenetic factors related to MHC genes elsewhere in the genome that
      might also have discrepant associations with gender.

      The study showed that, depending on how the family members were
      related, and on the genotype for a particular MS-associated MHC gene,
      the female-to-male ratio of those with the disease differed markedly.

      The female predominance was particularly great when affected members
      of families had the HLA-DRB1*15 genotype.

      There were also considerable differences in transmission of the
      genotype from one generation to the next according to the
      relationships between affected members.

      When member pairs were related more directly -- parent-child or
      sibling-sibling -- the odds of transmission across generations
      appeared lower than when the family structure was "collateral,"
      related as aunts-uncles-nieces-nephews or as cousins.

      Within nuclear families, the odds ratio for HLA-DRB1*15 transmission
      was 2.12, compared with 3.35 for the collateral families (P=0.0046 for
      the comparison).

      The odds of transmission also were greatest in both family types when
      affected relative pairs were both female.

      The findings, according to Ebers and colleagues, suggest that
      "differential transmission of the same haplotype in families with
      affected first-degree relatives versus those consisting of second- and
      third-degree relatives reflects the inheritance of putative epigenetic
      marks."

      The researchers suggested that DNA methylation -- which can be
      affected by environmental factors and is heritable -- could be the
      "epigenetic mark" responsible for these effects, although they
      acknowledged that supporting experimental data were still lacking.

      In an accompanying editorial, a Mayo Clinic researcher pointed out
      that epigenetics provide the only plausible mechanism that could
      account for the onset of female predominance in MS.

      "Given the rapidity of increase in the sex ratio, there does not seem
      to be enough evolutionary time to spread a purely genetic risk, and
      therefore [genomic-environmental interaction] seems to be the more
      likely explanation," wrote Orhun Kantarci, MD, of Mayo's branch in
      Rochester, Minn.

      Ebers and colleagues noted that MHC genes are believed to be the
      primary genetic drivers of other autoimmune diseases, such as systemic
      lupus erythematosus and rheumatoid arthritis, that also affect far
      more women than men.

      Primary source: Neurology
      Source reference:
      Chao M, et al "MHC transmission: Insights into gender bias in MS
      susceptibility" Neurology 2011; 76: 242–46.

      Neurology. 2011 Jan 5. [Epub ahead of print]
      MHC transmission: Insights into gender bias in MS susceptibility.
      Chao MJ,
      Ramagopalan SV,
      Herrera BM,
      Orton SM,
      Handunnetthi L,
      Lincoln MR,
      Dyment DA,
      Sadovnick AD,
      Ebers GC.
      From the Department of Clinical Neurology (M.J.C., S.V.R., B.M.H.,
      S.M.O., L.H., M.R.L., D.A.D., G.C.E.), University of Oxford, John
      Radcliffe Hospital, Oxford, UK; and Department of Medical Genetics and
      Faculty of Medicine (A.D.S.), Division of Neurology, University of
      British Columbia, Vancouver, Canada.

      Abstract
      OBJECTIVE:
      Major histocompatibility complex (MHC) genes dominate genetic
      susceptibility factors in multiple sclerosis (MS).
      Given the general consensus that incidence and prevalence of MS has
      been rising and specifically in women, we evaluated MHC-gender
      interactions.

      METHODS:
      In a large family-based cohort consisting of 7,093 individuals (2,127
      affected individuals) from 1,055 MS families, we examined MHC
      transmission by family structure and gender stratified by genetic
      distance of affected relatives from the MS proband.

      RESULTS:
      We found that affected individuals with HLA-DRB1*15-positive genotypes
      have higher female-to-male ratios as compared with affected
      individuals with HLA-DRB1*15-negative genotypes (χ(2) = 9.97, p =
      0.0015) with the exception of multiplex families with 3 or more
      affected across 2 generations.
      Transmission disequilibrium test results show that HLA-DRB1*15
      transmission was more distorted in collateral families vs nuclear
      families (χ(2) = 8.030, p = 0.0046), exclusively in affected
      female-female pairs (χ(2) = 7.81, p = 0.0051), but not in mixed gender
      pairs (χ(2) = 1.58, p = 0.21) or matched male pairs (Fisher p = 0.21).

      CONCLUSIONS:
      These observations implicate the MHC as the site of interactions and
      modifications mediating the female-to-male gender ratio in MS and its
      progressive increase.
      They further suggest this occurs via gene-environment interactions and
      epigenetic modifications in this region.
      The difference between collateral and nuclear families provides some
      insight into the inheritance, decay, and gender specificity of
      putative epigenetic marks.

      PMID: 21209377

      Additional source: Neurology
      Source reference:
      Kantarci O, "Sex-stratified inheritance of MS: New horizons from
      studies in MHC region" Neurology 2011; 76: 210-12.

      Neurology. 2011 Jan 5. [Epub ahead of print]
      Sex-stratified inheritance of MS: New horizons from studies in MHC region.
      Kantarci OH. kantarci.orhun@...
      http://www.mayoclinic.org/bio/12971634.html
      http://mayoresearch.mayo.edu/mayo/research/staff/Kantarci_OH.cfm
      From the Department of Neurology, Mayo Clinic College of Medicine,
      Rochester, MN.
      PMID: 21209375
      Orhun H. Kantarci, MD

      The study was funded by the Multiple Sclerosis Society of Canada and
      the Multiple Sclerosis Society of the United Kingdom.

      Ebers reported relationships with Roche, UCB, and Bayer Schering.
      Another author reported relationships with Bayer Canada, Teva, EMD
      Serono, and Biogen Idec.
      Other authors indicated they had no financial relationships with
      commercial entities.

      Kantarci reported research support from the Hilton Foundation and
      other nonprofit organizations.


      Congenital abnormalities and multiple sclerosis.
      Ramagopalan SV,
      Guimond C,
      Criscuoli M,
      Dyment DA,
      Orton SM,
      Yee IM,
      Ebers GC,
      Sadovnick D.
      BMC Neurol. 2010 Nov 16;10:115.
      PMID: 21080921 [PubMed - in process] Free Article

      BMC Neurol. 2010 Nov 16;10:115.
      Congenital abnormalities and multiple sclerosis.
      Ramagopalan SV, Guimond C, Criscuoli M, Dyment DA, Orton SM, Yee IM,
      Ebers GC, Sadovnick D.
      Wellcome Trust Centre for Human Genetics, University of Oxford,
      Oxford, OX3 7BN, UK.

      Abstract

      BACKGROUND:
      There is a strong maternal parent-of-origin effect in determining
      susceptibility to multiple sclerosis (MS).
      One hypothesis is that an abnormal intrauterine milieu leading to
      impaired fetal development could plausibly also result in increased
      susceptibility to MS.
      A possible marker for this intrauterine insult is the presence of a
      non-fatal congenital anomaly.

      METHODS:
      We investigated whether or not congenital anomalies are associated
      with MS in a population-based cohort.
      We identified 7063 MS index cases and 2655 spousal controls with
      congenital anomaly information from the Canadian Collaborative Project
      on Genetic Susceptibility to MS (CCPGSMS).

      RESULTS:
      The frequency of congenital anomalies were compared between index
      cases and controls.
      No significant differences were found.

      CONCLUSIONS:
      Congenital anomalies thus do not appear to be associated with MS.
      However, we did not have complete data on types and severity of
      congenital anomalies or on maternal birth history and thus this study
      should be regarded as preliminary.

      PMID: 2108092

      http://www.biomedcentral.com/1471-2377/10/115 free full text

      Sreeram V Ramagopalan 1,2 , sreeramr@...
      Colleen Guimond 3 ,
      Maria Criscuoli 3 ,
      David A Dyment 1,2 ,
      Sarah-Michelle Orton 1,2 , ortons@...
      Irene M Yee 3 ,
      George C Ebers 1,2

      http://www.well.ox.ac.uk/ebers/groupmembers.shtml
      http://www.well.ox.ac.uk/ebers/ info@...
      http://www.neuroscience.ox.ac.uk/directory/george-ebers
      neuroscience@...
      A. Dessa Sadovnick 3,4 sadovnik@...
      http://www.labome.org/expert/dessa/a-dessa-sadovnick-362731.html
      1 Wellcome Trust Centre for Human Genetics, University of Oxford,
      Oxford, OX3 7BN, UK
      2 Department of Clinical Neurology, University of Oxford, The West
      Wing, The John Radcliffe Hospital, Oxford, OX3 9DU, UK
      3 Department of Medical Genetics, University of British Columbia,
      G920, Detwiller Pavilion, VCHA - UBC Hospital, 2211 Wesbrook Mall,
      Vancouver, British Columbia, V6T 2B5, Canada
      4 Faculty of Medicine, Division of Neurology, University of British
      Columbia, G920, Detwiller Pavilion, VCHA - UBC Hospital, 2211 Wesbrook
      Mall, Vancouver, British Columbia, V6T 2B5, Canada
      _______________________________________________


      Rich Murray, MA
      Boston University Graduate School 1967 psychology,
      BS MIT 1964, history and physics,
      1943 Otowi Road, Santa Fe, New Mexico 87505
      505-819-7388 rmforall@...

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