formaldehyde is made in brain cells from methanol (wood alcohol) by ADH1 enzyme -- breakthrough paradigm by Prof. Woodrow C Monte: Rich Murray 2013.04.27
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formaldehyde is made in brain cells from methanol (wood alcohol) by ADH1 enzyme -- breakthrough paradigm by Prof. Woodrow C Monte: Rich Murray 2013.04.27
 
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formaldehyde is made in brain cells from methanol (wood alcohol) by ADH1 enzyme -- breakthrough paradigm by Prof. Woodrow C Monte: Rich Murray 2013.04.27 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 ..."
http://www.whilesciencesleeps.com/pdf/622.pdf 12 page full text 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 <ecourchesne@...>, http://www.whilesciencesleeps.com/pdf/570.pdf 9 page full text 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 <katesw@...>,
"...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 <sjwebb@...>, many strong birth defects in 336 rat fetuses, 3 g/kg bw oral methanol (not toxic dose) in 26 rat litters, thesis done 1987, WC Monte, M Hoque, L Black, CS Johnson: Rich Murray 2013.04.13
With years of expertise in testing toxins on rats, Prof. Woodrow C. Monte, Arizona State University, had his own lab, where he mentored graduate students. Vivid personal reports led him to test the possibility of birth defects from methanol, 11% of aspartame, 22 mg in the 200 mg aspartame in a 12-ounce can diet drink.
He was unaware that the FDA and Searle Corp. had hidden 6 of their studies that showed birth defects from aspartame in rabbits and mice in 1975. This dose was planned to swamp the catalase enzyme defense system, which, effective in rats and all animals, except the uniquely vulnerable human species, protects against harm from methanol being made into free floating formaldehyde inside cells with high levels of ADH1 enzyme, notably the inner walls of brain blood vessels and in retina rods and cones.
As the smallest organic molecule, methanol readily enters all cells, while it is carried to all parts of the body and the fetus with the bloodstream — in humans with a blood half-life of 3 hours, circulating through the whole body every minute.
A ten-fold lower dose of 0.3 g/kg body weight was used with 272 fetuses in 21 litters, producing a much lower number of birth defects, compared to 296 fetuses in 22 control litters with no methanol.
gives all photos and figures in “While Science Sleeps” textbook –
Figure 12.5 shows a damaged rat pup brain… 177. Hoque M., Monte WC., Black L., Johnston CS.
Methanol Neuropathy and Teratology A Histological Study on Long-Evans Rats. FASEB 1988;25(2(6)):A513. [ See also: Methyl alcohol ingestion as a model etiologic agent in multiple
sclerosis, WC Monte, D Glanzman, C Johnston; Methanol induced neuropathology in the mammalian central nervous system, Woodrow C. Monte, Renee Ann Zeising, both reports 1989.12.04: Murray 2007.12.28
2012.05.01
posted again Tuesday, May 1, 2012 Friday, December 28 2007 WC Monte finally got secret FDA memo 37 years after Searle Co. labs
found birth defects in rabbits from aspartame (methanol, becomes formaldehyde via ADH1 enzyme within human cells) and its phenylalanine: Rich Murray 2012.06.02
Fwd: Aspartame Submission from Prof. Woodrow C. Monte to EFSA: While Science Sleeps: A Sweetener Kills 241 p -- Ch 12 Autism and other Birth Defects 26 p -- 740 references full pdfs: Rich Murray
2011.11.03
Download Chapter 12 of the book "While Science Sleeps" "Autism and Other Birth Defects", with 100 free online full text references ] 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. 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 http://rmforall.blogspot.com/2013/03/smoke-from-pack-cigarettes-gives-40-mg.html
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 http://rmforall.blogspot.com/2013/02/welcome-to-wc-monte-methanol.html
Prof. Ruud A. Woutersen can confirm with C13, in humans methanol is made by ADH1 into formaldehyde inside cells in 20 specific tissues (Kun Lu, 2012) -- WC Monte paradigm -- Prof. Rolaf van Leeuwen will chair EFSA aspartame session Tuesday April 9: Rich Murray 2013.03.27 http://rmforall.blogspot.com/2013/03/prof-ruud-woutersen-can-confirm-with.html Paul Thomas MD Pediatrics & Integrative Medicine, Portland OR, praises
As an earnest medical layman, using John McDougall low fat, low protein, high starch organic vegan diet since January 1999, now 70, I started serving as a volunteer information activist on the Net, building up a large archive of long, detailed, fair, civil, balanced reviews of mostly mainstream medical research about aspartame (methanol, formaldehyde) toxicity: http://rmforall.blogspot.com -- since fall 2007 in close collaboration with Woodrow C. Monte. My posts usually have 50-100 page visits the first day, and continue to be read for years, being highly hyperlinked to each other. within the fellowship of service, Rich Murray, MA Boston University Graduate School 1967 psychology, BS MIT 1964 history and physics, 254-A Donax Avenue, Imperial Beach, CA 91932-1918 505-819-7388 cell 619-623-3468 home epigenetic DNA methylation causes autism in some identical twins, Jonathan Mill, Chloe C Y Wong, Institute of Psychiatry (IoP) at King's College London: Monte: Murray 2013.04.25
This highly skilled team could apply their copious genetic data to searching for similar patterns in autism in heavy users of aspartame and cigarettes -- the smoke from 2 cans aspartame diet drink gives the same methanol as a pack of cigarette smoke, about 40 mg -- also in Alzheimer's, depression, and multiple sclerosis.
free full text
Jonathan Mill <j.mill@...>, jonathan.mill@...,
Environment Interacts With Genes In Autism, Twin Study Shows Reuters | Posted: 04/23/2013 4:00 am EDT * Researchers analysed 50 sets of twins, some with autism
* Identical genes allow scientists to see other influences * Autism affects 1 in 100 in Europe, up to 1 in 50 in U.S. By Kate Kelland LONDON, April 23 (Reuters) -- Scientists have found patterns of change in gene activity involved in autism in a study that shed light on how environmental factors can work to turn certain genes on or off and contribute to the development of the brain disorder.
In the largest study of its kind, researchers analysed data from 50 sets of twins to try to find out what might have caused some of them to develop autism while their genetically identical siblings did not.
Chloe Wong, of the Institute of Psychiatry (IoP) at King's College London, who worked on the study, explained that epigenetic changes affected levels or activity of genes without changing the underlying DNA sequence. Scientists think they are one way in which the environment interacts with the genome.
Importantly, she said in a telephone interview, epigenetic changes are also potentially reversible, so finding out more about them may point researchers towards the development of new medicines or treatments.
People with autism have varying levels of impairment across three common areas- - social interaction and understanding, repetitive behaviour and interests, and language and communication. As many as one in 50 school age children in the United States are diagnosed with autism, although some of these will be milder cases that have been diagnosed partly because of better recognition of autism symptoms by carers and doctors. In Europe experts say the rate is around one in 100 children.
GENETIC CODE Previous studies have shown there is a strong genetic component to autism. In identical twins, in around 70 percent of cases where one twin has autism, so does the other. But in 30 percent of cases, one twin has autism while the other does not.
Because identical twins share the same genetic code, this suggests non-genetic, or epigenetic, factors may be important. Wong's team studied a particular epigenetic mechanism called DNA methylation, which acts to block the genetic sequences and can turn gene activity on or off.
They looked at DNA methylation at over 27,000 sites across the genome using samples taken from 50 identical twin pairs. Of the 50 pairs, 34 had one twin with autism and one without, five had both twins with autism, and 11 pairs were healthy controls with no autism traits or diagnoses.
The researchers found that DNA methylation at some genetic sites was consistently altered for all the children with autism, while differences at other sites were specific to certain groups of symptoms or traits of autism.
The number of DNA methylation sites across the genome was also linked to the severity of autism symptoms suggesting a quantitative relationship, said Wong, whose study was published in the journal Molecular Psychiatry on Tuesday.
"We identified distinctive patterns of DNA methylation associated with both autism diagnosis and related behaviour traits, and increasing severity of symptoms," she said. Jonathan Mill, of the IoP and the University of Exeter, who led the study, said research into the intersection between genetic and environmental influences was crucial "because risky environmental conditions can sometimes be avoided or changed".
He said the next step was to conduct larger studies to see whether researchers can identify key epigenetic changes that are common to the majority of people with autism and use them to help develop ways of preventing or treating the disorder.
It was too early in the process to identify which environmental factors may have had an impact. (Editing by Alison Williams) free full text Original Article Molecular Psychiatry advance online publication 23 April 2013; doi: 10.1038/mp.2013.41
Methylomic analysis of monozygotic twins discordant for autism spectrum disorder and related behavioural traits Open C C Y Wong 1, E L Meaburn 1,2,
A Ronald 1,2, T S Price 1,3, A R Jeffries 1, L C Schalkwyk 1, R Plomin 1 and J Mill 1,4 Jonathan Mill <jonathan.mill@...> , j.mill@..., Emma L Meaburn <e.meaburn@...>, Angelica Ronald <a.ronald@...>, Thomas S Price <thomas.price@...>, Leonard C Schalkwyk <leonard.schalkwyk@...>, Robert J. Plomin <robert.plomin@...>, Avshalom Caspi <avshalom.caspi@...>, Daniel H Geschwind <dhg@...>, 1 King's College London, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, De Crespigny Park, London, UK
2 Department of Psychological Sciences, Birkbeck, University of London, London, UK 3 Institute of Translational Medicine and Therapeutics, School of Medicine, University of Pennsylvania, PA, USA
4 University of Exeter Medical School, Exeter University, St Luke's Campus, Exeter, UK Correspondence: Dr J Mill, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King’s College London, Denmark Hill, De Crespigny Park, London SE5 8AF, UK. E-mail:jonathan.mill@... or j.mill@...
Received 27 November 2012; Revised 21 January 2013; Accepted 6 March 2013 Advance online publication 23 April 2013 Abstract Autism spectrum disorder (ASD) defines a group of common, complex neurodevelopmental disorders.
Although the aetiology of ASD has a strong genetic component, there is considerable monozygotic (MZ) twin discordance indicating a role for non-genetic factors. Because MZ twins share an identical DNA sequence, disease-discordant MZ twin pairs provide an ideal model for examining the contribution of environmentally driven epigenetic factors in disease.
We performed a genome-wide analysis of DNA methylation in a sample of 50 MZ twin pairs (100 individuals) sampled from a representative population cohort that included twins discordant and concordant for ASD, ASD-associated traits and no autistic phenotype.
Within-twin and between-group analyses identified numerous differentially methylated regions associated with ASD. In addition, we report significant correlations between DNA methylation and quantitatively measured autistic trait scores across our sample cohort.
This study represents the first systematic epigenomic analyses of MZ twins discordant for ASD and implicates a role for altered DNA methylation in autism. Keywords: ASD; autism; copy-number variation; DNA methylation; epigenetics; monozygotic twins
Acknowledgements This work was supported, in part, by the Autism Speaks Grant 4743 (RP, Principal Investigator). The twins were selected from the Twins Early Development Study which has been funded continuously since 1995 by a UK Medical Research Council (MRC) program grant to RP (G0901245, and previously G0500079), with additional support from the US National Institutes of Health (HD044454; HD046167).
We acknowledge the use of BRC Core Facilities provided by the financial support from the Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy’s and St Thomas’ NHS Foundation Trust in partnership with King’s College London and King’s College Hospital NHS Foundation Trust.
RP is supported by an MRC Research Professorship award (G19/2) and a European Advanced Investigator Award (295366). CCYW was a PhD student who was funded by the UK MRC. JM was supported by an NARSAD Young Investigator Award. Supplementary Information accompanies the paper on the Molecular Psychiatry website 1
Genetic and epigenetic associations of MAOA and NR3C1 with depression and childhood adversities. Melas PA, Wei Y, Wong CC, Sjöholm LK, Aberg E, Mill J, Schalling M, Forsell Y, Lavebratt C. Int J Neuropsychopharmacol. 2013 Mar 1:1-16. [Epub ahead of print]
PMID: 23449091 [PubMed - as supplied by publisher] Related citations Select item 23211398 2. Epigenetic studies of schizophrenia: progress, predicaments, and promises for the future.
Dempster E, Viana J, Pidsley R, Mill J. Schizophr Bull. 2013 Jan;39(1):11-6. doi: 10.1093/schbul/sbs139. Epub 2012 Dec 4. PMID: 23211398 [PubMed - in process] Related citations
Select item 22836009 3. SORL1 and SIRT1 mRNA expression and promoter methylation levels in aging and Alzheimer's Disease. Furuya TK, da Silva PN, Payão SL, Rasmussen LT, de Labio RW, Bertolucci PH, Braga IL, Chen ES, Turecki G, Mechawar N, Mill J, de Arruda Cardoso Smith M.
Neurochem Int. 2012 Dec;61(7):973-5. doi: 10.1016/j.neuint.2012.07.014. Epub 2012 Jul 23. PMID: 22836009 [PubMed - in process] Wong, C.C.Y., Meaburn, E.L., Ronald, A., Price, T.S., Schalkwyk, L.C., Plomin, R., Mill, J. (in preparation) Detection of substantial copy number-variations in a MZ concordant ASD twin pair. Wong, C.C.Y., Meaburn, E.L., Ronald, A., Price, T.S., Schalkwyk, L.C., Plomin, R., Mill, J. (in preparation) Differential allele-specific DNA methylation within MZ twins discordant for ASD. Wong, C.C.Y., Meaburn, E.L., Ronald, A., Price, T.S., Schalkwyk, L.C., Plomin, R., Mill, J. (in preparation) Genome-wide DNA methylation profiling of monozygotic twins discordant and Concordant for ASD and related traits. Chloe Chung Yi Wong
Post-Doctoral Research Worker 020 7848 0662 Chloe is a postdoctoral research fellow working in the Psychiatric Epigenetics Group at King's College London.
Her main research interest is the role of epigenetic factors in psychiatric disorders, with a particular focus on Autism Spectrum Disorder (ASD). She is currently undertaking a genome-wide investigation of DNA methylation in ASD post-mortem brain tissue (PIs: Professor Dan Geschwind, UCLA; Professor Jonathan Mill, King's College London, Exeter University).
She was recently awarded the UK Medical Research Council (MRC) Centenary Early Career Award (£15,000) to investigate dynamic DNA methylation changes in the development of autism using a longitudinal British Autism Study of Infant Siblings (BASIS) cohort. After graduating from King's College London (University of London) in 2007 with a BSc in Pharmacology & Molecular Genomics, Chloe was awarded a 1+3 PhD studentship from the MRC.
She achieved an MSc pass with distinction in Social, Genetic and Developmental Psychiatry in 2008 and subsequently started her PhD training under the supervision of Dr Jonathan Mill and Professor Avshalom Caspi.
During the course of her PhD, She investigated the role of DNA methylation differences in monozygotic and dizygotic twins in relation to psychiatric-related phenotypes including ASD and bullying victimisation.
Chloe's other research interest includes the dynamicity of DNA methylation and X-chromosome inactivation during childhood development. Chloe has extensive experience in cutting-edge methylomic profiling approaches and bioinformatic analyses.
She recently performed the first systemic genome-wide scan for DNA methylation changes associated with ASD and related phenotypic traits using discordant MZ twin samples (in press, Molecular Psychiatry). In addition, She has been involved in methodological advances in the field and has recently developed a pre-processing statistical pipeline for the Illumina Infinium HumanMethylation 450K microarray.
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Re: formaldehyde is made in brain cells from methanol (wood alcohol) by ADH1 enzyme -- breakthrough paradigm by Prof. Woodrow C Monte: Rich Murray 2013.04.27
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Very interesting! Thanks, Rich. It's amazing to me how biologically important formaldehyde is, not only as a toxin, but as a naturally occurring metabolite. I don't remember when I first heart the aphorism "The dose is the poison". But it comes up again and again. All the interesting chemicals are active and have "regimes" where they're negligible, interesting, and poisonous, at least in healthy organisms. Damn it. There's that magic number 3 again. ;-) On 04/27/2013 10:00 PM, Rich Murray wrote: > 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 ..." > > > http://www.whilesciencesleeps.com/pdf/622.pdf 12 page full text -- glen =><= Hail Eris! ============================================================ FRIAM Applied Complexity Group listserv Meets Fridays 9a-11:30 at cafe at St. John's College to unsubscribe http://redfish.com/mailman/listinfo/friam_redfish.com |
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