The End ME/CFS Project: History Taking Root
The history books record that in the nineteenth century Louis Pasteur formulated a “germ theory” of microbes as the causative agents of disease, and thus revolutionized medicine. His findings, along with his contemporary, John Snow (who linked cholera to infected water supply),...
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Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by sregan, May 6, 2013.

  1. sregan

    sregan Senior Member

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    After looking closely at a Methylation diagram it looks like just taking SAMe would get methylation going and that for those with the block that the SMP helps (Methionine synthase?) taking MCbl and MFolate will create more SAMe from recycled Homocysteine at the same time reducing a possibly harmful buildup of Homocysteine.

    I was wondering also if those on the SMP might need to supplement with methyl donors if somehow there could be a deficiency once methylation gets started again?

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  2. Lotus97

    Lotus97 Senior Member

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    sregan
    I think that might depend on a person's SNP. Rich recommends switching to methylcobalamin and raising methylfolate dosage if a person doesn't experience improvement with hydroxocobalamin and the starting dose of folinic acid and methylfolate. He's basing his recommendations on a study using an older version of his Simplified Methylation Protocol (SMP) in which SAMe and glutathione levels increased.
    http://www.mecfs-vic.org.au/sites/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf
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    The only study I could find using SAMe suggests SAMe doesn't raise or lower homocysteine. Perhaps taking SAMe in conjuction with a methylation protocol would produce different results
    http://www.ncbi.nlm.nih.gov/pubmed/19422296?dopt=Abstract
    Dietary supplement S-adenosyl-L-methionine (AdoMet) effects on plasma homocysteine levels in healthy human subjects: a double-blind, placebo-controlled, randomized clinical trial.
    OBJECTIVES: To determine if exogenous S-adenosyl-l-methionine (AdoMet), a commonly used nutritional supplement, increases the level of plasma homocysteine (Hcy), a potential cardiovascular risk factor, in healthy human subjects.
    DESIGN: Double-blind, placebo-controlled, randomized clinical trial.
    SETTING: Mayo Clinic, Rochester, Minnesota.
    SUBJECTS: Fifty-two (52) healthy human volunteers.
    INTERVENTION: Subjects received placebo or AdoMet (800 mg per day) for 4 weeks. Hcy levels were measured before and after administration of AdoMet or placebo.
    OUTCOME MEASURES: The primary outcome measure was change in Hcy level. Secondary outcome measures included an interim Hcy determination (at 2 weeks) and changes in levels of high-sensitivity C-reactive protein (hsCRP), lipids, and alanine aminotransferase.
    RESULTS: There was no statistically significant change in Hcy between groups. Similarly, no statistically significant differences in change in Hcy or hsCRP levels were observed at 2 or 4 weeks. There was a small but statistically significant increase (p < 0.04) in alanine aminotransferase at week 2 and a statistically significant decrease (p < 0.04) in total cholesterol in the AdoMet group compared with the placebo group.
    CONCLUSIONS: AdoMet at a daily dose of 800 mg for 4 weeks does not appear to significantly affect Hcy levels in the blood.
     

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