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Control of HIV latency and reactivation through methylation

Discussion in 'XMRV Research and Replication Studies' started by natasa778, May 30, 2010.

  1. natasa778

    natasa778 Senior Member

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  2. fred

    fred The game is afoot

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  3. natasa778

    natasa778 Senior Member

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    Assessing the Effects of High Methionine Intake on DNA Methylation

    Very long but few bits that stood out for me:

    ... this comparison illustrates that potential effects of dietary MET supplementation on transmethylation efficiency are complex and, in addition to being tissue specific, may also depend on multiple factors including age and overall dietary composition. The contradictory effects of MET supplementation on the [SAM]:[SAH] ratio suggest that high dietary intake of MET may induce DNA hypermethylation in some circumstances and hypomethylation in others.


    ... Environmental perturbations of DNA methylation do not appear to affect the entire genome to the same extent. Rather, genomic and/or epigenetic characteristics of specific loci render them especially susceptible to environmental perturbation (20). The challenge of nutritional epigenetics is to identify these epigenetically labile gene regions in humans. Adding further to the complexity, epigenetic gene regulation is, by nature, tissue specific and developmentally regulated. Hence, it is likely that specific environmental stimuli, such as high intake of dietary MET, will affect DNA methylation only in specific gene regions, in specific tissues, and during specific life stages. Metastable epialleles associated with transposable elements and genomically imprinted genes have been identified as two potential subsets of candidate genes with enhanced epigenetic lability to nutrition (20)...


    http://jn.nutrition.org/cgi/content/full/136/6/1706S

    also:
    MET excess and DNA methylation: Very few studies have examined the effects of high MET intake on DNA methylation. Several years ago, Tremolizzo et al. reviewed studies from the 1960s using high doses of MET in attempts at pharmacotherapy of schizophrenic patients and found that MET supplementation actually exacerbated the symptoms of schizophrenia (15). Based on this and other observations, they proposed that schizophrenia has an epigenetic basis and that, among genetically susceptible individuals, MET supplementation precipitates schizophrenic behavior by altering DNA methylation at specific gene regions.
     

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