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Thread: Accelerated 'aging' (or protection) in elite athletes

  1. #1
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    Glasgow, Scotland
    Y-DNA (P)
    mtDNA (M)

    Accelerated 'aging' (or protection) in elite athletes

    One study that has caught my eye is this one looking at some apparently contradictory data showing advanced methylation at key sites amongst elite athletes. One theory proposed is that the methylation far from reducing longevity is actually providing some protection against development of CAD.

    "More detailed analysis of the accelerated aging of elite athletes indicated by our model revealed that accelerated hypermethylation of TRIM59 and KLF14 were the principal cause of the changes. Both, are widely replicated age predictors used in various age estimation models based on DNA methylation analysis [2, 22, 28, 29]. Most studies have indicated longer life expectancy in top athletes compared to the general population and our finding of an accelerated epigenetic age of elite athletes seems to contradict these results...

    Wei et al showed that KLF14 may be involved in induction of inflammation and for this reason knockdown of this gene reduces pro-inflammatory cytokines and the formation of atherosclerotic lesions. This antiinflammatory effect was suggested to prevent atherosclerosis: a known chronic inflammatory disease [40]. "

    I checked my figures from the 5 sites they discuss. I'm a life long endurance runner (sub-elite) and have CAD. I put the average figures from the paper in brackets. I have *less* methylation in 4 of the 5 including both the key ones mentioned above. Perhaps I wasn't training hard enough.

    6:11044634 =76% methylated in me ELOVL2 (paper average 60%)
    1:207823681 =56% MIR29B2C (79%)
    3:160450199 =25% TRIM59 (31%)
    7:130734355 =0% KLF14 (5%)
    2:105399288 =17% FHL2 (36%)

    NB all five of these sites fell within the deep coverage part of my test and had ~40x read depth.
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