The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 13 No. 6 • December 2010


Human Longevity and Genes for Increased Disease Risk

Disease Risk Alleles Do Not Compromise
Human Longevity in Genome Study

You may assume that your family-associated increased risk of some diseases could have an effect on your likelihood of living a long lifespan. That may not be true, at least as suggested by a recent paper.1 In this study, a set of currently known alleles increasing the risk of coronary artery disease and type 2 diabetes that have been identified by genome-wide association studies were tested for compatibility with human longevity.

In the new study, the researchers showed that “nonagenarian siblings from long-lived families and singletons older than 85 y of age from the general population carry the same number of disease risk alleles as young controls. Longevity in this study population is not compromised by the cumulative effect of this set of risk alleles for common diseases.”

That appears to be good news. However, it is important to remember that regulation of DNA transcription by histones (and, hence, importantly, histone methylation and demethylation) is an important part of gene expression2–4 that would not be detected by identification of alleles alone. Hence, maintenance of appropriate levels of histone methylation and demethylation is an important part of what determines how your DNA eventually plays a role in whether you get diseases that you may be at risk for and how long you live. For a start, you might take (as we do) supplements of methyl-donating nutrients, such as choline (which we get from our sugar-free choline supplement and betaine and folic acid, as well as an important natural enzyme cofactor in the regulation of histone methylation, S-adenosylmethionine (SAMe).5–7

References

  1. Beekman et al. Genome-wide association study (GWAS)-identified disease risk alleles do not compromise human longevity. Proc Nat Acad Sci USA 107(42):18046-9 (2010).
  2. Bjornsson et al. Intra-individual changes over time in DNA methylation with familial clustering. JAMA 299(24):2877-83 (2008).
  3. Yang et al. Reversal of hypermethylation and reactivation of genes by dietary polyphenolic compounds. Nut Revs 66(Suppl. 1):S18-S20 (2008).
  4. Li et al. Age-dependent decreases in DNA methyltransferase levels and low transmethylation micronutrient levels synergize to promote overexpression of genes implicated in autoimmunity and acute coronary syndromes. Exper Geront 45:312-22 (2010).
  5. Priudova et al. S-adenosylmethionine stabilizes cystathionine beta-synthase and modulates redox capacity. Proc Nat Acad Sci USA 103(17):6489-94 (2006). “The transsulfuration pathway converts homocysteine to cysteine and represents the metabolic link between antioxidant and methylation metabolism.”
  6. Tchantchou et al. S-adenosylmethionine: a connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer’s disease. J Nutr 10(6):541-4 (2006).
  7. Morrison et al. Brain S-adenosylmethionine levels are severely decreased in Alzheimer’s disease. J Neurochem 67:1328-31 (1996).

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