Hormonal
Caloric restriction extends lifespan in humans by modulating epigenetic markers, specifically through DNA hypermethylation of the p16INK4a gene promoter and SIRT1-mediated deacetylation.
Research suggests that the longevity benefits of CR in humans may involve specific epigenetic changes, such as the silencing of the p16INK4a gene (a marker of cellular senescence) via DNA methylation and SIRT1 activation. This provides a biological basis for why CR might slow aging, though it does not yet translate to a guaranteed lifespan extension protocol for individuals.
In our current studies of human cells, DNA hypermethylation of an E2F-1 binding site was found in the promoter of the p16INK4a gene... resulting in p16INK4a downregulation, which contributes to CR-induced lifespan extension... CR-activated SIRT1 can directly bind to the p16INK4a promoter and decrease its expression through a deacetylation effect, which contributes to delaying the aging process and to lifespan extension [84].
Why this rating
Based on in vitro human cell studies and animal models; no long-term human lifespan data confirms this specific mechanism causes extended life.
Source
Epigenetic regulation of caloric restriction in aging
Yuanyuan Li et al. · BMC Medicine · 2011
DOI 10.1186/1741-7015-9-98
More from this paper
- Caloric restriction (CR) extends lifespan and delays aging-related diseases in mammals by reversing age-associated aberrant DNA methylation patterns and activating SIRT1-mediated histone deacetylation.Moderate
- Caloric restriction prevents or delays the onset of specific aging-related diseases, including cancer, diabetes, cardiovascular disease, and neurodegenerative disorders, in rodents and nonhuman primates.Moderate
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