Hormonal
Calorie restriction extends lifespan in yeast, C. elegans, and Drosophila by activating sirtuins (Sir2/SIRT1), which are NAD-dependent deacetylases that link metabolic state to aging.
Calorie restriction works in model organisms by activating sirtuins, which are enzymes that sense energy status via NAD+. This activation triggers mitochondrial biogenesis and stress resistance. While strict CR is difficult, the paper suggests that identifying molecules that activate sirtuins (like resveratrol) could offer similar health benefits without the dietary burden, though such drugs are not yet proven to replace healthy lifestyles in humans.
Sirtuin genes function as anti-aging genes in yeast, Caenorhabditis elegans, and Drosophila. The NAD requirement for sirtuin function indicates a link between aging and metabolism, and a boost in sirtuin activity may in part explain how calorie restriction extends life span.
Why this rating
Strong evidence across multiple model organisms (yeast, worms, flies, mice), though human data is limited to short-term metabolic markers.
Source
Sirtuins in Aging and Disease
Leonard Guarente · Cold Spring Harbor Symposia on Quantitative Biology · 2007
DOI 10.1101/sqb.2007.72.024
More from this paper
- SIRT1 activation via calorie restriction or resveratrol promotes mitochondrial biogenesis through PGC-1α deacetylation, which may reduce reactive oxygen species (ROS) production and mitigate aging.Moderate
- Resveratrol, a SIRT1 activator, counteracts adverse consequences of a high-calorie diet in mice, including extending lifespan and improving metabolic health, by promoting mitochondrial biogenesis.Moderate
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