WE ARE ANALOG, THEREFORE WE AGE. According to the Information Theory of Aging, we become old and susceptible to diseases because our cells lose youth… - David A. Sinclair

Aging is controlled by single genes
Aging is slowed by adversity
Aging regulators can be modulated by small molecules
Aging is slowed by eating stressed plants
Aging is largely epigenetic noise
Cellular damage accelerates epigenetic age
Aging is a disease
Aging is reversible

In animal studies, the key to engaging the sirtuin program appears to be keeping things on the razor's edge through calorie restriction — just enough food to function in healthy ways and no more. This makes sense. It engages the survival circuit, telling longevity genes to do what they have been doing since primordial times: boost cellular defenses, keep organisms alive during times of adversity, ward off disease and deterioration, minimize epigenetic change, and slow down aging.

But the true extent to which the survival circuit is conserved between yeast and humans wasn't fully known until 2017, when Eva Bober's team at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany, reported that sirtuins stabilize human rDNA.23 Then, in 2018, Katrin Chua at Stanford University found that, by stabilizing human rDNA, sirtuins prevent cellular senescence — essentially the same antiaging function as we had found for sirtuins in yeast twenty years earlier.24