Maximal human lifespan in light of a mechanistic model of aging
Abstract
Why has maximal human lifespan barely changed in the past two centuries? To understand this we make a mechanistic link between cellular damage, survival curves, and maximum lifespan using a validated stochastic model of damage accumulation and extensive human data. We show that maximal lifespan is set mainly by damage production and clearance rates, as in progeroid syndromes. In contrast, lifestyle factors such as exercise, nutrition, and sleep chiefly reduce stochastic noise and raise the damage level compatible with survival, shifting the median but not the maximum. Similar constraints arise in other mortality models. Our analysis predicts that lifestyle can extend maximal lifespan by at most ~1 year; substantial gains will require directly perturbing damage production or removal, suggesting specific molecular targets.
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Research summary
The paper claims that maximal human lifespan is primarily determined by damage production and clearance rates, with lifestyle factors only marginally extending lifespan. This research is relevant as it addresses the fundamental mechanisms of aging and suggests that significant lifespan extension requires targeting the biological processes of damage accumulation rather than merely improving lifestyle factors.
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