Aging of humans and other organisms shares nearly universal features, hinting at understandability.

With age, the risk of death and of many diseases rises exponentially, health differences between individuals widen, and timescales for recovery grow longer. Aging, at least in organisms such as mice, worms and flies, seems reversible to a certain extent, as evidenced by experiments which remove damaged cells or enhance repair. These features led us to a theory of the core processes of aging using a stochastic equation for damage accumulation, based on dynamic longitudinal damage experiments in mice and E coli, some of them done by our group. This theory, called the saturating removal model, explains the patterns of aging, and helps to identify the specific cellular and molecular drivers of aging in each organism. The mathematical approach explains the incidence curves of age-related diseases in humans, and the scaling and dynamics of survival curves under life-span-extending interventions in model organisms. We will discuss how this approach might guide future strategies to expand the health span and minimize the period of disability at the end of life.