Mathematical models of the way in which the world works, built from observed data and then manipulated to discover patterns, can teach us a great deal. The reliability theory of aging is one result of this approach: it doesn't tell us the exact mechanisms that cause us to age, but still sheds a lot of light on what those mechanisms could be. For example:

Living organisms seem to be formed with a high initial load of damage, and therefore their lifespan and aging patterns may be sensitive to early-life conditions that determine this initial damage load during early development. The idea of early-life programming of aging and longevity may have important practical implications for developing early-life interventions promoting health and longevity.

I noticed a paper today in which researchers modeling the Gompertz-Makeham law of mortality come to the same conclusion from the opposite direction in the modeling space. The important thing to remember here is that we all start with some non-zero mortality rate as a result of what reliability theory calls the high initial load of damage. Aging is then the increase in our current mortality rate as time goes by and we become more damaged.

A key goal of gerontology is to discover the factors that influence the rate of senescence, which in this context refers to the age-dependent acceleration of mortality, inversely related to the morality rate doubling time. In contrast factors that influence only initial mortality rate are thought to be less relevant to the fundamental processes of aging.

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Of particular interest, [our] improved estimates indicate that most genetic manipulations in mice that increase lifespan do so by decreasing initial mortality rate, not rate of senescence, whereas most genetic manipulations that decrease lifespan surprisingly do so by increasing the rate of senescence, not initial mortality rate.

This is a rather interesting conclusion, and certainly a novel way of looking at the varied gene-engineered mice strains that live longer, healthier lives. It suggests that some mutations are building better mice at the outset, but doing little to the aging process. Is this actually the case? More research is needed.