Science is as much about investigating what we do not see as it is about investigating what we do see. For example, from a recent open access paper:
Small rodents in captivity routinely reach ten times their mean life span in the wild. Why is it then that in human populations with an average life span of 40 to 80 years nobody has ever lived to 400 years old or more?
This is a fine and valid question. Why do we see little variation in human life span in comparison to that of smaller and more short-lived mammals?
The authors of this paper performed an analysis of mortality statistics across different species of mammal, the results of which lead into a very interesting and readable discussion on the interaction between evolutionary pressures and age-related frailty. This is all part of the larger question of why we age, and why we age in the way we do.
In particular, these researchers argue that the end stages of frailty in aging - senescence - do not result from a lack of evolutionary pressure later in life. But the fact that senescence still exists despite pressure for increased evolutionary fitness is telling us something important about the nature of mammalian biochemistry. From the paper:
A clear implication of our study, therefore, is that long-lived mammals are more likely than short-lived mammals to reach an age when their lives are affected by senescence (that is, an age closer to their maximum life span). In other words, our analysis suggests that senescence occurs at a much younger age, relative to the mean natural life span, in longer lived mammal species.
An age when senescence retards survival (i.e. near to the maximum life span) is reached by a higher proportion of individuals, and therefore remains under increasingly high selection pressure, in natural populations of longer lived mammal species ... This implies a minimum rate of senescence has been unavoidable in the evolution of mammals and could place a limit on their maximum life span, preventing humans from [naturally] reaching Methuselah-like ages. Because senescence affects survival in long-lived species despite relatively strong opposing selection pressure, they have probably evolved mechanisms to delay its negative effects. Retarding senescence further seems to be unavailable to natural selection.
This sort of theorizing is a sideline to the real work of extending healthy human longevity. We don't need to know how aging came to exist in its present form in order to be able to repair the biochemical damage that causes aging and thus reverse its effects. But it is nonetheless very interesting.
Turbill, C., & Ruf, T. (2010). Senescence Is More Important in the Natural Lives of Long- Than Short-Lived Mammals PLoS ONE, 5 (8) DOI: 10.1371/journal.pone.0012019