Michael Rae has posted some thoughts on known longevity mutations to the Immortality Institute forums. Cleaning it up a little, we have:
While laypeople and non-biogerontologist biologists often subscribe to the idea that we are 'programmed to age and die' (usually as a means to clear out the old to free up resources for the young, and/or to facilitate evolution by increasing the turnover of the generations), almost no gerontologists do: the idea is actually logically incoherent granted the basic logic of natural selection.
Instead, almost all biogerontologists subscribe to some version of the idea that aging is the result of stochastic molecular damage that is only partially prevented or repaired because to invest the resources into creating maintenance mechanisms powerful enough to obliterate such effects would be a waste - natural selection selects organisms that leave behind the most viable progeny, not those that win the longevity medal. Thus, evolution tends to select for maintenance systems that retard aging ENOUGH to let individuals live out a relatively long life - relative to what can be expected if they aren't killed by starvation, predation, exposure, etc - but not DRAMATICALLY more. The resources that would have been invested in repair are instead directed to either reproduction matters (fertility, attractiveness, etc) or line items related to surviving those other, grossly environmental threats (warmer fur, sharper claws, etc). Such ideas can be grouped under the "disposable soma theory," and mechanisms include the lack of selective pressure against mutations whose ill effects are felt only late in life -- most dramatically, in the case of "antagonistic pleiotropy," where a trait is selected because it has effects that are beneficial for fitness, but that cause negative consequences that are not normally felt in the wild. These negative consequences are only seen when the organism is sufficiently shielded from the natural environment to age significantly past its prime (e.g. growth hormone, sex steroids and reproductive and other cancers).
An apparent challenge to this has been raised by studies in C elegans (tiny roundworms) and other model organisms that have mutations that dramatically slow the rate of their aging, seemingly at no cost to fitness. However, studies have shown that this is often the result of the animals not being subjected to the rigors of a natural environment, and that when they have to compete under more natural conditions, they rapidly lose out to their wild-type cousins.
Which is why you don't see these sorts of mutations in the wild. Rae goes on to give examples - you should read the whole thing - and concludes:
This should give pause to those looking to intervene in aging by pharmaceutically exploiting these pathways (a standard strategy of the "gerontologist's school" of anti-aging biomedicine), and again reinforce the benefits of allowing metabolism to remain in its normal state, but cleaning up the ensuing damage directly, at the molecular level, iteratively pushing the level of damage beneath the threshold of pathology (the "engineer's school" of anti-aging biomedicine).
I'm not sure I agree with that conclusion as a blanket over the subject; after all, we're already very reliant upon technology to shield us from the consequences of not having technology - i.e. to have to endure the rigors of the environment and extremely poor control over basic needs for life. I'm sure we'd jump into the pool of being less generally resilient and more reliant on technology to live significantly longer in good health, given that we're pretty much already in that pool today. But that isn't the only option on the table, fortunately.
My arguments for the same conclusion as Rae above - let us primarily aim to repair damage rather than manipulate the rate at which damage happens - are primarily utilitarian. One path looks to be much easier than the other, and plausible arguments exist for it to produce more rapid gains per dollar invested in research. Furthermore, the resulting technology will likely be far more useful for those who are already old. Slowing the rate of further damage doesn't do much for those already greatly damaged.