I noticed an interesting idea in the form of a published research paper today. To what degree might we attribute the accelerating rise in human life span in recent centuries to an increased survival rate for people who bear gene variants that (a) harm the prospects for survival to adulthood in low-technology settings, but (b) lead to a longer life expectancy for those who do survive?
Healthy life span is rapidly increasing and human aging seems to be postponed. ... To explain current increase in longevity, I discuss that certain genetic variants such as hyper-active mTOR (mTarget of Rapamycin) may increase survival early in life at the expense of accelerated aging. In other words, robustness and fast aging may be associated and slow-aging individuals died prematurely in the past. Therefore, until recently, mostly fast-aging individuals managed to survive into old age. The progress of civilization (especially 60 years ago) allowed slow-aging individuals to survive until old age, emerging as healthy centenarians now.
This seems worth thinking about for at least a little while: examples of a trade-off between early life robustness and overall longevity abound in the animal kingdom, after all. Calorie restriction is one such example, in fact: an evolved way for individual animals to alter their metabolic settings in response to circumstances so as to focus resources on survival and procreation first and foremost when food is abundant, or on living longer to wait out a period of scarcity. A species that can do this has a considerable advantage over one that cannot.
I can't imagine that testing for signs of the revealed slow aging hypothesis would be straightforward, however. Identified genetic variants of human longevity found via centenarian studies and the like do not appear to have effects anywhere near as large as, say, regular exercise, calorie restriction, or the increase in medical technology and consequent avoidance of chronic disease across the past century. The current consensus is that common genetic differences do not affect life expectancy as greatly as do lifestyle choices. So could a genealogical study coupled with DNA analysis of living descendants be made sufficiently sensitive and statistically reliable to pull out small and changing contributions from different genetic variants over only a few generations? I would think that the best records for this purpose will be recent ones, such as can be found in countries like South Korea, where life expectancy has grown just as rapidly as the wealth of the population over the last 50 years.
With the cost of DNA sequencing falling rapidly, we will no doubt see such studies carried out in the years ahead, and possibly on a very large scale. You might look to the efforts of deCODE in Iceland, for example, as a precursor to this sort of project. It remains an open question as to what might turn up in the data collected - perhaps revealed slow aging, perhaps not.
Blagosklonny MV (2010). Why human lifespan is rapidly increasing: solving "longevity riddle" with "revealed-slow-aging" hypothesis. Aging, 2 (4), 177-82 PMID: 20404395