This piece arises from Future Tense, a collaboration among Arizona State University, the New America Foundation, and Slate. A Future Tense conference on life extension will be held at the New America Foundation on Tuesday, Nov. 16. (For more information and to sign up for the event, please visit the NAF Web site.) Read more of Slate's coverage on longevity.
Aging is bad for you. Whether you call it a disease, not a disease, a set of disease precursors, or some other variation on the theme, it is a medical condition, and thus a legitimate target—in principle—for medical intervention.
But is it a practical target? Medicine generally targets individual problems—a particular strain of virus, for example, or damage to a particular area of flesh. Aging seems like a huge number of progressive, chronic diseases all interacting with one another. Might such complexity be beyond the power of medicine—even medicine decades hence—to address?
Once these progressive, chronic diseases have become debilitating, piecemeal targeting of them is far less effective than medicine generally is against other, aging-independent diseases. The complexity is bad enough, but what's worse is that the diseases are progressive—they get harder to treat as time goes on, because they are simply the later stages of intrinsic, lifelong processes of accumulation of molecular and cellular damage.
Is there a way out? Biologists who study aging have long been impressed by the fact that aging seems orchestrated, and especially that the one manipulation that reliably postpones aging in laboratory animals—calorie restriction—is a very simple intervention that nonetheless elicits all the metabolic changes required to postpone age-related ill-health and extend life. This, the reasoning goes, suggests that medical interventions against aging could likewise be simpler than the phenomenon they target. But there are also persuasive counterarguments. First, the efficacy of calorie restriction is an exception, highly unlikely to be repeated by other simple interventions (except those that mimic it). Second, it is likely to work far less well in long-lived species such as humans than in mice or rats. And these arguments are robustly supported by available data.
However, in the past decade a new approach to medical intervention in aging has been explored: regenerative medicine. The attraction of this approach is that it acknowledges the irreducible complexity of aging but attacks the problem more pre-emptively than contemporary geriatric medicine does. Regenerative medicine can be defined as the restoration of structure to any damaged tissue or organ. As such, it encompasses molecular, cellular, and organ-level repair. As applied to aging, it amounts to preventative maintenance: periodic partial elimination of the accumulating damage of aging before that damage reaches a pathogenic level, thus postponing, maybe indefinitely, the age at which the ill-health of old age emerges.
OK, so it's an interesting new approach. But is it actually promising? Here's a selection of the reasons for optimism.
The classical areas of regenerative medicine have been moving ahead at an unprecedented pace in recent years. Some of the highlights have, with good reason, been celebrated in the mainstream media: The foremost example is the development by Shinya Yamanaka, and subsequent refinement by numerous groups, of a method to convert adult cells into a state very similar to embryonic stem cells. These cells, termed "induced pluripotent stem cells" or iPS cells, appear to have almost all the versatility of true embryonic stem cells, but can be obtained far more easily, in far greater numbers, and without the main ethical challenges that have confronted the embryonic stem cell field.
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