Living the life of Reilly...and lots of it!!

The science of 'aging' research has had its ups and downs, probably more downs than ups in a particular sense.  Aging researchers (that is, researchers on aging) have wanted their field to be a real science with some theory, some magic law-like explanations.  Theories have ranged from body size and metabolic rates specifying some 'maximum lifespan potential', to chromosome ends or a gene related to them (telomerase), to a specified tradeoff between being healthy when young and paying for it by aging, and more.  Behind many if not most such theories is the darwinist idea that lifespan is prescribed by some specific adaptive advantage, with humans being exceptional. 

But these haven't really worked (even if aging researchers, that is, researchers who have been aging over recent decades as one theory after another has faded), and one might think this was a dead-end area, so to speak.

One of the magical theories, of long-standing, has been that caloric restriction leads to an organism not burning itself out too quickly, and lasting longer.  It was once believed that mammals and some birds were endowed with a certain number of heart-beats, or calories burned, and that this could explain the typical lifespans of different species.  Body and/or brain size were thought to be correlated with these metabolic variables. As it turns out, and contrary to widespread mythology, even among professionals, we humans are barely--if at all--exceptional.  And some real exceptions were found, such as some very long-lived birds and tortoises.

NIH Nat'l Inst of Aging; NYT

However the idea lived on because of experiments in laboratory rodents that showed that restriction in calories consumed led to longer lifespans on average. There was then some preliminary suggestion that this held true for primates--rhesus monkeys, one of the practical preferred primate for such work, in particular.  Alas, living in privation (look at the faces on these poor animals; shouldn't the Institutional Review Board have prevented this study?) has failed over a long study time now, to show the effect.  I saw this in the NYT, though it's everywhere, but have not yet read the primary report.

 For 25 years, the rhesus monkeys were kept semi-starved, lean and hungry. The males’ weights were so low they were the equivalent of a 6-foot-tall man who tipped the scales at just 120 to 133 pounds. The hope was that if the monkeys lived longer, healthier lives by eating a lot less, then maybe people, their evolutionary cousins, would, too. Some scientists, anticipating such benefits, began severely restricting their own diets.

The results of this major, long-awaited study, which began in 1987, are finally in. But it did not bring the vindication calorie restriction enthusiasts had anticipated. It turns out the skinny monkeys did not live any longer than those kept at more normal weights. Some lab test results improved, but only in monkeys put on the diet when they were old. The causes of death — cancer, heart disease — were the same in both the underfed and the normally fed monkeys. 

Too bad!  Or is it?

This means that within reason at least we can live the life of Reilly--eat, drink, and be merry!  And still have our allotted time.  Well, up to a point....

Fortunately for science, if unfortunately for aging researchers and their simple theories, we really do have reasonable, if general and non-specific, non-selectionistic explanations.  There are many ways to go, and we die not because of a single aging clock, but because we statistically run out of the chance of avoiding all causes of death.  It only takes one to get you.  Now, there certainly does seem to be some general programming of our life-history, since our time to adulthood and so on is certainly associated with our body size, and this is generally true among mammals.  Thus, there must be some genetic basis for these characteristics.  But it need not be a single basis.  If there were advantage to being bigger and that led to living longer (perhaps to be able to raise offspring to their maturity, or for some other reasons) then any mechanisms that led to that would have been supported by selection.

That accounts in a very generic way for our body size and the general longevity associated with it.  But that fact does not suggest a simple calibration of lifespan (that is, death).  Despite some factors that do statistically increase some risks, what we die of is very variable from person to person, involving all body systems.  While there is a rough, body-size correlated calibration of all of this in some way, what ends life is not a death program, but the gradual running-out of the probability of escaping all causes, as we noted above. This is the 'competing causes' phenomenon of our lifespans.

There is no single death gene.  The theories and their evolutionary explanations never had any serious scientific backing, despite decades of being proffered to the profession, the public, and the NIH funders.  I know this, because I and others have been pointing out the counter arguments roughly presented above for decades.  But the reasoning and the data to support it were not convenient for those seeking for simple explanations.

Whatever calibrates our life-histories (including some of the suggested mechanisms as part of the story, as mentioned above), we still don't know.  But if we are conveniently prone for self-serving reasons to accept this latest study of rhesus monkeys, we can feel free now to go pop a cold one, and open that bag of chips!