August 17, 2009
Will Aging Decelerator Drugs Work?

Nicholas Wade of the New York Times has a pretty good article surveying efforts to translate research on resveratrol and other anti-aging compounds into drugs that slow the rate of aging. But resveratrol's mechanism of action is to mimic the effeects of life extending calorie restriction. One problem arises: calorie restriction might only work under special conditions that do not apply to humans.

Two experts on aging, Jan Vijg of the Albert Einstein College of Medicine and Judith Campisi of the Lawrence Berkeley National Laboratory, argued recently in Nature that the whole phenomenon of caloric restriction may be a misleading result unwittingly produced in laboratory mice. The mice are selected for quick breeding and fed on rich diets. A low-calorie diet could be much closer to the diet that mice are adapted to in the wild, and therefore it could extend life simply because it is much healthier for them.

“Life extension in model organisms may be an artifact to some extent,” they wrote. To the extent caloric restriction works at all, it may have a bigger impact in short-lived organisms that do not have to worry about cancer than in humans. Thus the hope of mimicking caloric restriction with drugs “may be an illusion,” they write.

Of course, humans in industrial societies eat rich diets rather than the sorts of diets we ate in our wilder ancestral past. Our ancestors were also hungry most of the time. So perhaps resveratrol still might help to slow down our aging by adapting our metabolism to our modern industrialized diets..

Biogerontologist Aubrey de Grey has long argued that he does not expect calorie restriction to extend life as much in humans percentage wise as in mice. This makes sense to me. First off, humans have many mutations for life extension that mice do not have. Some of the effects that calorie restriction can have on mouse metabolism to make them live longer are probably changes that our human metabolisms gained as permanent features as a result of mutations that enabled us to live far longer than mice. Second, calorie restriction's effects might be designed to enable an organism to survive until a better season of food supply. That suggests calorie restrictions benefits might be more tied to the length of seasons than to percentage of total life.

Some of the scientists in the article express skepticism at the arguments by evolutionary biologists that it'll be hard to extend life with simple drugs. The evolutionary biologists argue that if simple metabolic changes could extend life without substantial downsides then mutations to cause these changes would already have happened and spread. If the evolutionary biologists turn out to be wrong about these experimental drugs I can think of a reason: the drugs that extend life will exact some cost that matters far less for humans living in an industrial society. For example, they might make people less energetic or mentally more sluggish or perhaps increase the need for sleep. Or the drugs might increase risks of death in event of trauma of an accident. If mutations haven't already given us the same life-extending benefits that some drugs can provide then there's a decent chance there's a cost to those benefits.

What we need even more than drugs that slow aging: treatments that rejuvenate and reverse aging.

Share |      Randall Parker, 2009 August 17 11:48 PM  Aging Drugs


Comments
Jay said at August 18, 2009 4:16 AM:

Vijg and Campisi's comments seem to fly in the face of evidence on monkeys, which are not small animals. One lab which has fed monkeys a calorie restricted diet for many years is reporting substantial benefits compared with a control group.

Lou Pagnucco said at August 18, 2009 7:50 AM:

I agree with Jay. It seems unlikely that what works for higher primates would totally fail in humans. Also, the link with metabolic changes may not be causal.

For a species to be successful, longevity of the individual is incidental. Darwinian selection favors the best breeders - not necessarily those with the longest lifespan. I doubt evolution cares how long we live, just how many offspring we have and successfully raise.

Lou Pagnucco said at August 18, 2009 9:10 AM:

Postscript - I just found a recent paper examining evolutionary pressures and longevity:

"Adaptation, Aging, and Genomic Information"
http://www.impactaging.com/papers/v1/n5/pdf/100053.pdf

Excerpt:
"Thus it is easy for evolutionary biologists to deliberately produce organisms with slowed or postponed aging, as our publications have shown since 1980 [1, 4]. All we have to do is extend the period during which the forces of natural selection act with full force. Furthermore, it is clear that this entails genetic and functional changes involving many loci [10]"

David Govett said at August 18, 2009 1:32 PM:

As PacRim Jim says, "The best way to extend your life is to delay your birth as long as possible."

Ludwig Boltzmann said at August 19, 2009 2:53 PM:

Sadly I think there are thermodynamic/statistical mechanics reasons why this is not possible even if we can slow the aging process. If we had little nanomachines perhaps, but I don't think it will be possible to really "reverse aging" via manipulating the cellular machinery.

Roderick Reilly said at August 19, 2009 2:57 PM:

""""""I doubt evolution cares how long we live, just how many offspring we have and successfully raise.""""""

Than perhaps the solution to really great "longevity" is to acquire a new body entirely, transferring your cerebral database to a new home. Just make sure that your new body didn't used to belong to Henry Waxman or Rosie O'Donnell

Flash Program said at August 19, 2009 4:41 PM:

"Sadly I think there are thermodynamic/statistical mechanics reasons why this is not possible even if we can slow the aging process. If we had little nanomachines perhaps, but I don't think it will be possible to really "reverse aging" via manipulating the cellular machinery."-Ludwig Boltzmann

I don't see why not, most cells are replaceable, so genetically engineered cells can be introduced. So long as there is a way to either destroy or export molecular garbage, which doesn't seem like an impossible task, you only need to increase the error-correction capacity and fidelity of the DNA maintenance and replication machinery to a suitable level and it should last pretty much indefinitely.

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