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 evolutioin by increasing teh turnover of the generations), almost no gerontologists do: the idea is actually logically incoherent granted the basic logic of natural selection. Instead, almost noall biogerontologists subscribe to some version of the idea that aging is the result of stochastic molecular damage taht 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, because natural selection selects organisms that leave behind the most viable progeny. Thus, evolution tendds to select for maintenance systems that retard aging ENOUGH to let them 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, and to instedad invest the same resources in either things related to reproduction (fertility, attractiveness, etc) or things 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 thhe lack of selective pressure against mutations whose ill effects are felt only late in life -- most dramatically, inthe 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, but are seen when the organism is shielded from teh natural environment's hazards and are allowed to actually age (eg, growth hormone and 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 agign, 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 udner more natural conditions, they rapidly lose out to their wild-type cousins. Examples:
04/12/06 - REPOST "No Fitness Tradeoff for Longevity?" WAS Re: Prospects for aging medicine http://lists.milepos...ociety&P=R18040
04/12/06 - Longevity Mutants Lose Darwinian Fitness: More Evidence
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CR certainly seems to be another, less extreme example (because its detriments are more obvious). CR APPEARS to be a program that shifts resources away from reproduction and puts them into maintenance, allowing the organism to survive a famine intact, to breed another day. But clearly, if *perpetuated* in the wild, the CRed mouse's low fertility, body size, and temperature would make it a total loser if it had the CR phenotype when others didn't.
Now, here's another one:
Biol Lett. 2005 Jun 22;1(2):247-9.
The longevity of Caenorhabditis elegans in soil.
* Van Voorhies WA, Fuchs J, Thomas S.
... An important issue when interpreting results from these studies [of anti-aging interventions in C. elegans] is the similarity of the observed C. elegans We found that ... C. elegans mutants that live twice as long as wild-type worms in laboratory conditions typically die sooner than wild-type worms in a natural soil. ...
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).
PMID: 17148178 [PubMed - indexed for MEDLINE]