In <Pine.SOL.3.91.950422110448.24648A-100000 at corona> "Patrick O'Neil" <patrick at corona> writes:
>On Fri, 21 Apr 1995, Steve Chambers wrote:
>> In the hope of stimulating further debate, I'm going to play devil's
>> advocate. The following might be seen as evidence against such a
>> multiple process model of aging:
>> 1) It seems that homo sapiens' maximum lifespan may be double that of
>> his most immediate ancestor. Some might argue (notably Cutler) that
>> 150,000 years is such a short period of evolutionary history that
>> advantagous mutations could only have influenced a FEW aging processes.
>What data is there to support a doubled lifespan for modern humans vs
>their immediate ancestors?
Patrick
I always enjoy your posts and I appreciate the fact that you are arguing
in support of my earlier contentions. However, the arguments I presented
against a multiple process model for aging are very real and can't be
dismissed so easily.
For point (1)
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Cutler RG
Evolution of human longevity and the genetic complexity governing aging rate.
Proc Natl Acad Sci U S A; 1975 Nov; 72(11); P 4664-8
ABSTRACT
Genetic complexity of processes governing the aging rate of man was
estimated by determining the maximum rate lifespan has evolved along
the hominid ancestral-descendant sequence. Maximum lifespan potential
was found to have increased approximately 2-fold over the past 3 million
years, reaching a maximum rate of increase of 14 years per 100,000 years
about 100,000 years ago. It is estimated that about 0.6% of the total
functional genes have received substitutions leading to one or more
adaptive amino acid changes during this 100,000-year time-period.
This suggests that aging is not the result of an expression of a large
number of independently acting processes. Instead, primary aging processes
appear to exist where only a few genetic changes are necessary to decrease
uniformly the aging rate of many different physiological functions.
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I've not sighted the paper, but I believe the methods used were:
(1) a phylogenetic analysis of the MLP of present living species and
(2) an empirical equation using brain and body weight
estimates from fossils.
[snip]
>> 2) Calorie Restriction has a significant life-extending influence, and it
>> influences MANY age-related changes. The effect seems to be universal.
>> Some might offer this as evidence that there are only a FEW (and maybe
>> only one) underlying aging processes.
>Not necessarily. I would put forward the rather simple explanation of
>this effect as being due to a reduction in the rate of metabolism.
[snip]
This is not a new thought - but the jury's still out as to whether the
life-prolonging effects of CR can be attributed to a generally reduced
metabolism. It's hard to square such a theory with CR's effects on
glucose metabolism and the improvement in various immune functions.
Several studies have also shown no change in BMR/kg body weight for
CR animals.
>> 3) Recent evidence (eg. Carey et al, 1992; Curtsinger et al, 1992)
>> suggests that mortality rates may decline in late life of many species.
>> Some might suggest that this argues against there being MANY aging
>> processes.
>Hardly. Those who make it to old age and are still functional might well
>simply carry a slower developmental clock.
Quite so - there is plainly some development-program-linked component
to aging. But I can't see how it, per se, can provide a complete explanation
for a late-life reduction in mortality rates. It could only do so if it
was controlled by very few gene loci with very few alleles.
But hey, I'm open to suggestions...
Steve
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(I_lurk,_therefore_I_am!_\ ,,, Steve Chambers
(o o) steve at chambers.ak.planet.co.nz
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(c) Steve Chambers 1995. All rights reserved
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