AGING Processes - Many? A Definition?

Steve Chambers steve at chambers.ak.planet.co.nz
Wed May 3 23:00:33 EST 1995

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?  


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)
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 

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.

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.


>> 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.  


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...


(I_lurk,_therefore_I_am!_\ ,,,                    Steve Chambers
                          (o o)   steve at chambers.ak.planet.co.nz
(c) Steve Chambers                     1995. All rights reserved 

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