Learned Helplessness About Immortality (fwd)

Chris Patil cpatil at itsa.ucsf.edu
Mon Mar 4 22:37:00 EST 1996


In article <Pine.OSF.3.91.960302045820.24895B-100000 at beall.tenet.edu> dashley at TENET.EDU (Don Ashley) writes:

>The ends of chromosomes (telomeres) shorten with cell division under
>some circumstances, but it seems preposterous to think that this is
>happening in the reserve cells of skin, marrow, gut epithelium, and
>so forth.  Nor is it reasonable to believe that these cells can
>divide only fifty times (the "Hayflick phenomenon").

Telomeres absolutely do shorten in vivo, in all dividing cell lineages 
other than those in the germ line. This is far from preposterous. It 
still doesn't mean that telomere shortening causes aging, that telomere 
shortening is in any way responsible for the Hayflick limit, or that the 
Hayflick limit has anything to do with the aging process.

>Further, the cells that bear the brunt of aging (i.e., the brain
>cells) don't even divide.  The other familiar changes of aging are
>obviously programmed genetically (I'm thinking, for example, of the
>loss of receptors from the erectile tissues, which are also made up
>of non-dividing cells).
> 
>I appreciate anybody who wants to offer hope to others.  Sorry, but
>this particular hope is vain.  Our bodies are programmed to wear out.

Aging isn't "obviously" programmed genetically, except to the trivial 
extent that different organisms have different genomes and different 
lifespans. The question of whether aging is part of a developmental 
program, the consequence of accumulated damage to somatic tissues, or 
some combination of these factors is by all means an open question 

Population biology does predict that aging will evolve in a population 
that has a separation between soma and germ line, and in which genes 
influence fitness to different extents at different times in the life cycle
(an "age-structured population" in which reproductively mature 
individuals can be phenotypically distinguished on the basis of age); 
however, it doesn't say anything about the mechanism by which aging needs 
to take place. 

The model is open to the possibility that alleles that act to increase
reproductive success at later ages simply have less of an impact on
overall fitness (the intuitive explanation for this being the observation
that when two organisms are otherwise identical, the one with the shorter
generation time is more fit), and therefore aren't as vigorously selected
for. Alternatively (but hardly mutually exclusively), if there are alleles 
which confer early reproduction at the expense of later survival, these 
alleles will still be positively selected (a situation referred to as 
"antagonistic pleiotropy"). 

Neither of these classes of "aging genes"  necessarily amounts to a
developmental program which actively results in aging. An interesting 
question that may or may not reduce to a question of semantics is whether 
there's a difference between an active developmental program that results 
in senescence, and senescence due to a lack of effort put into 
maintenance (where such lack evolved as a result either of antagonistic 
pleiotropy or decay of late-acting alleles by neutral selection).






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