Learned Helplessness About Immortality (fwd)

David Kipling davidk at hgu.mrc.ac.uk
Tue Mar 5 07:28:57 EST 1996


I think Chris has made a very valid set of comments here.


> Chris Patil wrote:
> 
> 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").

(in reply to original post) Why is it preposterous?   50 divisions of a single cell produces 
about 1,000,000,000,000,000 offspring.   A pea-sized bit of tissue contains something of the 
order of 100,000,000 cells.  50 divisions therefore gives enough cells to make about 10 million 
pea-sized bits of tissue.  That's a lot of slack for development and regeneration to play with.  
 
> 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.

This of course is the crucial point, to what extent the Hayflick limit impacts upon organismal 
ageing.   It may in some tissues, whereas in other tissues damage to non-mitotic cells could be 
the major determinant (for point of argument).   Organismal ageing is probably too complex to be 
put down to a single mechanism.
 
> 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

The way I had it explained to me goes something like this:

An animal takes in resources (in the form of food).  These can be used for two main processes:  
repair to the somatic cells, and for producing offspring (e.g. growth of the embryo, post-natal 
care and feeding, etc.).    For every calorie you use for somatic repair, that's one less for the 
offspring.   On top of this you have the problem of predation.

So, if one is a mouse, there is no point in devoting vast amounts of resources to somatic repair 
- why live for 100 years if you are more than likely to be eaten in 12 months?  Better for you to 
devote more of those precious resources to making offspring as fast as possible.   In short, 
there is no selective advantage for a mouse to live for 100 years, but there is a selective 
*disadvantage* for it to use resources which would otherwise have been used for reproduction on 
useless somatic repair.

Note here that species with low levels of predation have longer lifespans - for example, 
ostriches are particularly short-lived birds (cannot fly so get eaten more often).  And so forth.

This is the "disposable soma" theory and suggests that ageing is a non-selected by-product of 
maximising the reproduction v. predation lifehistory, and also the fact that life is a 
compromise:  you cannot have maximum reproductive rates *and* maximum life spans at the same 
time.   


> 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).

The other thing we should remember as a general point is that ageing is probably a fairly recent 
process in human evolution.  We popularly think of age-related processes occurring in middle-age 
onwards, yet consider the fact that until the last few thousand years human life-spans have been 
very low.   Stone-age man was lucky to get past his early 20s by all accounts.  It is not until 
recent years that cultural advances have allowed massively extended lifespans, and with them 
ageing in the popularist definition.   In short, what we think of as "ageing" never really 
happened much during human evolution, so it is hard to see that it was actively "selected for" or 
"genetically programmed".   Better to imagine it as an unavoidable side-effect of other things 
being selected for, like reproductive success versus somatic repair.

David Kipling
MRC HGU Edinburgh




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