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Antiaging Research Priorities [was Re: Major Criticisms of

andrewmason at my-dejanews.com andrewmason at my-dejanews.com
Mon Sep 21 21:46:35 EST 1998


>  "David Lloyd-Jones"  wrote:

> I think this set of strategies is plausible as far as it goes -- but it only
> goes as far as cellular health. All "organisms", which is to say anything
> bigger than your friendly local e. coli, are alliances of cells, in the good
> metaphor of Lynn Margolis and her co-workers. Aging, it seems to me is as
> much or more an attribute of the alliance as it is of the individual cells.
>
> Thus cellular health would seem necessary but not sufficient for
> life-extension at the level of, say, the large mammal.


So you are proposing a sort of "Gaia" theory of aging? What are the specific
mechanisms for the degradation of the endocrine system you propose if they are
not simply caused by aging at the cellular level?


> Hence endocrinological strategies would seem to me to be a good place to
> look. (Sez the guy who made a fool of himself by writing in a moment of
> pique against the idea of mebabolic individuality a couple of weeks ago.
> :-) )  The essence of any alliance is the communication between the members,
> and for the body as a whole the endocrine system seems to be all the major
> media. The nerves may carry the mail, but the enzymes write the legislation
> and negotiate the treaties.

As I see it the problem with the Telomere theory of aging at the moment is the
lack of causation demonstrated between the shortening of telomeres and the
expression of genes responsible for the production of proteins and enzymes by
the cell. If it can be shown that shortened telomeres are responsible for a
reduction in the prodution of proteins and enzymes (particularly DNA repair
enzymes) then it would link "causes" of aging such as the decline in the
endocrine system directly to the telomere.

Aging manifests itself in many ways and many mechanisms are seen as causes -
free radical accumulation, mutation accumulation, declining enzyme
production, reduction in DNA repair, reduced cell turnover etc. etc. The
telomere theory potentially ties these together and gives them one central
cause, reducing them to merely explanations of "how" we age rather than "why"
we age.

Some researchers such as Hayflick are pessimistic about telomeres being
centrally responsible for all aging, others such as Dr. Michael Fossel (in
"Reversing Human Aging") are extremely optimistic. In the light of this I
think that cautious optimism (as displayed by Tom Mahoney) is appropriate.

As I see it the CR approach is stretching the time we have by slowing the
clock, rather than resetting the clock completely. It is a valid approach that
deserves attention, but don't lose sight of the main prize when there is
available a plausible, testable hypothesis that both simplifies and unifies
existing explanations for aging.

If the telomere theory of aging is wrong, lets disprove it and move on. If
it's right, the possibility of dramatically changing the aging process may
eventuate from it.

Andrew

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