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Antiaging Research Priorities [was Re: Major Criticisms of

Brian Manning Delaney bmdelaney at notarealaddr.ess
Fri Sep 18 03:55:18 EST 1998



Thomas Mahoney/ Excelife wrote:
> 
> In article <3.0.3.32.19980917132504.006dde00 at ac.ucr.edu>,
> browley at GALAXY.UCR.EDU says...
>
>> I think Tom Mahoney was making the point that CR
>> is an environmental, not genetic treatment for
>> aging.

> Quite correct.  Mice in the wild undoubtedly
> encounter periods where food is  scarce and the
> effects seen in CR are likely an adaptive
> response to these  conditions.  Thus the actual
> life span of the mice is that seen in CR.

I'm not sure how this way of looking at it is helpful.

If we had evolved a mechanism whereby certain chemicals
found in foods can be utilized by the body to slow free
radical damage in a systematic way that results in aging
being retarded, and then we put those chemicals in a pill,
and they increased longevity, would we not be increasng our
"actual life span" by taking this pill?

Take another example. Say we had evolved a mechanism whereby
eating a certain substance found in a now rare plant turns
on telomerase in enough cells, in the right way, to slow
aging. No one has been known to eat the substnce because our
dietary habits over the last few centuries have precluded
its consumption. But suddenly we discover it, and people
start taking it and living to be 140 years old. Since this
ability to age slowly under the conditions of the presence
of this substance is an evolutionary adaptive response,
would you say people living to 140 by means of this
substance aren't extending their life span?

How about if your lab creates the substance?

I don't think these questions are simple. But I do think, in
studies with mortality as an end-point, it makes sense to
differentiate between average and maximum life span, for
both the control and experimental groups. Going beyond that
-- like arguing that some experiments are merely reproducing
conditions that existed over the course of evolution, and
some aren't, and therefore some are extending our natural
life span and some aren't -- may be fruitful in certain
contexts, but I'm not sure how it bears on the question of
anti-aging research priorities.


> It might make it clearer if we looked at those
> mice who are fed regularly as  being overfed and
> dying earlier than their "normal" life span.

Definitely not clearer. The CR rodents are at close to
starvation-levels of eating, and the females can't even
reproduce. Maybe you can call the control rodents overfed,
but you can't call the CR rodents normal, given that they
aren't fit to reproduce. Therefore, their life spans are not
"normal."

(Pardon typos, it's late.)
Best,
Brian.

--
Brian Manning Delaney
My email address is here:
http://xyz.uchicago.edu/users/bmdelane/email4.htm
[Wrists: "Leave unambiguous typos."]
Note: All statements in this article are in jest; they
are not statements of fact.
"Mein Genie ist in meinen Nuestern." -Nietzsche.
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