Re: Re : Cornering the causes of aging (was Re: AGING: Accumulation of DNAdamage)

From: Joao Pedro de Magalhaes (
Date: Thu Jun 29 2000 - 22:30:30 MDT


CurtAdams wrote:
>I don't get this reference. Are you talking about lifetime vs. one-time
>reproduction in salmon?

For instance. Salmon's aging phenotype (amongst other iteroparous species)
is a good example of a very simple mechanism (and I'm certain you can't
tell me of a species with a very complex mechanism of aging; even if they
exist, none are known).

>Alleles which
>combine several systems together are much more difficult to evolve;

The body is an integrated collection of connected systems. If the immune
system degenerates with aging, the other systems will also be affected.

>There *are* thousands of pathologies. The phenetic variability of
>aging is a problem for *your* theory; you're the one claiming we
>all have the same aging system.

It's not a problem for my theory: since senescence affects the entire body
and all systems this leads to a large variety of pathologies. I was merely
pointing that the evolution of thousands of your proposed pathologies is
difficult (Strehler in 1986, Mechanisms of Aging . . . I believe does some
thinking about this).

>>(5) despite what I said in (1), in mammals that is not true.
>You've got to make up your mind here. If similarity of aging is evidence
>for your theory, variability (1) is evidence against it, and vice

Not really. Variability (1) is more likely to occur with simple aging
mechanisms. However, uniformity amongst a single phylum is also what is
expected assuming the causes of aging are the same for all species. You
see, it's two different phenomena: In (1) it is a comparison of different
causes of aging while in (5) it is a comparison between species that age
for the same reason.

>No; the simple explanation is that *everything* goes wrong. Mammals are
>all biologically very similar; they have the same things to go wrong.
>Non-replaceables wear out; proliferation slows, impairing repair,
>and cancer becomes more common. These are all very straightfoward.

But how do you explain that they occur in mice after 3 years and in humans
after 60? Something is the timekeeper of these events. You can say it's the
normal developmental program or whatever but something is controlling all
these events; they are not independant of one another.

I actually forgot another reason. If you are right and I'm wrong then every
single age-related pathology is independant (one gene for each pathology,
with, you might say, some exceptions). So how do you explain Werner's or
Hutchinson-Gilford's syndromes? Even if you don't think they are cases of
accelerated aging (which you'll obviously have to be ready to defend),
people with these diseases develop about 50% of all aging phenotypes (50%
of age-related pathologies you claim are independant). As you know,
Werner's syndrome is caused by one single gene. This alone rules out the
possibility that all age-related pathologies cannot have an upstream
regulator. In addition, it also provides strong evidence that other simple
(probably not with just one gene but a few more) mechanisms can be upstream
of most, if not all, aging pathologies. Finally, it demonstrates that
age-related pathologies do not develop independently and do not originate
in different genes (although other genes can affect their expression).

>He needs to read the literature: there have been many demonstrations
>of antagonistic pleiotropy. Offhand, I can recall Rose's and Partridge's;
>there are many, many others.

Can you mention them (particullarly in humans)? I couldn't find that many.
So far, I've got Lithgow, Rose, Partridge, Johnson, Austad, and Walker. In
humans all I've got is Hutchinson's disease increasing fertility.

>He doesn't mention that an aging population will be far less fit just
>because it has a higher death rate. If the situation is dire to the
>point a non-aging population can barely make it, the aging population
>will have negative growth due to the extra mortality, and will go

Good point. I discussed with Bowles a few months ago his article and I
don't agree with all his ideas. However, I think he mentions a few
interesting points regarding how aging can be advantageous in certain

>P.S. I'm not knocking Medical Hypotheses; there's a role for such
>journals. It's just that things published there aren't really evidence
>for anything.

I think there is a place for theoretical biology. In fact, I think there
should be more theoretical journals in biology. Physics, for example, has
many more people just working on theories. I think it's a pity that in
biology that doesn't happen; most biologists have to associate lab work
with thinking; which means the time biologists spend thinking is not as big
as physicists. That's probably why, on average, physicists are more
intelligent than biologists (taken from "The Bell Curve").

Best wishes.

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