>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).
>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
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").
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