In a message dated 6/30/00 3:37:30 AM, email@example.com writes:
>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).
How about us? Everything goes wrong, with a bewildering array of
interelated environmental and non-environmental causes, at widely
varying rates in different individuals.
Once-off reprocing, or semelparous, species, work as predicted; if
there's no chance of repeated reproduction there's no selection for
post-reproductive viability, so you get nearly instant death
(Pletcher and Curtsinger, 1998)
>>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.
The problem for "aging gene" theory is not so much the wide effects
of aging as the variability.
>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).
And I was pointing out it's not difficult; it's inevitable because
defective or inferior versions of *every* gene will be rattling around
in the population (unless pathologically inbred).
>>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.
If it's uniform within a phylum it's certainly going to be uniform
within a species.
>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
>normal developmental program or whatever but something is controlling all
>these events; they are not independant of one another.
The "timekeeper" is selective value: the detriment of one system failing
ahead of the general curve is very high, so "premature" death gets fixed.
The benefit of one system outlasting the curve is very small, so
extra-resilient mechanisms get lost.
>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
Not "cannot" in a mechanical sense (although even Werner's only does
*part* of aging), but "cannot" in an evolutionary sense: variation
in that helicase is not the cause of aging, and the helicase in the
normal population will be good enough to be a negligible cause of
mortality (which it is; in normal individuals you have many other
causes of DNA and chromosomal damage). I have to agree that you
could get an "aging clock"; it's not genetically impossible.
>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).
No, two genetic effects which produce many but not all aging phenotypes
don't prove that you can't produce those phenotypes by other mechanisms.
Indeed, every inbred mouse line seems to have a different way to get
>>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.
Well, calorie restriction works for just about
any species. One example is the marsupial mice (forget the name)
where the males a semelparous and the females iteroparous. The
males die from side-effects of hypertestosterone; crank down
their testosterone and they live several years too; but they
reproduce less. Nagai et al showed that when you breed mice
for extended survival you lose early fecundity. There are
sex hormone-survival tradeoffs in many species, including
human males at least.
>>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.
Medical Hypotheses is not unusual in being theoretical (there is
much theoretical work and even some theoretical journals). It's
unusual in publishing mildly crackpot theoretical work - stuff
that generates "oh please" or "who cares" responses from editors
of even third-string journals.
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