Evolution of aging (was Insulin Resistance and CR)
James
[sorry if you get two of these - my news server seems to be acting up
and at tthis point the one I posted before is not showing]
Zooko Journeyman wrote:
>
> Hang-Jun Jang <i...@chollian.net> wrote:
> >
> >Every organism
> >might be evolving to achieve eternal youth.
>
> Seems doubtful. Longevity beyond a certain point doesn't seem
> to be evolutionarily advantageous. If a species had infinite
> lifespan, it would evolve slowly or not-at-all after that!
[snip]
Neither of these theories are correct. Evolution does not favor eternal
youth, nor does it work against it. It simply does not care. Once you
have reproduced (and, in species where rearing the young is essential, I
imagine you must live long enough to do that as well) there are no
selective pressures either way. Without any selective pressures, the
result is aging and death since that is the result favored by chance
(since it takes a great deal of directed effort to maintain an organism,
entropy favors death).
The theory that old organisms dying to make room for their offspring is
beneficial can be disposed of by looking at mortality curves for various
organisms. Simply by looking at mortality rates in the wild for various
organisms you see that not very many individuals die of old age. They
die by accident or by predation at a relatively high rate, which would
leave plenty of room for future generations. Age-related death
contributes but a small amount to total death.
James
[sorry if you get two of these - my news server seems to be acting up
Zooko Journeyman
In article <3511D7...@nospam.com>, James <ja...@nospam.com> wrote:
>
>Zooko Journeyman wrote:
>>
>> Hang-Jun Jang <i...@chollian.net> wrote:
>> >
>> >Every organism
>> >might be evolving to achieve eternal youth.
>>
>> Seems doubtful. Longevity beyond a certain point doesn't seem
>> to be evolutionarily advantageous. If a species had infinite
>> lifespan, it would evolve slowly or not-at-all after that!
>
>[snip]
>
>Neither of these theories are correct. Evolution does not favor eternal
>youth, nor does it work against it. It simply does not care. Once you
>have reproduced (and, in species where rearing the young is essential, I
>imagine you must live long enough to do that as well) there are no
>selective pressures either way.
<snip>
Au contraire. Selective pressure can be applied upon a gene
even if the individual containing the gene never reproduces
again.
Imagine a gene which causes old, no-longer-reproducing
squirrels to go crazy and start biting the heads off of other
squirrels. This gene would receive negative selective pressure
over generations (because of its deleterious effects upon the
individual's family and neighbors) even though it has no effect
whatsoever during the reproductive cycle of the individual.
Not, of course, that living a long time is in any way
equivalent to biting the head off of a squirrel, but you get
the idea. Your argument that such a gene receives no selective
pressure, while intuitively appealing, is incorrect.
For related (?) perspectives, see Dawkins "The Extended
Phenotype" (1980's) and Baldwin (1880's).
Regards,
Zooko
"Half-assed programming is a time-filler that, like knitting,
must date to the beginning of the human experience."
-- Vernor Vinge, _A_Fire_Upon_the_Deep_
James
> Imagine a gene which causes old, no-longer-reproducing
> squirrels to go crazy and start biting the heads off of other
> squirrels. This gene would receive negative selective pressure
> over generations (because of its deleterious effects upon the
> individual's family and neighbors) even though it has no effect
> whatsoever during the reproductive cycle of the individual.
>
> Not, of course, that living a long time is in any way
> equivalent to biting the head off of a squirrel, but you get
> the idea. Your argument that such a gene receives no selective
> pressure, while intuitively appealing, is incorrect.
Sorry, but I think most current aging researchers would disagree with you on
this. If you want to argue the point on a pure logic basis (which I don't
feel is relevant) you might be correct, however when it comes to the real
world of aging you are not. As you point out, old squirrels don't bite the
heads off young ones -- nor does anything remotely similar happen -- so you
can't just generalize on the basis of some contrived situaiton. It is fairly
well accepted that aging occurs because, after successful reproduction,
selective pressure falls to levels that will not weed out deleterious
mutations.
References:
General: "Molecular Biology of Aging " (Rose),
Disposable Soma Theory: Kirkwood and Cremer, 1982.
Relationship bewtween adult mortality rates and maximum lifespan: Botkin and
Miller, 1974.
James
Ooops. That first reference should have been "Evolutionary Biology of Aging" by
Rose. By the way, this has the differential equations in it that describe the
reduction in selective pressure after reproduction.
Aubrey de Grey
Here is an ultra-potted history of ideas re the evolution of aging.
- Weissman 1881: Aging is selected for because old organisms compete
with young ones and diminish the adaptability of the species to
changing conditions, which is necessary for the species's long-term
survival. Broadly accepted until Medawar (1952) pointed out that
animals in the wild virtually always die very young, so that none
of the phenotypes of aging can possibly be causally relevant.
- Medawar 1952: selective pressure on late-onset phenotypes is so slight
that pro-aging mutations are not weeded out.
- Williams 1957: antagonistic pleiotropy. Since there is no selection
for late-onset phenotypes, the value in old age of genes which are
good for us in youth (so are selected for) varies. In particular, a
few (at least) are bad for us in old age (but without selection
against); these drive aging.
- Kirkwood 1977: disposable soma. Aging is selected for because it is
a result of sloppy maintenance, which is selected for because it
doesn't use up as much energy as good maintenance so leaves more
energy for reproduction.
The disposable soma theory is not currently disputed (though it has been
greatly refined and fleshed out in the past 20 years). It has elements of
what both James and Zooko (or, if you like, Medawar and Williams) said; I
hope this helps. I should mention, however, that it applies only to those
organisms in which sloppy maintenance causes aging. It is by no means
clear that this is universal in higher organisms: the curious phenomenon of
negligible senescence in some species with indeterminate growth (including
lobsters and some fish) may be an exception.
Aubrey de Grey
James
> The disposable soma theory is not currently disputed (though it has been
> greatly refined and fleshed out in the past 20 years). It has elements of
> what both James and Zooko (or, if you like, Medawar and Williams) said; I
> hope this helps. I should mention, however, that it applies only to those
> organisms in which sloppy maintenance causes aging. It is by no means
> clear that this is universal in higher organisms: the curious phenomenon of
> negligible senescence in some species with indeterminate growth (including
> lobsters and some fish) may be an exception.
Good summary Aubrey - Thanks! Question: Do you have references for the
negligible senesence in lobsters/fish? I have heard of this from time
to time, but haven't seen the primary literature. The only
multicellular organism that I know of that has been shown (to a fairly
high degree of certainty) to be immortal is hydra.
James
Steven B. Harris
In <6eutu8$ihh$1...@xs2.xs4all.nl> Zooko Journeyman <zo...@xs4all.nl>
writes:
>In article <3511D7...@nospam.com>, James <ja...@nospam.com>
wrote:
>>
>>Zooko Journeyman wrote:
>>>
>>> Hang-Jun Jang <i...@chollian.net> wrote:
>>> >
>>> >Every organism
>>> >might be evolving to achieve eternal youth.
>>>
>>> Seems doubtful. Longevity beyond a certain point doesn't seem
>>> to be evolutionarily advantageous. If a species had infinite
>>> lifespan, it would evolve slowly or not-at-all after that!
>>
>>[snip]
>>
>>Neither of these theories are correct. Evolution does not favor
eternal
>>youth, nor does it work against it. It simply does not care. Once
you
>>have reproduced (and, in species where rearing the young is
essential, I
>>imagine you must live long enough to do that as well) there are no
>>selective pressures either way.
>
><snip>
>
>Au contraire. Selective pressure can be applied upon a gene
>even if the individual containing the gene never reproduces
>again.
>
>
>squirrels to go crazy and start biting the heads off of other
>squirrels. This gene would receive negative selective pressure
>over generations (because of its deleterious effects upon the
>individual's family and neighbors) even though it has no effect
>whatsoever during the reproductive cycle of the individual.
>
>
>Not, of course, that living a long time is in any way
>equivalent to biting the head off of a squirrel, but you get
>the idea. Your argument that such a gene receives no selective
>pressure, while intuitively appealing, is incorrect.
It is true that through mechanisms of kin-selection, genes can have
influences independent of those that influence reproduction directly.
However, the influences are quite weak, especially if they don't
involve some kind of heavy nurturing or destructive behavior toward
relatives. Some gene that caused some kind of very diffuse advantage
or disadvantage for a *population* which carried it, would not give a
lot of selective pressure. And such influence as it DID have, would
only apply so long as the population which carried it was
reproductively isolated from others which didn't have it.
That, ultimately, is the fatal flaw in the old Weissman theory of
the evolution of aging, which posits that genes which cause aging were
selected for, because populations which carried them had a faster
turnover, and were more adaptable to environments. Nevermind that most
turnover in populations (deaths) have little to do with aging. Being
ageless is not the same as being immortal, and conditions being what
they are in the wild, average lifespan wouldn't be greatly different
for ageless animals (selective pressure is small, as discussed above).
The main problem is that the Weissman theory demands that the
detrimental effects of ageless members on a population is *so*
negative, that by kin selection alone it manages to outweigh the clear
reproductive advantages to the individuals who carry an ageless gene
(and who never suffer age-related infertility). This could happen only
if populations within the same species are not in reproductive contact.
Clearly, an "ageless" gene would confer short term benefits on
individuals, and spread through any population until it did away with
the allelic competition. All that would prevent such genes from
spreading throughout an entire species would be some kind of
reproductive isolation, allowing populations to "compete" with each
other indirectly, without ever having contact. After one population
died out, due to its burden of ageless individuals (we presume for the
sake of argument that the adaptive load on the population is this
severe), perhaps the other shorter-lived population could move in. Any
contact before that, however, and the whole thing is ruined: even one
inter-population mating per generation between "competing" populations
totally ruins any chance of a gene winning out by a positive advantage
in kin selection, when its direct reproductive effects are bad. On the
contrary, the reverse will happen. The problem with antagonistic
pleiotropy is that it works just as well on populations as it does on
individuals: if something helps a gene gain ground in a population in
the short term, that is what will happen, even if the gene is not good
for the population (or the species) in the long term. In humans and
other mammals, there is way too little genetic isolation between
populations for them ever to have competed strongly by means of kin
selection.
Steve Harris, M.D.
Zooko Journeyman
Steven B. Harris <sbha...@ix.netcom.com> wrote:
<snip>
Thanks to the several contributors for informed discussion of
the evolution of aging.
Do i understand correctly that the current scientific consensus
is that aging has little enough of a(n extended) phenotypic
effect upon other organisms that it can be considered
evolutionarily neutral? (Where the sloppy maintenance
hypothesis considers aging as such evolutionarily neutral, but
maintenance as evolutionarily significant.)
Regards,
Zooko
-------
Steven B. Harris
In <6f9j99$1me$1...@xs2.xs4all.nl> Zooko Journeyman <zo...@xs4all.nl>
writes:
>the evolution of aging.
>
>Do i understand correctly that the current scientific consensus
>is that aging has little enough of a(n extended) phenotypic
>effect upon other organisms that it can be considered
>evolutionarily neutral?
Comment:
That depends on what you consider "aging." In times past, the
time-dependent part of the mortality rise in the Gompertz-Makeham curve
was considered aging, and that term takes care of 90% of deaths in low
Makeham term conditions (low accidental mortality conditions). If this
is aging, it's probably caused by genetics (antagonistic pleiotropy
from genes important in youth) coupled with the effects of stochastic
(random) catastrophic failures which result from these-- such as cancer
promotion and initiation. Or fractures from osteoporosis caused by
bone loss at low estrogen levels (great for lactation, not so good for
granny).
Obviously, there are more than two aging processes, if the
mortalilty curve suffers an extra infection after 90% of animals have
died after good conditions, and now the force of mortality begins to
wayne. Perhaps this process, which kills the last 10 % of animals, and
is characterized by simply dropout and death and fibrosis fo cells in
all organs, wich attendent increasing dysfunction, has been going on
for all of the lifetime, and is more the "true" aging (since some lucky
people escape the premature death from pleiotropy problems, but nobody
escapes this latter process). And aging is nothing if not universal.
> (Where the sloppy maintenance
>hypothesis considers aging as such evolutionarily neutral, but
>maintenance as evolutionarily significant.)
Yes, this last kind of aging (disposable soma theory) has more to do
with the cost of maintennance, causing sloppy maintennence where good
maintainene is not needed, due to expected short mortalities from the
prospect of being lunch, rather than the prospect of immortality. But
sloppy maintainence here does not show up in just in one place-- rather
it shows up everywhere at roughly the same rate (why run maintainence
better in one place than another-- that's just wasted energy. Good
engineering never builds any part too much stronger than the others.
That is why people who die after the age of 100 die with everything
wrong with them, but nothing in particular.
In other words, you can look at a typical lifespan curve and guesss
that both major aging theories postulated in this decade are true.
It's the case of the seven blind men from Hindustan (Sach's poem), and
all are right. The antagonistic plieotropy theory of Medawar explains
time-dependent (exponential) increases in mortality during the first
90% of the way to maxiumum life span. But that's not all there is to
explain (though some texts simply ignore the tail).
If you escape all those bad genes (those that cause dessert
cravings, fast clot making, and so on), however, then the death of the
last 10% of your population sample, with it's much gentler increases in
force of mortality over time, are explained better by plain old wear
and tear. Which rate is amenable to evolutionary forces if predation
and stochastic mortality are low enough, and energy cost of upkeep is
low enough, that it's worth the while in reproductive and repair costs
to delay it wear and tear, when the organism can. But even here there
are apparently limits, as there are no basic designs which are built
using perfect repair as one of nature's designs for animals with
working brains or muscles. Or alveoli or glomeruli. Nature is
proflagate at building one-shot devices which give creatures short
term advantages, but can't be fixed anymore than that sealed factory
timeing box in the new cars. So, you can have agelessness if you don't
mind being a huckeberry or coral polyp or hydra. But what kind of a
deal is that? For the rest of us, nature can perhaps give you a slow in
aging and an increase in metabolic time of 2 or even 5 if you have a
big brain, or wings, or a shell. Further than that, and you'll have to
hope for nanotechnology and cryonics.
Steve Harris, M.D.
Gerontologist
Steven B. Harris
>In <6f9j99$1me$1...@xs2.xs4all.nl> Zooko Journeyman <zo...@xs4all.nl>
writes:
>Thanks to the several contributors for informed discussion of
>the evolution of aging.
>
>Do i understand correctly that the current scientific consensus
>is that aging has little enough of a(n extended) phenotypic
>effect upon other organisms that it can be considered
>evolutionarily neutral?
Comment:
That depends on what you consider "aging." In times past, the
time-dependent part of the mortality rise in the Gompertz-Makeham curve
was considered aging, and that term takes care of 90% of deaths in low
Makeham term conditions (low accidental mortality conditions). If this
is aging, it's probably caused by genetics (antagonistic pleiotropy
from genes important in youth) coupled with the effects of stochastic
(random) catastrophic failures which result from these-- such as cancer
promotion and initiation. Or fractures from osteoporosis caused by
bone loss at low estrogen levels (great for lactation, not so good for
granny).
Obviously, there are more than two "aging processes," if the
mortalilty curve suffers an extra infection after 90% of animals have
died after good conditions, and now the time dependent force of
mortality begins to wain. What, aging slows down? Naw-- more like
it's always been there since puberty, and has been covered up by
various other parasitic processes designed to make use work better then
young, but not survive long when old. Perhaps this process, which
kills the last 10 % of animals, and is characterized by simply dropout
and death and fibrosis fo cells in all organs, wich attendent
increasing dysfunction, has been going on for all of the lifetime, and
is more the "true" aging (since some lucky people escape the premature
death from pleiotropy problems, but nobody escapes this latter
process). And aging is nothing if not universal.
> (Where the sloppy maintenance
>hypothesis considers aging as such evolutionarily neutral, but
>maintenance as evolutionarily significant.)
Yes, this last kind of aging (disposable soma theory) has more to do
with the cost of maintennance, causing sloppy maintennence where good
maintainene is not needed, due to expected short mortalities from the
prospect of being lunch, rather than the prospect of immortality. But
sloppy maintainence here does not show up in just in one place-- rather
it shows up everywhere at roughly the same rate (why run maintainence
better in one place than another-- that's just wasted energy. Good
engineering never builds any part too much stronger than the others.
That is why people who die after the age of 100, typically die with
everything wrong with them, but nothing in particular.)
In other words, you can look at a typical lifespan curve and guesss
that both major aging theories postulated in this decade are true.
It's the case of the seven blind men from Hindustan (Sach's poem), and
all are right. The antagonistic plieotropy theory of Medawar explains
time-dependent (exponential) increases in mortality during the first
90% of the way to maxiumum life span. But that's not all there is to
explain about mortality changes with time (though some texts simply DO
ignore the tail).
If you escape all those bad genes (those that cause dessert
cravings, fast clot making, and so on), however, then the deaths of
your last 10% of your population sample, with it's much gentler
increases in force of mortality over time, are explained better by
plain old wear and tear. Which rate is amenable to evolutionary forces
if predation and stochastic mortality are low enough, and energy cost
of upkeep is low enough, that it's worth the while in reproductive and
repair costs to delay it wear and tear, when the organism can. But
even here there are apparently limits, as there are no basic designs
which are built using perfect repair as one of nature's designs for
animals with working brains or muscles. Or alveoli or glomeruli.
Nature is proflagate at building one-shot devices which give creatures
short term advantages, but can't be fixed anymore than that sealed
factory timeing box in the new cars. So, you can have agelessness if
you don't mind being a huckeberry or coral polyp or hydra. But what
kind of a deal is that? For the rest of us, nature can perhaps give you
a slow in aging and an increase in metabolic time of 2 or even 5 if you
have a big brain, or wings, or a shell. if you need more than
thatyou'll have to hope that cryonics and nanotechnology.
Steve Harris, M.D.
Gerontologist
>
>
>
>
>
Steven B. Harris
>Thanks to the several contributors for informed discussion of
>the evolution of aging.
>
>Do i understand correctly that the current scientific consensus
>is that aging has little enough of a(n extended) phenotypic
>effect upon other organisms that it can be considered
>evolutionarily neutral?
Comment (edited a bit for typos):
That depends on what you consider "aging." In times past, the
time-dependent part of the Gompertz-Makeham curve was considered
aging, and that term takes care of 90% of deaths in low Makeham-
term conditions (i.e., in low accidental mortality conditions,
such as populations in zoos, or populations getting good medical
care in industrialized countries). If this early time-dependent
exponential mortality is "aging," then "aging" is probably caused
by genetics (antagonistic pleiotropy from genes important in
youth but causing problems in old age) coupled with the effects of
stochastic (random) catastrophic failures which result from these.
Examples are cancer promotion and initiation. Or fractures from
osteoporosis caused by bone loss at low estrogen levels (great for
lactation, not so good for granny). Or emboli and infarctions caused
by a clotting system which works well at young ages, but not later.
Obviously, however, looking at real mortality curves shows
that they are not quite Gompertzian. If you look at the rise in
mortality, it is exponential up to a point, and then something
happens. There is, in short, more than one "aging processes," if
the mortality curve suffers an extra inflection after 90% of
animals have died after good conditions, and now the time
dependent force of mortality begins to wain. Which *is* what
happens in real mortality curves in everything from humans to
rats to fruitflies. What, you say--- aging slows down? A better
guess is that "aging" has always been there since puberty,
increasing chance of mortality slowly and perhaps linearly, but
has until very late in life (90% of max lifespan) been covered up
by late (and bad) effects of various other physiologic processes,
which are designed to make us work better then young, but which
become a hinderment (and exponentially risking source of
mortality risk) when we become old.
Perhaps this non-exponential aging process, the one that kills
the last 10% of animals in any population, and is characterized
by simple dropout and death and fibrosis of cells in all organs
(with attendant linearly increasing organ dysfunction), has been
going on for all of the lifetime, and is a better candidate for
"true" aging. After all, some lucky people escape the premature
death from pleiotropy problems (Jean Calmette), but nobody
escapes this latter process. And aging is nothing if not
universal.
> (Where the sloppy maintenance
>hypothesis considers aging as such evolutionarily neutral, but
>maintenance as evolutionarily significant.)
Yes, this last kind of aging (outlined in Kirkwood's
"disposable soma" theory, 1977) has more to do with the cost of
maintenance, because it results in sloppy maintenance where good
maintenance is not needed, due to expected short mortalities from
the prospect of being lunch, rather than the prospect of immorta-
lity. But sloppy maintenance in an animal of course does not
show up in just in one place-- rather it shows up everywhere at
roughly the same rate (why run maintenance better in one place
than another-- that's just wasted energy. Good engineering never
builds any part too much stronger than the others). That is why
people who die after the age of 100, typically die with
everything wrong with them, but nothing in particular.
In other words, you can look at a typical lifespan curve and
guess that both major aging theories postulated in this half of
the 20th century are true. It's the case of the seven blind men
from Hindustan (Sach's poem), and all are right. The
antagonistic pleiotropy theory of Medawar explains time-dependent
(exponential) increases in mortality during the first 90% of the
way to maximum life span, ala Gompertz. But that's not all there
is to explain about mortality changes with time (though some
texts simply DO ignore the mortality curve tail).
If you escape the bad geriatric effects all those genes that
help you in youth, but hurt later (those that cause dessert
cravings, fast clot making, and so on), then the deaths of your
last 10% of your population sample, with its much gentler
increases in force of mortality over time, are non-Gompertzian
mortality, and are explained better by plain old wear and tear.
Death here is stochastic, and results from random perturbations
of a system which has become fragile in all parts, due to bad
upkeep. The evolutionary rate of upkeep is amenable to
evolutionary forces. If predation and stochastic mortality are
low enough, and energy cost of upkeep is low enough, that it's
worth the while in reproductive and repair costs to delay wear
and tear, when the organism can. But even here there are
apparently limits, as we know of no designs built around perfect
or near perfect repair in nature's designs for animals with
working brains or muscles. Or alveoli or glomeruli. Nature is
profligate at building one-shot devices which give creatures
short term advantages, but can't be fixed any more than that
factory-sealed electronic-timing box in the new cars.
What this means is that you can have agelessness if you don't
mind being a huckleberry or coral polyp or hydra. But what kind
of a deal is that? For the rest of us, nature can perhaps give
you a slowdown in aging, and an increase in metabolic time of 2
or even 5, if you have a big brain, or wings, or a shell. if you
need more than that, you'll have to hope that cryonics and
nanotechnology succeed.
Steve Harris, M.D.
Zodor
James wrote:
>
> [sorry if you get two of these - my news server seems to be acting up
> and at this point the one I posted before is not showing]
>
> >
> > Hang-Jun Jang <i...@chollian.net> wrote:
> > >
> > >Every organism
> > >might be evolving to achieve eternal youth.
> >
> > Seems doubtful. Longevity beyond a certain point doesn't seem
> > to be evolutionarily advantageous. If a species had infinite
> > lifespan, it would evolve slowly or not-at-all after that!
>
> [snip]
>
> Neither of these theories are correct. Evolution does not favor eternal
> youth, nor does it work against it. It simply does not care. Once you
> have reproduced (and, in species where rearing the young is essential, I
> imagine you must live long enough to do that as well) there are no
> result is aging and death since that is the result favored by chance
> (since it takes a great deal of directed effort to maintain an organism,
> entropy favors death).
>
It takes vast amounts of energy to reduce entropy in order to build an
organism to begin with. In theory, it would not be unfeasible to have
an organism that would eat, use that energy to reduce entropy in order
to maintain its existance, and not physically degenerate to as great an
extent. That would seem to not be too much more than to have an
organism built from scratch to begin with.
The idea that there are no selective pressures either way is misleading.
If a very 'fit' organism lives indefinately, it can produce more
offspring than an organism that lives a finite amount of time, and then
has its genes in offspring.
The fit genes in the offspring can be shuffled around to greater extents
in offspring than in the first organism. If there are destructive
recessive genes in the long lived 'fit' organism, those recessive genes
could 'piggyback' on the 'fit' gene that increased the organism's
survivability and propogate along with the organism. A 'long necked
giraffe' in a forest with high leaves with a recessive gene for
hemophilia could propogate the hemophilia gene. With the reshuffling of
genes with each generation, these recessive destructive traits could
more thouroughly be weeded out. This would at least make longevity not
be selected for under some conditions.
Still, there is a need for a lengthened reproduction and longevity time
if there is much time needed to grow the organism to begin with. This
is evidenced by the fact that large organisms (whales) have longer
lifespans than smaller organisms (grasshoppers).
Humans have also in the past few million years of evolution had a factor
that has also selected for its longevity. Even considering captivity
and a sedentary lifestyle and medical procedures and the like, humans
have a somewhat longer lifespan than other organisms their size (chimps,
gazelles, pigs, dogs, lions and even whales). Only some tortises and
some fish and possibly lobsters can outlive a centegenarian. This has
been due to the fact that the organism (human) has increased
survivability when it can accumulate store and give out information over
a long time period.
The process may be extended further in the near future when over the
next several generations humanity genetically re-engineers itself to
have an indefinate potential lifespan.
James
> The idea that there are no selective pressures either way is misleading.
>
> If a very 'fit' organism lives indefinately, it can produce more
> offspring than an organism that lives a finite amount of time, and then
> has its genes in offspring.
No, it is not misleading, it is absolutely true. The concept that you
state is appealing at first glance, but it turns out that that just
isn't the way it works. I won't bother to debate about it further since
I have not been through the math that is applicable to this situation.
Suffice it to say that I don't think any mainstream aging researchers
would agree with you, so be careful what you state as fact.
Zodor
James wrote:
>
> > The idea that there are no selective pressures either way is misleading.
> >
>
> No, it is not misleading, it is absolutely true. ...
I would agree with you that in general evolution does not either favor
eternal youth or select against it. However, there are more specific
times where selection pressures may operate one way or the other.
Admittably, if an organism does not live long enough to reproduce that
is selected against.
> I have not been through the math that is applicable to this situation.
I am interested in the math. Do you have any good references on the
subject that I might use to learn more about the mathematics of
populations and genetic selection and the like?
James
> > I have not been through the math that is applicable to this situation.
>
> I am interested in the math. Do you have any good references on the
> subject that I might use to learn more about the mathematics of
> populations and genetic selection and the like?
I'm not sure where to find a really comprehensive treatment of the
subject, but Rose's "Evolutionary Biology of Aging" has a couple pages
on it along with the formulas.
Aubrey de Grey
James wrote:
> Do you have references for the
> negligible senesence in lobsters/fish?
Sorry for the delayed reply. Not nearly enough work has been done
on this, but two excellent places to find out what's known are:
- "Longevity, Senescence and the Genome", by Caleb Finch: University
of Chicago Press, 1990. This is a fantastically comprehensive
treatment of senescence in all manner of organisms, and deals
extensively with negligible senesence.
- Gerontology 40(2-4), 1994. This is a whole issue edited by B.K.
Patnaik, who with various colleagues has been working on aging
in lower vertebrates for many years.
Aubrey de Grey
Kate
Aubrey de Grey <ag...@mole.bio.cam.ac.uk> wrote in article
<6fub3r$hr8$1...@lyra.csx.cam.ac.uk>...
>
> James wrote:
>
> > Do you have references for the
> > negligible senesence in lobsters/fish?
>
A recent National Geographic has the name of a turtle researcher, Whit
Gibbons, at the University of Georgia, who claims they don't age.
Other researchers disagree and believe turtles do age.
Probably you could contact Whit Gibbons through the university.
Kate