| |
 |
|
|
Science Forum Index » Life Extension Forum » New special 'Longevity' issue of "Social Biology"
Page 1 of 1
|
| Author |
Message |
| Leonid Gavrilov |
 Posted: Sun Jan 04, 2004 5:02 pm |
|
|
|
Guest
|
Greetings,
I thought you might be interested to know about new special issue of
the journal "Social Biology" devoted to the problems of human
longevity. Details are attached below.
Best wishes for the New Year !
Kind regards,
-- Leonid Gavrilov
Author of the book "The Biology of Life Span"
http://longevity-science.org/index.html#Book
==================================
SOCIAL BIOLOGY, 49 (3-4): FAL-WIN 2002 (Released just recently):
--SPECIAL ISSUE: THE BIODEMOGRAPHY OF FERTILITY AND LONGEVITY -------
Biodemography: Consilience in action - An introduction to a special
issue of Social Biology
The effect of the nurturant bonding system on child security of
attachment and dependency
Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Fertility and post-reproductive longevity
Individual aging and mortality rate: How are they related?
Between nurture and nature: The shifting determinants of female
fertility in Danish twin cohorts
----------------THE END---------------------------------- |
|
|
| Back to top |
|
| DZ |
| Posted: Wed Jan 07, 2004 7:01 pm |
|
|
|
Guest
|
Leonid Gavrilov <gavrilov@aol.com> wrote:
Quote: Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Some of your research suggest that the increase in the (at least
father's) age of reproduction will decrease the offspring life span -
partly via the increase in the mutational load. By this mechanism the
life span decrease is expected to be heritable.
However, the population effect of this is ratchet-like. That is, since
younger than average age of reproduction does not increase the
expected life span (compared to the parental life expectancy), the
population mean life span should quickly decrease with
generations. This is so even when allowing for lower fertility of
offspring with the lower life expectancy.
For example, if the life expectancy is decreased on average by one
year when the reproduction event occurs after a threshold age, and if
the probability of such event (late reproduction) is 0.1, then the
population average life span will decrease by 5 years each 50
generations. Your numbers (of life span effect on daughters) imply
even sharper decrease.
How do you reconcile your theory with the observation that the life
expectancy in human populations is at least sustained?
DZ |
|
|
| Back to top |
|
| Tim Tyler |
| Posted: Wed Jan 07, 2004 8:06 pm |
|
|
|
Guest
|
In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Quote: Leonid Gavrilov <gavrilov@aol.com> wrote:
Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Some of your research suggest that the increase in the (at least
father's) age of reproduction will decrease the offspring life span -
partly via the increase in the mutational load. By this mechanism the
life span decrease is expected to be heritable.
However, the population effect of this is ratchet-like. That is, since
younger than average age of reproduction does not increase the
expected life span (compared to the parental life expectancy), the
population mean life span should quickly decrease with
generations. [...]
You are basically posing a specific instance of the general question
of how a population can maintain its genetic integrity in the face of
deleterious mutations.
The answer is much the same as normal: by those with too many deleterious
mutations failing to reproduce; by sexual recombination sometimes
randomly rearranging partially compromised parental genomes into intact
ones; and by sexual selection casuing those with mostly intact genomes
to seek each other out and have more offspring than is usual.
--
__________
|im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. |
|
|
| Back to top |
|
| DZ |
| Posted: Thu Jan 08, 2004 3:14 am |
|
|
|
Guest
|
Tim Tyler <tim@tt1lock.org> wrote:
Quote: In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Leonid Gavrilov <gavrilov@aol.com> wrote:
Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Some of your research suggest that the increase in the (at least
father's) age of reproduction will decrease the offspring life span -
partly via the increase in the mutational load. By this mechanism the
life span decrease is expected to be heritable.
However, the population effect of this is ratchet-like. That is, since
younger than average age of reproduction does not increase the
expected life span (compared to the parental life expectancy), the
population mean life span should quickly decrease with
generations. [...]
You are basically posing a specific instance of the general question
of how a population can maintain its genetic integrity in the face of
deleterious mutations.
The answer is much the same as normal: by those with too many deleterious
mutations failing to reproduce; by sexual recombination sometimes
randomly rearranging partially compromised parental genomes into intact
ones; and by sexual selection casuing those with mostly intact genomes
to seek each other out and have more offspring than is usual.
In this specific instance there is a strikingly large change in the
mean trait value: about 5% per generation, that occurs with the
probability equal to the chance of a late conception, which is itself
quite high. At the same time, being a trait with post-reproductive
manifestation, the decrease in the life span is only indirectly
related to fitness. Therefore, I would not expect the selection to be
strong enough to balance the mutational influx that is apparently
quite high. So, what is the decrease in reproduction probability among
those with the reduced life span due to late reproduction of their
parents?
As far as recombination is concerned, partially compromised parental
genomes can of course be rearranged in a way that would further
increase the number of mutations in offspring, rather than decrease
it. The selection here is essentially truncating, and the effect you
describe simply increases the population variance in the trait value.
Further, I doubt that substantial preferential mating of those with
"intact genomes" exists in humans, especially to the extent that would
offset the effect on the population life span value.
DZ |
|
|
| Back to top |
|
| DZ |
| Posted: Thu Jan 08, 2004 3:31 am |
|
|
|
Guest
|
Tim Tyler <tim@tt1lock.org> wrote:
Quote: In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Leonid Gavrilov <gavrilov@aol.com> wrote:
Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Some of your research suggest that the increase in the (at least
father's) age of reproduction will decrease the offspring life span -
partly via the increase in the mutational load. By this mechanism the
life span decrease is expected to be heritable.
However, the population effect of this is ratchet-like. That is, since
younger than average age of reproduction does not increase the
expected life span (compared to the parental life expectancy), the
population mean life span should quickly decrease with
generations. [...]
You are basically posing a specific instance of the general question
of how a population can maintain its genetic integrity in the face of
deleterious mutations.
The answer is much the same as normal: by those with too many deleterious
mutations failing to reproduce; by sexual recombination sometimes
randomly rearranging partially compromised parental genomes into intact
ones; and by sexual selection casuing those with mostly intact genomes
to seek each other out and have more offspring than is usual.
In this specific instance there is a strikingly large change in the
trait value: about 5% in a single generation, that occurs with the
probability equal to the chance of a late conception, which is itself
quite high. At the same time, being a trait with post-reproductive
manifestation, the decrease in the life span is only indirectly
related to fitness. Therefore, I would not expect the selection to be
strong enough to balance the mutational influx that is apparently
quite high. So, what is the decrease in reproduction probability among
those with the reduced life span due to late reproduction of their
parents?
As far as recombination is concerned, partially compromised parental
genomes can of course be rearranged in a way that would further
increase the number of mutations in offspring, rather than decrease
it. The selection here is essentially truncating, and the effect you
describe simply increases the population variance in the trait value.
Further, I doubt that substantial preferential mating of those with
"intact genomes" exists in humans, especially to the extent that would
offset the effect on the population life span value.
DZ |
|
|
| Back to top |
|
| Tim Tyler |
| Posted: Thu Jan 08, 2004 6:18 am |
|
|
|
Guest
|
In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Quote: Tim Tyler <tim@tt1lock.org> wrote:
In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Leonid Gavrilov <gavrilov@aol.com> wrote:
Genealogical data and the biodemography of human longevity
--- (http://longevity-science.org/SocialBiology-03.pdf)
Parents' age at birth of their offspring and child survival
Some of your research suggest that the increase in the (at least
father's) age of reproduction will decrease the offspring life span -
partly via the increase in the mutational load. By this mechanism the
life span decrease is expected to be heritable.
However, the population effect of this is ratchet-like. That is, since
younger than average age of reproduction does not increase the
expected life span (compared to the parental life expectancy), the
population mean life span should quickly decrease with
generations. [...]
You are basically posing a specific instance of the general question
of how a population can maintain its genetic integrity in the face of
deleterious mutations.
The answer is much the same as normal: by those with too many deleterious
mutations failing to reproduce; by sexual recombination sometimes
randomly rearranging partially compromised parental genomes into intact
ones; and by sexual selection casuing those with mostly intact genomes
to seek each other out and have more offspring than is usual.
In this specific instance there is a strikingly large change in the
trait value: about 5% in a single generation, that occurs with the
probability equal to the chance of a late conception, which is itself
quite high. At the same time, being a trait with post-reproductive
manifestation, the decrease in the life span is only indirectly
related to fitness.
*If* the adverse effects on lifespan are the /only/ deleterious
effects of the mutution. There is also the possibility that such
mutations have their negative effect on LS by comproming function
in other ways - ways that can more obviously be selected against.
I think also the idea that the "decreased lifespan" as a post-reproductive
manifestation *may* come from looking at the large magnitude of the
/average/ lifespan figures for the group.
However, a small decrease in average lifespan might easily be
effected by an increase in infant mortality - and any such
component could be affected more easily by selection.
Quote: Therefore, I would not expect the selection to be strong enough to
balance the mutational influx that is apparently quite high. So, what
is the decrease in reproduction probability among those with the
reduced life span due to late reproduction of their parents?
As far as recombination is concerned, partially compromised parental
genomes can of course be rearranged in a way that would further
increase the number of mutations in offspring, rather than decrease
it. The selection here is essentially truncating, and the effect you
describe simply increases the population variance in the trait value.
Yes - sex creates some individuals with more mutations than normal
and other ones with less mutations than normal. The agent that
removes the mutations from the population is still selection - but
sex gives selection it more chance to work - by concentrating the
mutations in some individuals, allowing selection to kill them -
or at least stop them reproducing.
Quote: Further, I doubt that substantial preferential mating of those with
"intact genomes" exists in humans, especially to the extent that would
offset the effect on the population life span value.
IMO, those (say) with good disease resistant genes do seek out others
in a similarly healthy state to mate with in human populations -
though I will make no claims about the magnitude of the effect.
If the answer you are apparently looking for is that the human
population is (uniquely in modern times) under a mutational load
that's not being redressed properly by selective forces - then
that /is/ a point of view held by some other writers
(e.g. W. D. Hamilton in v.1 of his selected papers).
If true, the consequence of such decay in terms of LS would be that
people might not "naturally" have such good live expectancy in the
future.
Their *actual* lifespans might still be much greater - due to
much the same technological interventions that allowed their
equally sickly parents to survive until reproductive age.
--
__________
|im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. |
|
|
| Back to top |
|
| DZ |
| Posted: Thu Jan 08, 2004 8:22 pm |
|
|
|
Guest
|
Tim Tyler <tim@tt1lock.org> wrote:
Quote: In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
In this specific instance there is a strikingly large change in the
trait value: about 5% in a single generation, that occurs with the
probability equal to the chance of a late conception, which is itself
quite high. At the same time, being a trait with post-reproductive
manifestation, the decrease in the life span is only indirectly
related to fitness.
*If* the adverse effects on lifespan are the /only/ deleterious
effects of the mutution. There is also the possibility that such
mutations have their negative effect on LS by comproming function
in other ways - ways that can more obviously be selected against.
I think also the idea that the "decreased lifespan" as a post-reproductive
manifestation *may* come from looking at the large magnitude of the
/average/ lifespan figures for the group.
However, a small decrease in average lifespan might easily be
effected by an increase in infant mortality - and any such
component could be affected more easily by selection.
The data from the studied samples list offspring age at death that
start at 30. So, the samples and results are conditional on offspring
survival through adulthood, and infant mortality doesn't seem to
affect offspring's probability of reproduction. What is this
probability is important, however I can't find it in the papers listed
on longevity-science.org. It needs to be low, low enough to be seen
from the data, for the theory of mutational accumulation to be able to
explain lack of observable decrease in the population mean life
span. If both parents were affecting the life span decrease in the
same way, the proportional decrease in probability of no reproduction
of offspring should be equal to the proportion of late conceptions,
for the extreme of the free recombination. Motoo Kimura described this
as well as the other extreme case of asexual reproduction, which by
the way gives the same result when there is no epistasis.
DZ |
|
|
| Back to top |
|
| Tim Tyler |
| Posted: Sun Jan 11, 2004 6:44 am |
|
|
|
Guest
|
In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted:
Quote: Tim Tyler wrote:
If the answer you are apparently looking for is that the human
population is (uniquely in modern times) under a mutational load
that's not being redressed properly by selective forces [...]
I'm interested in what is the relative contribution of two following
mechanisms that can explain life span shortening due to late
conception:
1) Life span decrease as attributed to accumulation of deleterious
mutations throughout parental life.
2) Life span decrease caused by non-genetic mechanisms, such as
non-coding modifications / damage to sex cells and worsened
environment during the early development.
It sounds as though you could do with data from adoptees.
--
__________
|im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. |
|
|
| Back to top |
|
| |
|
Page 1 of 1
All times are GMT - 5 Hours
The time now is Fri Nov 21, 2008 8:21 pm
|
|