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Medical Forum / General / General / January 2004New special 'Longevity' issue of "Social Biology"
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---------------------------------- > 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 In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >> Genealogical data and the biodemography of human longevity >> --- (http://longevity-science.org/SocialBiology-03.pdf) >> [quoted text clipped - 10 lines] > 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.  Signature__________ |im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. > In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >>> Genealogical data and the biodemography of human longevity [quoted text clipped - 23 lines] > 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 > In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >>> Genealogical data and the biodemography of human longevity [quoted text clipped - 23 lines] > 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 In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >> In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >>>> Genealogical data and the biodemography of human longevity >>>> --- (http://longevity-science.org/SocialBiology-03.pdf) >>>> [quoted text clipped - 27 lines] > 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. > Therefore, I would not expect the selection to be strong enough to > balance the mutational influx that is apparently quite high. So, what [quoted text clipped - 6 lines] > 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. > 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. Signature__________ |im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. > In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: >> In this specific instance there is a strikingly large change in the [quoted text clipped - 16 lines] > 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 > 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). 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. DZ In sci.life-extension DZ <netsink@nc.rr.com> wrote or quoted: > > If the answer you are apparently looking for is that the human > > population is (uniquely in modern times) under a mutational load [quoted text clipped - 10 lines] > 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. Signature__________ |im |yler http://timtyler.org/ tim@tt1lock.org Remove lock to reply. > > Genealogical data and the biodemography of human longevity > > --- (http://longevity-science.org/SocialBiology-03.pdf) [quoted text clipped - 24 lines] > > DZ *** Good point ! We addressed this issue in the following publication: Gavrilov, L.A., Gavrilova, N.S. How human longevity and species survival could be compatible with high mutation rates. Journal of Anti-Aging Medicine, 1999, 2(2): 153-154. http://longevity-science.org/JAAM-Mutation.pdf Kind regards, -- Leonid Gavrilov Author of the book "The Biology of Life Span" http://longevity-science.org/index.html#Book > > > Genealogical data and the biodemography of human longevity > > > --- (http://longevity-science.org/SocialBiology-03.pdf) [quoted text clipped - 32 lines] > Journal of Anti-Aging Medicine, 1999, 2(2): 153-154. > http://longevity-science.org/JAAM-Mutation.pdf Thanks. This article explains the mechanism of sustaining high mutational load - in the population genetic sense of decrease of population fitness through elimination of deleterious mutations. You suggest the mechanism of early elimination. This is fine explanation. What I'm wondering about is the following. In Biodemography-2001.pdf you show that offspring of late conceptions that survive through adulthood still exhibit substantial decrease in longevity. So this observable decrease in just a single generation is not accounted by development failures or by early death. Then this effect must accumulate in generations unless there is substantially lower probability of reproduction for these offspring. Is there? DZ > Kind regards, > > -- Leonid Gavrilov > Author of the book "The Biology of Life Span" > http://longevity-science.org/index.html#Book > > > > Genealogical data and the biodemography of human longevity > > > > --- (http://longevity-science.org/SocialBiology-03.pdf) [quoted text clipped - 47 lines] > > DZ *** Yes, this is an important question, and we planned to study it. Surprisingly it proved to be difficult to get a research funding for this particular study, which required labor-intensive and time-consuming data collection on *correct* numbers of children, etc. (high data quality comes with a cost). Perhaps we need to look for an alternative sources of support for this research project elsewhere... We would appreciate any help in connecting us with foundations or private sponsors keen to support such a study. Thank you ! Kind regards, -- Leonid Gavrilov Author of the book "The Biology of Life Span" http://longevity-science.org/index.html#Book > > > > Genealogical data and the biodemography of human longevity > > > > --- (http://longevity-science.org/SocialBiology-03.pdf) [quoted text clipped - 47 lines] > > DZ *** Yes, this is an important question, and we planned to study it. Surprisingly it proved to be difficult to get a research funding for this particular study, which required labor-intensive and time-consuming data collection on *correct* numbers of children, etc. (high data quality comes with a cost). Perhaps we need to look for an alternative sources of support for this research project elsewhere... We would appreciate any help in connecting us with foundations or private sponsors keen to support such a study. Thank you ! Kind regards, -- Leonid Gavrilov Author of the book "The Biology of Life Span" http://longevity-science.org/index.html#Book |
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