Sociality, Hierarchy, Health Comparative Biodemography: A Collection of Papers (2014) / Chapter Skim
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2 Alleles, Mortality Schedules, and the Evolutionary Theory of Senescence--Kenneth W. Wachter
2 Alleles, Mortality Schedules, and the Evolutionary Theory of Senescence--Kenneth W. Wachter
Pages 17-38
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From page 17... ...
Demographic thinking stood in need of greater clarity about the distinct roles of genetic variation maintained in equilibrium and erstwhile genetic variants, now omnipresent or gone to "fixation." "Allele" in the title is a word for a genetic variant. In this paper, I generally refer to the most common kind of alleles, found in Single Nucleotide Polymorphisms (SNPs)
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From page 18... ...
They scrutinize research aimed at making sense of specific contrasts, the differences in adaptive strategies and body plans that separate flies, worms, elephants, and humans. A rich literature drawing on a long tradition of fieldwork in biology employs the tools of optimal life history theory.
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From page 19... ...
It is the accumulation of large numbers of somewhat independent small age-specific effects, whose distribution has been shaped over long stretches of time by natural selection, that seems most plausibly responsible for shared regularities in age-specific demographic schedules. The obvious comparison is with the heights of members of a population, going back to Francis Galton, where the observation of Gaussian distributions among adult members of populations is not ascribed to the detailed action of a few alleles but to the Central Limit Theorem applying to a large collection of small statistically independent contributions.
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From page 20... ...
It concludes with a glance at early results from genome sequencing and the promise they hold for connecting some biodemographic models with empirical genetic data. HETEROGENEITY: LIFELUCK, RISK, AND FRAILTY Natural selection operates on phenotypic variability correlated with genetic variation.
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From page 21... ...
In this metric, for studying frailty distributions, populations with different baseline hazard functions can be pooled. Variance in frailty manifests itself in a tendency for aggregate population hazard functions to taper off into plateaus at extreme ages.
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From page 22... ...
STOCHASTIC VITALITY In stochastic vitality models of survival through the lifecourse, heterogeneity present at birth is supplemented age by age by systematic trends and random shocks, usually modeled with a Markov process. Vitality may be modeled as a high-dimensional vector including physiological indices whose transitions can be estimated from longitudinal surveys, as in the sophisticated stochastic risk factors models of Kenneth Manton, Anatoli Yashin, and their collaborators.
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From page 23... ...
Vitalities at the low end of the distribution are removed by death but replenished by the random arrival of individuals whose state of health is going downhill. The move from fixed frailty to stochastic vitality avoids the drawback I have discussed from implausibly low mortality rates at early ages from individuals at the extremes of low frailty.
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From page 24... ...
Each specific causal effect presumably has its own specific age pattern and presumably depends heavily on environmental context, affecting the hazard rates of nematode worms in different ways than, say, Icelanders. Understanding such effects is important for health and welfare, but it is not the big part of evolutionary demography.
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From page 25... ...
A hazard function constant over age implies an exponentially decreasing proportion of survivors by age. If fertility rates are more or less constant over ages with significant numbers of survivors, then a burst of mortality at a single age implies a loss in net reproduction that is an exponentially decreasing function of age.
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From page 26... ...
Charlesworth went on to observe that one could optionally posit a small fixed selective cost to every allele on top of the age-specific costs, and the result would be hazard functions whose exponential increases tapered into p lateaus at extreme ages as observed. Later parts of this section describe results that put these ideas in a new light.
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From page 27... ...
This finding explains that a far-reaching demographic difference emerges from what has seemed to be a minor difference for phenotypes, namely whether there are non-negligible deleterious effects at young ages for most alleles whose primary action is to raise hazard rates at old ages. Small earlyage consequences of deleterious alleles can, in principle, exert small but sufficient selective pressure to keep the representation of these alleles in check
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From page 28... ...
A better understanding of how genetic load interacts with optimal life history allocations and strategies in the presence of environmental variation across time and space is a high priority. By the same token, combination of mutation accumulation with stochastic vitality models likely holds a key to understanding the present-day post-reproductive signatures of deleterious alleles whose equilibrium frequencies were established over evolutionary time when their lethal consequences were often felt at prime reproductive and nurturing ages.
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From page 29... ...
For natural selection to do its work, deleterious effects of mutant a lleles have to be ultimately expressed in fertility and survival. But it makes sense to think of the effects of alleles operating through a number of inter mediate causal pathways that might be reflected in the transition rates for a tochastic vitality model.
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From page 30... ...
3. The theory proposes that most relevant alleles arose from muta tions fairly far in the past, well before dramatic reductions in human mortality and likely before many of the transformations accompanying sustained population growth, leading to the hypoth esis that age estimates for relevant alleles should often come out at more than several hundreds of generations.
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From page 31... ...
What makes alleles deleterious t are effects on the net reproduction of those who carry them, either on adult survival, on infant and child survival, on fertility and mating success, or on some combination. The term "MA-alleles" denotes the subset of deleterious alleles that affect adult hazard functions and, under equilibrium conditions, are held in equilibrium by mutation-selection balance.
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From page 32... ...
The application of the principle proceeds from a comparison of a hypothetical baseline survival schedule dominated by exogenous mortality in the absence of MA-alleles with a hypothetical observable mortality schedule for populations over evolutionary time when mutation-selection equilibria could have prevailed. Guesses at the hypothetical observable schedule can be informed by anthropological lifetable estimates for presentday hunter-gatherers summarized, for example, by Gurven and Kaplan (2007)
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From page 33... ...
The age distribution of a lleles is shaped by drift and by effective population size over time as well as by selective cost. However, the quantities of demographic interest are not frequencies of alleles at single genetic sites but aggregated counts of sets or "teams" of alleles sharing a single age-specific effect profile.
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From page 34... ...
Variations around this average are bound to be large, both because of the variations in selective costs between alleles whose actions on hazard rates are concentrated at different ages and because of the intrinsic randomness of natural selection. However, it does appear that a substantial portion of genetic load affecting adult hazard rates is a legacy from long before the transformations of modern times.
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From page 35... ...
Biodemographers have an agenda for combining mutation accumulation theory with stochastic vitality models to relate present-day patterns of post-reproductive survival to earlier patterns of reproductive-age survival over evolutionary time. We have an account that links the ubiquity of Gompertzian increases in hazard rates at mediumold ages to the plateaus at older ages.
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From page 36... ...
. Neutral genomic regions refine models of recent rapid human population growth.
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From page 37... ...
. The age-specific force of natural selection and biodemographic walls of death.
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