Evolution, mutations, and human longevity : European royal and noble families. Gavrilova, N., S., Gavrilov, L., A., Evdokushkina, G., N., Semyonova, V., G., Gavrilova, A., L., Evdokushkina, N., N., Kushnareva, Y., E., Kroutko, V., N., & Andreyev, A., Y. Hum Biol, 70(4):799-804, 1998.
abstract   bibtex   
The evolutionary theory of aging predicts that the equilibrium gene frequency for deleterious mutations should increase with age at onset of mutation action because of weaker (postponed) selection against later-acting mutations. According to this mutation accumulation hypothesis, one would expect the genetic variability for survival (additive genetic variance) to increase with age. The ratio of additive genetic variance to the observed phenotypic variance (the heritability of longevity) can be estimated most reliably as the doubled slope of the regression line for offspring life span on paternal age at death. Thus, if longevity is indeed determined by late-acting deleterious mutations, one would expect this slope to become steeper at higher paternal ages. To test this prediction of evolutionary theory of aging, we computerized and analyzed the most reliable and accurate genealogical data on longevity in European royal and noble families. Offspring longevity for each sex (8409 records for males and 3741 records for females) was considered as a dependent variable in the multiple regression model and as a function of three independent predictors: paternal age at death (for estimation of heritability of life span), paternal age at reproduction (control for parental age effects), and cohort life expectancy (control for cohort and secular trends and fluctuations). We found that the regression slope for offspring longevity as a function of paternal longevity increases with paternal longevity, as predicted by the evolutionary theory of aging and by the mutation accumulation hypothesis in particular.
@article{
 title = {Evolution, mutations, and human longevity : European royal and noble families},
 type = {article},
 year = {1998},
 keywords = {Europe,European royal and noble families,Evolution,Evolutionary theories,Genealogy,Genetics,Human,Life Expectancy,Lifespan,Longevity,Mutation,Offspring,Paternal age at death,Sex difference},
 pages = {799-804},
 volume = {70},
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 abstract = {The evolutionary theory of aging predicts that the equilibrium gene frequency for deleterious mutations should increase with age at onset of mutation action because of weaker (postponed) selection against later-acting mutations. According to this mutation accumulation hypothesis, one would expect the genetic variability for survival (additive genetic variance) to increase with age. The ratio of additive genetic variance to the observed phenotypic variance (the heritability of longevity) can be estimated most reliably as the doubled slope of the regression line for offspring life span on paternal age at death. Thus, if longevity is indeed determined by late-acting deleterious mutations, one would expect this slope to become steeper at higher paternal ages. To test this prediction of evolutionary theory of aging, we computerized and analyzed the most reliable and accurate genealogical data on longevity in European royal and noble families. Offspring longevity for each sex (8409 records for males and 3741 records for females) was considered as a dependent variable in the multiple regression model and as a function of three independent predictors: paternal age at death (for estimation of heritability of life span), paternal age at reproduction (control for parental age effects), and cohort life expectancy (control for cohort and secular trends and fluctuations). We found that the regression slope for offspring longevity as a function of paternal longevity increases with paternal longevity, as predicted by the evolutionary theory of aging and by the mutation accumulation hypothesis in particular.},
 bibtype = {article},
 author = {Gavrilova, N S and Gavrilov, L A and Evdokushkina, G N and Semyonova, V G and Gavrilova, A L and Evdokushkina, N N and Kushnareva, Y E and Kroutko, V N and Andreyev, A Y},
 journal = {Hum Biol},
 number = {4}
}

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