Biomedical subjects
L A Gavrilov
Publications and source records attributed to L A Gavrilov.
[Evolution theory, mutations, and human life span].
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Evolution, mutations, and human longevity: European royal and noble families.
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.
[Regularities in the inheritance of human life expectancy: contribution of paternal and maternal longevity on life span of offspring].
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Mutation load and human longevity.
Since paternal age at reproduction is considered to be the main factor determining human spontaneous mutation rate (Crow, J. (1993) Environ. Mol. Mutagenesis, 21, 122-129), the effect of paternal age on human longevity was studied on 8,518 adult persons (at age 30 and above) from European aristocratic families with well-known genealogy. The daughters born to old fathers (50-59 years) lose about 4.4 years of their life compared to daughters of young fathers (20-29 years) and these losses are highly statistically significant, while sons are not significantly affected. Since only daughters inherit the paternal X chromosome, this sex-specific decrease in daughters' longevity might indicate that human longevity genes (crucial, house-keeping genes) sensitive to mutational load might be located in this chromosome.
[Maternal age and lifespan of the offspring].
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[Paternal age and lifespan of the offspring].
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Epidemiologic approach to the biology of human life span.
The present work suggests a new, epidemiologic approach to the study of the biological mechanisms determining human life span. The proposed approach is based on revealing the biological component of human mortality with a subsequent analysis of its regional and sex variability. The biological component of mortality is defined as a component which is age-dependent, but historically stable with respect to socio-economic transformations. It has been shown that the Gompertz function elaborated in the Gompertz-Makeham Law known since 1860 can serve as the biological component. The Gompertz function values, being historically stable. For the first time ever, biological mortality maps have been drawn for the male and female population of Europe. Possible mechanisms of these regional and sex-related biological distinctions are likewise considered.
Human life span stopped increasing: why?
To account for the cessation of human life span increase in developed countries, we have studied the Swedish vital statistics over the period of 1901-1978. Approximating age-related mortality dynamics as the sum of the constant (age-independent mortality) and exponential (age-dependent mortality), we have discovered a striking phenomenon consisting in historical stability of age-dependent mortality. It appeared that decrease in total mortality was exclusively due to age-independent mortality which is close now to the limiting (zero) level. The results obtained prove the existence of the biological limit for the average life span and show that the conventional reserves for decrease in mortality have been exhausted. Thus, the problem of life prolongation requires a new way of thinking.
[Determination of the specific duration of life].
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[Kinetic patterns of human mortality in historical perspective].
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[Mathematical model of aging in animals].
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[Does a limit of the life span really exist?].
Mathematical models of aging are in conflict with real data on centenarian's survival, when these models are based on the concept of maximal life span potential. It seems that there is no absolute superior limit for the duration of life.
[Diploid cell cultures as an object for the study of the molecular mechanisms of aging].
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