ArticleEvolutionary applications2019
Parents of early-maturing girls die younger.
Article in Evolutionary applications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Mothers of small-bodied children and fathers of vigorous sons live longer.Frontiers in public health · 2023Article
- Anthropometrics of Estonian children in relation to family disruption: Thrifty phenotype and Trivers-Willard effects.Evolution, medicine, and public health · 2021Article
- Morphometric traits predict educational attainment independently of socioeconomic background.BMC public health · 2019Article
- Parents of early-maturing girls die younger.Evolutionary applications · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to the life-history theory, rates of sexual maturation have coevolved with mortality rates so that individuals who mature faster tend to die younger. We used two data sets, providing different markers for the speed of pubertal development to test whether rates of sexual maturation of women predict the age at death of their parents. In the data set of Estonian schoolgirls born between 1936 and 1961, the rate of breast development predicted lifespan of both mothers and fathers (irrespectively of their socio-economic position), so that parents of rapidly maturing girls died at younger age. This finding supports the view that fast maturation rates in humans have coevolved with short lifespans and that such trade-offs can be detected as intergenerational phenotypic correlations in modern populations. Menarcheal age of participants of Estonian Biobank (born between 1925 and 1996) did not predict the age of death of their mothers; however, it did predict survival of their fathers, but only in environment where the genetic variation is exposed (families where at least one parent had tertiary education). In such families (where girls also matured 0.2-0.4 years earlier than in poorly educated families), 1-year delay in daughter's menarche corresponded to 9% lower hazard of father's death. Heritability of menarcheal age was also highest in well-educated families. The latter findings are consistent with the idea that genetic differences in the rate of pubertal maturation may be expressed most clearly in well-off families because in such families, the contribution of environmental variance to total phenotypic variance in menarcheal age is smallest. Our findings suggest that with global improvement and equalization of growth conditions, reductions of environmental variation in the rate of maturation increasingly expose the genetic differences in menarcheal age to selection. Under such conditions, selection on menarcheal age has a potential to affect the evolution of lifespan.
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