“…Individual‐level associations between lifespan and rate of sexual maturation may reflect either within‐population polymorphisms in antagonistic pleiotropic effects (Corbett, Courtiol, Lummaa, Moorad, & Stearns, ; Laisk et al, ) or induced phenotypic responses to womb or childhood environment (Lea, Tung, Archie, & Alberts, ; Wells, ). For instance, the risk of developing diseases related to metabolic syndrome among early‐maturing women might appear inevitable consequence of (initially adaptive) plastic response of a “thrifty phenotype” to low maternal investment in utero (Wells, ), but also result from the overlap of genomic loci associated with early menarche with genes implicated in metabolic diseases (Day et al, ; Perry et al, ).…”