Reported early family environment covaries with menarcheal age as a function of polymorphic variation in estrogen receptor-α

Abstract

Age at menarche, a sentinel index of pubertal maturation, was examined in relation to early family relationships (conflict, cohesion) and polymorphic variation in the gene encoding estrogen receptor-α (ESR1) in a midlife sample of 455 European American women. Consistent with prior literature, women who reported being raised in families characterized by close interpersonal relationships and little conflict tended to reach menarche at a later age than participants reared in families lacking cohesion and prone to discord. Moreover, this association was moderated by ESR1 variation, such that quality of the family environment covaried positively with menarcheal age among participants homozygous for minor alleles of the two ESR1 polymorphisms studied here (rs9304799, rs2234693), but not among women of other ESR1 genotypes. In addition, a) family relationship variables were unrelated to ESR1 variation, and b) genotype-dependent effects of childhood environment on age at menarche could not be accounted for by personality traits elsewhere shown to explain heritable variation in reported family conflict and cohesion. These findings are consistent with theories of differential susceptibility to environmental influence, as well as the more specific hypothesis (by Belsky) that girls differ genetically in their sensitivity to rearing effects on pubertal maturation.

Environmental Factors and Puberty Onset: An Update

“…This link is regulated by polymorphic variation in the gene encoding estrogen receptor-α (ESR1). Moreover correlated variations of family environment positively regulated menarcheal age in those applicants homozygous for minor alleles (rs9304799, rs2234693), but not in women having different genotypes (Manuck et al, 2011). These findings are consistent with hypothesis of Belsky and Pluess, 2009 who found that girls differ genetically in their sensitivity to rearing effects on pubertal maturation.…”

Family Experience and Pubertal Development in Evolutionary Perspective

“…Similarly, the recently published research is also noteworthy, inspired by evolutionary reasoning, showing that children appear to be differentially susceptible to effects of rearing on puberty because of their genetic make-up and physiological reactivity to stress [17][18][19][20][21]. Such data raise the prospect that many existing studies both over-and underestimate environmental effects on pubertal timing by failing to distinguish those least and most susceptible to such influences, respectively.…”

Toward a new biology of social adversity

“…Such individuals thus show either the least or most adaptive outcomes within the population, depending on the character of the proximal social contexts in which they are reared. Studies demonstrating this greater susceptibility of neurobiologically responsive children to both positive and negative aspects of their environments have implicated a wide variety of stressors and adversities, including paternal depression (67), marital conflict (68,69), parental psychopathology (70), and overall family distress (71); of positive environmental features, including parental warmth (72) and supportive interventions (73); and of defining biological parameters, including physiological reactivity (e.g., 74, 75), differences in brain circuitry (76), and gene polymorphisms (77,78). Most importantly, highly susceptible children show bidirectional effects on outcomes in contrasting low-and high-stress settings, not simply an attenuation of negative effects in low-stress circumstances.…”