Is reproductive development adaptively calibrated to early experience? Evidence from a national sample of females.

Abstract

Many developmental theories have not been sufficiently evaluated using designs that control for unobserved familial confounds. Our long-term goal is to determine the causal structure underlying associations between early environmental conditions and later psychosocial and health outcomes. Our overall objective in this study was to further evaluate predictions derived from applications of life history theory to female reproductive development, key among them that reproductive milestones translate early environmental risk into fertility, health, and behavioral outcomes. To this end, we used female data from the National Longitudinal Survey of Youth 1979 and structural equation modeling to conduct increasingly severe tests, beginning with covariate control and then progressing to sibling control and behavioral genetic designs. After adjusting for confounds varying between sets of siblings, we did not find evidence that age at menarche reflected components of early environment or that any focal outcomes reflected early fragmented family structure (birth to age nine). Although we detected no links between measured environment and individual differences in age at sexual debut, we did find that it reflected both shared and nonshared influences in our behavior genetic models. Interestingly, delayed sexual debut (into young adulthood) reflected identification of parents as the greatest influences and forecasted an array of fertility-related outcomes. Taken together, these findings challenge theories suggesting menarche timing is adaptively calibrated to early environment. They also highlight the need for more research using sibling control and related designs to examine the roles of environments in development. Public Significance StatementEstimates from sibling control and ACE models suggest that age at menarche did not play an important role in linking components of the early environment to fertility, health, and behavioral outcomes later in life. Small associations between age at sexual debut and number of pregnancies, number of children, mental health, depression, and binge drinking survived sibling controls. ACE models implicated both shared and nonshared environmental influences in the etiology of age at sexual debut. However, associations between measured environments and this milestone (in the normal range of ages at debut) did not survive sibling controls, although for socioeconomic status this may be due to a lack of variance within sibling sets. Results call into question adaptive theories of the timing of age at menarche and suggest they may not provide information that is useful in public health efforts.