Life history models of sexual development are popular for understanding female sexual development as it relates to early experiences in the rearing environment. Broadly speaking, life history models suppose that early stressful environments will lead to accelerated maturation, manifesting as earlier timing of menarche, which subsequently leads to earlier age at first sex, and more unrestricted (and risky) sexual behavior.
Although there are subtle differences between the three primary life history developmental models (see Figure 1 for a conceptual depiction of predictions across the three models), they all have in common the prediction that menarche timing is, in part, regulated by early environmental stress, such that stress and father absence – a particular variable of interest within the literature – predict earlier menarche timing.
The effect of father absence on menarche timing has been enjoying a rich discussion in recent years, with criticisms ranging from genetic confounding (which my colleagues and I outline here) to WEIRD effects not found in cross-cultural data. Other criticisms have focused on the issue of broader confounding factors such as socioeconomic status and body mass index. Although each of these criticisms and alternative explanations for menarche timing have been investigated independently in previous research, no previous study has attempted to comprehensively evaluate a broad array of proposed effects of life history antecedents on menarche timing (that are derived from life history developmental models) with a genetically informative research design.
In our recent research, we (co-authors, George Richardson, Joe Nedelec, & Hexuan Lui) sought to test a comprehensive model of theoretically relevant life history predictors on menarche timing and subsequent sexual behavior in girls using a twin subsample from Add Health. We took a two-stage approach to test the associations between father absence, specifically, and environmental stress, broadly, with age at menarche and sexual debut, and to identify potential genetic confounding of those associations.
In the first stage we tested and refined a measurement model specifying a latent environmental stress factor, and then built and tested a comprehensive structural equation model to test our life history hypotheses (see Figure 2). What is most striking about these results is what effects are not detected. There are no significant effects of environmental stress or father absence on age at menarche; only BMI is a significant predictor (a well-known predictor in the pediatrics literature.) There were, however, significant effects of early environmental stress on sexual debut, consistent with recent work in a Canadian sample.
In the next stage, we used univariate and multivariate behavior genetic models to identify whether significant associations between BMI and age at menarche, and between age at sexual debut and number of sexual partners and risky sexual behavior, were confounded by shared genetic covariation. Results here did not provide evidence of a nonshared environmental association (i.e., an association that survived control of genetic and shared environmental factors), suggesting the effect of BMI on age at menarche in our nongenetically informative model is likely spurious. Findings also did not provide evidence of a nonshared environmental association between age at sexual debut and risky sexual behavior. However, the association between age at sexual debut and number of sexual partners did survive control of genetic and shared environmental factors, suggesting it may reflect a causal effect of the former on the latter.
This study tested many other predictions in addition to the key findings presented above. Below in Table 1 is the tl;dr version of our primary aims and results summary.
What do all these results mean for life history models of sexual development? First, and in my view, most importantly, is that the null association between early environmental stress and father absence with menarche timing (the latest null result in a growing list) calls into question each of the three life history developmental models. Why? Because parental investment theory, psychosocial acceleration theory, and child development theory all rely on menarche timing as a key regulatory mechanism linking early environments to adolescent sexual behavior. (In our paper we discuss at great length the implications for each theory on preprint pp. 20-23).
Our behavior genetic models offer some interesting insights to life history models, too – just not for age at menarche. The evidence associated with age at sexual debut does suggest sexual behavior may be, in part, responsive to early environmental stress. Unlike age at menarche, age at sexual debut does reflect the shared environment in all the models we tested. Again, however, life history developmental models will have to reconcile the fact that the key regulatory mechanism of menarche timing is missing. Additionally, these results also do not provide evidence for my own hypothesis that the association between father absence and age at menarche is genetically confounded – because there appears to be no such association to confound!
This paper, currently under peer-review, contributes to the ongoing critical discussions in the life history literature particularly regarding developmental models, facultative adjustment, and genetic confounding. We look forward to hearing your comments!