While effects of AD on reproductive timing appear robust against a host of correlated sociodemographic, psychiatric, and family and childhood risks, mechanisms underlying observed associations between reproductive onset and AD remain largely unknown. Results are consistent with alcohol- but not smoking-related reproductive dysfunctions, although other unmeasured factors may also contribute to reproductive delay. In addition to biological consequences of drinking, a common inherited liability to later reproduction and AD risk is possible. Although genetic effects were nonsignificant when examined in subsidiary analyses, results for women in the older cohort were of modest magnitude. Given imprecise estimates (95% CIs are wide), genetic sources of covariation could go undetected in the current sample.
