Twin data provided the opportunity to investigate these mechanisms by examining the sources of common variance among drinking onset, SLE, and past year alcohol consumption. Our estimates of the contribution of genetic and environmental influences on alcohol consumption are consistent with those reported in other twin studies (see review by Dick et al., 2010). The degree of overlap between age at drinking onset and PYDD was modest and primarily attributable to genetic influences contributing to both measures. This reflects that among MZ pairs, past-year drinking of twin A is about as strongly related to the drinking onset age of twin B as it is to twin A’s own onset age. In our prior study of the shared variance between onset age and lifetime alcohol abuse/dependence, the overlap was much greater (women: 38%, men: 23%; Prescott and Kendler, 1999) than between onset age and PYDD in the current study (women: 2.8 to 4.1%, men: 2.9 to 3.1%). However, this is not surprising because PYDD is only a “snapshot” of drinking during a single year. The association between SLE and alcohol consumption
