and colleagues (1992) demonstrating that shared environmental influences on alcohol-related symptomatology may be more prominent in women while genetic influences are more pronounced in men, particularly those with early onset of AD symptoms and with work by Prescott and colleagues (1994a, 1994b) that found no evidence for shared environment on alcohol-problems but reported significant shared environmental influences on lifetime abstinence (which is correlated with lifetime ever drinking) as well as on past year alcohol consumption, where shared environmental influences on the latter were only significant in women. It is notable that, in the present study, sex differences were attributable to non-shared environmental factors, which were somewhat higher in male twins – to what extent this sex difference refers to reduced measurement precision in males reporting on their AD symptoms, particularly when they initiate drinking later in life, or to important individual-specific environmental incidents (e.g. trauma) that impact male drinking more distinctly than they do female, drinking warrants further exploration. Furthermore, while parameters from the bivariate moderation model appeared largely consistent across the sexes, AD symptom-specific genetic factors in males were not moderated by age at 1st drink – this may have been due to the high genetic overlap between age
