Our main goal was to study the temporal pattern of genetic factors for AAD symptoms during the critical developmental period from adolescence into early adulthood. Studying age-related changes was allowed, since the CAGE assessed the same phenotype across age 15–32 and across men and women, as indicated by the analyses on measurement invariance. In particular, we wanted to discriminate between the developmentally stable and developmentally dynamic hypotheses that predict quite different patterns for cross age genetic effects on symptoms of AAD. Genetic innovation was not detected, which provides evidence in favor of the developmentally stable hypothesis. That is, genetic risk factors for symptoms of AAD appear to be temporally stable across the key developmental period from mid-adolescence into early adulthood. The same genetic risk factors are important at younger and older ages. This is in line with Sartor et al. (2008) who found that one common genetic factor could explain the rate of progression from age at alcohol initiation to age at occurrence of the first symptom of AAD and age at onset of an alcohol dependence diagnosis. Although in
