In this article, the primary goal is to investigate how genetic risk factors for symptoms of AAD change across age. In particular, we seek to discriminate between two hypotheses about the developmental pattern of genetic risk factors for AAD symptoms in the key time period of adolescence and early adulthood. In this period drinking habits are commonly formed, levels of alcohol consumption typically peak (Koppes et al. 2000; Midanik and Clark 1994; Moore et al. 2005; Poelen et al. 2005) and symptoms of AAD usually begin (Harford et al. 2005; Schuckit et al. 1998). The developmentally stable hypothesis predicts that a single set of genetic risk factors will impact on AAD symptoms from late adolescence through early adulthood. By contrast, the developmentally dynamic hypothesis predicts that new genetic influences on AAD symptoms “come on line” at a particular age. These genetic innovations give rise to a qualitative change in genetic effects. Regardless of qualitative change, the importance of genetic risk factors may change quantitatively over time. This can result from genetic amplification, if the importance of genetic influences increases over age, or from genetic attenuation if the importance of genetic factors declines during development.
