These longitudinal data have been instrumental in COGA's ability to chart the etiology and course of alcohol use and AUD across the lifecourse. For instance, our early family data documented the increased co‐aggregation of multiple SUDs in AUD probands and their first degree relatives, relative to comparison families, providing initial support for familial clustering of and potential genetic influences on the comorbidity across AUD and SUDs (e.g., References 21, 22). We have since conducted several studies that have disentangled family history into elements of genetic liability, nurture and density of risk (e.g., References 23, 24, 25). Our data on adolescent offspring of individuals with AUD documented the role of behavioral precursors, such as externalizing problems, and social environments, such as peers and parents, in trajectories that separated persisting drinking problems from developmentally‐delimited heavy alcohol use (e.g., References 26, 27, 28). We were also able to examine the risk posed by early initiation of alcohol use on later drinking milestones using several analytic paradigms (e.g., References 29, 30). More recently, our longitudinal design has facilitated characterizations of remission and recovery in
