significant, did not mediate genetic risk on externalizing behavior. Thus, while a variety of adolescent problem behaviors are significantly correlated, the structure of that association may differ as a function of phenotype (e.g., comorbid HYP/IMP and CDP vs. comorbid CDP and AlcProb) and developmental course (childhood, adolescence and adulthood), a finding that could inform different approaches to research, treatment, and prevention. For example, when considering risk for alcohol problems in adolescence, early identification efforts might focus on conduct problems and environmental factors common to both. Additionally, focusing on shared genetic factors that influence a spectrum of externalizing behaviors, may aid in identifying susceptibility genes and understanding the biological pathways that affect vulnerability for a variety of poor outcomes (Dick et al., 2008). To conclude, a greater understanding of the structure of comorbidity can have an important impact on public health and remediation efforts of the deleterious effects of behavioral disorders such that information on the underlying covariance structure can provide information on (i) putative risk factors (biological and/or environmental) for disorders, and (ii) clinical treatment, including medication (e.g., treatments efficacious for one disorder should be investigated as a potential treatment for the other disorder).
