in each gender. Third, covariates of substance addiction, such as attention deficit hyperactivity disorder (Disney et al., 1999; Elkins et al., 2007), delinquency, conduct disorder, depression, and antisocial tendencies (Fu et al., 2002) were not included in this study. Though this is a limitation to this study, the focus of this paper was to determine the extent to which genetic and environmental risk factors for dependence symptoms in young adulthood are relevant, and the extent to which they are correlated across substances; additional studies are needed to tease apart the comorbidity between substance use disorders and other externalizing problems. Lastly, low prevalence rates and endorsement of symptoms make it difficult to explore these hypotheses using multivariate threshold models without model fit issues. This limitation also affects our ability to compare our results to that of past studies, particularly, the examination of individual symptoms. For example, studies examining the variability of DSM symptoms reveal that for alcohol and tobacco, heritability estimates vary by DSM symptom and phenotype definition (Hardie et al., 2008; Lessov et al., 2004; Slutske et al., 1999). Limitations aside, this community-based study provides evidence for a genetically influenced substance dependence vulnerability underlying DSM-IV tobacco, alcohol, and cannabis dependence
