Research has documented a strong association between early adolescent problem behavior and adult disinhibitory psychopathology, leading some to suggest that the latter can be reduced by preventing or delaying the former. But the prevention implications of this association necessarily depend upon the causal mechanisms that produce it. The current study was designed to test implications of a model that posits that early problem behavior and disinhibitory psychopathology are associated because they are both manifestations of a common inherited liability. At their age-17 assessment, 1080 twins from the older cohort of the Minnesota Twin Family Study reported whether and the age at which they first: drank alcohol, used tobacco, used illicit drugs, had sexual intercourse, and had police contact. An Early Problem Behavior index was computed by summing the number of these experiences each participant reported having before age 15. Outcome measures of disinhibitory psychopathology were assessed by clinical interview at the age-20 follow-up and included number of symptoms of nicotine dependence, alcohol abuse and dependence, drug abuse and dependence, and adult antisocial behavior. Biometric analysis of the multivariate twin data showed that: (1) early adolescent problem behavior is weakly heritable (approximately 20%), (2) the common factor underlying disinhibitory psychopathology is strongly heritable (approximately 75%), and (3) the phenotypic correlation between early adolescent problem behavior and disinhibitory psychopathology was strong (approximately 0.60) and accounted for primarily by genetic factors common to the two domains. Findings are discussed in the context of research on the prevention and developmental nature of substance use disorders and related psychopathology.
KeywordsAdolescent problem behavior; disinhibitory psychopathology; externalizing; twin studies Behavioral genetic research has established the importance of both heritable and non-heritable influences on the development of adult substance use disorders (SUDs) including: nicotine dependence (Heath and Madden, 1995;Kendler et al., 1999), alcohol dependence Kendler et al., 1992;McGue, 1999;, and illicit substance abuse and dependence (Ball and Collier, 2002;Kendler and Prescott, 1998;Lynskey et al., 2002;McGue et al., 2000;Tsuang et al., 1996). Current behavioral genetic research aims to build on these findings by identifying the specific genetic and environmental factors that affect SUD risk and by characterizing their joint mechanisms of actions (Rutter et al., 2001). While much of this effort appropriately involves the use of molecular approaches to identify the specific genes that contribute to SUD risk (Goldman et al., 2005), complementary approaches * To whom correspondence should be addressed at Department of Psychology, University of Minnesota, 75 East River Rd., Minneapolis, MN, 55455, USA. Tel.: +612-625-8305; Fax: +612-626-2079; e-mail: mcgue001@umn.edu. An observation critical to understanding the developmental nature of SUD...