The Adolescent Origins of Substance Use Disorders: A Behavioral Genetic Perspective

Over the past twenty years there has been an increasing recognition within the substance abuse research field that substance use disorders (SUDs) are usefully conceptualized within a developmental framework. That is, initiation of substance use in adolescence and escalation to substance abuse in early adulthood are strongly age-graded, with the relevant behavioral risk and protective factors manifesting early in development, often prior to substance use onset. In this chapter we review a program of research that seeks to provide a behavioral genetic perspective on the development of SUDs. 

The Minnesota Center for Twin and Family Research (MCTFR) undertakes longitudinal research on families including twins, adopted siblings and non-adopted siblings spanning early adolescence through early adulthood. A total of nearly 10,000 individuals in 2500 families have participated in MCTFR research. 

We review findings from the MCTFR to establish four general features of the development of SUDs informed by behavioral genetic research: 

1. Both general and specific processes contribute to the aggregation of SUDs in families; 
2. Genetic contributions to SUD risk appear to be primarily at the general factor level, although the contribution of the general factor appears to decrease with age;
3. SUD risk is manifested before initiation of substance use in terms of elevated levels of externalizing psychopathology and personality characteristics indicative of low self-control; and
4. he genetic factors that contribute to SUD risk appear to be numerous with very small phenotypic effects, making them difficult to identify.

Below:  Mapping substance use disorders onto the dimensions of internalizing and externalizing psychopathology. Model based on findings from Krueger (1999), Vollebergh et al. (2001), and Kendler et al.(2003). Figure reproduced with permission from McGue and Irons (2013).

Below:  Biometric latent model of externalizing psychopathology. The associations among the five observed phenotypes can be accounted for by a single externalizing factor with variance apportioned as 81% to additive genetic factors (a2), 0% to shared environmental factors (c2), and 19% to nonshared environmental factors (e2). Based on findings from Krueger et al. (R. F. Krueger et al., 2002).

Full article at:  http://goo.gl/rgV5o2

By:  Matt McGue, Dan Irons, and William G. Iacono

Department of Psychology University of Minnesota

Correspondence: Matt McGue Department of Psychology University of Minnesota 75 East River Rd. Minneapolis, MN 55455 (612)-625-8305 (Voice); (612)-626-2079 (FAX) Email: ude.nmu.@100eugcm

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