The Developmental Behavior Genetics of Drug Involvement: Overview and Comments

Abstract

The papers in this special issue have in common an interest in developmental variations in the heritability of substance use, abuse, and problems. A number of the studies are longitudinal, and even those that are cross-sectional are analytically focused on whether heritability, shared, and nonshared environmentality effects are constant or change over the period from onset of use to the time when problem use is more constant. This commentary provides an overview of the work from a developmental psychopathology perspective. Findings are linked to the existing longitudinal/ developmental literature on the epigenesis of substance use disorders and similarities and contradictions are noted. Suggestions for next step work, involving the need for increased differentiation of the substance abuse phenotypes, the utilization of phenotypic measures that delineate heterogeneity of course, and more precise definition of the specific environmental variations that underlie shared and nonshared environmental liability, are provided. KeywordsDevelopmental genetics; Substance use; Substance abuse; Phenotype definition Over the past decade, a good deal of evidence from a number of heritability studies has accumulated that suggests the genetic risk for substance use disorders is carried through one major common factor and a number of specific factors, whose relative role and type varies with drug of abuse (Karkowski et al. 2000;Kendler et al. 2003;Tsuang et al. 1998). The common factor has been identified as an externalizing one, marked at the behavioral level by symptoms of undercontrol and behavioral dysregulation. Although less well known, the nongenetic evidence is even more compelling for a common causal factor cutting across drugs of abuse. This work, coming from six long term prospective studies (Caspi et al. 1996(Caspi et al. , 2002Eron et al. 1987;Mayzer et al. 2002Mayzer et al. , 2003Masse and Tremblay 1997;Cloninger et al. 1988) carried out over the past quarter century, provides a remarkable convergence with the genetic literature in demonstrating that externalizing symptomatology appearing in early childhood is predictive of SUD outcomes some 15-20 years after the first appearance of the drug-nonspecific behavioral risk (see Zucker 2006 for a review of this work). Moreover, these traits (a) are known to be relatively stable over the course of childhood and adolescence (Fuller et al. 2003;Olweus, 1979); are most likely to show a continuity pattern among individuals who thereafter develop the more chronic and severe forms of SUD (Biglan et al. 2004; Campbell et al. 2000).These predictive relationships are not directly informative about the developmental topography of drug involvement, from exposure to onset of use, from onset of use to progression into

Underage Drinking: A Developmental Framework

“…76 Of particular interest here is emerging interest in specific genes that may interact with experience over the course of development to increase or to decrease the likelihood of alcohol use and AUD and interest in the effects of ethanol exposure on gene expression across development. There is keen interest in identifying the chemical processes, brain functions, and behaviors that are serving as intermediaries of gene-environment interactions, because the genes of 1 person do not interact directly with the genes of other people or directly with the external environment.…”

Simultaneous Versus Concurrent Use of Alcohol and Cannabis in the National Alcohol Survey

“…Individuals who use both cannabis and alcohol may be inherently more susceptible to poly-substance use because of common genetic vulnerabilities or behavioral under-control (McGue and Iacono, 2005; McGue et al, 2006; Zucker, 2006). Studies comparing alcohol only users to poly-substance users have found that those who use both alcohol and cannabis are more likely to be male and younger than those who use only alcohol (Harrington et al, 2012; Midanik et al, 2007).…”

The role of early childhood ADHD and subsequent CD in the initiation and escalation of adolescent cigarette, alcohol, and marijuana use.

“…Though children with ADHD likely share a common biological risk for substance use, environmental factors at home, at school, and in peer settings appear to moderate outcome (Zucker, 2006). Within the home setting, family conflict and parenting practices, such as monitoring, may moderate an adolescent with ADHD’s risk for deviant behavior (Molina et al, 2012; Patterson, DeGarmo, & Knutson, 2000).…”

“…However, without a longitudinal perspective, these effects are difficult to disentangle statistically because individuals with childhood CD but without ADHD are uncommon, and the shared variance between ADHD and CD is therefore very large (Derefinko & Pelham, in press; Plizska, Carlson, & Swanson, 1999; Waschbusch, 2002). These above-mentioned studies suggest that ADHD and substance use relate in a complicated manner, perhaps involving comorbid CD under some circumstances but not others (Zucker, 2006). …”