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Interaction of Genes and Environment in Adolescent Substance Use: Opportunities and Implications for Interventions

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Richard Rende
Added: 25 July 2011

Introduction

Clinical, developmental, and public health perspectives all converge on the idea that early use of substances (the most common being tobacco, alcohol, and marijuana)—and particularly onset in early adolescence—is problematic and portends poorly for functioning later in life. Although experimentation in adolescence was once considered normative, there is increasing recognition that use of substances is not inherently benign, especially as some youth may be at biological—and particularly—genetic risk for rapid escalation. As such, there have been strong suggestions that early psychosocial interventions are of extreme importance for reducing the likelihood of progression to higher levels of use, abuse, and dependence.1–4

Abstract

It is well recognized that adolescence is now a period of development in which the roots of substance abuse and dependence are put down. As such, there is an appreciation of the importance of delivering psychosocial interventions that could curtail adolescent use and prevent escalation into problematic levels of use. This paper reviews the rationale of psychosocial interventions from the perspective of genetic epidemiology. Genetically informative studies are discussed as laying a foundation that emphasizes the importance of shared environmental influences as targets for psychosocial interventions that could reduce early levels of substance use in adolescence, and serve as a blockade for the activation of genes that underlie progression to heavier use, as well as abuse and dependence. Recent conceptual and empirical approaches to gene-environment interplay are discussed with reference to the specific case of delivering psychosocial interventions. The implications for merging the intervention mindset with the tools of genetic epidemiology are discussed.

Keywords

adolescence, substance use, intervention, genetic epidemiology, gene-environment interplay