Environmental Adversity and Increasing Genetic Risk for Externalizing Disorders

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Abstract
Various lines of evidence testify that genetic and environmental factors contribute to psychiatric and substance use disorders.1 Recently, psychiatric genetic research has evolved beyond simple estimates of heritable and nonheritable influences to investigations that begin to delineate the mechanisms of gene-environment interplay. This includes studies using the specific gene × measured environment design,2 with the most well-known example being that variants of the 5-HTT gene increase risk for major depression in the context of stressful life events.3,4 In addition, there is an accumulating literature of quantitative genetic studies5-9 that use twin, adoption, and family designs to delineate processes of gene-environment interplay, such as how the relative contribution of genetic and environmental risk factors changes as a function of the environmental context. Although there has been a veritable explosion in studies of gene-environment interplay in psychopathology in recent years, there have been few attempts to integrate findings in an effort to articulate more general principles of gene-environment influence across different environmental variables and psychiatric disorders.10-12 Key questions that remain unanswered include the following: Is the mechanism of environmental influence the same regardless of the environmental variable such as parenting, peers, or stressful life events? Or, do different environmental variables exhibit varying mechanisms of influence? Also, are the mechanisms of gene-environment influence the same for all types of psychiatric disorders? For example, are processes of gene-environment interplay the same or different for internalizing (major depression and anxiety disorders) vs externalizing (antisocial behavior and substance use) disorders?