Environmental adversity and increasing genetic risk for externalizing disorders

Abstract

Context: Studies of gene-environment interplay in the development of psychiatric and substance use disorders are rapidly accumulating. However, few attempts have been made to integrate findings and to articulate general mechanisms of gene-environment influence in the emergence of psychopathology.

Objective: To identify patterns of gene-environment interplay between externalizing disorders (antisocial behavior and substance use) and several environmental risk factors.

Design: We used quantitative genetic models to examine how genetic and environmental risk for externalizing disorders changes as a function of environmental context.

Setting: Participants were recruited from the community and took part in a daylong assessment at a university laboratory.

Participants: The sample consisted of 1315 male and female twin pairs participating in the assessment of the Minnesota Twin Family Study at age 17 years.

Main outcome measures: Multiple measures and informants were used to construct a composite of externalizing disorders and composite measures of 6 environmental risk factors, including academic achievement and engagement, antisocial and prosocial peer affiliations, mother-child and father-child relationship problems, and stressful life events.

Results: A significant gene x environment interaction was detected between each environmental risk factor and externalizing such that greater environmental adversity was associated with increased genetic risk for externalizing.

Conclusions: In the context of environmental adversity, genetic factors become more important in the etiology of externalizing disorders. The consistency of the results further suggests a general mechanism of environmental influence on externalizing disorders regardless of the specific form of the environmental risk.

Figure 1

EXT = Externalizing disorders composite. Full model of moderation of the genetic and environmental influences on EXT as a function of different levels of Antisocial Peers. A refers to additive genetic effects, C to shared environmental effects, and E to nonshared environmental effects. The parameters a₂₁, c₂₁, and e₂₁ include genetic and environmental influences that overlap between Antisocial Peers and EXT (i.e., can be used to derive the genetic and environmental covariance), while a₂₂, c₂₂, and e₂₂ are genetic and environmental influences unique to EXT. Antisocial Peers can moderate either the common variance with EXT or the unique variance of EXT. The β's indicate the direction (+ or -) and magnitude of any moderation effects on the paths from the ACE effects to EXT, while M indicates the level of the moderator, that is, the number of antisocial peers.

Figure 2

Changes in the unstandardized variance of Externalizing (EXT) as a function of environmental risk factors for the best fitting model. All environmental risk factors have been coded so that higher levels are associated with greater environmental adversity.