Childhood Adversity, Monoamine Oxidase A Genotype, and Risk for ConductDisorder

Abstract

There is a long history of research on risk factors for conduct disorder,^1-3 in part because of thedeleterious effects of aggressive, antisocial, and criminal acts on individualsand society at large. Evidence for aggregate genetic effects has been reportedby many twin, family, and adoption studies, based on the pattern of resemblancebetween different classes of relatives, but reliable evidence for specificgenetic effects is limited. Recently, an interaction between a functionalpolymorphism in the promoter of the monoamine oxidase A (MAO-A) gene and childhoodmaltreatment was reported to be associated with a significantly increasedrisk for antisocial behavior in boys from the Dunedin Multidisciplinary Healthand Development Study.⁴ There was an independenteffect of maltreatment but no independent effect of low MAO-A activity onrisk for antisocial behavior. Low MAO-A activity was therefore a detectablerisk factor only in the presence of an adverse childhood environment, andthe effect was not trivial. Individuals with both the low-activity MAO-A genotypeand maltreatment accounted for 12% of the birth cohort but 44% of the cohort'sviolent convictions. A genotype-environment interaction may therefore accountfor a significant portion of individual variation in risk for antisocial behavior.This finding is a rare example of a measured gene and a measured environmentjointly affecting human behavior. Such effects have been documented in experimentalorganisms⁵ and described in theoretical treatises,⁶ but they have rarely been explored and replicatedin studies of human behavior.