The X-linked MAOA gene has a repeat promoter polymorphism (MAOA-LPR) that influences gene activity. Several studies have shown G×E effects on childhood conduct and hyperactivity disorders, predictors of AUDs and DD [25], and on antisocial behavior that is often comorbid. Longitudinal G×E studies have shown that childhood maltreatment [82–84] and family adversity [85] interact with the MAOA-LPR low-activity variant to predict childhood conduct disorder and adult antisocial behavior. In the ALSPAC longitudinal study, the low-activity variant was associated with increased hyperactivity at age 7 years in children exposed to multiple SLE in the first 3 years of life [24]. One retrospective study showed an effect on AD: in women from a Southwestern American Indian tribe, the low-activity allele was associated with AD, particularly antisocial alcoholism, but only in women exposed to CSA [86]. Other retrospective studies have yielded mixed G×E results for antisocial behavior [9•]. Further studies have looked at G×E effects on drinking behaviors. In a large Swedish study of high school students, psychosocial risk (quality of family relations, sexual abuse) was associated with high alcohol consumption in boys
