Identifying the specific etiological factors that contribute to the development of attention-deficit hyperactivity disorder (ADHD) holds great promise for future innovations regarding the conceptualization of the disorder as well as prevention and treatment measures. A wealth of evidence has demonstrated that genetic factors make large contributions to ADHD, yet numerous environmental risk factors have also been identified. Uncovering the nature of the exchange processes that are involved in the development of ADHD via investigation of gene x environment interactions (GxE) represents an important step forward in research involving the causal mechanisms of the disorder. Risk factors related to the family environment may be particularly important for the development of behavioral and emotional regulation capabilities. In particular, conflict in the home has emerged as an important correlate of both symptom severity and impairment for child problems and represents a potential putative environmental risk factor for ADHD. The current research examined the potential etiological role of children's cognitive appraisals self-blame in relation to their parents' marital conflict in ADHD via tests of GxE effects using two complementary methodologies: behavioral and molecular genetics. However, prior to these tests, the phenotypic relationships among children's appraisals of marital conflict and externalizing behaviors were examined. In Study 1, the unique relationships between appraisals of self-blame and ADHD symptoms was replicated, indicating that self-blame was related to ADHD symptoms even when oppositional and conduct are controlled. In Study 2, behavioral genetic methods for testing GxE effects were conducted in a twin sample of 248 twin pairs. Self-blame emerged as a significant moderator of latent genetic and environmental influences on parent rated ADHD symptoms on the Child Behavior Checklist DSM-IV ADHD Scale, such that genetic influences decreased but non-shared environmental influences increased with higher reports of self-blame. In Study 3, tests of GxE effects involving a specific genetic marker, the promoter polymorphism of the serotonin transporter gene (5HTTLPR) were conducted in a completely independent sample of n=304 youth, of whom n=151 had ADHD. That analysis revealed significant interactions, such that increases in teacher-rated DSM-IV ADHD symptoms corresponded with increases in self-blame, but only for individuals with the low and high serotonin-activity genotypes. Findings from both studies are complementary and suggest that self-blame may indeed have a specific role in the etiology of ADHD via moderating of genetic effects. Results suggest that different exchange processes (i.e., genetic main effects, environmental main effects, GxE interaction effects) may be differentially important for the etiology of ADHD and provide support for an etiological role of self-blame in ADHD. More broadly, these findings offer an innovative approach for understanding the interactional processes between genetic and environmental risk factors and their contributions to ADHD.
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