Quantitative genetic studies (i.e., twin and adoption studies) suggest that genetic influences contribute substantially to the development of attention deficit hyperactivity disorder (ADHD). Over the past 15 years, considerable efforts have been made to identify genes involved in the etiology of this disorder resulting in a large and often conflicting literature of candidate gene associations for ADHD. The first aim of the present study was to conduct a comprehensive meta-analytic review of this literature to determine which candidate genes show consistent evidence of association with childhood ADHD across studies. The second aim was to test for heterogeneity across studies in the effect sizes for each candidate gene as its presence might suggest moderating variables that could explain inconsistent results. Significant associations were identified for several candidate genes including DAT1, DRD4, DRD5, 5HTT, HTR1B, and SNAP25. Further, significant heterogeneity was observed for the associations between ADHD and DAT1, DRD4, DRD5, DBH, ADRA2A, 5HTT, TPH2, MAOA, and SNAP25, suggesting that future studies should explore potential moderators of these associations (e.g., ADHD subtype diagnoses, gender, exposure to environmental risk factors). We conclude with a discussion of these findings in relation to emerging themes relevant to future studies of the genetics of ADHD.

Variation in central serotonin levels due to genetic mutations or experimental modifications has been associated with the manifestation of aggression in humans and animals. Many studies have examined whether common variants in serotonergic genes are implicated in aggressive or antisocial behaviors (ASB) in human samples. The two most commonly studied polymorphisms have been the serotonin transporter linked polymorphic region of the serotonin transporter gene (5HTTLPR) and the 30 base pair variable number of tandem repeats of the monoamine oxidase A gene (MAOA-uVNTR). Despite the aforementioned theoretical justification for these polymorphisms, findings across studies have been mixed and are thus difficult to interpret. A meta-analysis of associations of the 5HTTLPR and MAOA-uVNTR with ASB was conducted to determine: (1) the overall magnitude of effects for each polymorphism, (2) the extent of heterogeneity in effect sizes across studies and the likelihood of publication bias, and (3) whether sample-level or study-level characteristics could explain observed heterogeneity across studies. Both the 5HTTLPR and the MAOA-uVNTR were significantly associated with ASB across studies. There was also significant and substantial heterogeneity in the effect sizes for both markers, but this heterogeneity was not explained by any sample-level or study-level characteristics examined. We did not find any evidence for publication bias across studies for the MAOA-uVNTR, but there was evidence for an oversampling of statistically significant effect sizes for the 5HTTLPR. These findings provide support for the modest role of common serotonergic variants in ASB. Implications regarding the role of serotonin in antisocial behavior and the conceptualization of antisocial and aggressive phenotypes are discussed.

Although advances in neonatal care over the past century have resulted in increased rates of survival among at-risk births, including infants with low birth weight, we have much to learn about the psychological outcomes in this population. In particular, although it appears that there is growing evidence that low birth weight may be associated with an increased risk for Attention-Deficit/Hyperactive Disorder (ADHD) symptoms in childhood, few studies have examined birth weight as a risk factor for disruptive disorders that commonly co-occur with ADHD [e.g. Oppositional Defiant Disorder (ODD) or Conduct Disorder (CD)]. In addition, the etiology of the relation between birth weight and these disorders is unknown. The current investigation aimed to better understand the putative role of birth weight in disruptive behavior disorders in the context of potentially confounding genetic and environmental influences by examining phenotypic associations between birth weight and disruptive disorder symptoms across families (using generalized linear models with generalized estimating equations) as well as within families (using linear regression) in two independent twin samples (Sample 1: N = 1676 individuals; Sample 2: N = 4038 individuals). We found negative associations between birth weight and several childhood disruptive disorder symptom dimensions, including inattentive, hyperactive-impulsive, and broad externalizing symptoms in both samples. Nonetheless, the overall magnitude of these associations was very small, contributing to less than 1% of the variance in these symptom dimensions. Within-family associations between birth weight and disruptive disorder symptoms did not differ for monozygotic and dizygotic twin pairs, suggesting that nonshared environmental influences rather than common genetic influences are responsible for these associations. These consistent albeit weak associations between birth weight and disruptive disorder symptoms suggest that, at least in the general population, low birth weight does not represent a major risk factor in the development of these symptoms.

Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disorder characterized by inattention, impulsivity, and/or hyperactivity in children and adults. Putative environmental risk factors for ADHD include toxin and prenatal smoke exposure, low socioeconomic status, and parental marital instability and discord. Genetic associations with ADHD have been found in the dopaminergic, serotonergic, and noradrenergic neurotransmitter systems, but findings are inconsistent across studies. Herein, we review studies of gene-environment interactions for ADHD to better understand how genetic and environmental risk factors may contribute to the disorder in a nonindependent fashion, which may account in part for the inconsistent findings on genetic associations. Although evidence of interactions between prenatal substance exposure and the dopamine genes DAT1 and DRD4 was found, findings across studies have been mixed. We discuss these findings and the future directions and limitations of current gene-environment research.

Few studies have examined the etiology of psychopathic traits in youth, and even fewer have tested whether the genetic and environmental influences underlying these traits differ for boys and girls. We tested for sex differences in the etiology of 3 trait dimensions-impulsivity, narcissism, and callous-unemotionality (CU)-previously found to underlie youth psychopathy in our sample. Using biometric modeling we tested whether constraining the genetic and environmental influences for each dimension across sex reduced model fit. We also tested for qualitative sex differences in the influences underlying these dimensions by allowing the genetic and environmental correlations between opposite sex dizygotic twins to be less than their respective values in same-sex dizygotic twins. Although the magnitudes of the genetic and environmental influences underlying the CU and narcissistic trait dimensions did not differ for boys and girls, nonshared environmental influences contributed significantly greater variance to impulsive traits in boys. No qualitative sex differences were found in the influences underlying any of the 3 trait dimensions, suggesting that the same genes and environments contribute to these psychopathic traits in males and females.