Modern research acknowledges that psychopathology and individual differences in normal development are the joint products of both biological and social influences. Although there have been numerous publications on Gene × Environment interactions in the past decade, gene–environment correlation is another important form of gene–environment interplay that has received less attention. This Special Section demonstrates, using a range of methodological approaches, the importance of gene–environment correlation in developmental psychopathology. Several types of gene–environment correlation are described, including passive, evocative, and active. Other studies highlight the potential for gene–environment correlation to obscure associations between risk exposures and child psychopathology. Future directions for gene–environment correlation research are discussed.

Gene–environment correlation (rGE) exists both within and between families. Between families, accumulating rGE has been used to explain dramatic changes in phenotypic means over time. The Dickens and Flynn model of increases in cognitive ability over generational time, for example, suggests that small changes in phenotype can lead to subsequent reallocation of environmental resources. This process sets up a reciprocal feedback loop between phenotype and environment, producing accumulating rGE that can cause large changes in the mean of ability, even though ability remains highly heritable in cross-sectional data. We report simulations suggesting that similar processes may operate within twin and sibling pairs. Especially in dizygotic twins and siblings, small differences in phenotype can become associated with reallocations of environmental resources within families. We show that phenotype–environment effects can account for age-related increases in rGE, rapid differentiation of siblings raised together, and widely reported increases in the heritability of behavior during childhood and adolescence.

Teenage childbirth is a risk factor for poor offspring outcomes, particularly offspring antisocial behavior. It is not clear, however, if maternal age at first birth (MAFB) is causally associated with offspring antisocial behavior or if this association is due to selection factors that influence both the likelihood that a young woman gives birth early and that her offspring engage in antisocial behavior. The current study addresses the limitations of previous research by using longitudinal data from Swedish national registries and children of siblings and children of twins comparisons to identify the extent to which the association between MAFB and offspring criminal convictions is consistent with a causal influence and confounded by genetic or environmental factors that make cousins similar. We found offspring born to mothers who began childbearing earlier were more likely to be convicted of a crime than offspring born to mothers who delayed childbearing. The results from comparisons of differentially exposed cousins, especially born to discordant monozygotic twin sisters, provide support for a causal association between MAFB and offspring criminal convictions. The analyses also found little evidence for genetic confounding due to passive gene–environment correlation. Future studies are needed to replicate these findings and to identify environmental risk factors that mediate this causal association.

Parental depression is associated with disruptions in the parent–child relationship, exposure to stressful family life events, and offspring depressive symptoms. Evidence suggests that intergenerational transmission of depression involves environmental and inherited contributions. We sought to evaluate the role of passive gene–environment correlation (rGE) in relation to depression, family life events that were due to parental behavior, and parental positivity in a sample where children varied in genetic relatedness to their rearing parents. Our study included 865 families with children born through assisted conception (444 related to both parents, 210 related to the mother only, 175 related to the father only, and 36 related to neither parent). Consistent with previous studies, the intergenerational transmission of depressive symptoms was largely due to environmental factors, although parent and child gender influenced results. Maternal and paternal depressive symptoms were associated with reduced positivity and increased parentally imposed life events regardless of parent–child relatedness. Results of path analysis were consistent with passive rGE for both maternal and paternal positivity in that positivity partially mediated the link between maternal/paternal depression and child depression only in genetically related parent–child pairs. Results also suggested passive rGE involving parentally imposed life events for mothers and fathers although passive rGE effects were smaller than for positivity.

Biological parents pass on genotypes to their children, as well as provide home environments that correlate with their genotypes; thus, the association between the home environment and children's temperament can be genetically (i.e., passive gene–environment correlation) or environmentally mediated. Furthermore, family environments may suppress or facilitate the heritability of children's temperament (i.e., gene–environment interaction). The sample comprised 807 twin pairs (mean age = 7.93 years) from the longitudinal Wisconsin Twin Project. Important passive gene–environment correlations emerged, such that home environments were less chaotic for children with high effortful control, and this association was genetically mediated. Children with high extraversion/surgency experienced more chaotic home environments, and this correlation was also genetically mediated. In addition, heritability of children's temperament was moderated by home environments, such that effortful control and extraversion/surgency were more heritable in chaotic homes, and negative affectivity was more heritable under crowded or unsafe home conditions. Modeling multiple types of gene–environment interplay uncovered the complex role of genetic factors and the hidden importance of the family environment for children's temperament and development more generally.

Married men engage in significantly less antisocial behavior than unmarried men, but it is not clear whether this reflects a causal relationship. Instead, the relationship could reflect selection into marriage whereby the men who are most likely to marry (men in steady employment with high levels of education) are the least likely to engage in antisocial behavior. The relationship could also be the result of reverse causation, whereby high levels of antisocial behavior are a deterrent to marriage rather than the reverse. Both of these alternative processes are consistent with the possibility that some men have a genetically based proclivity to become married, known as an active genotype–environment correlation. Using four complementary methods, we tested the hypothesis that marriage limits men's antisocial behavior. These approaches have different strengths and weaknesses and collectively help to rule out alternative explanations, including active genotype–environment correlations, for a causal association between marriage and men's antisocial behavior. Data were drawn from the in-home interview sample of the National Longitudinal Study of Adolescent Health, a large, longitudinal survey study of a nationally representative sample of adolescents in the United States. Lagged negative binomial and logistic regression and propensity score matching models (n = 2,250), fixed-effects models of within-individual change (n = 3,061), and random-effects models of sibling differences (n = 618) all showed that married men engaged in significantly less antisocial behavior than unmarried men. Our findings replicate results from other quasiexperimental studies of marriage and men's antisocial behavior and extend the results to a nationally representative sample of young adults in the United States.

Early disruptive behaviors, such as aggressive and hyperactive behaviors, known to be influenced by genetic factors, have been found to predict early school peer relation difficulties, such as peer rejection and victimization. However, there is no consensus regarding the developmental processes underlying this predictive association. Genetically informative designs, such as twin studies, are well suited for investigating the underlying genetic and environmental etiology of this association. The main goal of the present study was to examine the possible establishment of an emerging gene–environment correlation linking disruptive behaviors to peer relationship difficulties during the first years of school. Participants were drawn from an ongoing longitudinal study of twins who were assessed with respect to their social behaviors and their peer relation difficulties in kindergarten and in Grade 1 through peer nominations measures and teacher ratings. As predicted, disruptive behaviors were concurrently and predictively associated with peer relation difficulties. Multivariate analyses of these associations indicate that they were mainly accounted for by genetic factors. These results emphasize the need to adopt an early and persistent prevention framework targeting both the child and the peer context to alleviate the establishment of a negative coercive process and its consequences.

Depression is known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene–environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene–environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.

The behavior genetic literature suggests that genetically influenced characteristics of the child elicit specific behaviors from the parent. However, little is known about the processes by which genetically influenced child characteristics evoke parental responses. Interpersonal theory provides a useful framework for identifying reciprocal behavioral processes between children and mothers. The theory posits that, at any given moment, interpersonal behavior varies along the orthogonal dimensions of warmth and control and that the interpersonal behavior of one individual tends to elicit corresponding or contrasting behavior from the other (i.e., warmth elicits warmth, whereas control elicits submission). The current study thus examined these dimensions of interpersonal behavior as they relate to the parent–child relationship in 546 twin families. A computer joystick was used to rate videos of mother–child interactions in real time, yielding information on mother and child levels of warmth and control throughout the interaction. Analyses indicated that maternal control, but not maternal warmth, was influenced by evocative gene–environment correlational processes, such that genetic influences on maternal control and child control were largely overlapping. Moreover, these common genetic influences were present both cross-sectionally and over the course of the interaction. Such findings not only confirm the presence of evocative gene–environment correlational processes in the mother–child relationship but also illuminate at least one of the specific interpersonal behaviors that underlie this evocative process.

We used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene–environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.

This study examined genetic and environmental influences on associations among marital conflict about the child, parental monitoring, sibling relationship negativity, and peer delinquency during adolescence and initiation of illegal drug use by young adulthood. The sample comprised data collected longitudinally from same-sex sibling pairs and parents when the siblings were 10–18 years old (M = 14.5 and 12.9 years for Child 1 and Child 2, respectively) and 20–35 years old (M = 26.8 and 25.5 years for Child 1 and Child 2, respectively). Findings indicate four factors that explain the initiation of illegal drug use: two shaped by genetic influences and two shaped by environments shared by siblings. The two genetically shaped factors probably have distinct mechanisms: one a child-initiated coercive process in the family and the other parent and peer processes shaped by the child's disclosure. The environmentally influenced factors seem distinctively shaped by poor parental monitoring of both sibs and the effects of siblings on each other's deviancy.

Self-control, involving processes such as delaying gratification, concentrating, planning, following instructions, and adapting emotions and behavior to situational requirements and social norms, may have a profound impact on children's adjustment. The importance of self-control suggests that parents are likely to modify their parenting based on children's ability for self-control. We study the effect of children's self-control, a trait partially molded by genetics, on their mothers' parenting, a process of evocative gene–environment correlation. Israeli 3.5-year-old twins (N = 320) participated in a lab session in which their mothers' parenting was observed. DNA was available from most children (N = 228). Mothers described children's self-control in a questionnaire. Boys were lower in self-control and received less positive parenting from their mothers, in comparison with girls. For boys, and not for girls, the serotonin transporter linked polymorphic region gene predicted mothers' levels of positive parenting, an effect mediated by boys' self-control. The implications of this evocative gene–environment correlation and the observed sex differences are discussed.

The dopamine active transporter 1 (DAT1) gene is implicated in psychopathology risk. Although the processes by which this gene exerts its effects on risk are poorly understood, a small body of research suggests that the DAT1 gene influences early emerging negative emotionality, a marker of children's psychopathology risk. As child negative emotionality evokes negative parenting practices, the DAT1 gene may also play a role in gene–environment correlations. To test this model, children (N = 365) were genotyped for the DAT1 gene and participated in standardized parent–child interaction tasks with their primary caregiver. The DAT1 gene 9-repeat variant was associated with child negative affect expressed toward the parent during parent–child interactions, and parents of children with a 9-repeat allele exhibited more hostility and lower guidance/engagement than parents of children without a 9-repeat allele. These gene–environment associations were partially mediated by child negative affect toward the parent. The findings implicate a specific polymorphism in eliciting negative parenting, suggesting that evocative associations play a role in elevating children's risk for emotional trajectories toward psychopathology risk.

Gene–environment correlations (rGE) have been demonstrated in behavioral genetic studies, but rGE have proven elusive in molecular genetic research. Significant gene–environment correlations may be difficult to detect because potential moderators could reduce correlations between measured genetic variants and the environment. Molecular genetic studies investigating moderated rGE are lacking. This study examined associations between child catechol-O-methyltransferase genotype and aspects of positive parenting (responsiveness and warmth), and whether these associations were moderated by parental personality traits (neuroticism and extraversion) among a general community sample of third, sixth, and ninth graders (N = 263) and their parents. Results showed that parent personality traits moderated the rGE association between youths' genotype and coded observations of positive parenting. Parents with low levels of neuroticism and high levels of extraversion exhibited greater sensitive responsiveness and warmth, respectively, to youth with the valine/valine genotype. Moreover, youth with this genotype exhibited lower levels of observed anger. There was no association between the catechol-O-methyltransferase genotype and parenting behaviors for parents high on neuroticism and low on extraversion. Findings highlight the importance of considering moderating variables that may influence child genetic effects on the rearing environment. Implications for developmental models of maladaptive and adaptive child outcomes, and interventions for psychopathology, are discussed within a developmental psychopathology framework.

This review discusses neurobiological studies of oppositional defiant disorder and conduct disorder within the conceptual framework of three interrelated mental domains: punishment processing, reward processing, and cognitive control. First, impaired fear conditioning, reduced cortisol reactivity to stress, amygdala hyporeactivity to negative stimuli, and altered serotonin and noradrenaline neurotransmission suggest low punishment sensitivity, which may compromise the ability of children and adolescents to make associations between inappropriate behaviors and forthcoming punishments. Second, sympathetic nervous system hyporeactivity to incentives, low basal heart rate associated with sensation seeking, orbitofrontal cortex hyporeactiviy to reward, and altered dopamine functioning suggest a hyposensitivity to reward. The associated unpleasant emotional state may make children and adolescents prone to sensation-seeking behavior such as rule breaking, delinquency, and substance abuse. Third, impairments in executive functions, especially when motivational factors are involved, as well as structural deficits and impaired functioning of the paralimbic system encompassing the orbitofrontal and cingulate cortex, suggest impaired cognitive control over emotional behavior. In the discussion we argue that more insight into the neurobiology of oppositional defiance disorder and conduct disorder may be obtained by studying these disorders separately and by paying attention to the heterogeneity of symptoms within each disorder.

A fundamental question in the discipline of developmental psychopathology is whether early interpersonal experiences influence maladaptation in enduring or transient ways. We address this issue by applying a structural modeling approach developed by us to examine data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development on maternal sensitivity in the first 3 years of life and its association with symptoms of psychopathology through age 15. Results suggest that there may be enduring effects of early caregiving experiences on symptomatology as rated by teachers, although such effects were not found for maternal report. Additional analyses indicated that enduring associations found via teacher report could not be fully accounted for by continuity in caregiving experiences or by early contextual adversity.

Recent evidence suggests that impulsivity and sensation seeking are not stable risk factors for substance use among adolescents and early adults but rather that they undergo significant developmental maturation and change. Further, developmental trends of both personality facets may vary across individuals. In the current investigation, we used longitudinal data from ages 15 to 26 on 5,632 individuals drawn from the offspring generation of the National Longitudinal Survey of Youth to examine whether interindividual differences in intraindividual change in impulsivity and sensation seeking predicted the escalation of alcohol, marijuana, and cigarette use in adolescence and early adulthood. Latent growth curve models revealed significant individual differences in rates of change in both personality and substance use. Age-related changes in personality were positively associated with individual differences in substance-use change. Individuals who declined more slowly in impulsivity increased in alcohol, marijuana, and cigarette more rapidly, whereas individuals who declined more slowly in sensation seeking increased more rapidly in alcohol use only. Although risk for substance use across the population may peak during adolescence and early adulthood, this risk may be highest among those who decline more gradually in impulsivity.

Although the sensitization hypothesis is fundamental to process-oriented explanations of the effects of marital conflict on children, few longitudinal tests of the theory's propositions have been conducted. Hierarchical linear modeling was used in this prospective, longitudinal study (n = 297 families) to assess changes in the dimensions of responding to conflict (i.e., emotional, cognitive, and behavioral) for 3 consecutive years in youths between the ages of 8 and 19 years. Moreover, to test the notion of sensitization, analyses were conducted to examine whether change in marital conflict predicted change in children's responding across middle childhood and adolescence. Supporting the sensitization hypothesis, increases in exposure to hostile marital conflict were associated with increases in children's negative emotionality, threat, self-blame, and skepticism about resolution. With a few exceptions, the effects were largely consistent for boys and girls and for younger and older children.

Williams syndrome is a neurodevelopmental genetic disorder caused by a hemizygous deletion on chromosome 7q11.23, resulting in atypical brain structure and function, including abnormal morphology of the corpus callosum. An influence of handedness on the size of the corpus callosum has been observed in studies of typical individuals, but handedness has not been taken into account in studies of callosal morphology in Williams syndrome. We hypothesized that callosal area is smaller and the size of the splenium and isthmus is reduced in individuals with Williams syndrome compared to healthy controls, and examined age, sex, and handedness effects on corpus callosal area. Structural magnetic resonance imaging scans were obtained on 25 individuals with Williams syndrome (18 right-handed, 7 left-handed) and 25 matched controls. We found that callosal thickness was significantly reduced in the splenium of Williams syndrome individuals compared to controls. We also found novel evidence that the callosal area was smaller in left-handed participants with Williams syndrome than their right-handed counterparts, with opposite findings observed in the control group. This novel finding may be associated with LIM-kinase hemizygosity, a characteristic of Williams syndrome. The findings may have significant clinical implications in future explorations of the Williams syndrome cognitive phenotype.

To better understand mechanisms underlying the intergenerational transmission of social anxiety, we used a prospective adoption design to examine the roles of genetic influences (inferred from birth mothers' social phobia) and rearing environment (adoptive mothers' and fathers' responsiveness) on the development of socially inhibited, anxious behaviors in children between 18 and 27 months of age. The sample consisted of 275 adoption-linked families, each including an adopted child, adoptive parents, and a birth mother. Results indicated that children whose birth mothers met criteria for the diagnosis of social phobia showed elevated levels of observed behavioral inhibition in a social situation at 27 months of age if their adoptive mothers provided less emotionally and verbally responsive rearing environments at 18 months of age. Conversely, in the context of higher levels of maternal responsiveness, children of birth mothers with a history of social phobia did not show elevated levels of behavioral inhibition. These findings on maternal responsiveness were replicated in a model predicting parent reports of child social anxiety. The findings are discussed in terms of gene–environment interactions in the intergenerational transmission of social anxiety.