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.

Developmental psychopathology is not characterized by adherence to one specific theory but instead serves as an organizational framework in which research is driven by a number of key assumptions. In the developmental psychopathology approach, two primary assumptions emphasize the importance of systems thinking and the utility of multilevel analyses. As will be illustrated here, these emphases are inextricably linked: a systems approach necessitates a multilevel approach, such that a level of organization must bring coherence to a level of mechanisms. Given this assumption, coming to an integrative understanding of the relation between levels is of central importance. One broad framework for this endeavor is relational developmental systems, which has been proposed by certain theorists as a new paradigm for developmental science. The implications of embracing this framework include the potential to connect developmental psychopathology with other approaches that emphasize systems thinking and that take an integrative perspective on the problem of levels of analysis.

The development of emotional regulation capacities in children at high versus low risk for externalizing disorder was examined in a longitudinal study investigating: (a) whether disturbances in emotion regulation precede and predict the emergence of externalizing symptoms and (b) whether sensitive maternal behavior is a significant influence on the development of child emotion regulation. Families experiencing high (n = 58) and low (n = 63) levels of psychosocial adversity were recruited to the study during pregnancy. Direct observational assessments of child emotion regulation capacities and maternal sensitivity were completed in early infancy, at 12 and 18 months, and at 5 years. Key findings were as follows. First, high-risk children showed poorer emotion regulation capacities than their low-risk counterparts at every stage of assessment. Second, from 12 months onward, emotion regulation capacities showed a degree of stability and were associated with behavioral problems, both concurrently and prospectively. Third, maternal sensitivity was related to child emotion regulation capacities throughout development, with poorer emotion regulation in the high-risk group being associated with lower maternal sensitivity. The results are consistent with a causal role for problems in the regulation of negative emotions in the etiology of externalizing psychopathology and highlight insensitive parenting as a potentially key developmental influence.

Symptoms of anxiety and depression are prevalent among adolescents and associated with impairment in multiple domains of functioning. Moreover, anxiety and depression frequently co-occur, with estimated comorbidity rates as high as 75%. Whereas previous research has shown that anxiety symptoms predict increased depressive symptoms over time, the relation between depressive symptoms and later anxiety symptoms has been inconsistent. The present study examined dynamic relations between anxiety and depressive symptoms across adolescence and explored whether these longitudinal relations were moderated by maternal history of anxiety, family relationship quality, or children's attributional style. Participants included 240 children (M age = 11.86 years; 53.9% female) and their mothers, who were assessed annually for 6 years. Children reported on their depressive symptoms and mothers reported on their child's anxiety symptoms. Dynamic latent change score models indicated that anxiety symptoms predicted subsequent elevations in depressive symptoms over time. Depressive symptoms predicted subsequent elevations in anxiety symptoms among children who had mothers with a history of anxiety, reported low family relationship quality, or had high levels of negative attributions. Thus, whereas anxiety symptoms were a robust predictor of later depressive symptoms during adolescence, contextual and individual factors may be important to consider when examining relations between depressive symptoms and subsequent change in anxiety symptoms.

Although family support reliably predicts the development of adolescent depression and suicidal behaviors, relatively little is known about the interplay of family support with potential genetic factors. We tested the association of the 44 base pair polymorphism in the serotonin transporter linked promoter region gene (5-HTTLPR), family support (i.e., cohesion, communication, and warmth), and their interaction with self-reported depression symptoms and risk for suicide in 1,030 Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health. High-quality family support predicted fewer symptoms of depression and reduced risk for suicidality. There was also a significant interaction between 5-HTTLPR and family support for boys and a marginally significant interaction for girls. Among boys with poor family support, youth with at least one short allele had more symptoms of depression and a higher risk for suicide attempts relative to boys homozygous for the long allele. However, in the presence of high family support, boys with the short allele had the fewest depression symptoms (but not suicide attempts). Results suggest that the short allele may increase reactivity to both negative and positive family influences in the development of depression. We discuss the potential role of interactive exchanges between family support and offspring genotype in the development of adolescent depression and suicidal behaviors.

The biological sensitivity to context hypothesis posits that high physiological reactivity (i.e., increases in arousal from baseline) constitutes heightened sensitivity to environmental influences, for better or worse. To test this hypothesis, we examined the interactive effects of family cohesion and heart rate reactivity to a public speaking task on aggressive/rule-breaking and prosocial behavior in a large sample of adolescents (N = 679; M age = 16.14). Multivariate analyses revealed small- to medium-sized main effects of lower family cohesion and lower heart rate reactivity on higher levels of aggressive/rule-breaking and lower levels of prosocial behavior. Although there was some evidence of three-way interactions among family cohesion, heart rate reactivity, and sex in predicting these outcome variables, these interactions were not in the direction predicted by the biological sensitivity to context hypothesis. Instead, heightened reactivity appeared to operate as a protective factor against family adversity, rather than as a susceptibility factor. The results of the present study raise the possibility that stress reactivity may no longer operate as a mechanism of differential susceptibility in adolescence.

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.

Since this journal's inception, the field of adolescent brain development has flourished, as researchers have investigated the underpinnings of adolescent risk-taking behaviors. Explanations based on translational models initially attributed such behaviors to executive control deficiencies and poor frontal lobe function. This conclusion was bolstered by evidence that the prefrontal cortex and its interconnections are among the last brain regions to structurally and functionally mature. As substantial heterogeneity of prefrontal function was revealed, applications of neuroeconomic theory to adolescent development led to dual systems models of behavior. Current epidemiological trends, behavioral observations, and functional magnetic resonance imaging based brain activity patterns suggest a quadratic increase in limbically mediated incentive motivation from childhood to adolescence and a decline thereafter. This elevation occurs in the context of immature prefrontal function, so motivational strivings may be difficult to regulate. Theoretical models explain this patterning through brain-based accounts of subcortical–cortical integration, puberty-based models of adolescent sensation seeking, and neurochemical dynamics. Empirically sound tests of these mechanisms, as well as investigations of biology–context interactions, represent the field's most challenging future goals, so that applications to psychopathology can be refined and so that developmental cascades that incorporate neurobiological variables can be modeled.

Poor self-regulation has been implicated as a significant risk factor for the development of multiple forms of psychopathology. This research examined the proposition that self-regulation deficits differentially predict aggressive behavior and depressive symptoms, depending on children's social approach versus avoidance motivation. A prospective, multiple-informant approach was used to test this hypothesis in 419 children (M age = 8.92, SD = 0.36). Parents rated children's inhibitory control. Children completed measures of social approach–avoidance motivation and depressive symptoms. Teachers rated children's aggressive behavior. As anticipated, poor inhibitory control predicted aggressive behavior in boys with high but not low approach motivation and low but not high avoidance motivation, whereas poor inhibitory control predicted depressive symptoms in girls with high but not low avoidance motivation. This research supports several complementary theoretical models of psychopathology and provides insight into the differential contributions of poor self-regulation to maladaptive developmental outcomes. The findings suggest the need for targeted intervention programs that consider heterogeneity among children with self-regulatory deficits.

This study examined the psychometric properties of the DSM-oriented scales of the Child Behavior Checklist (Achenbach, Dumenci, & Rescorla, 2003) using confirmatory factor analysis to compare the six-factor structure of the DSM-oriented scales to competing models consistent with developmental theories of symptom differentiation. We tested these models on both clinic-referred (N = 757) and school-based, nonreferred (N = 713) samples of youths in order to assess the generalizability of the factorial structures. Although previous research has supported the fit of the six-factor DSM-oriented structure in a normative sample of youths ages 7 to 18 (Achenbach & Rescorla, 2001), tripartite model research indicates that anxiety and depressive symptomology are less differentiated among children compared to adolescents (Jacques & Mash, 2004). We thus examined the relative fit of a six- and a five-factor model (collapsing anxiety and depression) with younger (ages 7–10) and older (ages 11–18) youth subsamples. The results revealed that the six-factor model fit the best in all samples except among younger nonclinical children. The results extended the generalizability of the rationally derived six-factor structure of the DSM-oriented scales to clinic-referred youths and provided further support to the notion that younger children in nonclinical samples exhibit less differentiated symptoms of anxiety and depression.

We studied the developmental trends of temperament and character in a longitudinal population-based sample of Finnish men and women aged 20–45 years using the Temperament and Character Inventory model of personality. Personality was assessed in 1997, 2001, and 2007 (n = 2,104, 2,095, and 2,056, respectively). Mean-level changes demonstrated qualitatively distinct developmental patterns for character (self-directedness, cooperativeness, and self-transcendence) and temperament (novelty seeking, harm avoidance, reward dependence, and persistence). Character developed toward greater maturity, although self-transcendence decreased with age. However, self-transcendence was the strongest predictor of overall personality change. Cohort effects indicated lower level of self-transcendence and higher level of self-directedness and cooperativeness in younger birth cohorts. Regarding temperament, novelty seeking decreased and persistence increased slightly with age. Both high novelty seeking and high persistence predicted overall personality change. These findings suggest that temperament and character traits follow different kinds of developmental trajectories.

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.

The endophenotype is central to modern developmental psychopathology studies. It is used in studies seeking to connect the genetic substrates of the panoply of major mental disorders with processes, tapped by laboratory and other assessment measures, in the genotype to a behavior/psychopathology pathway. Proposed originally by Gottesman and Shields (1972; Shields & Gottesman, 1973) 41 years ago, the endophenotype concept has gained widespread traction in psychopathology research since the Gottesman and Gould (2003) review. Other concepts broadly related to the endophenotype notion have also generated discussion in experimental and developmental psychopathology research. One is the intermediate phenotype, a concept proffered as a putative alternative formulation to the endophenotype. Another concept in this intellectual vein is biomarker. The terms endophenotype, intermediate phenotype, and biomarker have often been used interchangeably in the psychiatric literature, yielding conceptual confusion. However, these three terms are not fungible. The recent Research Domain Criteria proposal from the National Institute of Mental Health has emphasized selected underlying processes thought to be of developmental etiologic significance to psychopathology. These selected processes will be the focus of energetic future research efforts, many of which will make use of the endophenotype and biomarker research paradigms. In this context, the concepts of endophenotype, intermediate phenotype, and biomarker are examined critically and contrasted in terms of meaning, intention, clarity, and intellectual history. This analysis favors use of the endophenotype concept in genetically informed laboratory and neuroscience studies of psychopathology. The term intermediate phenotype is perhaps best restricted to its originally defined meaning in genetics. Biomarker is used to denote objectively measured biological antecedents or consequences of normal or pathogenic processes or a physiologic response to a therapeutic intervention.

Earlier age of menarche is believed to confer greater vulnerability to depressive symptoms via increased reactivity to stressors associated with adolescence. In this longitudinal study, we measured depressive symptoms and salivary cortisol levels in 198 boys and 142 girls between the ages of 11 and 13 tested four times during Grade 7 as they transitioned from elementary school to secondary school as per Quebec's education system. Results showed that girls who had already reached menarche before starting secondary school had significantly higher depressive symptoms and salivary cortisol levels across the school year in comparison to girls who had not reached menarche, who in turn presented higher depressive scores than boys. When we divided menarcheal girls as a function of menarcheal timing in subanalyses, we found that girls with early menarche presented consistently elevated depressive symptoms across the school year while girls with on-time menarche presented transient depressive symptoms but no differences in salivary cortisol levels. Collectively, these results show that early menarche is associated with high depressive symptoms and cortisol levels in adolescent girls. This developmental milestone may render girls more vulnerable to environmental stressors and therefore represents a critical period to intervene to promote mental health.

We investigated the roles of sex and respiratory sinus arrhythmia (RSA), an index of autonomic parasympathetic nervous system activity, as predictors of codeveloping externalizing and internalizing symptoms in middle childhood. We expected that sex, baseline RSA (RSA-B), and RSA reactivity (RSA-R) to two types of tasks would interact to differentiate co-occurring trajectories of symptoms. We tested these hypotheses by combining longitudinal data from two independent samples (n = 390; 210 girls, 180 boys) with repeated measures at ages 8, 9, 10, and 11. RSA-R was measured in response to a socially stressful and frustrating stressor. Indicators of growth in externalizing and internalizing symptoms were derived from multiple domain growth models and used in person-centered growth mixture analyses. Three groups of externalizing and internalizing trajectories were found. Profile membership was predicted by several two-way interactions among sex, RSA-B, or RSA-R but was not predicted by three-way interactions. Children with low RSA-B and strong RSA withdrawal, girls with low RSA-B, and girls with strong RSA withdrawal were more likely to be on a developmental trajectory of low externalizing symptoms and moderately elevated internalizing symptoms. Membership in the high externalizing and high internalizing trajectory was predicted by weak RSA withdrawal for boys and strong RSA withdrawal for girls. The type of stressor task also played a role in predicting probability of profile membership. Results are discussed in the context of developmental psychobiology and implications for the codevelopment of psychopathology symptoms in childhood.

Emotional distress experienced by mothers increases young children's risk of externalizing problems through suboptimal parenting and child self-regulation. An integrative structural equation model tested hypotheses that mothers’ parenting (i.e., low levels of inductive discipline and maternal warmth) would mediate adverse effects of early maternal distress on child effortful control, which in turn would mediate effects of maternal parenting on child externalizing behavior. This longitudinal study spanning ages 3, 6, and 10 included 241 children, mothers, and a subset of teachers. The hypothesized model was partially supported. Elevated maternal distress was associated with less inductive discipline and maternal warmth, which in turn were associated with less effortful control at age 3 but not at age 6. Inductive discipline and maternal warmth mediated adverse effects of maternal distress on children's effortful control. Less effortful control at ages 3 and 6 predicted smaller relative decreases in externalizing behavior at 6 and 10, respectively. Effortful control mediated effects of inductive discipline, but not maternal warmth, on externalizing behavior. Findings suggest elevated maternal distress increases children's risk of externalizing problems by compromising early parenting and child self-regulation.

Substance use is a major contributor to morbidity and mortality among American adolescents. Conduct problems and depressive symptoms have each been found to be associated with adolescent substance use. Although they are highly comorbid, the role of the interaction of conduct problems and depressive symptoms in substance use is not clear. In national samples of 8th-, 10th-, and 12th-grade students from the Monitoring the Future study, latent moderated structural equation modeling was used to estimate the association of conduct problems, depressive symptoms, and their interaction to the use of alcohol (including binge drinking), cigarettes, and marijuana. Moderation by age and sex was tested. The interaction of conduct problems with depressive symptoms was a strong predictor of substance use, particularly among younger adolescents. With few exceptions, adolescents with high levels of both conduct problems and depressive symptoms used substances most frequently. Conduct problems were a strong positive predictor of substance use, and depressive symptoms were a weak positive predictor. Whereas conduct problems are often thought to be a primary predictor of substance use, this study revealed that depressive symptoms potentiate the relation of conduct problems to substance use. Therefore, substance use prevention efforts should target both depressive symptoms and conduct problems.

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.

Research on the hypothalamic–pituitary–adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology in the past 25 years. Extensive animal research has provided knowledge of the substrates and physiological mechanisms that guide development of stress reactivity and regulation using methods that are not feasible in humans. Recent advances in understanding the anatomy and physiology of the HPA axis in humans and its interactions with other stress-mediating systems, including accurate assessment of salivary cortisol, more sophisticated neuroimaging methods, and a variety of genetic analyses, have led to greater knowledge of how psychological and biological processes impact functioning. A growing body of research on HPA axis regulation and reactivity in relation to psychopathology has drawn increased focus on the prenatal period, infancy, and the pubertal transition as potentially sensitive periods of stress system development in children. Theories such as the allostatic load model have guided research by integrating multiple physiological systems and mechanisms by which stress can affect mental and physical health. However, almost none of the prominent theoretical models in stress physiology are truly developmental, and future work must incorporate how systems interact with the environment across the life span in normal and atypical development. Our theoretical advancement will depend on our ability to integrate biological and psychological models. Researchers are increasingly realizing the importance of communication across disciplinary boundaries in order to understand how experiences influence neurobehavioral development. It is important that knowledge gained over the past 25 years has been translated to prevention and treatment interventions, and we look forward to the dissemination of interventions that promote recovery from adversity.

This study tested a theoretical model of continuity in anxious emotion and its links to academic achievement in disaster-exposed youth. An urban school based sample of youths (n = 191; Grades 4–8) exposed to Hurricane Katrina were assessed at 24 months (Time 1) and then again at 30 months (Time 2) postdisaster. Academic achievement was assessed through end of the school year standardized test scores (~31 months after Katrina). The results suggest that the association of traumatic stress to academic achievement was indirect via linkages from earlier (Time 1) posttraumatic stress disorder symptoms that predicted later (Time 2) test anxiety. Time 2 test anxiety was then negatively associated with academic achievement. Age and gender invariance testing suggested strong consistency across gender and minor developmental variation in the age range examined. The model presented advances the developmental understanding of the expression of anxious emotion and its links to student achievement among disaster-exposed urban school children. The findings highlight the importance of identifying heterotypic continuity in anxiety and suggest potential applied and policy directions for disaster-exposed youth. Avenues for future theoretical refinement are also discussed.