This study examined developmentally salient risk and protective factors of adolescent substance use assessed during early childhood and early adolescence using a sample of 310 low-income boys. Child problem behavior and proximal family risk and protective factors (i.e., parenting and maternal depression) during early childhood, as well as child and family factors and peer deviant behavior during adolescence, were explored as potential precursors to later substance use during adolescence using structural equation modeling. Results revealed that early childhood risk and protective factors (i.e., child externalizing problems, mothers' depressive symptomatology, and nurturant parenting) were indirectly related to substance use at the age of 17 via risk and protective factors during early and middle adolescence (i.e., parental knowledge and externalizing problems). The implications of these findings for early prevention and intervention are discussed.

Building on research on cumulative risk and psychopathology, this study examines how cumulative risk exposure is associated with altered diurnal cortisol rhythms in an ethnically diverse, low-income sample of youth. In addition, consistent with a diathesis-stress perspective, this study explores whether the effect of environmental risk is moderated by allelic variation in the serotonin transporter linked polymorphic region (5-HTTLPR) gene. Results show that youth with greater cumulative risk exposure had flatter diurnal cortisol slopes, regardless of 5-HTTLPR genotype. However, the association of cumulative risk with average cortisol output (area under the curve [AUC]) was moderated by the 5-HTTLPR genotype. Among youth homozygous for the long allele, greater cumulative risk exposure was associated with lower cortisol AUC, driven by significant reductions in cortisol levels at waking. In contrast, there was a trend-level association between greater cumulative risk and higher cortisol AUC among youth carrying the short allele, driven by a trend-level increase in bedtime cortisol levels. Findings are discussed with regard to the relevance of dysregulated diurnal cortisol rhythms for the development of psychopathology and the implications of genetically mediated differences in psychophysiological adaptations to stress.

Structural and functional alterations in a variety of brain regions have been associated with depression and risk for depression across the life span. A majority of these regions are associated with emotion reactivity and/or regulation. However, it is generally unclear what mechanistic role these alterations play in the etiology of depression. A first step toward understanding this is to characterize the relationships between variation in brain structure/function and individual differences in depression severity and related processes, particularly emotion regulation. To this end, the current study examines how brain structure and function predict concurrent and longitudinal measures of depression symptomology and emotion regulation skills in psychiatrically healthy school-age children (N = 60). Specifically, we found that smaller hippocampus volumes and greater responses to sad faces in emotion reactivity regions predict increased depressive symptoms at the time of scan, whereas larger amygdala volumes, smaller insula volumes, and greater responses in emotion reactivity regions predict decreased emotion regulation skills. In addition, larger insula volumes predict improvements in emotion regulation skills even after accounting for emotion regulation at the time of scan. Understanding brain–behavior relationships in psychiatrically healthy samples, especially early in development, will help inform normative developmental trajectories and neural alterations in depression and other affective pathology.

A growing body of research has documented structural and functional brain development during adolescence, yet little is known about neurochemical changes that occur during this important developmental period. Magnetic resonance spectroscopy (MRS) is a well-developed technology that permits the in vivo quantification of multiple brain neurochemicals relevant to neuronal health and functioning. However, MRS technology has been underused in exploring normative developmental changes during adolescence and the onset of alcohol and drug use and abuse during this developmental period. This review begins with a brief overview of normative cognitive and neurobiological development during adolescence, followed by an introduction to MRS principles. The subsequent sections provide a comprehensive review of the existing MRS studies of development and cognitive functioning in healthy children and adolescents. The final sections of this article address the potential application of MRS in identifying neurochemical predictors and consequences of alcohol use and abuse in adolescence. MRS studies of adolescent populations hold promise for advancing our understanding of neurobiological risk factors for psychopathology by identifying the biochemical signatures associated with healthy brain development, as well as neurobiological and cognitive correlates of alcohol and substance use and abuse.

Founded in the social process model, the aim of this study was to identify whether the associations of relational aggression with concurrent and subsequent relational victimization differed depending on early adolescents' personal vulnerabilities and gender. The vulnerabilities of interest were social-information processing variables that convey greater emotional sensitivity, including rejection sensitivity, fear of negative evaluation, and avoidance of intimacy. Participants were 358 early adolescents (176 boys, 178 girls) aged 9 to 13 years. Relational aggression and victimization were assessed via peer nominations, whereas the three indicators of emotional sensitivity were assessed via self-report. Overall, results revealed greater relational aggression at Time 1 to be associated with greater relational victimization at both Time 1 and Time 2. However, this finding was qualified by both emotional sensitivity and gender. When considered separately, girls who were relationally aggressive and emotionally sensitive were at increased risk of victimization at both assessment points. In contrast, no link was found between relational aggression and victimization for boys, although relational vulnerabilities did have unique associations with boys' relational victimization. These findings have implications for our understanding of relational aggression and victimization, as well as for the development of interventions aimed at reducing these problems.

Anxiety disorders are associated with abnormalities in amygdala function and prefrontal cortex–amygdala connectivity. The majority of functional magnetic resonance imaging studies have examined mean group differences in amygdala activation or connectivity in children and adolescents with anxiety disorders relative to controls, but emerging evidence suggests that abnormalities in amygdala function are dependent on the timing of the task and may vary across the course of a scanning session. The goal of the present study was to extend our knowledge of the dynamics of amygdala dysfunction by examining whether changes in amygdala activation and connectivity over scanning differ in pediatric anxiety disorder patients relative to typically developing controls during an emotion processing task. Examining changes in activation over time allows for a comparison of how brain function differs during initial exposure to novel stimuli versus more prolonged exposure. Participants included 34 anxiety disorder patients and 19 controls 7 to 19 years old. Participants performed an emotional face-matching task during functional magnetic resonance imaging scanning, and the task was divided into thirds in order to examine change in activation over time. Results demonstrated that patients exhibited an abnormal pattern of amygdala activation characterized by an initially heightened amygdala response relative to controls at the beginning of scanning, followed by significant decreases in activation over time. In addition, controls evidenced greater context-modulated prefrontal cortex–amygdala connectivity during the beginning of scanning relative to patients. These results indicate that differences in emotion processing between the groups vary from initial exposure to novel stimuli relative to more prolonged exposure. Implications are discussed regarding how this pattern of neural activation may relate to altered early-occurring or anticipatory emotion-regulation strategies and maladaptive later-occurring strategies in children and adolescents with anxiety disorders.

Physically maltreated children are at risk for developing externalizing behavioral problems characterized by reactive aggression. The current experiment tested the relationships between individual differences in a neural index of social information processing, histories of child maltreatment, child negative affect, and aggressive behavior. Fifty boys (17 maltreated) performed an emotion recognition task while the P3b component of the event-related potential was recorded to index attention allocation to angry faces. Children then participated in a peer-directed aggression task. Negative affect was measured by recording facial electromyography, and aggression was indexed by the feedback that children provided to a putative peer. Physically maltreated children exhibited greater negative affect and more aggressive behavior, compared to nonmaltreated children, and this relationship was mediated by children's allocation of attention to angry faces. These data suggest that physical maltreatment leads to inappropriate regulation of both negative affect and aggression, which likely place maltreated children at increased risk for the development and maintenance of externalizing behavior disorders.

Consistent research shows that peer victimization predicts internalizing symptoms in childhood and adolescence, but the extent to which peer victimization and its harmful effects on mental health persists into young adulthood is unclear. The current study describes patterns of physical and relational victimization during and after high school, and examines concurrent and prospective associations between internalizing symptoms (depressive and anxious symptoms) and peer victimization (physical and relational) from adolescence to young adulthood (ages 12–27). Data were collected from the Victoria Healthy Youth Survey, a five-wave multicohort study conducted biennially between 2003 and 2011 (N = 662). Physical victimization was consistently low and stable over time. Relational victimization increased for males after high school. Both types of victimization were associated concurrently with internalizing symptoms across young adulthood for males and for females. Although sex differences were important, victimization in high school also predicted increases in internalizing problems over time.

Developmental–ecological models are useful for integrating risk factors across multiple contexts and conceptualizing mediational pathways for adolescent alcohol use, yet these comprehensive models are rarely tested. This study used a developmental–ecological framework to investigate the influence of neighborhood, family, and peer contexts on alcohol use in early adolescence (N = 387). Results from a multi-informant longitudinal cross-lagged mediation path model suggested that high levels of neighborhood disadvantage were associated with high levels of alcohol use 2 years later via an indirect pathway that included exposure to delinquent peers and adolescent delinquency. Results also indicated that adolescent involvement with delinquent peers and alcohol use led to decrements in parenting, rather than being consequences of poor parenting. Overall, the study supported hypothesized relationships among key microsystems thought to influence adolescent alcohol use, and thus findings underscore the utility of developmental–ecological models of alcohol use.

We utilized a longitudinal twin study (N = 2,510) to identify the child characteristics present prior to initiation of substance use that best predicted later substance use disorders. Two independent traits accounted for the majority of premorbid risk: socialization (conformity to rules and conventional values) and boldness (sociability and social assurance, stress resilience, and thrill seeking). Low socialization was associated with disruptive behavior disorders, parental externalizing disorders, and environmental adversity and exhibited moderate genetic (0.45) and shared environmental influences (0.30). Boldness was highly heritable (0.71) and associated with less internalizing distress and environmental adversity. In combination, these traits exhibited robust associations with adolescent and young adult substance use disorders (R = .48 and .50, respectively) and incremental prediction over disruptive behavior disorders, parental externalizing disorders, and environmental adversity. The results were replicated in an independent sample. Socialization and boldness offer a novel conceptualization of underlying risk for substance use disorders that has the potential to improve prediction and theory with implications for basic research, prevention, and intervention.

The bully/victim relationship was studied in a sample of elementary school children (N = 1,289 in first, third, and fifth grades). Three questions were tested. Does bullying involve a power differential between bully and victim? Are bully/victim dyads participants in a relationship, whether mutual liking or disliking? Does the gender composition of the bully/victim dyad moderate power differential and relational context patterns? Hierarchical linear modeling was used to analyze predictors of the reputational strength of bully/victim ties. The findings revealed that the bully/victim dyads most frequently nominated by peers were characterized by asymmetries in social status, where bullies were increasingly more popular than their victims, and by asymmetries in aggression, where bullies were increasingly less aggressive than their victims. Bullies and victims were likely to select one another as among the children that they least like. Most effects with respect to aggression, popularity, and relationships were moderated by the gender composition of the bully/victim dyad. Implications for a developmental psychopathology perspective on peer bullying and victimization are highlighted.

Integrative, multilevel approaches investigating neurobiological systems relevant to threat detection promise to advance understanding of the pathophysiology of major depressive disorder (MDD). In this study we considered key neuronal and hormonal systems in adolescents with MDD and healthy controls (HC). The goals of this study were to identify group differences and to examine the association of neuronal and hormonal systems. MDD and HC adolescents (N = 79) aged 12–19 years were enrolled. Key brain measures included amygdala volume and amygdala activation to an emotion face-viewing task. Key hormone measures included cortisol levels during a social stress task and during the brain scan. MDD and HC adolescents showed group differences on amygdala functioning and patterns of cortisol levels. Amygdala activation in response to emotional stimuli was positively associated with cortisol responses. In addition, amygdala volume was correlated with cortisol responses, but the pattern differed in depressed versus healthy adolescents, most notably for unmedicated MDD adolescents. The findings highlight the value of using multilevel assessment strategies to enhance understanding of pathophysiology of adolescent MDD, particularly regarding how closely related biological threat systems function together while undergoing significant developmental shifts.

The link between the experience of peer victimization (PV) and future psychological maladjustment has been consistently documented; however, little is known about intermediary cognitive processes that underlie this relation or how these processes vary across childhood. The present study examined the prospective relations between physical and relational PV and the development of negative and positive automatic thoughts and self-cognitions. Self-reports of cognitions and peer nomination measures of victimization were obtained from 1,242 children and young adolescents (Grades 3 through 6) in a two-wave longitudinal study. The results revealed that PV predicted significant increases in negative views of the self, world, and future and decreases in self-perceived competence for girls under 11 years of age, with the effect being stronger for younger girls. PV was not significantly associated with changes in positive or negative self-cognitions for older girls or for boys of any age. These findings support the hypothesis that PV may be linked to future psychopathology through its influence on self-cognitions, but only for girls.

Emotion knowledge in childhood has been shown to predict social functioning and psychological well-being, but relatively little is known about parental factors that influence its development in early childhood. There is some evidence that both parenting behavior and maternal depression are associated with emotion recognition, but previous research has only examined these factors independently. The current study assessed auditory and visual emotion recognition ability among a large sample of preschool children to examine typical emotion recognition skills in children of this age, as well as the independent and interactive effects of maternal and paternal depression and negative parenting (i.e., hostility and intrusiveness). Results indicated that children were most accurate at identifying happy emotional expressions. The lowest accuracy was observed for neutral expressions. A significant interaction was found between maternal depression and negative parenting behavior: children with a maternal history of depression were particularly sensitive to the negative effects of maladaptive parenting behavior on emotion recognition ability. No significant effects were found for paternal depression. These results highlight the importance of examining the effects of multiple interacting factors on children's emotional development and provide suggestions for identifying children for targeted preventive interventions.

The current study investigated the longitudinal relationships among behavioral inhibition (BI), life events, and anxiety in a sample of 102 BI children and 100 behaviorally uninhibited (BUI) children aged 3 to 4 years. Children's parents completed questionnaires on BI, stressful life events, and anxiety symptoms, and were administered a diagnostic interview three times in a 5-year period. In line with our hypotheses, negative life events, particularly negative behavior-dependent life events (i.e., life events that are related to the children's own behaviors), and the impact of negative life events were predictive of increases in subsequent anxiety symptoms, the likelihood of having an anxiety disorder, and increased number of anxiety diagnoses over the 5-year follow-up period. Experiencing more positive, behavior-independent life events decreased the risk of being diagnosed with an anxiety disorder. Furthermore, differences were found in life events between BI and BUI children. That is, BI children experienced fewer positive and specifically positive behavior-dependent life events, and the impact of these positive life events was also lower in BI children than in BUI children. However, BI did not interact with life events in the prediction of anxiety problems as hypothesized. Therefore, this study seems to indicate that BI and life events act as additive risk factors in the development of anxiety problems.

Many African American adolescents experience racial discrimination, with adverse consequences; however, stability and change in these experiences over time have not been examined. We examined longitudinal patterns of perceived racial discrimination assessed in Grades 7–10 and how these discrimination trajectories related to patterns of change in depressive and anxious symptoms and aggressive behaviors assessed over the same 4-year period. Growth mixture modeling performed on a community epidemiologically defined sample of urban African American adolescents (n = 504) revealed three trajectories of discrimination: increasing, decreasing, and stable low. As predicted, African American boys were more frequent targets for racial discrimination as they aged, and they were more likely to be in the increasing group. The results of parallel process growth mixture modeling revealed that youth in the increasing racial discrimination group were four times more likely to be in an increasing depression trajectory than were youth in the low stable discrimination trajectory. Though youth in the increasing racial discrimination group were nearly twice as likely to be in the high aggression trajectory, results were not statistically significant. These results indicate an association between variation in the growth of perceived racial discrimination and youth behavior and psychological well-being over the adolescent years.

In the current study, we addressed several issues related to the forms (physical and relational) and functions (reactive and proactive) of aggression in community (n = 307), voluntary residential (n = 1,917), and involuntarily detained (n = 659) adolescents (ages 11–19 years). Across samples, boys self-reported more physical aggression and girls reported more relational aggression, with the exception of higher levels of both forms of aggression in detained girls. Further, few boys showed high rates of relational aggression without also showing high rates of physical aggression. In contrast, it was not uncommon for girls to show high rates of relational aggression alone, and these girls tended to also have high levels of problem behavior (e.g., delinquency) and mental health problems (e.g., emotional dysregulation and callous–unemotional traits). Finally, for physical aggression in both boys and girls, and for relational aggression in girls, there was a clear pattern of aggressive behavior that emerged from cluster analyses across samples. Two aggression clusters emerged, with one group showing moderately high reactive aggression and a second group showing both high reactive and high proactive aggression (combined group). On measures of severity (e.g., self-reported delinquency and arrests) and etiologically important variables (e.g., emotional regulation and callous–unemotional traits), the reactive aggression group was more severe than a nonaggressive cluster but less severe than the combined aggressive cluster.

The most commonly reported socially aberrant behavior in postinstitutionalized (PI) children is disinhibited social engagement (DSE; also known as indiscriminate friendliness). There is no gold standard for measurement of this phenomenon nor agreement on how to differentiate it from normative behavior. We adopted a developmental psychopathology approach (Cicchetti, 1984) to study this phenomenon by comparing it to normative social development and by studying its patterns over time in 50 newly adopted PI children (16–36 months at adoption) compared with 41 children adopted early from foster care overseas and 47 nonadopted (NA) controls. Using coded behavioral observations of the child's interaction with an unfamiliar adult, atypical behaviors were differentiated from normative behaviors. Principal components analysis identified two dimensions of social disinhibition. The nonphysical social dimension (e.g., initiations, proximity) showed wide variation in NA children and is therefore considered a typical form of sociability. Displays of physical contact and intimacy were rare in NA children, suggesting that they represent an atypical pattern of behavior. Both adopted groups demonstrated more physical DSE behavior than NA children. There were no group differences on the nonphysical factor, and it increased over time in all groups. Implications for understanding the etiology of DSE and future directions are discussed.

Can atypical patterns of parasympathetic nervous system activity serve as endophenotypes for depression? Using respiratory sinus arrhythmia (RSA) as an index of parasympathetic nervous system function, we examined this question in two studies: one involving mothers with and without depression histories and their offspring (at high and low risk for depression, respectively), and a further study of adolescent sibling pairs concordant and discordant for major depression. In both studies, subjects were exposed to sad mood induction; subjects' RSA was monitored during rest periods and in response to the mood induction. We used Gottesman and Gould's (2003) criteria for an endophenotype and a priori defined “atypical” and “normative” RSA patterns (combinations of resting RSA and RSA reactivity). We found that atypical RSA patterns (a) predicted current depressive episodes and remission status among women with histories of juvenile onset depression and healthy controls, (b) predicted longitudinal trajectories of depressive symptoms among high- and low-risk young offspring, (c) were concordant across mothers and their juvenile offspring, (d) were more prevalent among never-depressed youth at high risk for depression than their low-risk peers, and (e) were more concordant across adolescent sibling pairs in which both versus only one had a history of major depression. Thus, the results support atypical RSA patterns as an endophenotype for depression. Possible mechanisms by which RSA patterns increase depression risk and their genetic contributors are discussed.

The long-term sequelae of adolescent depressive symptoms were examined in a multimethod, multireporter study of a diverse community sample of 179 adolescents followed from age 14 to 24. Mild to moderate levels of early adolescent depressive symptoms were found to predict lower maternal relationship quality, less positive interactions with romantic partners, and greater loneliness in adulthood even after accounting for prior levels of social functioning and for concurrent levels of adult depressive symptoms. Predictions were partially mediated via late adolescent avoidance of social interactions and poor maternal relationship quality. Results are interpreted as suggesting the potential impact of depressive symptoms on adolescent social development and the need to consider treatment for even mild symptoms and their social concomitants.