Premorbid risk for major depressive disorder (MDD) and predictors of an earlier onset and recurrent course were examined in two studies in a large, community-based sample of parents and offspring, prospectively assessed from late childhood into adulthood. In Study 1 (N = 2,764 offspring and their parents), parental psychiatric status, offspring personality at age 11, and age 11 offspring internalizing and externalizing symptoms predicted the subsequent development of MDD, as did poor quality parent–child relationships, poor academic functioning, early pubertal development, and childhood maltreatment by age 11. Parental MDD and adult antisocial behavior, offspring negative emotionality and disconstraint, externalizing symptoms, and childhood maltreatment predicted an earlier onset of MDD, after accounting for course; lower positive emotionality, trait anxiety, and childhood maltreatment predicted recurrent MDD, after accounting for age of onset. In Study 2 (N = 7,146), we examined molecular genetic risk for MDD by extending recent reports of associations with glutamatergic system genes. We failed to confirm associations with MDD using either individual single nucleotide polymorphism based tests or gene-based analyses. Overall, results speak to the pervasiveness of risk for MDD, as well as specific risk for early onset MDD; risk for recurrent MDD appears to be largely a function of its often earlier onset.

In this investigation, gene–environment–gender interaction effects in predicting child borderline personality disorder symptomatology among maltreated and nonmaltreated low-income children (N = 1,051) were examined. In the context of a summer research camp, adult-, peer-, and self-report assessments of borderline precursor indicators were obtained, as well as child self-report on the Borderline Personality Features Scale for Children. Genetic variants of the oxytocin receptor genotype and the FK506 binding protein 5 gene CATT haplotype were investigated. Children who self-reported high levels of borderline personality symptomatology were differentiated by adults, peers, and additional self-report on indicators of emotional instability, conflictual relationships with peers and adults, preoccupied attachment, and indicators of self-harm and suicidal ideation. Maltreated children also were more likely to evince many of these difficulties relative to nonmaltreated children. A series of analyses of covariance, controlling for age and ancestrally informative markers, indicated significant Maltreatment × Gene × Gender three-way interactions. Consideration of the maltreatment parameters of subtype, onset, and recency expanded understanding of variation among maltreated children. The three-way interaction effects demonstrated differential patterns among girls and boys. Among girls, the gene–environment interaction was more consistent with a diathesis-stress model, whereas among boys a differential-sensitivity interaction effect was indicated. Moreover, the genetic variants associated with greater risk for higher borderline symptomatology, dependent on maltreatment experiences, were opposite in girls compared to boys. The findings have important implications for understanding variability in early predictors of borderline personality pathology.

The current study filled significant gaps in our knowledge of developmental psychopathology by examining the influence of multilevel risk factors and developmental assets on longitudinal trajectories of internalizing symptoms and self-esteem in an exceptionally culturally diverse sample of rural adolescents. Integrating ecological and social capital theories, we explored if positive microsystem transactions are associated with self-esteem while negative microsystem transactions increase the chances of internalizing problems. Data came from the Rural Adaptation Project, a 5-year longitudinal panel study of more than 4,000 middle school students from 28 public schools in two rural, disadvantaged counties in North Carolina. Three-level hierarchical linear modeling models were estimated to predict internalizing symptoms (e.g., depression, anxiety) and self-esteem. Relative to other students, risk for internalizing problems and low self-esteem was elevated for aggressive adolescents, students who were hassled or bullied at school, and those who were rejected by peers or in conflict with their parents. Internalizing problems were also more common among adolescents from socioeconomically disadvantaged families and neighborhoods, among those in schools with more suspensions, in students who reported being pressured by peers, and in youth who required more teacher support. It is likely that these experiences left adolescents disengaged from developing social capital from ecological microsystems (e.g., family, school, peers). On the positive side, support from parents and friends and optimism about the future were key assets associated with lower internalizing symptoms and higher self-esteem. Self-esteem was also positively related to religious orientation, school satisfaction, and future optimism. These variables show active engagement with ecological microsystems. The implications and limitations were discussed.

Nonsuicidal self-injury (NSSI) is a common behavior among females that has been shown to confer risk for continued self-injury and suicidal attempts. NSSI can be viewed conceptually as behavior that is pathognomonic with aggression and/or depression. Empirical research on concurrent correlates supports this concept: numerous and diverse factors are shown to be significantly associated with self-harm, including depression, emotion dysregulation, impulsivity, and aggression and other conduct problems, as well as environmental stressors such as bullying, harsh parenting, and negative life events. In the present study, we test hypotheses regarding developmental precursors (measured from ages 8 to 12 years) to NSSI in young adolescent girls (ages 13–14 years), specifically whether aggression, depression, and environmental stressors distinguish girls with and without self-harm, and whether there is evidence for multiple developmental pathways to NSSI. Data were derived from the longitudinal Pittsburgh Girls Study. In this community sample of girls, the prevalence of NSSI at ages 13 or 14 years of age was 6.0%. Initial levels in dimensions measured within the depression, aggression, and environmental stressor domains accounted for variance in NSSI in early adolescence. Changes over time in relational aggression and assertiveness were also significantly associated with risk for NSSI. To a large extent, adolescent NSSI was predicted by psychological deficits and stress exposure that began early in childhood. Risk indices were calculated using the 85th or 15th percentile. Close to 80% of girls who engaged in NSSI during adolescence were identified by at least one risk domain in childhood. A sizable proportion of adolescent girls who later engaged in NSSI had childhood risk scores in all three domains; the remaining girls with adolescent NSSI were relatively evenly distributed across the other risk domain profiles. The observation that multiple pathways to NSSI exist suggests that deficits underlying the behavior may vary and require different modes of prevention.

Dispositional trait frameworks offer great potential to elucidate the nature and development of psychopathology, including the construct of relational aggression. The present study sought to explore the dispositional context of relational aggression across three dispositional frameworks: temperament, personality, and personality pathology. Participants comprised a large community sample of youth, aged 6 to 18 years (N = 1,188; 51.2% female). Ratings of children's relational aggression, temperament, personality, and personality pathology traits were obtained through parent report (86.3% mothers). Results showed convergence and divergence across these three dispositional frameworks. Like other antisocial behavior subtypes, relational aggression generally showed connections with traits reflecting negative emotionality and poor self-regulation. Relational aggression showed stronger connections with temperament traits than with personality traits, suggesting that temperament frameworks may capture more relationally aggressive content. Findings at the lower order trait level help differentiate relational aggression from other externalizing problems by providing a more nuanced perspective (e.g., both sociability and shyness positively predicted relational aggression). In addition, there was little evidence of moderation of these associations by gender, age, or age2, and findings remained robust even after controlling for physical aggression. Results are discussed in the broader context of conceptualizing relational aggression in an overarching personality-psychopathology framework.

The majority of aggressive children exhibit symptoms of anxiety, yet none of our developmental models of aggression incorporate the role of anxiety, and our treatments ignore this comorbidity. This article outlines a novel theoretical model that specifies three hypotheses about comorbid anxious and aggressive children: (a) unpredictable parenting induces anxiety in children that in turn triggers aggressive behavior; (b) prolonged periods of anxiety deplete children's capacity to inhibit impulses and trigger bouts of aggression, and aggression in turn functions to regulate levels of anxiety; and (c) minor daily stressors give rise to anxiety while cognitive perseveration maintains anxious moods, increasingly disposing children to aggress. Little or no research has directly tested these hypotheses. Extant research and theory consistent with these claims are herein reviewed, and future research designs that can test them specifically are suggested. The clinical implications most relevant to the hypotheses are discussed, and to improve the efficacy of treatments for childhood aggression, it is proposed that anxiety may need to be the primary target of treatment.

Anxious mothers' parenting, particularly transfer of threat information, has been considered important in their children's risk for social anxiety disorder (SAnxD), and maternal narratives concerning potential social threat could elucidate this contribution. Maternal narratives to their preschool 4- to 5-year-old children, via a picture book about starting school, were assessed in socially anxious (N = 73), and nonanxious (N = 63) mothers. Child representations of school were assessed via doll play (DP). After one school term, mothers (Child Behavior Checklist [CBCL]) and teachers (Teacher Report Form) reported on child internalizing problems, and child SAnxD was assessed via maternal interview. Relations between these variables, infant behavioral inhibition, and attachment, were examined. Socially anxious mothers showed more negative (higher threat attribution) and less supportive (lower encouragement) narratives than controls, and their children's DP representations SAnxD and CBCL scores were more adverse. High narrative threat predicted child SAnxD; lower encouragement predicted negative child CBCL scores and, particularly for behaviorally inhibited children, Teacher Report Form scores and DP representations. In securely attached children, CBCL scores and risk for SAnxD were affected by maternal anxiety and threat attributions, respectively. Low encouragement mediated the effects of maternal anxiety on child DP representations and CBCL scores. Maternal narratives are affected by social anxiety and contribute to adverse child outcome.

Learning to respond to others' distress with well-regulated empathy is an important developmental task linked to positive health outcomes and moral achievements. However, this important interpersonal skill set may also confer risk for depression and anxiety when present at extreme levels and in combination with certain individual characteristics or within particular contexts. The purpose of this review is to describe an empirically grounded theoretical rationale for the hypothesis that empathic tendencies can be “risky strengths.” We propose a model in which typical development of affective and cognitive empathy can be influenced by complex interplay among intraindividual and interindividual moderators that increase risk for empathic personal distress and excessive interpersonal guilt. These intermediate states in turn precipitate internalizing problems that map onto empirically derived fear/arousal and anhedonia/misery subfactors of internalizing disorders. The intraindividual moderators include a genetically influenced propensity toward physiological hyperarousal, which is proposed to interact with genetic propensity to empathic sensitivity to contribute to neurobiological processes that underlie personal distress responses to others' pain or unhappiness. This empathic personal distress then increases risk for internalizing problems, particularly fear/arousal symptoms. In a similar fashion, interactions between genetic propensities toward negative thinking processes and empathic sensitivity are hypothesized to contribute to excess interpersonal guilt in response to others' distress. This interpersonal guilt then increases the risk for internalizing problems, especially anhedonia/misery symptoms. Interindividual moderators, such as maladaptive parenting or chronic exposure to parents' negative affect, further interact with these genetic liabilities to amplify risk for personal distress and interpersonal guilt as well as for consequent internalizing problems. Age-related increases in the heritability of depression, anxiety, and empathy-related constructs are consistent with developmental shifts toward greater influence of intraindividual moderators throughout childhood and adolescence, with interindividual moderators exerting their greatest influence during early childhood. Efforts to modulate neurobiological and behavioral expressions of genetic dysregulation liabilities and to promote adaptive empathic skills must thus begin early in development.

Research findings in psychoneuroimmunology document reliable, bidirectional linkages among psychological processes, the nervous system, and the immune system. However, available data are based almost entirely on animal and adult human studies; the application to children and adolescents is uncertain. We capitalized on the experimental leverage provided by a routine vaccination to examine the link between mood symptoms and the immune response to a vaccine challenge in early adolescence. One hundred twenty-six 11-year-olds for whom vaccine response data were available were assessed at prevaccination and 4 weeks, 3 months, and 6 months following vaccination; self-report ratings of depression and anxiety as well as measures of psychosocial and somatic risk were assessed prior to vaccine response. Analyses indicated that children's internalizing mood symptoms were associated with elevated and persistently higher antibody responses, with evidence extending to two of the four serogroups. The associations remained after controlling for multiple possible confounders (social class, body mass index, sleep, psychosocial risk, and pubertal status). The observed enhanced vaccine response associated with depressive and anxious symptoms in early adolescence may reflect an important developmental difference in immune system–brain interplay between adults and children, and it underscores the need for further developmental studies of psychoneuroimmunology.