Cross-sectional and longitudinal research has shown that race-related stress is associated with increased depressive symptoms among racial/ethnic minorities. Rumination has long been considered a maladaptive self-regulatory response to race-related stress, and growing evidence suggests that it may be an important link in the relation between race-related stress and depression. More adaptive forms of self-regulation, such as active coping, may counteract the negative impact of rumination. We examined the influence of rumination on the relation between race-related stress and depressive symptoms in a sample (N = 69) of young adult (mean age = 20 ± 1.5 years) African American women. We also considered the possible moderating effects of John Henryism, a form of persistent and determined goal striving, and vagally mediated heart rate variability, a purported biomarker of coping. Anticipatory race-related stress was indirectly associated with depressive symptoms through rumination: estimate = 0.07, 95% confidence interval [0.01, 0.16]. Both John Henryism and vagally mediated heart rate variability moderated the relationship between race-related stress and rumination; however, only John Henryism reliably influenced the indirect association between race-related stress and depression through rumination. We discuss these findings in the context of growing research examining the interplay between cultural and biological factors in the risk for poorer mental health.

There is increasing interest among developmental psychopathologists in broad transdiagnostic factors that give rise to a wide array of clinical presentations (multifinality), but little is known about how these processes lead to particular psychopathological manifestations over the course of development. We examined whether individual differences in the error-related negativity (ΔERN), a neural indicator of error monitoring, predicts whether early persistent irritability, a prototypical transdiagnostic construct, is associated with later internalizing versus externalizing outcomes. When children were 3 years old, mothers were interviewed about children's persistent irritability and completed questionnaires about their children's psychopathology. Three years later, EEG was recorded while children performed a go/no-go task to measure the ΔERN. When children were approximately 9 years old, mothers again completed questionnaires about their children's psychopathology. The results indicated that among children who were persistently irritable at age 3, an enhanced or more negative ΔERN at age 6 predicted the development of internalizing symptoms at age 9, whereas a blunted or smaller ΔERN at age 6 predicted the development of externalizing symptoms. Our results suggest that variation in error monitoring predicts, and may even shape, the expression of persistent irritability and differentiates developmental trajectories from preschool persistent irritability to internalizing versus externalizing outcomes in middle to late childhood.

The purpose of this study was to examine the association between paternal alcohol use and the mother-infant relationship. A related goal was to investigate the role of maternal depression and marital satisfaction in moderating this relationship. Subjects were 55 mother-infant dyads (12–24-month-old infants) who were observed in the Strange Situation paradigm to assess infant attachment and in structured play interactions. There were 23 families with heavy drinking fathers and 32 with light drinking fathers. As predicted, infants of heavy drinking fathers were more likely to be insecurely attached compared to infants of light drinking fathers. Contrary to expectations, neither maternal depression nor marital interaction mediated the relationship between paternal alcohol use and mother-infant interactions. However, maternal depression did interact with paternal alcohol use to predict infant attachment security and maternal sensitivity. There was also an interactive effect of marital satisfaction and paternal alcohol use on maternal sensitivity. The results suggest that paternal alcohol use may influence family functioning and the mother-child relationship as early as infancy and suggest one possible pathway toward maladjustment among infants of heavy drinking fathers. However, in addition to investigating the impact of paternal alcohol use on the father-infant relationship, the influence of various familial factors associated with paternal alcohol use need to be more closely examined from a longitudinal perspective.

In this study, we employed an eye-gaze paradigm to explore whether children (ages 8–12) and adolescents (ages 12–18) with autism spectrum disorders (ASDs) are able to use prosodic cues to determine the syntactic structure of an utterance. Persons with ASD were compared to typically developing (TD) peers matched on age, IQ, gender, and receptive language abilities. The stimuli were syntactically ambiguous but had a prosodic break that indicated the appropriate interpretation (feel the frog … with the feather vs. feel … the frog with the feather). We found that all groups were equally sensitive to the initial prosodic cues that were presented. Children and teens with ASD used prosody to interpret the ambiguous phrase as rapidly and efficiently as their TD peers. However, when a different cue was presented in subsequent trials, the younger ASD group was more likely to respond in a manner consistent with the initial prosodic cue rather than the new one. Eye-tracking data indicated that both younger groups (ASD and TD) had trouble shifting their interpretation as the prosodic cue changed, but the younger TD group was able to overcome this interference and produce an action consistent with the prosodic cue.

Although there is considerable evidence that relational victimization is associated with depressive symptoms in youth, our understanding about the mechanisms by which victimization and depressive symptoms are linked is limited. The current study explored ruminating about victimization experiences as a potential mechanism that might contribute to an understanding of the association between relational victimization and depressive symptoms. We also tested the specificity of the proposed models by controlling for and testing parallel models of a highly related behavior: relational aggression. A sample of 499 adolescents from sixth through eighth grades participated. Teacher reports were used to assess relational victimization and relational aggression. Self-reports were used to assess depressive symptoms and rumination. The results showed that rumination partially mediated the association between relational victimization and depressive symptoms. No moderation effect was found. In contrast, rumination moderated the association between relational aggression and depressive symptoms. Specifically, relational aggression was associated with depressive symptoms for those adolescents who were also ruminators. Thus, ruminating about victimization experiences appears to be an important mechanism that functions differently for relational aggression and relational victimization in conferring risk for depressive symptoms. The findings offer important practical implications for those working with adolescents and also lay the groundwork for future research.

The literature on developmental psychopathology has been criticized for its limited integration of culture and, particularly, the lack of research addressing cultural development in relation to psychopathology. In this paper, I present how the study of ethnic–racial identity provides a heuristic model for how culture can be examined developmentally and in relation to psychopathology. In addition, I introduce the Identity Project intervention program and discuss how its findings provide empirical support for the notions that cultural development can be modified with intervention, and that such modifications can lead to psychosocial benefits for adolescents. Finally, I discuss existing challenges to advancing this work and important future directions for both basic and translational research in this area.

Attention-deficit/hyperactivity disorder (ADHD) is associated with self-harm during adolescence and young adulthood, especially among females. Yet little is known about the developmental trajectories or childhood predictors/moderators of self-harm in women with and without childhood histories of ADHD. We characterized lifetime risk for nonsuicidal self-injury (NSSI), suicidal ideation (SI), and suicide attempts (SA), comparing female participants with (n = 140) and without (n = 88) childhood ADHD. We examined theory-informed childhood predictors and moderators of lifetime risk via baseline measures from childhood. First, regarding developmental patterns, most females with positive histories of lifetime self-harm engaged in such behaviors in adolescence yet desisted by adulthood. Females with positive histories of self-harm by late adolescence emanated largely from the ADHD-C group. Second, we found that predictors of NSSI were early externalizing symptoms, overall executive functioning, and father's negative parenting; predictors of SI were adverse childhood experiences and low self-esteem; and predictors of SA were early externalizing symptoms, adverse childhood experiences, and low self-esteem. Third, receiver operating characteristics analyses helped to ascertain interactive sets of predictors. Findings indicate that pathways to self-harm are multifaceted for females with ADHD. Understanding early childhood predictors and moderators of self-harm can inform both risk assessment and intervention strategies.

It is possible that findings suggesting a link between prenatal maternal stress (PNMS) and anxiety symptoms in offspring are confounded by postnatal and/or shared mother–child heritability effects. Following exposure to a natural disaster, the Queensland Flood Study investigated the unique and additive effects of various types of disaster-related PNMS (objective hardship, cognitive appraisal, and subjective distress) on childhood anxiety symptomatology (internalizing and/or anxiety symptom measures). Timing of flood exposure during pregnancy and child sex were examined as potential moderators. After controlling for maternal psychosocial factors, greater objective hardship as a result of the floods was significantly associated with greater anxiety symptoms (N = 114) and marginally associated with greater internalizing behaviors (N = 115). Earlier timing of the flood in pregnancy was associated with greater anxiety symptoms. No such associations were found between any PNMS measure and teacher-rated child internalizing behaviors (N = 90). Sex and timing did not moderate associations. Our findings suggest that, in isolation, increased maternal hardship due to exposure to an independent stressor, during pregnancy, may have a programming effect on childhood anxiety symptoms.

The prevalence of depression rises steeply during adolescence. Family processes have been identified as one of the important factors that contribute to affect (dys)regulation during adolescence. In this study, we explored the affect expressed by mothers, fathers, and adolescents during a problem-solving interaction and investigated whether the patterns of the affective interactions differed between families with depressed adolescents and families with nondepressed adolescents. A network approach was used to depict the frequencies of different affects, concurrent expressions of affect, and the temporal sequencing of affective behaviors among family members. The findings show that families of depressed adolescents express more anger than families of nondepressed adolescents during the interaction. These expressions of anger co-occur and interact across time more often in families with a depressed adolescent than in other families, creating a more self-sustaining network of angry negative affect in depressed families. Moreover, parents’ angry and adolescents’ dysphoric affect follow each other more often in depressed families. Taken together, these patterns reveal a particular family dynamic that may contribute to vulnerability to, or maintenance of, adolescent depressive disorders. Our findings underline the importance of studying affective family interactions to understand adolescent depression.

The emerging field of neurogenetics seeks to model the complex pathways from gene to brain to behavior. This field has focused on imaging genetics techniques that examine how variability in common genetic polymorphisms predict differences in brain structure and function. These studies are informed by other complimentary techniques (e.g., animal models and multimodal imaging) and have recently begun to incorporate the environment through examination of Imaging Gene × Environment interactions. Though neurogenetics has the potential to inform our understanding of the development of psychopathology, there has been little integration between principles of neurogenetics and developmental psychopathology. The paper describes a neurogenetics and Imaging Gene × Environment approach and how these approaches have been usefully applied to the study of psychopathology. Six tenets of developmental psychopathology (the structure of phenotypes, the importance of exploring mechanisms, the conditional nature of risk, the complexity of multilevel pathways, the role of development, and the importance of who is studied) are identified, and how these principles can further neurogenetics applications to understanding the development of psychopathology is discussed. A major issue of this piece is how neurogenetics and current imaging and molecular genetics approaches can be incorporated into developmental psychopathology perspectives with a goal of providing models for better understanding pathways from among genes, environments, the brain, and behavior.

Children entering out-of-home (OoH) care have often experienced multiple forms of maltreatment and are at risk of psychiatric disorder and poor long-term outcome. Recent evidence shows high rates of disinhibited attachment disorder (DAD) among maltreated adolescents in UK OoH care (Kay & Green, 2013). This study aimed to further understand the mechanisms of outcome in this group through investigation of social cognitive functioning. Patterns of theory of mind (ToM) and social information processing were assessed alongside DAD behavior and psychopathology in 63 adolescents in UK OoH care (mean age = 176 months, SD = 22; 48% male; 89% White British) and 69 low-risk comparison adolescents (mean age = 171 months, SD = 17; 46% male; 87% White British). Compared to low risk, OoH adolescents showed a hostile attribution bias and ToM deficit, but this was confounded by language ability. ToM was associated with reduced hostile attribution and responding biases and increased social competence, which was further associated with lower levels of externalizing psychopathology. There was no association between social cognition and core features of DAD. Social cognitive deficits and biases may play a role in the high rates of externalizing psychopathology and relationship functioning difficulties in maltreated samples. Future research should assess alternative cognitive mechanisms for DAD.

Different dimensions of adversity may affect mental health through distinct neurobiological mechanisms, though current supporting evidence consists largely of cross-sectional associations between threat or deprivation and fronto-limbic circuitry. In this exploratory three-wave longitudinal study spanning ages 9–19 years, we examined the associations between experiences of unpredictability, threat, and deprivation with the development of functional connectivity within and between three brain networks implicated in psychopathology: the salience (SAL), default mode (DMN), and fronto-parietal (FPN) networks, and tested whether network trajectories moderated associations between adversity and changes in internalizing symptoms. Connectivity decreased with age on average; these changes differed by dimension of adversity. Whereas family-level deprivation was associated with lower initial levels and more stability across most networks, unpredictability was associated with stability only in SAL connectivity, and threat was associated with stability in FPN and DMN-SAL connectivity. In youth exposed to higher levels of any adversity, lower initial levels and more stability in connectivity were related to smaller increases in internalizing symptoms. Our findings suggest that whereas deprivation is associated with widespread neurodevelopmental differences in cognitive and emotion processing networks, unpredictability is related selectively to salience detection circuitry. Studies with wider developmental windows should examine whether these neurodevelopmental alterations are adaptive or serve to maintain internalizing symptoms.

This paper uses a functionalist view of emotion to consider family factors that create risk for depressive symptoms in adolescents. Two adolescent siblings and their mothers were assessed for emotion regulation during autonomy-related communication tasks, whereas their mother's attachment- and intimacy-related functioning was assessed through interview and self-report. The results indicate that older teens' failure to establish autonomous stances during communication and their mothers' dissatisfaction with intimate relationships increase risk for teenagers reporting depressive symptoms. Further, mothers' preoccupation attachment-related issues was found to be associated with less autonomous communication from older teenagers. Implications of these findings and future directions for investigating the family factors associated with adolescent depression are discussed.

We examine resilience in relation to one type of risk — familial risk — from a genetic perspective. Specifically, we ask why only some children growing up with the same familial risk develop psychopathology. Unlike environmental theories, genetics predicts that children in the same family will differ in their outcomes. That is, some children in a family at risk are unaffected not because they are resilient but because they are not at risk genetically. Eventually, some of the genes responsible for genetic risk will be identified, making it possible to predict which children in a family will be affected. Resilience from a genetic perspective can be viewed as the extent to which children at genetic risk are not affected. In addition, there may be genetic contributions to resilience that protect some individuals in high-risk families. Finally, genetic research has shown that salient environment influences often operate in a nonshared manner, making children in the same family different. Research on nonshared environmental factors will advance our understanding of environmental origins of resilience by focusing on environmental reasons why children growing up in high-risk families have such different outcomes.

Previous research documented a robust link between difficulties in self-regulation and development of externalizing problems (i.e., aggression and delinquency). In this study, we examined the longitudinal additive and interactive genetic and environmental covariation underlying this well-established link using a twin design. The sample included 131 pairs of monozygotic twins and 173 pairs of same-sex dizygotic twins who participated in three waves of annual assessment. Mothers and fathers provided reports of externalizing problems. Teacher report and observer rating were used to assess twin's attention regulation. The etiology underlying the link between externalizing problems and attention regulation shifted from a common genetic mechanism to a common environmental mechanism in the transition across middle childhood. Household chaos moderated the genetic variance of and covariance between externalizing problems and attention regulation. The genetic influence on individual differences in both externalizing problems and attention regulation was stronger in more chaotic households. However, higher levels of household chaos attenuated the genetic link between externalizing problems and attention regulation.

Theoretical models and empirical studies suggest that there are a number of distinct pathways of aggressive behavior development in childhood that place youth at risk for antisocial outcomes in adolescence and young adulthood. The prediction of later antisocial behavior based on these early pathways, although substantial, is not perfect. The goal of the present study was to identify factors that explain why some boys on a high-risk developmental trajectory in middle childhood do not experience an untoward outcome, and, conversely, why some boys progressing on a low-risk trajectory do become involved in later antisocial behavior. To that end, we explored a set of theoretically derived predictors measured at entrance to elementary and middle school and examined their utility in explaining discordant cases. First-grade reading achievement, race, and poverty status proved to be significant early predictors of discordance, whereas the significant middle-school predictors were parent monitoring, deviant peer affiliation, and neighborhood level of deviant behavior.This research was supported by grants from the National Institutes of Mental Health (RO1 MH42968 to Sheppard G. Kellam, PI, and T-32 MH18834 to Nick Ialongo, PI) and the Centers for Disease Control and Prevention (R49/CCR318627-03). We thank the Baltimore City Public Schools for their continuing collaborative efforts and the parents, children, teachers, principals, and school psychologists and social workers who participated.

Deferred imitation and object permanence (OP) were tested in 48 young children with Down syndrome (DS), ranging from 20 to 43 months of age. Deferred imitation and high-level OP (invisible displacements) have long been held to be synchronous developments during sensory-motor “Stage 6” (18–24 months of age in unimpaired children). The results of the current study demonstrate deferred imitation in young children with DS, showing they can learn novel behaviors from observation and retain multiple models in memory. This is the first demonstration of deferred imitation in young children with DS. The average OP level passed in this sample was A-not-B, a task passed at 8–12 months of age in normally developing infants. Analyses showed that individual children who failed high-level OP (invisible displacements) could still perform deferred imitation. This indicates that deferred imitation and OP invisible displacements are not synchronous developments in children with DS. This asynchrony is compatible with new data from unimpaired children suggesting that deferred imitation and high-level OP entail separate and distinctive kinds of memory and representation

This study examined developmental processes linking competence and psychopathology in an urban sample of girls during their transition to adolescence. Longitudinal associations among indices of externalizing symptoms, social competence, and internalizing symptoms were also tested within contexts of family adversity and girls’ pubertal status. Child, parent, and teacher report were employed to assess core constructs across six annual assessment waves, starting at age 9. Results revealed the significant effect of prior levels of externalizing symptoms on changes in social competence and internalizing symptoms, as well as reciprocal relations between social competence and internalizing symptoms. In addition, girl's maladaptive functioning predicted increases in family adversity exposure over time. Last, more mature pubertal status in early assessment waves was linked to an increase in internalizing symptoms; however, this association was reversed by the last assessment, when most girls had reached advance stages of puberty. The timing of these effects reveals important targets for future interventions aimed at promoting the successful adaptation of girls in adolescence.

The amygdala has received great interest as a possible neurophysiological substrate of bipolar disorder (BD). This review summarizes information about the structure and function of the amygdala with attention to its role in experienced emotion and mood. We review the evidence for amygdala pathology in psychiatric conditions and discuss the role of the amygdala in BD during development. There appear to be consistent findings in the neuroimaging literature that suggest an etiological model for BD that involves abnormalities in the structure and function of the amygdala, but also depends on the failure of prefrontal cortical regions to modulate amygdala activity. In addition, evidence is accumulating to suggest that this model has flexible outcomes, depending on factors intrinsic and extrinsic to BD, and may follow several possible paths across the course of maturational development.