In this study, we used a stress test to investigate endocrinological and subjective stress responses of 8- to 14-year-old children with internalizing or externalizing disorders and healthy controls. The sample (N = 170) consisted of clinical and community children. Parents were given a diagnostic interview to diagnose their children's psychiatric condition. We measured saliva cortisol and subjectively experienced arousal in children before and after the Trier Social Stress Test for Children. Children also rated their performance immediately after the stress test, and 1 hr later they rated their positive and negative thoughts about this stressful event. Children with internalizing or externalizing disorders exhibited a blunted cortisol response compared to healthy controls. Depressed children rated their test performance lower and reported more negative thoughts after the test in comparison to healthy controls, anxious children reported more arousal before and after the task, and children with externalizing disorders reported more positive thoughts. In regression analyses, cortisol and subjective stress responses were both predictive of psychiatric disorders. The study extends previous work on the relation between psychiatric disorders and children's stress responses to an experimentally induced stress task by including a broad range of psychiatric disorders and by integrating endocrinological and subjective stress responses.

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.

Prenatal exposure to maternal mood disturbances shapes children's cognitive development reflected in the critical construct of executive functions (EFs). Little is known, however, about underlying mechanisms. By examining cortisol responses in both everyday and lab challenge settings, we tested whether the child/offspring hypothalamic–pituitary–adrenal axis mediates effects of prenatal maternal mood on child EFs at age 6. In 107 Canadian children born to women with a wide range of anxious and depressive symptoms during pregnancy, we found that in boys but not girls, depressed and/or anxious prenatal maternal mood is associated with heightened diurnal cortisol levels in everyday settings, as well as heightened cortisol reactivity to a lab challenge and that this heightened reactivity was associated with poorer EFs. Among boys we also observed that cortisol reactivity but not diurnal cortisol mediated the association between depressed and/or anxious prenatal maternal mood and EFs. Depressed and/or anxious prenatal maternal mood was related to child EFs for both girls and boys. To our knowledge, this is the first study to demonstrate a mediating role for child stress regulation in the association between prenatal maternal stress-related mood disturbances and child EFs, providing evidence of a mechanism contributing to fetal programming of cognition.

The current study used data from two longitudinal samples to test whether self-regulation, depressive symptoms, and aggression/antisociality were mediators in the relation between a polygenic score indexing serotonin (5-HT) functioning and alcohol use in adolescence. The results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create 5-HT polygenic risk scores. Adolescents and/or parents reported on adolescents’ self-regulation (Time 1), depressive symptoms (Time 2), aggression/antisociality (Time 2), and alcohol use (Time 3). The results showed that 5-HT polygenic risk did not predict self-regulation. However, adolescents with higher levels of 5-HT polygenic risk showed greater depression and aggression/antisociality. Adolescents’ aggression/antisociality mediated the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. Pathways to alcohol use were especially salient for males from families with low parental education in one of the two samples. The results provide insights into the longitudinal mechanisms underlying the relation between 5-HT functioning and alcohol use (i.e., earlier aggression/antisociality). There was no evidence that genetically based variation in 5-HT functioning predisposed individuals to deficits in self-regulation. Genetically based variation in 5-HT functioning and self-regulation might be separate, transdiagnostic risk factors for several types of psychopathology.

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.

The prenatal environment shapes the offspring's phenotype; moreover, transgenerational stress and stress during pregnancy may play a role. Brain-derived neurotrophic factor (BDNF) and glucocorticoids influence neurodevelopment during pregnancy, and there is evidence that BDNF in amniotic fluid is mainly of fetal origin, while the source of glucocorticoids is maternal. We tested the hypothesis that maternal early life stress, psychiatric diagnoses, anxiety, perceived stress, and socioeconomic status influence BDNF and glucocorticoid concentrations in amniotic fluid in the second trimester. We studied 79 pregnant women who underwent amniocentesis in the early second trimester and analyzed BDNF, cortisol, and cortisone concentrations in amniotic fluid. The endocrine data were related to maternal early life adversities (Childhood Trauma Questionaire), perceived stress (Perceived Stress Scale), anxiety, socioeconomic status (family income), and the presence of psychiatric diseases. We found BDNF in amniotic fluid to be positively related to maternal early adversity (Childhood Trauma Questionaire). Low family income (socioeconomic status) was related to high amniotic fluid glucocorticoid concentrations. Neither glucocorticoid concentrations nor hydroxy steroid dehydrogenase (HSD2) activity could be related to BDNF concentrations in amniotic fluid. Early maternal adverse events may be reflected in the fetal BDNF regulation, and it should be tested whether this relates to differences in neurodevelopment.

A growing number of research studies have examined the intradyadic coregulation (or attunement) of hypothalamus–pituitary–adrenal axis functioning in mothers and their children. However, it is unclear how early this coregulation may be present in dyads at clinical high risk and whether certain factors, such as maternal depression or positive parenting, are associated with the strength of this coregulation. The present study examined cortisol attunement within mother–infant dyads in a high-risk sample of 233 mothers who received treatment for psychiatric illness during pregnancy and whose infants were 6 months old at the study visit. Results showed that maternal and infant cortisol covaried across four time points that included a stressor paradigm and a mother–infant interaction task. Greater maternal positive affect, but not depression, predicted stronger cortisol attunement. In addition, infants’ cortisol level following separation from the mother predicted mothers’ cortisol level at the next time point. Mothers’ cortisol level following the separation and the laboratory stress paradigm predicted infants’ cortisol levels at each successive time point, over and above infants’ own cortisol at the previous time point. These findings suggest that maternal and infant cortisol levels influence one another in a bidirectional fashion that may be temporally and context dependent.

High conflict and low warmth in families may contribute to immune cells developing a tendency to respond to threats with exaggerated inflammation that is insensitive to inhibitory signaling. We tested associations between family environments and expression of genes bearing response elements for transcription factors that regulate inflammation: nuclear factor kappa B (NF-κB) and glucocorticoid receptor. The overall sample (47 families) completed interviews, questionnaires, and 8-week daily diary assessments of conflict and warmth, which were used to create composite family conflict and warmth scores. The diaries assessed upper respiratory infection (URI) symptoms, and URI episodes were clinically verified. Leukocyte RNA was extracted from whole blood samples provided by a subsample of 42 children (8–13 years of age) and 73 parents. In children, higher conflict and lower warmth were related to greater expression of genes bearing response elements for the proinflammatory transcription factor NF-κB, and more severe URI symptoms. In parents, higher conflict and lower warmth were also related to greater NF-κB–associated gene expression. Monocytes and dendritic cells were implicated as primary cellular sources of differential gene expression in the sample. Consistent with existing conceptual frameworks, stressful family environments were related to a proinflammatory phenotype at the level of the circulating leukocyte transcriptome.

Adolescence is a sensitive period for sociocultural development in which facets of social identity, including social status and race, become especially salient. Despite the heightened importance of both social status and race during this developmental period, no known work has examined how individual differences in social status influence perceptions of race in adolescents. Thus, in the present study, we investigated how both subjective social status and objective socioeconomic status (SES) influence neural responses to race. Twenty-three Mexican American adolescents (15 females; mean age = 17.22 years) were scanned using functional magnetic resonance imaging while they viewed Black and White faces in a standard labeling task. Adolescents rated their subjective social status in US society, while their parents responded to questions about their educational background, occupation, and economic strain (objective SES). Results demonstrated a negative association between subjective social status and neural responses in the amygdala, fusiform face area, and medial prefrontal cortex when adolescents viewed Black (relative to White) faces. In other words, adolescents with lower subjective social status showed greater activity in neural regions involved in processing salience, perceptual expertise, and thinking about the minds of others when they viewed images of Black faces, suggesting enhanced salience of race for these youth. There was no relationship between objective SES and neural responses to the faces. Moreover, instructing participants to focus on the gender or emotion expression on the face attenuated the relationship between subjective social status and neural processing of race. Together, these results demonstrate that subjective social status shapes the way the brain responds to race, which may have implications for psychopathology.

Childhood maltreatment, including abuse and neglect, may have sustained effects on the integrity and functioning of the brain, alter neurophysiological responsivity later in life, and predispose individuals toward psychiatric conditions involving socioaffective disturbances. This meta-analysis aims to quantify associations between self-reported childhood maltreatment and brain function in response to socioaffective cues in adults. Seventeen functional magnetic resonance imaging studies reporting on data from 848 individuals examined with the Childhood Trauma Questionnaire were included in a meta-analysis of whole-brain findings, or a review of region of interest findings. The spatial consistency of peak activations associated with maltreatment exposure was tested using activation likelihood estimation, using a threshold of p < .05 corrected for multiple comparisons. Adults exposed to childhood maltreatment showed significantly increased activation in the left superior frontal gyrus and left middle temporal gyrus, and decreased activation in the left superior parietal lobule and the left hippocampus. Although hyperresponsivity to socioaffective cues in the amygdala and ventral anterior cingulate cortex in correlation with maltreatment severity is a replicated finding in region of interest studies, null results are reported as well. The findings suggest that childhood maltreatment has sustained effects on brain function into adulthood, and highlight potential mechanisms for conveying vulnerability to development of psychopathology.

Extant research consistently links youth externalizing problems and later maladaptive outcomes, and these behaviors are particularly detrimental given their relative stability across development. Although an array of risk and protective factors for externalizing problems have been identified, few studies have examined factors reflecting the multiple social–ecological levels that influence child development and used them to predict longitudinal trajectories of externalizing problems. The current study examined externalizing behavior trajectories in a sample of 1,094 at-risk youth (539 boys, 555 girls) from the Longitudinal Studies in Child Abuse and Neglect multisite longitudinal study of child maltreatment. Normed Child Behavior Checklist externalizing scores were used to estimate group trajectories via growth-based trajectory modeling at ages 10, 12, 14, and 16 using the SAS PROC TRAJ procedure. Model fit was assessed using the Bayes information criterion and the Akaike information criterion statistics. Analyses revealed optimal fit for five distinct behavioral trajectories: low stable, mid-increasing, mid-decreasing, medium high, and high stable. Multinomial logistic regressions revealed that a combination of risk and protective factors at individual, family, school, and neighborhood levels contribute to distinct trajectories of externalizing problems over time. Predictors of low and decreasing trajectories can inform interventions aimed at addressing externalizing problems among high-risk adolescents.

This study examined the impact of the middle school transition on general anxiety trajectories from middle childhood to middle adolescence, as well as how youths’ individual vulnerability and exposure to contextual stressors were associated with anxiety trajectories. Participants were 631 youth (47% boys, M age = 7.96 years at Time 1), followed for 7 successive years from second to eighth grade. Teachers reported on youths’ individual vulnerability to anxiety (anxious solitude) in second grade; youth reported on their anxiety in second to eighth grade and aspects of their social contexts particularly relevant to the school transition (school hassles, peer victimization, parent–child relationship quality, and friendship quality) in sixth to eighth grade. The results revealed two subgroups that showed either strongly increasing (5%) or decreasing (14%) levels of anxiety across the transition and two subgroups with fairly stable levels of either high (11%) or low (70%) anxiety over time. Youth in the latter two subgroups could be distinguished based on their individual vulnerability to anxiety, whereas youth with increasing anxiety reported more contextual stressors and less contextual support than youth with decreasing anxiety. In sum, findings suggest that the middle school transition has the potential to alter developmental trajectories of anxiety for some youth, for better or for worse.

Prenatal maternal stress (PNMS) has been associated with postnatal behavioral alterations that may be partly explained by interactions between the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal (HPG) axes. Yet it remains unclear whether PNMS leads to enduring HPA–HPG alterations in the offspring, and whether HPA–HPG interactions can impact behavior during development, in particular levels of aggression in childhood. Here we investigated the relationship between a marker for HPG axis function (baseline testosterone) and a marker for HPA axis response (cortisol area under the curve) in 11½-year-olds whose mothers were exposed to the 1998 Quebec ice storm during pregnancy (n = 59 children; 31 boys, 28 girls). We examined (a) whether the degree of objective or subjective PNMS regulates the testosterone–cortisol relationship at age 11½, and (b) whether this testosterone–cortisol relationship is associated with differences in aggressive behavior. We found that, at lower levels of subjective PNMS, baseline testosterone and cortisol reactivity were positively correlated; in contrast, there was no relationship between these hormones at higher levels of subjective PNMS. Cortisol response moderated the relationship between testosterone and aggression. These results support the notion PNMS may explain variance in fetal HPA–HPG interactions, and that these interactions may be associated with aggressive behavior in late childhood.

A great deal of research has focused on acculturation and enculturation, which represent the processes of adapting to a new culture. Despite this growing literature, results have produced inconsistent findings that may be attributable to differences in terms of the instruments used to assess acculturation and enculturation. Utilizing a 3-year longitudinal data set (with 1-year lags between assessments), the present study explored the psychometric properties of the Bicultural Involvement Questionnaire—Short Version (BIQ-S) and the Acculturation Rating Scale for Mexican Americans II (ARSMA-II) and examined the overlap between changes in these measures as they relate to internalizing and externalizing problem behavior. The present sample consisted of 216 immigrant Latino youth (43% boys; mean age 13.6 years at baseline; SD = 1.44 years, range 10 to 17). Exploratory structural equation modeling identified factor structures for the BIQ-S and ARSMA-II that diverged from their hypothesized structure. Growth curve models also indicate divergence between the BIQ-S and ARSMA-II in terms of change in acculturation and enculturation processes. Finally, the present findings emphasized that measures of acculturation and enculturation are not equivalent in terms of their effects on internalizing and externalizing problems.

The offspring of parents with bipolar disorder (OBD) are at high risk for developing mental disorders. In addition to genetic factors, environmental risk is purported to be associated with these negative outcomes. However, few studies have examined this relation. Using concurrent and longitudinal data, we examined if support, structure, and control provided by parents in middle childhood mediated the relation between having a parent with or without bipolar disorder, and offspring mental health. The sample included 145 offspring (77 OBD, 68 controls) aged 4 to 14 years and their parents. Parent and teacher ratings of child behavior were collected, and diagnostic assessments were conducted in offspring 12 years later (n = 101). Bootstrapping analyses showed that low levels of structure mediated the relation between having a parent with bipolar disorder and elevated internalizing and externalizing difficulties during middle childhood. For the longitudinal outcomes, parental control emerged as the strongest mediator of the relation between parents’ bipolar disorder and offspring psychopathology. Suboptimal childrearing may have different immediate and enduring consequences on mental health outcomes in the OBD. Parental structure has robust effects on emotional and behavioral problems in middle childhood, while levels of control promote psychological adjustment in the OBD as they mature.

Although substantial human and animal evidence suggests a role for the amygdala in anxiety, literature linking amygdala volume to anxiety symptomatology is inconclusive, with studies finding positive, negative, and null results. Clarifying this brain–behavior relation in middle to late childhood is especially important, as this is a time both of amygdala structural maturation and the emergence of many anxiety disorders. The goal of the current study was to clarify inconsistent findings in previous literature by identifying factors moderating the relation between amygdala volume and anxiety traits in a large sample of typically developing children aged 6–13 years (N = 72). In particular, we investigated the moderating effects of informant (parent vs. child), age, and sex. We found that children's reports (i.e., self-reports) were related to amygdala volume; children who reported higher anxiety levels had smaller amygdalae. This negative relation between amygdala volume and anxiety weakened with age. There was also an independent effect of sex, such that relations were stronger in males than in females. These results indicate the importance of considering sample and informant characteristics when charting the neurobiological mechanisms underlying developmental anxiety.

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.

This paper aims to advance the scientific understanding of the role of culture, particularly cultural orientation, in development and psychopathology. We advance a theoretical framework that conceptualizes cultural orientation as a developmental construct represented by multiple psychological dimensions and social identities, and influenced by the contexts in which individuals are embedded. This perspective suggests that cultural orientation changes within individuals over time as a function of their experiences with and memberships in multiple groups, including the mainstream and ethnic culture groups, as well as a function of their normative developmental changes (i.e., the development of cognitive, social, and emotional capabilities). In addition, this framework places the development of an ethnic culture social identity (e.g., an ethnic identity) and a mainstream culture social identity in broader developmental perspectives that recognize these as two of the many social identities that are simultaneously embedded within the individual's self-concept and that simultaneously influence one's cultural orientation. To support the successful integration of culture into the study of development and psychopathology, we describe how highly reliable and valid measures of cultural orientation, indexed by individuals’ social identities, are essential for generating a scientifically credible understanding of the role of cultural orientation in development and psychopathology. Further, we detail some best research practices associated with our developmental and contextual framework, and note some important considerations for researchers interested in studying cultural orientation, development, and psychopathology.

The current project seeks to integrate literatures on personality risk for antisocial behavior (ASB) by examining how callous–unemotional traits relate to (a) the development of disinhibited traits and (b) the association between disinhibited traits and ASB. In Study 1, using a nationally representative sample of youth (N > 7,000), we examined whether conduct problems and lack of guilt assessed during ages 4–10 years predicted levels of and changes in disinhibited traits over the course of adolescence, and moderated associations between these traits and ASB. High levels of childhood conduct problems were associated with higher levels of impulsivity, sensation seeking, and ASB in early adolescence, whereas lack of guilt was associated with lower levels of sensation seeking. Neither conduct problems nor lack of guilt significantly predicted changes in impulsivity or sensation seeking, and associations among changes in sensation seeking, impulsivity, and ASB were also consistent across levels of conduct problems and lack of guilt. In Study 2, using a cross-sectional sample of adolescents (N = 970), we tested whether callous–unemotional traits moderated associations between disinhibited traits and ASB. Consistent with the results of Study 1, associations between disinhibited personality and ASB were consistent across a continuous range of callous–unemotional traits.

Maltreated children in foster care are at high risk for dysregulated hypothalamus–pituitary–adrenal (HPA) axis functioning and educational difficulties. The present study examined the effects of a short-term school readiness intervention on HPA axis functioning in response to the start of kindergarten, a critical transition marking entry to formal schooling, and whether altered HPA axis functioning influenced children's school adjustment. Compared to a foster care comparison group, children in the intervention group showed a steeper diurnal cortisol slope on the first day of school, a pattern previously observed among nonmaltreated children. A steeper first day of school diurnal cortisol slope predicted teacher ratings of better school adjustment (i.e., academic performance, appropriate classroom behaviors, and engagement in learning) in the fall of kindergarten. Furthermore, the children's HPA axis response to the start of school mediated the effect of the intervention on school adjustment. These findings support the potential for ameliorative effects of interventions targeting critical transitional periods, such as the transition of formal schooling. This school readiness intervention appears to influence stress neurobiology, which in turn facilitates positive engagement with the school environment and better school adjustment in children who have experienced significant early adversity.