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

The purpose of this study was to examine child, maternal, and family antecedents of children's early affect dysregulation within the mother–child relationship and later cognitive and socioemotional correlates of affect dysregulation. Children's affect dysregulation at 24 and 36 months was defined in the context of mother–child interactions in semistructured play and toy cleanup. Dyads were classified as dysregulated at each age based on high negative affect. Affect dysregulation was associated with less maternal sensitivity and stimulation, more maternal depressive symptoms, and lower family income over the first 36 months of life. Children with early negative mood, lower Bayley Mental Development Index scores and insecure-avoidant (15 months) or insecure-resistant attachment classifications (36 months) were more likely to be in an affect-dysregulated group. Controlling for family and child variables, affect-dysregulated children had more problematic cognitive, social, and behavioral outcomes at 54 months, kindergarten, and first grade. The findings are discussed in terms of the early role played by parents in assisting children with affect regulation, the reciprocal nature of parent–child interactions, and the contribution of affect regulation to children's later cognitive, social, and behavioral competence.This study is directed by a Steering Committee and supported by NICHD through a cooperative agreement (U10), which calls for scientific collaboration between the grantees and the NICHD staff. Participating investigators, listed in alphabetical order, are Virginia Allhusen, University of California, Irvine; Jay Belsky, University of London; Cathryn L. Booth, University of Washington; Robert Bradley, University of Arkansas, Little Rock; Celia A. Brownell, University of Pittsburgh; Margaret Burchinal, University of North Carolina, Chapel Hill; Susan B. Campbell, University of Pittsburgh; K. Alison Clarke–Stewart, University of California, Irvine; Martha Cox, University of North Carolina, Chapel Hill; Sarah L. Friedman, NICHD, Bethesda, Maryland; Kathyrn Hirsh–Pasek, Temple University; Aletha Huston, University of Texas, Austin; Elizabeth Jaeger, Temple University; Jean F. Kelly, University of Washington; Bonnie Knoke, Research Triangle Institute, Research Triangle, North Carolina; Nancy Marshall, Wellesley College; Kathleen McCartney, Harvard University; Marion O'Brien, University of Kansas; Margaret Tresch Owen, University of Texas, Dallas; Chris Payne, University of North Carolina, Greensboro; Deborah Phillips, National Research Council, Washington, DC; Robert Pianta, University of Virginia; Wendy Robeson, Wellesley College; Susan Spieker, University of Washington; Deborah Lowe Vandell, University of Wisconsin, Madison; and Marsha Weinraub, Temple University. The authors express appreciation to the study coordinators at each site who supervised the data collection, the research assistants who collected the data, and especially the families and child care providers who welcomed the authors into their homes and workplaces and cooperated willingly with repeated requests for information.

Past studies have shown that aggressive children exhibit rigid (rather than flexible) parent–child interactions; these rigid repertoires may provide the context through which children fail to acquire emotion-regulation skills. Difficulties in regulating emotion are associated with minimal activity in dorsal systems in the cerebral cortex, for example, the anterior cingulate cortex. The current study aimed to integrate parent–child and neurocognitive indices of emotion regulation and examine their associations for the first time. Sixty children (8–12 years old) referred for treatment for aggression underwent two assessments. Brain processes related to emotion regulation were assessed using dense-array EEG with a computerized go/no-go task. The N2 amplitudes thought to tap inhibitory control were recorded, and a source analysis was conducted. In the second assessment, parents and children were videotaped while trying to solve a conflict topic. State space grids were used to derive two dynamic flexibility parameters from the coded videotapes: (a) the number of transitions between emotional states and (b) the dispersion of emotional states, based on proportional durations in each state. The regression results showed that flexibility measures were not related to N2 amplitudes. However, flexibility measures were significantly associated with the ratio of dorsal to ventral source activation: for transitions, ΔR2 = .27, F (1, 34) = 13.13, p = .001; for dispersion, ΔR2 = .29, F (1, 35) = 14.76, p < .001. Thus, in support of our main hypothesis, greater dyadic flexibility was associated with a higher ratio of dorsomedial to ventral activation, suggesting that children with more flexible parent–child interactions are able to recruit relatively more dorsomedial activity in challenging situations.

Transactional processes between parental support and adolescents’ depressive symptoms might differ in the short term versus long term. Therefore, this multi-sample study tested bidirectional within-family associations between perceived parental support and depressive symptoms in adolescents with datasets with varying measurement intervals: Daily (N = 244, Mage = 13.8 years, 38% male), bi-weekly (N = 256, Mage = 14.4 years, 29% male), three-monthly (N = 245, Mage = 13.9 years, 38% male), annual (N = 1,664, Mage = 11.1 years, 51% male), and biennial (N = 502, Mage = 13.8 years, 48% male). Preregistered random-intercept cross-lagged panel models (RI-CLPMs) showed negative between- and within-family correlations. Moreover, although the preregistered models showed no within-family lagged effect from perceived parental support to adolescent depressive symptoms at any timescale, an exploratory model demonstrated a negative lagged effect at a biennial timescale with the annual dataset. Concerning the reverse within-family lagged effect, increases in adolescent depressive symptoms predicted decreases in perceived parental support 2 weeks and 3 months later (relationship erosion effect). Most cross-lagged effects were not moderated by adolescent sex or neuroticism trait level. Thus, the findings mostly support adolescent-driven effects at understudied timescales and illustrate that within-family lagged effects do not generalize across timescales.

This study examined whether individual differences in affective reactivity, defined as changes in positive or negative affect in response to daily racial discrimination, predicted subsequent depressive symptoms. Participants were African American graduate and postgraduate students (N = 174; M age = 30 years) recruited for a measurement-burst study. Data on depressive symptoms were gathered at two assessment points 1 year apart. Affective reactivity data was obtained from participants via a 14-day diary study of daily racial discrimination and affect. Participants who experienced pronounced increases in negative affect on days when racial discrimination occurred had elevated depressive symptoms 1 year later. Heightened positive affect reactivity was also associated with more depressive symptoms at follow-up. The results suggest that affective reactivity (either greater increases in negative affect or greater decreases in positive affect in the context of racial discrimination) may be an underlying psychological mechanism that confers vulnerability to future depressive symptoms.

The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother–infant dyads. Prenatal distress was assessed at 17 and 29 weeks’ gestational age (GA). Infant structural data were collected via diffusion tensor imaging (DTI) at 42–45 weeks’ postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks’ GA was associated with increased fractional anisotropy, b = .283, t(64) = 2.319, p = .024, and with increased axial diffusivity, b = .254, t(64) = 2.067, p = .043, within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks’ GA, or earlier in gestation.

We examined facial emotion recognition in 12-year-olds in a longitudinally followed sample of children with and without exposure to early life psychosocial deprivation (institutional care). Half of the institutionally reared children were randomized into foster care homes during the first years of life. Facial emotion recognition was examined in a behavioral task using morphed images. This same task had been administered when children were 8 years old. Neutral facial expressions were morphed with happy, sad, angry, and fearful emotional facial expressions, and children were asked to identify the emotion of each face, which varied in intensity. Consistent with our previous report, we show that some areas of emotion processing, involving the recognition of happy and fearful faces, are affected by early deprivation, whereas other areas, involving the recognition of sad and angry faces, appear to be unaffected. We also show that early intervention can have a lasting positive impact, normalizing developmental trajectories of processing negative emotions (fear) into the late childhood/preadolescent period.

In this review we examine factors hypothesized to affect children's memory for traumatic events. Theoretical ideas on the processing and remembering of trauma are presented and critiqued. We review research on how psychopathology may generally influence and dissociation and posttraumatic stress disorder may specifically influence children's memory and suggestibility. The special case of child maltreatment is addressed as it relates to interviewing children about traumatic life experiences. Throughout we draw on current developmental, cognitive, social, and clinical theory and research. The review covers a controversial and exciting area of psychological inquiry.

Emerging research in epigenetics has shown that there is variability in how environmental exposures “get under the skin” through mechanisms like DNA methylation to influence gene expression that may lead to differential adaptations to stress. This is the first study to examine prospectively the relationship between DNA methylation at birth and resilience to prenatal environmental stressors in several domains (conduct, hyperactivity, emotional problems, and global symptomatology) in middle childhood. We focused on DNA methylation in the vicinity of the oxytocin receptor (OXTR) gene as it has been previously associated with impairments in social–cognitive processes that may underlie a wide range of childhood psychopathology. Participants were 91 youth exposed to pre- and postnatal adversity with established conduct problem trajectories drawn from the Avon Longitudinal Study of Parents and Children. Consistent with our hypothesis, OXTR DNA methylation was predictive of resilience in the conduct problems domain in middle childhood. DNA methylation profiles did not predict resilience in domains of emotional, hyperactivity, and global symptomatology, suggesting a potential role for OXTR in the development of conduct problems in particular. However, individuals who were resilient to conduct problems were also broadly resilient across multiple domains. Therefore, future research should elucidate the biological pathways between OXTR DNA methylation and gene expression and its relation to impairments in social behavior.

Culturally linked family influences during adolescence are important predictors of health and well-being for Latino youth, yet few studies have examined whether these familial influences are associated with indicators of typical physiological stress processes. Following a cultural neurobiology framework, we examined the role of family in the everyday lives of Latino adolescents (N = 209; Mage = 18.10; 85.1% Mexican descent; 64.4% female) by investigating familism values and perceptions of parent support as well as daily family assistance behaviors in relation to hypothalamic–pituitary–adrenal axis diurnal patterns, indexed by salivary cortisol five times a day for 3 weekdays. Three-level growth curve analyses revealed that perceptions of parental support were associated with greater cortisol awakening responses, whereas familism values were not associated with diurnal cortisol patterns. In day-to-day analyses, assisting family during the day (compared to not assisting family) was associated with lower waking cortisol levels and flatter diurnal slopes the next day. Our findings highlight the dynamic associations and multiple time courses between cultural values and behaviors, daily experiences, and physiological stress processes for Latino adolescents. Further, we identified important cultural risk and promotive factors associated with physiological regulation in daily life and potential pathways toward health outcomes in adulthood.

In postconflict settings risk factors at multiple levels of the social ecology, including community, family, and relationship factors, potentially affect children's mental health. In addition, intergenerational risk factors such as guardians’ history of childhood family violence, war exposure, and psychopathology may contribute to children's psychopathological symptoms. In this study, we aimed to identify risk constellations that predict child internalizing and externalizing behavior problems, depression, and posttraumatic stress symptoms in the postconflict setting of northern Uganda. In a cross-sectional epidemiological study, 513 second-grade students and their female guardians were interviewed using standardized clinical questionnaires. A higher exposure to traumatic events, more witnessed or experienced violence within the family, and lower child-reported care from female guardians independently predicted psychopathological symptoms in children. While controlling for intergenerational risk factors in female guardians, serial mediation modeling revealed that the effect of trauma exposure on children's psychopathological symptoms was partially mediated by higher exposure to family violence and lower child-perceived care from female guardians. The mediation appeared to be stronger for children's depression symptoms and internalizing and externalizing behavior problems than for posttraumatic stress symptoms. The current findings support the need for targeted interventions at the individual and family system levels that are matched to children's psychopathological symptoms.

We conducted a developmental analysis of genetic moderation of the effect of the Fast Track intervention on adult externalizing psychopathology. The Fast Track intervention enrolled 891 children at high risk to develop externalizing behavior problems when they were in kindergarten. Half of the enrolled children were randomly assigned to receive 10 years of treatment, with a range of services and resources provided to the children and their families, and the other half to usual care (controls). We previously showed that the effect of the Fast Track intervention on participants' risk of externalizing psychopathology at age 25 years was moderated by a variant in the glucocorticoid receptor gene. Children who carried copies of the A allele of the single nucleotide polymorphism rs10482672 had the highest risk of externalizing psychopathology if they were in the control arm of the trial and the lowest risk of externalizing psychopathology if they were in the treatment arm. In this study, we test a developmental hypothesis about the origins of this for better and for worse Gene × Intervention interaction (G × I): that the observed G × I effect on adult psychopathology is mediated by the proximal impact of intervention on childhood externalizing problems and adolescent substance use and delinquency. We analyzed longitudinal data tracking the 270 European American children in the Fast Track randomized control trial with available genetic information (129 intervention children, 141 control group peers, 69% male) from kindergarten through age 25 years. Results show that the same pattern of for better and for worse susceptibility to intervention observed at the age 25 follow-up was evident already during childhood. At the elementary school follow-ups and at the middle/high school follow-ups, rs10482672 predicted better adjustment among children receiving the Fast Track intervention and worse adjustment among children in the control condition. In turn, these proximal G × I effects early in development mediated the ultimate G × I effect on externalizing psychopathology at age 25 years. We discuss the contribution of these findings to the growing literature on genetic susceptibility to environmental intervention.

Children who spend their early lives in institutions experience profound psychosocial deprivation that is associated with altered stress response system development. Here, we used data from a longitudinal randomized controlled trial of foster care for institutionally reared children to examine whether caregiving quality and stressful life events (SLEs) in early adolescence (age 12) influence patterns of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) reactivity. Controlling for the effect of institutional care, higher caregiving quality at age 12 was associated with heightened cortisol and SNS reactivity. However, moderation analysis revealed that the latter effect was only observed among never-institutionalized children, whereas ever-institutionalized children demonstrated a persistently blunted SNS response regardless of recent caregiving quality. Among institutionally reared children, SLEs interacted with prior random assignment to foster care, such that those placed in foster care early in development had a SNS response that approximated never-institutionalized children when SLEs at age 12 were low. In contrast, SNS reactivity was persistently blunted among those with prolonged deprivation, regardless of recent SLEs. Early-life deprivation is associated with persistent blunting of stress response systems, but normalization may be achievable if SLEs are limited following placement into enriched family-based care.

Cluster A odd or eccentric personality disorder (PD) symptoms may reflect a schizophrenia spectrum biological vulnerability in at least some persons. Consequently, this symptom pattern may have particularly negative effects on the transition from adolescent to adult roles. A general population sample of 200 young adults was assessed on Cluster A PD at mean ages 17 and 22, and subsequently provided detailed narratives about their monthly experiences and behaviors between these two ages. Adolescent Cluster A PD was related to the developmental trajectories of residential, career, financial, romantic, and family formation roles during this period, and trajectories were related to a change in symptoms over this period. Symptoms were associated with early parenthood and less advanced education, but for other developmental outcomes tended to differ for men and women. These gender differences were attributable, in part, to the differential meaning and consequences of early parenthood for men and women.This work was funded by NIMH Grant MH-54161 to Patricia Cohen, and by the New York State Office of Mental Health.

There is an extensive literature describing the detrimental effects of adverse childhood experiences (ACE; e.g., abuse, neglect, and household dysfunction) on physical and mental health. However, few large-scale studies have explored these associations longitudinally in urban minority cohorts or assessed links to broader measures of well-being such as educational attainment, occupation, and crime. Although adversity and resilience have long been of interest in developmental psychology, protective and promotive factors have been understudied in the ACE literature. This paper investigates the psychosocial processes through which ACEs contribute to outcomes, in addition to exploring ways to promote resilience to ACEs in vulnerable populations. Follow-up data were analyzed for 87% of the original 1,539 participants in the Chicago Longitudinal Study (N = 1,341), a prospective investigation of the impact of an Early Childhood Education program and early experiences on life-course well-being. Findings suggest that ACEs impact well-being in low-socioeconomic status participants above and beyond the effects of demographic risk and poverty, and point to possible mechanisms of transmission of ACE effects. Results also identify key areas across the ecological system that may promote resilience to ACEs, and speak to the need to continue to support underserved communities in active ways.

Manuck, Craig, Flory, Halder, and Ferrell (2011) reported that a theoretically anticipated effect of family rearing on girls' menarcheal age was genetically moderated by two single nucleotide polymorphisms (SNPs) of the estrogen receptor-α gene. We sought to replicate and extend these findings, studying 210 White females followed from birth. The replication was general because a different measure of the rearing environment was used in this inquiry (i.e., maternal sensitivity) than in the prior one (i.e., family cohesion). Extensions of the work included prospective rather than retrospective measurements of the rearing environment, reports of first menstruation within a year of its occurrence rather than decades later, accounting for some heritability of menarcheal age by controlling for maternal age of menarche, and using a new model-fitting approach to competitively compare diathesis–stress versus differential-susceptibility models of Gene × Environment interaction. The replication/extension effort proved successful in the case of both estrogen receptor-α SNPs, with the Gene × Environment interactions principally reflecting diathesis–stress: lower levels of maternal sensitivity predicted earlier age of menarche for girls homozygous for the minor alleles of either SNP but not for girls carrying other genotypes. Results are discussed in light of the new analytic methods adopted.

Cognitive impairment has been identified as an important aspect of major depressive disorder (MDD). We tested two theories regarding the association between MDD and cognitive functioning using data from longitudinal cohort studies. One theory, the cognitive reserve hypothesis, suggests that higher cognitive ability in childhood decreases risk of later MDD. The second, the scarring hypothesis, instead suggests that MDD leads to persistent cognitive deficits following disorder onset. We tested both theories in the Dunedin Study, a population-representative cohort followed from birth to midlife and assessed repeatedly for both cognitive functioning and psychopathology. We also used data from the Environmental Risk Longitudinal Twin Study to test whether childhood cognitive functioning predicts future MDD risk independent of family-wide and genetic risk using a discordant twin design. Contrary to both hypotheses, we found that childhood cognitive functioning did not predict future risk of MDD, nor did study members with a past history of MDD show evidence of greater cognitive decline unless MDD was accompanied by other comorbid psychiatric conditions. Our results thus suggest that low cognitive functioning is related to comorbidity, but is neither an antecedent nor an enduring consequence of MDD. Future research may benefit from considering cognitive deficits that occur during depressive episodes from a transdiagnostic perspective.

Research shows that childhood dysregulation is associated with later psychiatric disorders. It does not yet resolve discrepancies in the operationalization of dysregulation. It is also far from settled on the origins and implications of individual differences in dysregulation. This study tested several operational definitions of dysregulation using Achenbach attention, anxious/depressed, and aggression subscales. Individual growth curves of dysregulation were computed, and predictors of growth differences were considered. The study also compared the predictive utility of the dysregulation indexes to standard externalizing and internalizing indexes. Dysregulation was indexed annually for 24 years in a community sample (n = 585). Hierarchical linear models considered changes in dysregulation in relation to possible influences from parenting, family stress, child temperament, language, and peer relations. In a test of the meaning of dysregulation, it was related to functional and psychiatric outcomes in adulthood. Dysregulation predictions were further compared to those of the more standard internalizing and externalizing indexes. Growth curve analyses showed strong stability of dysregulation. Initial levels of dysregulation were predicted by temperamental resistance to control, and change in dysregulation was predicted by poor language ability and peer relations. Dysregulation and externalizing problems were associated with negative adult outcomes to a similar extent.

This article investigates the impact of ego development on the course of psychiatric illness in a group of 37 psychiatrically hospitalized adolescents ages 12 to 16. The subjects, 21 males and 16 females, were evaluated at time of admission and again after 9 months of hospitalization. Using the Loevinger Sentence Completion Test (Loevinger, Wessler, & Redmore, 1970), two ego pathway groups were defined: progressors, those subjects who had advanced at least one-half stage in ego development, and nonprogressors, those who did not progress at least one-half state in ego development. Significant differences in clinical course were found between the two groups. Progressors demonstrated more significant decreases in psychiatric symptoms as measured by the Achenbach and Edelbrock (1987) Youth Self Report and had a significant change in their use of coping and defense processes compared with the nonprogressors. The findings are discussed in the context of a constructivist approach to developmental psychopathology.