Two disorders of attachment have been consistently identified in some young children following severe deprivation in early life: reactive attachment disorder and disinhibited social engagement disorder. However, less is known about whether signs of these disorders persist into adolescence. We examined signs of reactive attachment disorder and disinhibited social engagement disorder at age 12 years in 111 children who were abandoned at or shortly after birth and subsequently randomized to care as usual or to high-quality foster care, as well as in 50 comparison children who were never institutionalized. Consistent with expectations, those who experienced institutional care in early life had more signs of reactive attachment disorder and disinhibited social engagement disorder at age 12 years than children never institutionalized. In addition, using a conservative intent-to-treat approach, those children randomized to foster care had significantly fewer signs of reactive attachment disorder and disinhibited social engagement disorder than those randomized to care as usual. Analyses within the ever institutionalized group revealed no effects of the age of placement into foster care, but number of caregiving disruptions experienced and the percentage of the child's life spent in institutional care were significant predictors of signs of attachment disorders assessed in early adolescence. These findings indicate that adverse caregiving environments in early life have enduring effects on signs of attachment disorders, and provide further evidence that high-quality caregiving interventions are associated with reductions in both reactive attachment disorder and disinhibited social engagement disorder.

Early caregiving adversity is associated with increased risk for social difficulties. The ventral striatum and associated corticostriatal circuitry, which have demonstrated vulnerability to early exposures to adversity, are implicated in many aspects of social behavior, including social play, aggression, and valuation of social stimuli across development. Here, we used resting-state functional magnetic resonance imaging to assess the degree to which early caregiving adversity was associated with altered coritocostriatal resting connectivity in previously institutionalized youth (n = 41) relative to youth who were raised with their biological families from birth (n = 47), and the degree to which this connectivity was associated with parent-reported social problems. Using a seed-based approach, we observed increased positive coupling between the ventral striatum and anterior regions of medial prefrontal cortex (mPFC) in previously institutionalized youth. Stronger ventral striatum–mPFC coupling was associated with parent reports of social problems. A moderated-mediation analysis showed that ventral striatal–mPFC connectivity mediated group differences in social problems, and more so with increasing age. These findings show that early institutional care is associated with differences in resting-state connectivity between the ventral striatum and the mPFC, and this connectivity seems to play an increasingly important role in social behaviors as youth enter adolescence.

This study reports findings from the administration of a social problem-solving training (SPST) intervention to juvenile detainees in the Connecticut Youth Detainee Program. SPST is a cognitive behavioral intervention that teaches children and youth how to more effectively cope with interpersonal stress and conflict. In the current study, we tested whether SPST could decrease depressive symptoms in a sample of detained adolescent offenders. The study used a randomized-control design with detention staff administering the intervention. The results showed that SPST, as a main effect, was not more effective in reducing depressive symptoms than treatment as usual. However, the effectiveness of SPST was moderated by fluid intelligence. Juvenile detainees with high intelligence scores were most likely to benefit from SPST compared to treatment as usual. It was surprising that, for those with lower intelligence scores, SPST increased depressive symptoms relative to treatment as usual. These results help fill a critical need for intervention effectiveness data on juvenile detainees and indicate that SPST may not be useful for reducing outcomes such as depression.

The link between parental depressive history and parenting styles is well established, as is the association of parenting with child psychopathology. However, little research has examined whether a depressive history in one parent predicts the parenting style of the other parent. As well, relatively little research has tested transactional models of the parenting–child psychopathology relationship in the context of parents' depressive histories. In this study, mothers and fathers of 392 children were assessed for a lifetime history of major depression when their children were 3 years old. They then completed measures of permissiveness and authoritarianism and their child's internalizing and externalizing symptoms when children were 3, 6, and 9 years old. The results showed that a depressive history in one parent predicted the other parent's permissiveness. Analyses then showed that child externalizing symptoms at age 3 predicted maternal permissiveness and authoritarianism and paternal permissiveness at age 6. Maternal permissiveness at age 6 predicted child externalizing symptoms at age 9. No relationships in either direction were found between parenting styles and child internalizing symptoms. The results highlight the importance of considering both parents' depressive histories when understanding parenting styles, and support transactional models of parenting styles and child externalizing symptoms.

Despite major advances in the development of interventions for youth anxiety and depression, approximately 30% of youths with anxiety do not respond to cognitive behavioral treatment, and youth depression treatments yield modest symptom decreases overall. Identifying networks of modifiable risk and maintenance factors that contribute to both youth anxiety and depression (i.e., internalizing problems) may enhance and broaden treatment benefits by informing the development of mechanism-targeted interventions. A particularly powerful network is the rich array of family processes linked to internalizing problems (e.g., parenting styles, parental mental health problems, and sibling relationships). Here, we propose a new theoretical model, the triadic modelof family process, to organize theory and evidence around modifiable, transdiagnostic family factors that may contribute to youth internalizing problems. We describe the model's implications for intervention, and we propose strategies for testing the model in future research. The model provides a framework for studying associations among family processes, their relation to youth internalizing problems, and family-based strategies for strengthening prevention and treatment.

Comorbidity of internalizing and externalizing problems and its risk and protective factors have not been well incorporated into developmental research, especially among racial minority youth from high-poverty neighborhoods. The present study identified a latent comorbid factor as well as specific factors underlying internalizing and externalizing problems among 592 African American adolescents living in economically disadvantaged neighborhoods (291 male; M age = 15.9 years, SD = 1.43 years). Stressful life events and racial discrimination were associated with higher comorbid problems, whereas stressful life events and exposure to violence were associated with higher specific externalizing problems. Collective efficacy was associated with both lower specific externalizing problems and lower comorbid problems. Moreover, high collective efficacy buffered the risk effects of stressful life events and racial discrimination on comorbid problems. Our results demonstrated the advantages of latent variable modeling to understanding comorbidity by articulating impacts of risk factors on comorbid and specific components underlying internalizing and externalizing problems. They also highlighted the protective effect of collective efficacy in mitigating risks for these problems. These findings broadly call for more studies on comorbidities in developmental psychopathology among youth from diverse sociocultural backgrounds.

This study tested a hypothesized cascade in which children's insecure representations of the interparental relationship increase their school problems by altering children's cortisol reactivity to stress and their executive functioning. Participants included 235 families. The first of five measurement occasions occurred when the children were in kindergarten (M age = 6 years), and they were followed through the transition to high school. The results indicated that children's histories of insecure representations of the interparental relationship during the early school years were associated with executive functioning difficulties in adolescence (M age = 14 years). This in turn predicted subsequent increases in school adjustment difficulties 1 year later. In addition, elevated cortisol reactivity to interadult conflict mediated the association between early histories of insecurity and subsequent executive function problems in adolescence.

Theory suggests that early experiences may calibrate the “threshold activity” of the hypothalamus–pituitary–adrenal axis in childhood. Particularly challenging or particularly supportive environments are posited to manifest in heightened physiological sensitivity to context. Using longitudinal data from the Family Life Project (N = 1,292), we tested whether links between maternal sensitivity and hypothalamus–pituitary–adrenal axis activity aligned with these predictions. Specifically, we tested whether the magnitude of the within-person relation between maternal sensitivity and children's cortisol levels, a proxy for physiological sensitivity to context, was especially pronounced for children who typically experienced particularly low or high levels of maternal sensitivity over time. Our results were consistent with these hypotheses. Between children, lower levels of mean maternal sensitivity (7–24 months) were associated with higher mean cortisol levels across this period (measured as a basal sample collected at each visit). However, the magnitude and direction of the within-person relation was contingent on children's average levels of maternal sensitivity over time. Increases in maternal sensitivity were associated with contemporaneous cortisol decreases for children with typically low-sensitive mothers, whereas sensitivity increases were associated with cortisol increases for children with typically high-sensitive mothers. No within-child effects were evident at moderate levels of maternal sensitivity.

Childhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus–pituitary–adrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14–17 years (cortisol n = 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk.

Using a population-based birth cohort in upstate New York (2008–2010), we examined the determinants of brain-derived neurotrophic factor (BDNF) measured in newborn dried blood spots (n = 2,637). We also examined the association between neonatal BDNF and children's development. The cohort was initially designed to examine the influence of infertility treatment on child development but found no impact. Mothers rated children's development in five domains repeatedly through age 3 years. Socioeconomic and maternal lifestyle determinants of BDNF were examined using multivariable linear regression models. Generalized linear mixed models estimated odds ratios for neonatal BDNF in relation to failing a developmental domain. Smoking and drinking in pregnancy, nulliparity, non-White ethnicity/race, and prepregnancy obesity were associated with lower neonatal BDNF. Neonatal BDNF was not associated with failure for developmental domains; however, there was an interaction between BDNF and preterm birth. In preterm infants, a higher BDNF was associated with lower odds of failing any developmental domains, after adjusting for confounders and infertility treatment. This result was particularly significant for failure in communication. Our findings suggest that BDNF levels in neonates may be impacted by maternal lifestyle characteristics. More specifically, lower neonatal BDNF might be an early marker of aberrant neurodevelopment in preterm infants.

This study used a prospective longitudinal design to examine the early developmental pathways that underlie language growth in infants at high risk (n = 50) and low risk (n = 34) for autism spectrum disorder in the first 18 months of life. While motor imitation and responding to joint attention (RJA) have both been found to predict expressive language in children with autism spectrum disorder and those with typical development, the longitudinal relation between these capacities has not yet been identified. As hypothesized, results revealed that 15-month RJA mediated the association between 12-month motor imitation and 18-month expressive vocabulary, even after controlling for earlier levels of RJA and vocabulary. These results provide new information about the developmental sequencing of skills relevant to language growth that may inform future intervention efforts for children at risk for language delay or other developmental challenges.

Maltreatment is associated with chronic depression, high negative self-attributions, and lifetime psychopathology. Adolescence is a sensitive period for the formation of self-concept. Identifying neurobiomarkers of self-processing in depressed adolescents with and without maltreatment may parse the effects of trauma and depression on self-development and chronic psychopathology. Depressed adolescents (n = 86) maltreated due to omission (DO, n = 13) or commission (DCM, n = 28) or without maltreatment (DC, n = 45), and HCs (HC, n = 37) appraised positive and negative self-descriptors in the scanner. DCM and DO showed hypoactivity in the dorsal anterior cingulate cortex (dACC) while processing positive versus negative self-descriptors compared to DC youth, who in turn showed reduced dACC recruitment versus HC. HC youth showed the highest activation in the dACC and striatum during positive self-descriptors; these regions showed a linear decline in activity across DC, DO, and DCM. Low dACC activity to positive versus negative self-descriptors was linked to inadequate coregulation of children's emotions by parents. Negative self-cognitions prevalent in DCM and DO adolescents may be perpetuated by activity in the dACC and striatum. Reduced activation of the dACC and striatum for positive self-descriptors, coupled with enhanced activity for negative self-descriptors, may heighten the risk for persistent depression.

Individuals who have experienced high levels of childhood stress are at increased risk for a wide range of behavioral problems that persist into adulthood, yet the neurobiological and molecular mechanisms underlying these associations remain poorly understood. Many of the difficulties observed in stress-exposed children involve problems with learning and inhibitory control. This experiment was designed to test individuals' ability to learn to inhibit responding during a laboratory task. To do so, we measured stress exposure among a community sample of school-aged children, and then followed these children for a decade. Those from the highest and lowest quintiles of childhood stress exposure were invited to return to our laboratory as young adults. At that time, we reassessed their life stress exposure, acquired functional magnetic resonance imaging data during an inhibitory control task, and assayed these individuals' levels of methylation in the FK506 binding protein 5 (FKBP5) gene. We found that individuals who experienced high levels of stress in childhood showed less differentiation in the dorsolateral prefrontal cortex between error and correct trials during inhibition. This effect was associated only with childhood stress exposure and not by current levels of stress in adulthood. In addition, FKBP5 methylation mediated the association between early life stress and inhibition-related prefrontal activity. These findings are discussed in terms of using multiple levels of analyses to understand the ways in which adversity in early development may affect adult behavioral adaptation.

While striving to succeed in the face of adversity may provide individuals with outward benefits, it may come at a cost to individuals’ physical health. The current study examines whether striving predicts greater physiological or psychosocial costs among those who experienced child maltreatment, a stressor that disrupts the caregiving environment and threatens relationship security. Using data from the National Longitudinal Study of Adolescent to Adult Health, we tested whether greater striving after childhood maltreatment would come at a cost, increasing underlying cardiovascular disease (CVD) risk and depressive symptoms despite showing outward success via income and college degree attainment. The study included 13,341 Black, Hispanic, and White adolescents who self-reported striving and their experiences of childhood neglect, physical abuse, and sexual abuse. As young adults, participants reported depressive symptoms, income, and college degree attainment and completed a health assessment from which a 30-year Framingham-based CVD risk score was calculated. Higher striving was associated with lower CVD risk and depressive symptoms, and higher income and college degree attainment, regardless of maltreatment history. These findings highlight the potential for striving as a target for interventions and support the need to examine multiple biological and behavioral outcomes to understand the multifaceted nature of resilience.

This study assessed attachment representation and attachment-related autonomic regulation in a sample of 38 maltreating and 35 nonmaltreating mothers. Mothers’ state of mind regarding attachment was measured using the Adult Attachment Interview. They further watched an attachment-based comfort paradigm, during which we measured skin conductance and vagal tone. More maltreating mothers (42%) than nonmaltreating mothers (17%) had an unresolved/disoriented attachment classification. Attachment representation was related to physiology during the comfort paradigm: an unresolved state of mind and a nonautonomous classification were associated with a decrease in skin conductance during the comfort paradigm, specifically during the responsive caregiver scenario. However, physiology did not differ between maltreating and nonmaltreating mothers. The decrease in skin conductance of unresolved mothers during the comfort paradigm might be indicative of a deactivating response, which is congruent with the dissociative nature of the unresolved state of mind. The results point to the potential utility of interventions focused on attachment representations for maltreating mothers.