Background

Despite the high prevalence of childhood adversity and well-documented associations with poor academic achievement and psychopathology, effective, scalable interventions remain largely unavailable. Existing interventions targeting growth mindset—the belief that personal characteristics are malleable—have been shown to improve academic achievement and symptoms of psychopathology in youth.

Objective

The present study examines growth mindset as a potential modifiable mechanism underlying the associations of two dimensions of childhood adversity—threat and deprivation—with academic achievement and internalizing psychopathology.

Participants and setting

Participants were 408 youth aged 10–18 years drawn from one timepoint of two longitudinal studies of community-based samples recruited to have diverse experiences of childhood adversity.

Method

Experiences of threat and deprivation were assessed using a multi-informant, multi-method approach. Youth reported on growth mindset of intelligence and symptoms of anxiety and depression. Parents provided information about youths' academic performance.

Results

Both threat and deprivation were independently associated with lower growth mindset, but when accounting for co-occurring adversities, only the association between threat and lower growth mindset remained significant. Lower growth mindset was associated with worse academic performance and greater symptoms of both anxiety and depression. Finally, there was a significant indirect effect of experiences of threat on both lower academic performance and greater symptoms of anxiety through lower growth mindset.

Conclusions

Findings suggest that growth mindset could be a promising target for efforts aimed at mitigating the impact of childhood adversity on academic achievement and psychopathology given the efficacy of existing brief, scalable growth mindset interventions.

Strong in-group bonds, facilitated by implicit favoritism for in-group members (i.e., in-group bias), promote mental health across development. Yet, we know little about how the development of in-group bias is shaped by early-life experiences. Childhood violence exposure is known to alter social information processing biases. Violence exposure may also influence social categorization processes, including in-group biases, in ways that influence risk for psychopathology. We examined associations of childhood violence exposure with psychopathology and behavioral and neural indices of implicit and explicit bias for novel groups in children followed longitudinally across three time points from age 5 to 10 years old (n=101 at baseline; n=58 at wave 3). To instantiate in-group and out-group affiliations, youths underwent a minimal group assignment induction procedure, in which they were randomly assigned to one of two groups. Youth were told that members of their assigned group shared common interests (in-group) and members of the other group did not (out-group). In pre-registered analyses, violence exposure was associated with lower implicit in-group bias, which in turn was associated prospectively with higher internalizing symptoms and mediated the longitudinal association between violence exposure and internalizing symptoms. During an fMRI task examining neural responses while classifying in-group and out-group members, violenceexposed children did not exhibit the negative functional coupling between vmPFC and amygdala to in-group vs. out-group members that was observed in children without violence exposure. Reduced implicit in-group bias may represent a novel mechanism linking violence exposure with the development of internalizing symptoms.

Macrostructural characteristics, such as cost of living and state-level anti-poverty programs relate to the magnitude of socioeconomic disparities in brain development and mental health. In this study we leveraged data from the Adolescent Brain and Cognitive Development (ABCD) study from 10,633 9-11 year old youth (5115 female) across 17 states. Lower income was associated with smaller hippocampal volume and higher internalizing psychopathology. These associations were stronger in states with higher cost of living. However, in high cost of living states that provide more generous cash benefits for low-income families, socioeconomic disparities in hippocampal volume were reduced by 34%, such that the association of family income with hippocampal volume resembled that in the lowest cost of living states. We observed similar patterns for internalizing psychopathology. State-level anti-poverty programs and cost of living may be confounded with other factors related to neurodevelopment and mental health. However, the patterns were robust to controls for numerous state-level social, economic, and political characteristics. These findings suggest that state-level macrostructural characteristics, including the generosity of anti-poverty policies, are potentially relevant for addressing the relationship of low income with brain development and mental health.

Experiencing adversity in childhood and adolescence, including stressful life events (SLEs), may accelerate the pace of development, leading to adverse mental and physical health. However, most research on adverse early experiences and biological aging (BA) in youths relies on cross-sectional designs. In 171 youths followed for approximately 2 years, we examined if SLEs over follow-up predicted rate of change in two BA metrics: epigenetic age and Tanner stage. We also investigated if rate of change in BA was associated with changes in depressive symptoms over time. Youths aged 8–16 years at baseline self-reported Tanner stage and depressive symptoms at baseline and follow-up and provided saliva samples for DNA at both assessments. Horvath epigenetic age estimates were derived from DNA methylation data measured with the Illumina EPIC array. At follow-up, contextual threat interviews were administered to youths and caregivers to assess youths’ experiences of past-year SLEs. Interviews were objectively coded by an independent rating team to generate a SLE impact score, reflecting the severity of all SLEs occurring over the prior year. Rate of change in BA metrics was operationalized as change in epigenetic age or Tanner stage as a function of time between assessments. Higher objective SLE impact scores over follow-up were related to a greater rate of change in epigenetic age (β = 0.21, p = .043). Additionally, among youths with lower—but not higher—Tanner stage at baseline, there was a positive association of SLE impact scores with rate of change in Tanner stage (Baseline Tanner Stage × SLE Impact Score interaction: β = − 0.21, p = .011). A greater rate of change in epigenetic age was also associated with higher depressive symptom levels at follow-up, adjusting for baseline symptoms (β = 0.15, p = .043). Associations with epigenetic age were similar, although slightly attenuated, when adjusting for epithelial (buccal) cell proportions. Whereas much research in youths has focused on severe experiences of early adversity, we demonstrate that more commonly experienced SLEs during adolescence may also contribute to accelerated BA. Further research is needed to understand the long-term consequences of changes in BA metrics for health.

Earlier pubertal development appears to be one pathway through which childhood trauma contributes to psychopathology in adolescence. Puberty-related changes in neural networks involved in emotion processing, namely the amygdala-medial prefrontal (mPFC) circuit, may be a potential mechanism linking trauma and adolescent psychopathology. Our participants were 227 youth between 10 and 13 years of age who completed assessments of threat and deprivation-related experiences of adversity, pubertal stage, and internalizing and externalizing symptoms. A subset (n = 149) also underwent a functional MRI scan while passively viewing fearful and calm faces. Potential mechanisms linking childhood trauma with psychopathology, encompassing earlier pubertal timing and neural response to aversive stimuli were explored. Earlier pubertal development was associated with childhood trauma as well as increased externalizing symptoms in boys only. Earlier pubertal timing in males and females was negatively associated with activation in bilateral amygdala, hippocampal, and fusiform regions when comparing fearful and calm faces. However, amygdala-mPFC connectivity showed no association with pubertal timing or psychopathology symptoms. These findings do not support accelerated amygdala-mPFC development as a mechanism linking childhood trauma and psychopathology, but instead provide support for the role of pubertal development in normative decreases in limbic activation across development.

We examined whether family care following early-life deprivation buffered the association between stressful life events (SLEs) and executive functioning (EF) in adolescence. In early childhood, 136 institutionally reared children were randomly assigned to foster care or care-as-usual; 72 never-institutionalized children served as a comparison group. At age 16 years, adolescents (n = 143; 54% female; 67.1% Romanian) self-reported recent SLEs, completed a battery of memory and EF tasks, and completed a go/nogo task in which mediofrontal theta power (MFTP) was measured using electroencephalogram. More independent SLEs predicted lower EF and more dependent SLEs predicted lower MFTP, but only among adolescents with prolonged early deprivation. Findings provide preliminary evidence that family care following early deprivation may facilitate resilience against stress during adolescence on EF.

The dimensional model of adversity proposes that experiences of threat and deprivation have distinct neurodevelopmental consequences. We examined these dimensions, separately and jointly, with brain structure in a sample of 149 youth aged 8–17—half recruited based on exposure to threat-related experiences. We predicted that greater threat would be uniquely associated with reduced cortical thickness and surface area in brain regions associated with salience processing including ventromedial prefrontal cortex (vmPFC), anterior cingulate cortex (ACC), and insula, and that deprivation experiences would be uniquely associated with reductions in cortical thickness and surface area in frontoparietal areas associated with cognitive control. As predicted, greater threat was associated with thinner cortex in a network including areas involved in salience processing (anterior insula, vmPFC), and smaller amygdala volume (particularly in younger participants), after controlling for deprivation. Contrary to our hypotheses, threat was also associated with thinning in the frontoparietal control network. However, these associations were reduced following control for deprivation. No associations were found between deprivation and brain structure. This examination of deprivation and threat concurrently in the same sample provided further evidence that threat-related experiences influence the structure of the developing brain independent of deprivation.

Purpose

Early life adversity (ELA) is associated with sexual risk, but ELA dimensions—and potential mechanisms—have been less examined. We evaluated associations between threat and deprivation—two key ELA dimensions—and sexual behaviors in adolescents. Secondary analyses investigated age at menarche as a mechanism linking ELA with sexual outcomes in girls. We predicted associations between threat and sexual behaviors, with younger age at menarche as a pathway.

Methods

Data were from the National Comorbidity Survey, Adolescent Supplement. Adolescents and caregivers reported on youths' ELA experiences, which were categorized as threat- or deprivation-related. Adolescents reported if they engaged in sex (N = 9,937) and on specific sexual risk indicators, including age at first sex, number of past-year sexual partners, and condom use consistency (“always” vs. “not always” used). Girls reported age at menarche.

Results

Threat (odds ratio [OR] = 1.76 [95% confidence interval [CI], 1.62–1.92]) and deprivation (OR = 1.51 [95% CI, 1.24–1.83]) were each linked with engagement in sex, ps<.05. Threat-related experiences were associated with multiple sexual risk markers, even when accounting for deprivation: earlier age at first sex (b = −0.20 [95% CI, −0.27 to 0.13]), greater number of partners (b = 0.17 [95% CI, 0.10–0.25]), and inconsistent condom use (OR = 0.72 [95% CI, 0.64–0.80]), ps <.001. Deprivation was not associated with sexual risk when adjusting for threat. We observed no significant indirect effects through age at menarche.

Discussion

Although threat and deprivation were related to engagement in sexual activity, threat-related experiences were uniquely associated with sexual risk. Screening for threat-related ELA may identify adolescents at-risk for poor sexual health.

Child abuse is associated with elevated risk for psychopathology. The current study examined the role of automatic emotion regulation as a potential mechanism linking child abuse with internalizing psychopathology. A sample of 237 youth aged 8–16 years and their caregivers participated. Child abuse severity was assessed by self-report questionnaires, and automatic emotion regulation was assessed using an emotional Stroop task designed to measure adaptation to emotional conflict. A similar task without emotional stimuli was also administered to evaluate whether abuse was uniquely associated with emotion regulation, but not cognitive control applied in a nonemotional context. Internalizing psychopathology was assessed concurrently and at a 2-year longitudinal follow-up. Child abuse severity was associated with lower emotional conflict adaptation but was unrelated to cognitive control. Specifically, the severity of emotional and physical abuse, but not sexual abuse, were associated with lower emotional conflict adaptation. Emotional conflict adaptation was not associated with internalizing psychopathology prospectively. These findings suggest that childhood emotional and physical abuse, in particular, may influence automatic forms of emotion regulation. Future work exploring the socioemotional consequences of altered automatic emotion regulation among youth exposed to child abuse is clearly needed.