Exposure to childhood adversity is a powerful risk factor for psychopathology. Despite extensive efforts, we have not yet identified effective or scalable interventions that prevent the emergence of mental health problems in children who have experienced adversity. In this modified Delphi study, we identified intervention strategies for effectively targeting both the neurodevelopmental mechanisms linking childhood adversity and psychopathology – including heightened emotional reactivity, difficulties with emotion regulation, blunted reward processing, and social information processing biases, as well as a range of psychopathology symptoms. We iteratively synthesized information from experts in the field and relevant meta-analyses through three surveys, first with experts in intervention development, prevention, and childhood adversity (n = 32), and then within our study team (n = 8). The results produced increasing stability and good consensus on intervention strategy recommendations for specific neurodevelopmental mechanisms and symptom presentations and on strength of evidence ratings of intervention strategies targeting youth and parents. More broadly, our findings highlight how intervention decision making can be informed by meta-analyses, enhanced by aggregate group feedback, saturated before consensus, and persistently subjective or even contradictory. Ultimately, the results converged on several promising intervention strategies for prevention programming with adversity-exposed youth, which will be tested in an upcoming clinical trial.
Adolescents exposed to violence are at elevated risk of developing most forms of psychopathology, including depression, anxiety, and alcohol abuse. Prior research has identified emotional reactivity and difficulties with emotion regulation as core mechanisms linking violence exposure with psychopathology. Scant research has examined behavioral responses to distress as a mechanism in this association. This study examined the association of violence exposure with distress tolerance—the ability to persist in the face of distress—and whether lower distress tolerance linked violence exposure with subsequent increases in depression, anxiety, and alcohol abuse problems during adolescence. Data were collected prospectively in a sample of 287 adolescents aged 16–17 (44.3% male; 40.8% White). At Time 1, participants provided self-report of demographics, violence exposure, and psychopathology, and completed a behavioral measure of distress tolerance, the Paced Auditory Serial Addition Task. Four months later, participants (n = 237) repeated the psychopathology assessments. Violence exposure was associated with lower distress tolerance (β = -.21 p = .009), and elevated concurrent psychopathology (β = .16-.45, p = .001-.004). Low distress tolerance was prospectively associated with greater likelihood of abusing alcohol over time (OR = .63, p = .021), and mediated the association between violence exposure and greater levels (β = .02, 95% CI [.001, .063]) and likelihood (OR = .03, 95% CI [.006, .065]) of alcohol use over time. In contrast, low distress tolerance was not associated concurrently or prospectively with internalizing symptoms. Results persisted after controlling for socio-economic status. Findings suggest that distress tolerance is shaped by early experiences of threat and plays a role in the association between violence exposure and development of problematic alcohol use in adolescence.
Exposure to stressful life events is strongly associated with internalizing psychopathology, and identifying factors that reduce vulnerability to stress-related internalizing problems is critical for development of early interventions. Drawing on research from affective science, we tested whether high emotion differentiation—the ability to specifically identify one’s feelings—buffers adolescents from developing internalizing symptoms when exposed to stress. Thirty adolescents completed a laboratory measure of emotion differentiation before an intensive yearlong longitudinal study in which exposure to stress and internalizing problems were assessed at both the moment level (n = 4,921 experience-sampling assessments) and month level (n = 355 monthly assessments). High negative and positive emotion differentiation attenuated moment-level coupling between perceived stress and feelings of depression, and high negative emotion differentiation eliminated month-level associations between stressful life events and anxiety symptoms. These results suggest that high emotion differentiation buffers adolescents against anxiety and depression in the face of stress, perhaps by facilitating adaptive emotion regulation.
Attention biases to emotion are associated with symptoms of internalizing and externalizing psychopathology in children and adolescents. It is unknown whether attention biases to emotion and their associations with different symptoms of psychopathology vary across development from early childhood through young adulthood. We examine this age-related variation in the current study. Participants (N = 190; ages: 4–25) completed survey-based psychopathology symptom measures and a dot-probe task to assess attention bias to happy, sad, and angry relative to neutral faces. We tested whether linear or non-linear (e.g., spline-based models) associations best characterized age-related variation in attention to emotion. We additionally examined whether attention biases were associated with depression, anxiety, and externalizing symptoms and whether these associations varied by age. No age-related differences in attention biases were found for any of the emotional faces. Attention biases were associated with psychopathology symptoms, but only when examining moderation by age. Biased attention to angry faces was associated with greater symptoms of anxiety and depression in adolescents and young adults, but not children. Similarly, biased attention to happy faces was associated with externalizing symptoms in adolescents and young adults, but not in children. In contrast, biased attention to happy faces was associated with greater anxiety symptoms in children, but not in adolescents or young adults. Biased attention toward social threat and reward becomes more strongly coupled with internalizing and externalizing symptoms, respectively, during the transition to adolescence. These findings could inform when interventions such as attention bias modification training may be most effective.
The depression gap refers to higher rates of depression among women than men. Change in the depression gap over time may elucidate social causes of this disparity—such as unequal college attendance or employment status. We conducted a meta-regression analysis to estimate variation in the depression gap over time by age, accounting for potential sources of variation between studies. Electronic databases and bibliographies were searched for English language studies from January 1980–October 2019. 144 independent estimates from United States-representative samples met selection criteria (n=813,189). The depression gap was summarized as prevalence ratios (PR) among studies using diagnostic instruments, and standardized mean differences among symptom-based studies. Primary study measures were baseline study year (range: 1982-2017), and age (range: 10-60+). Compared with respondents ages 60+, depression prevalence was greater among respondents aged 10-19 (PR=1.26; 95% CI=1.02, 1.56). Over time, the depression gap did not change among adults, but increased among adolescents (age by time interaction PR=1.05; 95% CI=1.01, 1.08). Results were similar for symptom-based studies. The present study finds no evidence of a change in the depression gender gap for US adults, however, the gap increased among adolescents. Greater attention to factors driving this widening disparity in adolescent depression is needed.
Although increasing numbers of children have socially transitioned to live in line with their gender identities, little is known about factors associated with their wellbeing. This study examines the associations between parent-reported family, peer, and school support for a youth’s gender identity, as well as an objective measure of state-level support, with parent-reported internalizing symptoms in 265 transgender youth (67.2% transgender girls, 32.8% transgender boys), ages 3–15 years (M = 9.41, SD = 2.62). Parents who reported higher levels of family, peer, and school support for their child’s gender identity also reported fewer internalizing symptoms; the objective measure of state-level support was not related to internalizing symptoms. Additionally, peer and school support buffered against the association between gender-related victimization and internalizing symptoms, as reported by parents. This work demonstrates that even among transgender youth with families who supported their transitions, parents see better well-being in their children when they also see more support for the child’s gender identity from family, peers, and schools.
Children raised in families with low socioeconomic status (SES) are more likely to exhibit symptoms of psychopathology. However, the strength of this association, the specific indices of SES most strongly associated with childhood psychopathology, and factors moderating the association are strikingly inconsistent across studies. We conducted a meta-analysis of 120 estimates of the association between family SES and child psychopathology in 13 population-representative cohorts of children studied in the US since 1980. Among 26,715 participants aged 3–19 years, we observed small to moderate associations of low family income (g = 0.19), low Hollingshead index (g = 0.21), low subjective SES (g = 0.24), low parental education (g = 0.25), poverty status (g = 0.25), and receipt of public assistance (g = 0.32) with higher levels of childhood psychopathology. Moderator testing revealed that receipt of public assistance showed an especially strong association with psychopathology and that SES was more strongly related to externalizing than internalizing psychopathology. Dispersion in our final, random effects, model suggested that the relation between SES and child psychopathology is likely to vary in different populations of children and in different communities. These findings highlight the need for additional research on the mechanisms of SES-related psychopathology risk in children in order to identify targets for potential intervention.
Background: Adolescence has been proposed to be a period of heightened sensitivity to environmental influence. If true, adolescence may present a window of opportunity for recovery for children exposed to early-life adversity. Recent evidence supports adolescent recalibration of stress response systems following early-life adversity. However, it is unknown whether similar recovery occurs in other domains of functioning in adolescence. Methods: We use data from the Bucharest Early Intervention Project – a randomized controlled trial of foster care for children raised in psychosocially depriving institutions – to examine the associations of the caregiving environment with reward processing, executive functioning, and internalizing and externalizing psychopathology at ages 8, 12, and 16 years, and evaluate whether these associations change across development. Results: Higher quality caregiving in adolescence was associated with greater reward responsivity and lower levels of internalizing and externalizing symptoms, after covarying for the early-life caregiving environment. The associations of caregiving with executive function and internalizing and externalizing symptoms varied by age and were strongest at age 16 relative to ages 8 and 12 years. This heightened sensitivity to caregiving in adolescence was observed in both children with and without exposure to early psychosocial neglect. Conclusions: Adolescence may be a period of heightened sensitivity to the caregiving environment, at least for some domains of functioning. For children who experience early psychosocial deprivation, this developmental period may be a window of opportunity for recovery of some functions. Albeit correlational, these findings suggest that it may be possible to reverse or remediate some of the lasting effects of early-life adversity with interventions that target caregiving during adolescence. Keywords: Institutionalization; reward; executive function; psychopathology; adolescence.
Background Early adversity consistently predicts youth psychopathology. However, the pathways linking unique dimensions of early adversity, such as deprivation, to psychopathology are understudied. Here, we evaluate a theoretical model linking early deprivation exposure with psychopathology prospectively through language ability. Methods Participants included 2,301 youth (47.5% female) enrolled in the Fragile Families and Child Wellbeing Study. We include data from assessment points at ages 1, 3, 5, 9, and 15. Latent factors for deprivation and threat were modeled from multiple indicators at ages 1 and 3. Youth language ability was assessed at Age 5. Indicators of psychopathology were assessed at ages 5, 9, and 15. A structural equation model tested longitudinal paths to internalizing and externalizing psychopathology from experiences of deprivation and threat. Results Deprivation from birth to Age 3 was associated with an indirect effect on internalizing and externalizing symptoms in early childhood (Age 5), later childhood (Age 9), and adolescence (Age 15) via language ability in early childhood (Age 5). Early threat exposure was associated with increased internalizing and externalizing psychopathology across all ages. There was no significant indirect effect from threat to psychopathology via language ability. Conclusions The effects of deprivation on psychopathology during early childhood, late childhood, and adolescence are explained, in part, through early childhood language ability. Results provide insight into language ability as a possible opportunity for intervention.
BACKGROUND: Disruptions in neural circuits underlying emotion regulation (ER) may be a mechanism linking child maltreatment with psychopathology. We examined the associations of maltreatment with neural responses during passive viewing of negative emotional stimuli and attempts to modulate emotional responses. We investigated whether the influence of maltreatment on neural activation during ER differed across development and whether alterations in brain function mediated the association between maltreatment and a latent general psychopathology ('p') factor. METHODS: Youth aged 8-16 years with (n = 79) and without (n = 72) exposure to maltreatment completed an ER task assessing neural responses during passive viewing of negative and neutral images and effortful attempts to regulate emotional responses to negative stimuli. P-factor scores were defined by a bi-factor model encompassing internalizing and externalizing psychopathology. RESULTS: Maltreated youth had greater activation in left amygdala and salience processing regions and reduced activation in multiple regions involved in cognitive control (bilateral superior frontal gyrus, middle frontal gyrus, and dorsal anterior cingulate cortex) when viewing negative v. neutral images than youth without maltreatment exposure. Reduced neural recruitment in cognitive control regions mediated the association of maltreatment with p-factor in whole-brain analysis. Maltreated youth exhibited increasing recruitment with age in ventrolateral prefrontal cortex during reappraisal while control participants exhibited decreasing recruitment with age. Findings were similar after adjusting for co-occurring neglect. CONCLUSIONS: Child maltreatment influences the development of regions associated with salience processing and cognitive control during ER in ways that contribute to psychopathology.
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.
Sensitive periods neurobiologically encode environmental experiences to facilitate plasticity and learning in human development. Knowledge of human sensitive periods has largely come from methods developed in animal models and remains limited in many domains. We provide a framework and suite of approaches to study these phenomena in humans to stimulate progress in understanding human sensitive periods. To do so, we evaluate how current research approaches can shed light on different aspects of human sensitive period processes. These approaches comprise environmental manipulations like deprivation and substitution paradigms, pharmacological manipulations, and computational modeling. Finally, we propose three novel approaches rooted in human neuroscience—including impoverished environments, enriched environmental interventions, and individual differences in stress—to motivate future research on sensitive period mechanisms.
This longitudinal study examined early social–cognitive markers that might be associated with the emergence of childhood depression and anxiety. At 5 years of age, 137 children completed an implicit self-esteem measure. At 9 years of age, the same children completed measures of implicit self-esteem, explicit self-esteem, depression, and anxiety. Two novel findings emerged. First, higher implicit self-esteem at age 5 than explicit self-esteem at age 9 (implicit \textgreater explicit discrepancy) was associated with depressive symptoms at age 9, but not with symptoms of anxiety. Second, this cross-age implicit \textgreater explicit discrepancy was associated with depressive symptoms more strongly than was the same implicit \textgreater explicit discrepancy measured concurrently at age 9. The overall pattern suggests that the appearance of depressive symptoms in children is associated with discrepancies between implicit and explicit self-esteem and not just lower levels of implicit self-esteem or lower levels of explicit self-esteem taken alone. It is the direction and discrepancy across time that is particularly informative, such that discrepancies between early implicit representations and later explicit reports of self-worth reflect a developmental pathway associated with elevated risk for depressive symptoms. Taken altogether, this study illustrates the benefits of combining work in developmental, child-clinical, and social psychology to provide a more complete view of the developing child. We believe that combining implicit and explicit measures of self-esteem across developmental time points can be used to examine early markers of depression in children at younger ages than typically possible with explicit measures alone.
Childhood adversity is common and strongly associated with risk for psychopathology. Identifying factors that buffer children from experiencing psychopathology following adversity is critical for developing more effective intervention approaches. In the present study, we examined several behavioral metrics of reward processing reflecting global approach motivation for reward and the degree to which reward responses scaled with reward value (i.e., behavioral sensitivity to reward value) as potential moderators of the association of multiple dimensions of adversity including trauma, caregiver neglect, and food insecurity with depression and externalizing psychopathology in a sample of youths ages 8 to 16 (n = 132). Trauma exposure and externalizing problems were positively associated at low and moderate levels of reward reactivity, but this association became nonsignificant at high levels of reward reactivity. Our findings extend prior work by demonstrating that high behavioral sensitivity to reward value may buffer against externalizing problems following exposure to trauma.
Life history theory argues that exposure to early life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 54 studies (n = 116,010) examining associations of ELA with pubertal timing and cellular aging (telomere length and DNA methylation age), systematically review 25 studies (n = 3,253) examining ELA and neural markers of accelerated development (cortical thickness and amygdala-prefrontal cortex functional connectivity) and evaluate whether associations of ELA with biological aging vary according to the nature of adversity experienced. ELA overall was associated with accelerated pubertal timing (d = −0.10) and cellular aging (d = −0.21), but these associations varied by adversity type. Moderator analysis revealed that ELA characterized by threat was associated with accelerated pubertal development (d = −0.26) and accelerated cellular aging (d = −0.43), but deprivation and SES were unrelated to accelerated development. Systematic review revealed associations between ELA and accelerated cortical thinning, with threat-related ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks. There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention. (PsycInfo Database Record (c) 2020 APA, all rights reserved)
Children who are victims of interpersonal violence have a markedly elevated risk of engaging in aggressive behavior and perpetrating violence in adolescence and adulthood. Although alterations in social information processing have long been understood as a core mechanism underlying the link between violence exposure and externalizing behavior, scant research has examined more basic social cognition abilities that might underlie this association. To that end, this study examined the associations of interpersonal violence exposure with cognitive and affective theory of mind (ToM), core social-cognitive processes that underlie many aspects of social information processing. In addition, we evaluated whether difficulties with ToM were associated with externalizing psychopathology. Data were collected in a community-based sample of 246 children and adolescents aged 8–16 who had a high concentration of exposure to interpersonal violence. Violence exposure was associated with lower accuracy during cognitive and affective ToM, and the associations persisted after adjusting for co-occurring forms of adversity characterized by deprivation, including poverty and emotional neglect. Poor ToM performance, in turn, was associated with externalizing behaviors. These findings shed light on novel pathways that increase risk for aggression in children who have experienced violence.
Background: Stressful life events are more likely to trigger depression among individuals exposed to childhood adversity. However, the mechanisms underlying this stress sensitization remain largely unknown. Any such mechanism must be altered by childhood adversity and interact with recent stressful life events, magnifying their association with depression.
Aim: This study investigated whether reduced hippocampal and amygdala volume are potential mechanisms underlying stress sensitization following childhood violence exposure.
Method: A sample of 149 youth (aged 8-17 years), with (N = 75) and without (N = 74) exposure to physical abuse, sexual abuse, or domestic violence participated. Participants completed a structural MRI scan and assessments of depression. Approximately 2 years later, stressful life events were assessed along with depression symptoms in 120 participants (57 violence exposed).
Results: Childhood violence exposure was associated with smaller hippocampal and amygdala volume. Stressful life events occurring during the follow-up period predicted worsening depression over time, and this association was magnified among those with smaller hippocampal and amygdala volumes. Significant moderated mediation models revealed the indirect effects of violence exposure on increasing depression over time through hippocampal and amygdala volumes, particularly among youths who experienced more stressful life events.
Conclusions: These results provide evidence for reduced hippocampal and amygdala volume as potential mechanisms of stress sensitization to depression following exposure to violence. More broadly, these patterns suggest that hippocampal and amygdala-mediated emotional and cognitive processes may confer vulnerability to stressful life events among children who have experienced violence.
The depression gap (i.e., higher rates of depression among women than men) represents an important mental health disparity in the US. Differences in gendered social position (i.e., the roles, responsibilities, and opportunities available to women and men), which have been changing since the mid-20th Century may contribute to this gender gap. The present study examined the evidence for a changing depression gap across birth cohorts and tested the extent to which any changes over time were mediated by changes in relative social position between women and men. Data were from the National Longitudinal Surveys. The depression gap was defined as differences in mean CESD scores for women vs. men. The analytic sample included 13,666 respondents interviewed from 1992 to 2014. Hierarchical mixed models estimated the magnitude of the gender depression gap over time, its association with 10-year birth cohort (range: 1957–1994), and whether any variation was mediated by ratios among women relative to men of obtaining a college degree, being employed full-time, and the average number of hours spent doing housework per week, three indicators of gendered social position. There was a linear decrease in the depression gap by 0.18 points across birth cohort (95% CI = −0.26, −0.10). The results of the mediation analysis estimated that an increasing ratio of college degree attainment mediated 39% of the gender depression gap across cohorts (95% CI = 0.18, 0.78). There was no evidence of mediation due to changing employment or housework ratios. These findings partially support the hypothesis that the depression gap is changing over time and is meaningfully related to the social environment. Understanding the social causes of the depression gap can illuminate the fundamental processes through which depression disparities may be perpetuated or attenuated over time and may aid in the identification of strategies to reduce them.
\textlessh2\textgreaterAbstract\textless/h2\textgreater\textlessh3\textgreaterPurpose\textless/h3\textgreater\textlessp\textgreaterSchools provide access to mental health services for traditionally underserved youth. However, there is variability in the types of school-based services students receive (e.g., school counseling, services in separate classrooms, or schools serving students with psychiatric disorders). Prior research has typically not distinguished among these different types of school-based services. The present study examines sociodemographic characteristics and disorders associated with the types of services received in schools.\textless/p\textgreater\textlessh3\textgreaterMethods\textless/h3\textgreater\textlessp\textgreaterData were analyzed from a sample of adolescent–parent pairs in the U.S. National Comorbidity Survey Adolescent Supplement who received school mental health services (N = 1,204). DSM-IV diagnoses were based on the Composite International Diagnostic Interview administered to adolescents and questionnaires self-administered to parents. Adolescents (aged 13–18 years) and parents also responded to questions about lifetime school-based mental health service receipt.\textless/p\textgreater\textlessh3\textgreaterResults\textless/h3\textgreater\textlessp\textgreaterAmong those receiving school-based mental health services, almost one-third (29.7%) received services in a separate classroom and almost one-fourth (22.3%) in a separate school. Increased likelihood of lifetime placement in a separate classroom or school was detected among older youth, males, blacks, Latinos, youth with learning disabilities, those whose parents had fewer years of education, and those who received community-based mental health services. Oppositional defiant disorder was associated with increased lifetime placement in a separate school.\textless/p\textgreater\textlessh3\textgreaterConclusions\textless/h3\textgreater\textlessp\textgreaterThe results advance the evidence base by indicating that racial/ethnic minority youth and those whose parents have fewer years of education were more likely to receive school-based mental health services in separate settings. These results provide more context to studies of school-based mental health service receipt.\textless/p\textgreater