Exposure to chronic or severe stressful life events during childhood and adolescence—frequently referred to as early life stress (ELS) or childhood adversity—has powerful andlasting associations with psychopathology across the life course. This chapter reviews thegrowing body of research on ELS and psychopathology across the life course, with aparticular focus on the mechanisms that explain the strong associations between ELS andpsychopathology. To address these questions, I review evidence on the links between ELSand psychopathology and highlight divergent conceptual models of ELS that advocatedifferent approaches to uncovering these mechanisms. I end by addressing differentapproaches to the measurement and analysis of ELS that have emerged from theseconceptual frameworks.

Low socioeconomic status (SES) is associated with greater risk for symptoms of attention-deficit/hyperactivity disorder (ADHD). One mechanism through which SES may confer risk for ADHD is by influencing brain structure. Alterations to cortical thickness, surface area and subcortical volume have been associated with low SES and with the presence of ADHD across multiple studies. The current study examined whether cortical thickness, surface area or subcortical volume mediate the associations between SES and ADHD in youth 3–21 years old (N = 874) from the Pediatric Imaging, Neurocognition and Genetics Study. Freesurfer was used to estimate cortical thickness, surface area and subcortical volume from structural magnetic resonance imaging. Parents reported on demographics, family SES, ADHD diagnoses and the presence of child attention problems. Statistical mediation was assessed using a bootstrap resampling procedure. Controlling for parental ADHD, child age, gender, birth weight and scanner, children in low SES families were more likely to be in the ADHD group. Consistent with previous reports in this sample, low SES was associated with reduced surface area across the frontal lobe and reduced subcortical volume in the amygdala, cerebellum, hippocampus and basal ganglia. Of these regions, a significant indirect effect of SES on ADHD status through subcortical volume was observed for the left cerebellum (95% confidence interval: 0.004, 0.022), the right cerebellum (95% confidence interval: 0.006, 0.025), and the right caudate (95% confidence interval: 0.002, 0.022). Environmentally mediated changes in the cerebellum and the caudate may be neurodevelopmental mechanisms explaining elevated risk of ADHD in children in low SES families.

Background

Adolescence is characterized by substantial changes in sleep behavior, heightened exposure to stressful life events (SLEs), and elevated risk for internalizing problems like anxiety and depression. Although SLEs are consistently associated with the onset of internalizing psychopathology, the mechanisms underlying this relationship remain poorly understood, especially at the within-person level. Here, we leverage a high-frequency longitudinal design to examine sleep as a potential mechanism linking SLEs to increases in anxiety and depression symptoms over a one-year period.

Methods

Thirty female adolescents aged 15–17 years completed 12 monthly in-laboratory assessments of exposure to SLEs and symptoms of anxiety and depression (n = 355 monthly assessments), and wore an actigraphy wristband for continuous monitoring of sleep for the duration of the study (n = 6,824 sleep days). Multilevel models examined concurrent and lagged within-person associations between SLEs, sleep duration and timing regularity, and anxiety and depression symptoms.

Results

Within-person fluctuations in SLEs were associated with variability in sleep duration both concurrently and prospectively, such that when adolescents experienced greater SLEs than was typical for them, they exhibited more variable sleep duration that same month as well as the following month. In turn, within-person increases in sleep duration variability predicted greater anxiety symptoms in the same month and mediated the association between SLEs and anxiety.

Conclusions

These findings highlight sleep disruptions as a mechanism underlying the longitudinal associations between SLEs and anxiety symptoms, and suggest that interventions promoting sleep schedule consistency may help mitigate risk for stress-related psychopathology in adolescence.

Exposure to childhood adversity is common and associated with a host of negative developmental outcomes. The most common approach used to examine the consequences of adversity exposure is a cumulative risk model. Recently, we have proposed a novel approach, the dimensional model of adversity and psychopathology (DMAP), where different dimensions of adversity are hypothesized to impact health and well-being through different pathways. We expect deprivation to primarily disrupt cognitive processing, whereas we expect threat to primarily alter emotional reactivity and automatic regulation. Recent hypothesis-driven approaches provide support for these differential associations of deprivation and threat on developmental outcomes. However, it is not clear whether these patterns would emerge using data-driven approaches. Here we use a network analytic approach to identify clusters of related adversity exposures and outcomes in an initial study (Study 1: N = 277 adolescents aged 16–17 years; 55.1% female) and a replication (Study 2: N = 262 children aged 8–16 years; 45.4% female). We statistically compare our observed clusters with our hypothesized DMAP model and a clustering we hypothesize would be the result of a cumulative stress model. In both samples we observed a network structure consistent with the DMAP model and statistically different than the hypothesized cumulative stress model. Future work seeking to identify in the pathways through which adversity impacts development should consider multiple dimensions of adversity.

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.

Studies of posttraumatic stress disorder (PTSD) report volume abnormalities in multiple regions of the cerebral cortex. However, findings for many regions, particularly regions outside commonly studied emotion-related prefrontal, insular, and limbic regions, are inconsistent and tentative. Also, few studies address the possibility that PTSD abnormalities may be confounded by comorbid depression. A mega-analysis investigating all cortical regions in a large sample of PTSD and control subjects can potentially provide new insight into these issues. Given this perspective, our group aggregated regional volumes data of 68 cortical regions across both hemispheres from 1379 PTSD patients to 2192 controls without PTSD after data were processed by 32 international laboratories using ENIGMA standardized procedures. We examined whether regional cortical volumes were different in PTSD vs. controls, were associated with posttraumatic stress symptom (PTSS) severity, or were affected by comorbid depression. Volumes of left and right lateral orbitofrontal gyri (LOFG), left superior temporal gyrus, and right insular, lingual and superior parietal gyri were significantly smaller, on average, in PTSD patients than controls (standardized coefficients = −0.111 to −0.068, FDR corrected P values \textless 0.039) and were significantly negatively correlated with PTSS severity. After adjusting for depression symptoms, the PTSD findings in left and right LOFG remained significant. These findings indicate that cortical volumes in PTSD patients are smaller in prefrontal regulatory regions, as well as in broader emotion and sensory processing cortical regions.

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

Transdiagnostic processes confer risk for multiple types of psychopathology and explain the co-occurrence of different disorders. For this reason, transdiagnostic processes provide ideal targets for early intervention and treatment. Childhood trauma exposure is associated with elevated risk for virtually all commonly occurring forms of psychopathology. We articulate a transdiagnostic model of the developmental mechanisms that explain the strong links between childhood trauma and psychopathology as well as protective factors that promote resilience against multiple forms of psychopathology. We present a model of transdiagnostic mechanisms spanning three broad domains: social information processing, emotional processing, and accelerated biological aging. Changes in social information processing that prioritize threat-related information—such as heightened perceptual sensitivity to threat, misclassification of negative and neutral emotions as anger, and attention biases towards threat-related cues—have been consistently observed in children who have experienced trauma. Patterns of emotional processing common in children exposed to trauma include elevated emotional reactivity to threat-related stimuli, low emotional awareness, and difficulties with emotional learning and emotion regulation. More recently, a pattern of accelerated aging across multiple biological metrics, including pubertal development and cellular aging, has been found in trauma-exposed children. Although these changes in social information processing, emotional responding, and the pace of biological aging reflect developmental adaptations that may promote safety and provide other benefits for children raised in dangerous environments, they have been consistently associated with the emergence of multiple forms of internalizing and externalizing psychopathology and explain the link between childhood trauma exposure and transdiagnostic psychopathology. Children with higher levels of social support, particularly from caregivers, are less likely to develop psychopathology following trauma exposure. Caregiver buffering of threat-related processing may be one mechanism explaining this protective effect. Childhood trauma exposure is a powerful transdiagnostic risk factor associated with elevated risk for multiple forms of psychopathology across development. Changes in threat-related social and emotional processing and accelerated biological aging serve as transdiagnostic mechanisms linking childhood trauma with psychopathology. These transdiagnostic mechanisms represent critical targets for early interventions aimed at preventing the emergence of psychopathology in children who have experienced trauma.

This study examines racial/ethnic differences in perceived need for mental health treatment, barriers to treatment receipt, and reasons for dropout. Data are from the Collaborative Psychiatric Epidemiology Studies, a pooled dataset from three U.S. nationally-representative adult samples. Among respondents with a 12-month psychiatric disorder who received no treatment (N = 1417), Asians and Latinos reported lower perceived need than Blacks and Whites, and Latinos reported the fewest attitudinal barriers. Among those with a 12-month disorder who dropped out of treatment, Asians and Latinos gave more reasons for dropping out. Significant interactions of race/ethnicity with other characteristics identified subpopulations with high unmet need.

This study examined two facets of emotion development: emotion word comprehension (knowing the meaning of emotion words such as “anger” or “excitement”) and emotion concept abstraction (representing emotions in terms of internal psychological states that generalize across situations). Using a novel emotion vocabulary assessment, we captured how a cross-sectional sample of participants aged 4-25 (N=196) defined 24 emotions. Smoothing spline regression models suggested that emotion comprehension followed an emergent shape: knowledge of emotion words increased across childhood and plateaued around age 11. Human coders rated the abstractness of participants’ responses, and these ratings also followed an emergent shape but plateaued significantly later than comprehension, around age 18. An automated linguistic analysis of abstractness supported coders’ perceptions of increased abstractness across age. Finally, coders assessed the definitional “strategies” participants used to describe emotions. Young children tended to describe emotions using concrete strategies such as providing example situations that evoked those emotions or by referring to physiological markers of emotional experiences. Whereas use of these concrete strategies decreased with age, the tendency to use more abstract strategies such as providing general definitions that delineated the causes and characteristics of emotions or by providing synonyms of emotion words increased with age. Overall, this work (i) provides a tool for assessing definitions of emotion terms, (ii) demonstrates that emotion concept abstraction increases across age, and (iii) suggests that adolescence is a period in which emotion words are comprehended but their level of abstraction continues to mature.

{BackgroundAlthough early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA – threat and deprivation – have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology.MethodsData were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders.ResultsGreater exposure to threat was associated with earlier AAM (B = −0.1

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.