Autonomic nervous system reactivity has been posited to be a mechanism contributing to social and emotional problems among children exposed to early adversity. Leveraging data from the Bucharest Early Intervention Project, a longitudinal randomized controlled trial of foster care versus institutional care of abandoned children in Romania, we assessed whether altered sympathetic reactivity to peer rejection feedback in early adolescence mediated the relation between early institutional rearing and peer problems in later adolescence. We also assessed whether adolescent friendship quality or randomized placement in foster care early in life moderated these associations. Participants include 68 institutionalized children randomized to care as usual, 68 institutionalized children randomized to foster care, and 135 never-institutionalized children. At age 12, participants reported friendship quality with respect to a best friend and completed a social rejection task while electrocardiogram and impedance cardiography were recorded. Sympathetic nervous system reactivity to rejection feedback was assessed using preejection period (PEP). At ages 12 and 16, peer problems were reported by parents. Mediation analysis revealed that less PEP reactivity to social rejection at age 12 partially mediated the association between early institutionalization and greater peer problems at age 16. Further moderated mediation analysis revealed that this indirect effect was evidenced among previously institutionalized youths with low, but not high, quality friendships. We did not observe foster care intervention effects. These findings suggest that altered sympathetic reactivity to social rejection might be a mechanism linking early institutionalization to social difficulties into adolescence, however, positive adolescent friendships may buffer these effects. (PsycInfo Database Record (c) 2022 APA, all rights reserved)
Identifying the potential pathways linking childhood abuse to depression and suicidal ideation is critical for developing effective interventions. This study investigated implicit self-esteem—unconscious valenced self-evaluation—as a potential pathway linking childhood abuse with depression and suicidal ideation. A sample of youth aged 8–16 years (N = 240) completed a self-esteem Implicit Association Test (IAT) and assessments of abuse exposure, and psychopathology symptoms, including depression, suicidal ideation, anxiety, and externalizing symptoms. Psychopathology symptoms were re-assessed 1–3 years later. Childhood abuse was positively associated with baseline and follow-up depression symptoms and suicidal ideation severity, and negatively associated with implicit self-esteem. Lower implicit self-esteem was associated with both depression and suicidal ideation assessed concurrently and predicted significant increases in depression and suicidal ideation over the longitudinal follow-up period. Lower implicit self-esteem was also associated with baseline anxiety, externalizing symptoms, and a general psychopathology factor (i.e. p-factor). We found an indirect effect of childhood abuse on baseline and follow-up depression symptoms and baseline suicidal ideation through implicit self-esteem. These findings point to implicit self-esteem as a potential mechanism linking childhood abuse to depression and suicidal ideation.
Environmental experiences early in life have strong and enduring consequences for cognitive, emotional, and neurobiological development and related physical and mental health trajectories. The powerful influence of early caregiver nurturance and stimulation on promoting positive neurodevelopmental outcomes has been demonstrated across species. These findings elucidate the environmental conditions known to facilitate healthy neurodevelopment and underscore the potential for modifiable psychosocial factors in the environment to be harnessed to inform early preventive interventions to promote health and adaptive development. A framework for early preventive interventions to enhance nurturing and responsive caregiving for implementation during early sensitive periods of brain develop- ment delivered within existing health or educational infrastructures is proposed. Emotional development during sensitive periods is an important, under-recognized, and abundantly modifiable predictor of mental and physical health outcomes that warrants investment of resources and integration of interventions into public health infra- structure for children worldwide. Future studies are needed to further clarify whether and when sensitive periods are present for key developmental domains to inform the optimal timing and targets of these interventions. Numerous available empirically supported early interventions may be modified and applied in briefer and more feasible mo- dalities of delivery to broader populations of developing children. As well established in growth and development across species, essential environmental inputs that are particularly important at specified developmental periods facilitate optimal growth trajectories. Such principles hold great potential in application to early child neuro- development to facilitate a thriving and resilient human population.
The COVID-19 pandemic has introduced widespread societal changes that have required ongoing adaptation. Unsurprisingly, stress-related psychopathology has increased during the pandemic, in both children and adults. We review these patterns through the lens of several leading conceptual models of the link between stress and psychopathology. Some of these models focus on characteristics of environmental stressors—including cumulative risk, specific stressor types, and stress sensitization approaches. Understanding the specific aspects of environmental stressors that are most likely to lead to psychopathology can shed light on who may be in most need of clinical intervention. Other models center on factors that can buffer against the onset of psychopathology following stress and the mechanisms through which stressors contribute to emergent psychopathology. These models highlight specific psychosocial processes that may be most usefully targeted by interventions to reduce stress-related psychopathology. We review evidence for each of these stress models in the context of other widescale community-level disruptions, like natural disasters and terrorist attacks, alongside emerging evidence for these stress pathways from the COVID-19 pandemic. We discuss clinical implications for developing interventions to reduce stress-related psychopathology during the pandemic, with a focus on brief, digital interventions that may be more accessible than traditional clinical services.
The central goal of clinical psychology is to reduce the suffering caused by mental health conditions. Anxiety, mood, psychosis, substance use, personality, and other mental disorders impose an immense burden on global public health and the economy. Tackling this burden will require the development and dissemination of intervention strategies that are more effective, sustainable, and equitable. Clinical psychology is uniquely poised to serve as a transdisciplinary hub for this work. But rising to this challengerequires an honest reckoning with the strengths and weaknesses of current training practices. Building on new data, we identify the most important challenges to training the next generation of clinical scientists. We provide specific recommendations for the full spectrum of stakeholders—from funders, accreditors, and universities to program directors, faculty, and students—with an emphasis on sustainable solutions that promote scientific rigor and discovery and enhance the mental health of clinical scientists and the public alike.
Exposure to childhood adversity has been consistently associated with poor devel- opmental outcomes, but it is unclear whether these associations vary across dif- ferent forms of adversity. We examined cross-sectional and longitudinal associa- tions between threat and deprivation with cognition, emotional processing, and psy- chopathology in a middle-income country. The sample consisted of 2511 children and adolescents (6–17 years old) from the Brazilian High-Risk Cohort for Mental Condi- tions. Parent reports on childhood adversity were used to construct adversity latent constructs. Psychopathology was measured by the Child Behavior Checklist (CBCL) to generate a measure of general psychopathology (the “p” factor). Executive function (EF) and attention orienting toward angry faces were assessed using cognitive tasks. All measures were acquired at two time-points 3 years apart and associations were tested using general linear models. Higher levels of psychopathology were predicted by higher levels of threat cross-sectionally and longitudinally, and by deprivation longi- tudinally. For EF, worse performance was associated only with deprivation at baseline and follow-up. Finally, threat was associated with attention orienting towards angry faces cross-sectionally, but neither form of adversity was associated with changes over time in attention bias. Our results suggest that threat and deprivation have dif- ferential associations with cognitive development and psychopathology. Exposure to adversity during childhood is a complex phenomenon with meaningful influences on child development. Because adversity can take many forms, dimensional models might help to disentangle the specific developmental correlates of different types of early experience. A video abstract of this article can be viewed at https://www.youtube.com/ watch?v=uEU0L8exyTM.
Exposure to early-life adversity (ELA) is associated with elevated risk for depression and anxiety disorders in adolescence. Identifying mechanisms through which ELA contributes to the emergence of depression and anxiety is necessary to design preventive interventions. One potential mechanism linking exposure to ELA with psychopathology is accelerated pubertal development. Exposure to trauma—specifically interpersonal violence—is associated with earlier pubertal timing, which in turn predicts adolescent-onset depression and anxiety disorders. We review the recent literature on adversity and accelerated pubertal development, exploring specific associations between trauma and accelerated pubertal development as a mechanism linking adversity with depression and anxiety disorders in adolescence. Finally, we suggest future directions for research exploring mechanisms linking ELA with accelerated pubertal development as well as pubertal timing and psychopathology in adolescence.
Background: Altered DNA methylation (DNAm) may be one pathway through which early-life adversity (ELA) contributes to adverse mental and physical health outcomes. This study investigated whether the presence versus absence of ELA experiences reflecting the dimensions of threat and deprivation were associated with epigenome- wide DNAm cross-sectionally and longitudinally in a community-based sample of children and adolescents.
Methods: In 113 youths aged 8–16 years with wide variability in ELA, we examined associations of abuse (physical, sexual, emotional; indicating threat-related experiences) and neglect (emotional, physical; indicating deprivation- related experiences) with DNAm assessed with the Illumina EPIC BeadChip array, with DNA derived from saliva. In cross-sectional epigenome-wide analyses, we investigated associations of lifetime abuse and neglect with DNAm at baseline. In longitudinal epigenome-wide analyses, we examined whether experiencing abuse and neglect over an approximately 2-year follow-up were each associated with change in DNAm from baseline to follow-up.
Results: In cross-sectional analyses adjusting for lifetime experience of neglect, lifetime experience of abuse was associated with DNAm for four cytosine-phosphodiester-guanine (CpG) sites (cg20241299: coefficient = 0.023, SE = 0.004; cg08671764: coefficient = 0.018, SE = 0.003; cg27152686: coefficient = − 0.069, SE = 0.012; cg24241897: coefficient = − 0.003, SE = 0.001; FDR < .05). In longitudinal analyses, experiencing neglect over follow-up was associ- ated with an increase in DNAm for one CpG site, adjusting for abuse over follow-up (cg03135983: coefficient = 0.036, SE = 0.006; FDR < .05).
Conclusions: In this study, we identified examples of epigenetic patterns associated with ELA experiences of threat and deprivation that were already observable in youth. We provide novel evidence for change in DNAm over time in relation to ongoing adversity and that experiences reflecting distinct ELA dimensions may be characterized by unique epigenetic patterns.
Keywords: Threat, Deprivation, Abuse, Neglect, DNA methylation
Background: Posttraumatic stress disorder (PTSD) is accompanied by disrupted cortical neuroanatomy. We investigated alteration in covariance of structural networks associated with PTSD in regions that demonstrate the case-control differences in cortical thickness (CT) and surface area (SA).
Methods: Neuroimaging and clinical data were aggregated from 29 research sites in >1,300 PTSD cases and >2,000 trauma-exposed controls (age 6.2-85.2 years) by the ENIGMA-PGC PTSD working group. Cortical regions in the network were rank-ordered by effect size of PTSD- related cortical differences in CT and SA. The top-n (n = 2 to 148) regions with the largest effect size for PTSD > non-PTSD formed hypertrophic networks, the largest effect size for PTSD < non-PTSD formed atrophic networks, and the smallest effect size of between-group differences formed stable networks. The mean structural covariance (SC) of a given n-region network was the average of all positive pairwise correlations and was compared to the mean SC of 5,000 randomly generated n-region networks.
Results: Patients with PTSD, relative to non-PTSD controls, exhibited lower mean SC in CT- based and SA-based atrophic networks. Comorbid depression, sex and age modulated covariance differences of PTSD-related structural networks.
Conclusions: Covariance of structural networks based on CT and cortical SA are affected by PTSD and further modulated by comorbid depression, sex, and age. The structural covariance networks that are perturbed in PTSD comport with converging evidence from resting state functional connectivity networks and networks impacted by inflammatory processes, and stress hormones in PTSD.
This study examined whether COVID-19-related maternal mental health changes contributed to changes in adolescent psychopathology.
A community sample of 226 adolescents (12 years old before COVID-19) and their mothers were asked to complete COVID-19 surveys early in the pandemic (April–May 2020, adolescents 14 years) and approximately 6 months later (November 2020–January 2021). Surveys assessed pandemic-related stressors (health, financial, social, school, environment) and mental health.
Lower pre-pandemic family income-to-needs ratio was associated with higher pre-pandemic maternal mental health symptoms (anxiety, depression) and adolescent internalizing and externalizing problems, and with experiencing more pandemic-related stressors. Pandemic-related stressors predicted increases in maternal mental health symptoms, but not adolescent symptoms when other variables were covaried. Higher maternal mental health symptoms predicted concurrent increases in adolescent internalizing and externalizing. Maternal mental health mediated the effects of pre-pandemic income and pandemic-related stressors on adolescent internalizing and externalizing problems.
Results indicate that adolescent mental health is closely tied to maternal mental health during community-level stressors such as COVID-19, and that pre-existing family economic context and adolescent symptoms increase risk for elevations in symptoms of psychopathology.
Two extant frameworks – the harshness-unpredictability model and the threat-deprivation model – attempt to explain which dimensions of adversity have distinct influences on development. These models address, respectively, why, based on a history of natural selection, develop- ment operates the way it does across a range of environmental contexts, and how the neural mechanisms that underlie plasticity and learning in response to environmental experiences influence brain development. Building on these frameworks, we advance an integrated model of dimensions of environmental experience, focusing on threat-based forms of harshness, deprivation-based forms of harshness, and environ- mental unpredictability. This integrated model makes clear that the why and the how of development are inextricable and, together, essential to understanding which dimensions of the environment matter. Core integrative concepts include the directedness of learning, multiple levels of developmental adaptation to the environment, and tradeoffs between adaptive and maladaptive developmental responses to adversity. The integrated model proposes that proximal and distal cues to threat-based and deprivation-based forms of harshness, as well as unpredictability in those cues, calibrate development to both immediate rearing environments and broader ecological contexts, current and future. We high- light actionable directions for research needed to investigate the integrated model and advance understanding of dimensions of environmental experience.
Altered aversive learning represents a potential mechanism through which childhood trauma (CT) might influence risk for psychopathology. This study examines the temporal dynamics of neural activation and patterns of functional connectivity during aversive learning in children with and without exposure to CT involving interpersonal violence and evaluates whether these neural patterns mediate the association of CT with psychopathology in a longitudinal design.
Childhood socioeconomic status (SES) is related to disparities in the development of both language and executive functioning (EF) skills. Emerging evidence suggests that language development may precede and provide necessary scaffolding for EF development in early childhood. The present preregistered study investigates how these skills co-develop longitudinally in early childhood and whether language development explains the relationship between SES and EF development. A socioeconomically diverse sample of 305 children completed repeated assessments of language (sentence comprehension) and EF (cognitive flexibility, behavioral inhibition, and cognitive inhibition) at four waves spaced 9 months apart from ages 3 to 5 years. Bivariate latent curve models with structured residuals were estimated to disaggregate between-person and within-person components of stability and change. Results revealed bidirectional relationships between language and EF across all waves. However, at 3 years, language comprehension more strongly predicted EF than the reverse; yet by 5 years, the bidirectional effects across domains did not significantly differ. Children from higher-SES backgrounds exhibited higher initial language and EF skills than children from lower-SES families, though SES was not associated with either rate of growth. Finally, early language-mediated the association between SES and early EF skills, and this model outperformed a reverse direction mediation. Together, results suggest that EF development is driven by early language development, and that SES disparities in EF are explained, at least in part, by early differences in language comprehension. These findings have implications for early interventions to support children's language skills as a potential pathway to improving early EF development.
Low childhood socioeconomic status (SES) is associated with increased risk for psychopathology, because in part of heightened exposure to environmental adversity. Adverse experiences can be characterized along dimensions, including threat and deprivation, that contribute to psychopathology via distinct mechanisms. The current study investigated a neural mechanism through which threat and deprivation may contribute to socioeconomic disparities in psychopathology. Participants were 177 youths (83 girls) aged 10-13 years recruited from a cohort followed since the age of 3 years. SES was assessed using the income-to-needs ratio at the age of 3 years. At the age of 10-13 years, retrospective and current exposure to adverse experiences and symptoms of psychopathology were assessed. At this same time point, participants also completed a face processing task (passive viewing of fearful and neutral faces) during an fMRI scan. Lower childhood SES was associated with greater exposure to threat and deprivation experiences. Both threat and deprivation were associated with higher depression symptoms, whereas threat experiences were uniquely linked to posttraumatic stress disorder symptoms. Greater exposure to threat, but not deprivation, was associated with higher activation in dorsomedial pFC to fearful compared with neutral faces. The dorsomedial pFC is a hub of the default mode network thought to be involved in internally directed attention and cognition. Experiences of threat, but not deprivation, are associated with greater engagement of this region in response to threat cues. Threat-related adversity contributes to socioeconomic disparities in adolescent psychopathology through distinct mechanisms from deprivation.
Despite the clear importance of a developmental perspective for understanding the emergence of psychopathology across the life-course, such a perspective has yet to be integrated into the RDoC model. In this paper, we articulate a framework that incorporates developmentally-specific learning mechanisms that reflect experience-driven plasticity as additional units of analysis in the existing RDoC matrix. These include both experience-expectant learning mechanisms that occur during sensitive periods of development and experience-dependent learning mechanisms that may exhibit substantial variation across development. Incorporating these learning mechanisms allows for clear integration not only of development but also environmental experience into the RDoC model. We demonstrate how individual differences in environmental experiences—such as early-life adversity—can be leveraged to identify experience-driven plasticity patterns across development and apply this framework to consider how environmental experience shapes key biobehavioral processes that comprise the RDoC model. This framework provides a structure for understanding how affective, cognitive, social, and neurobiological processes are shaped by experience across development and ultimately contribute to the emergence of psychopathology. We demonstrate how incorporating an experience-driven plasticity framework is critical for understanding the development of many processes subsumed within the RDoC model, which will contribute to greater understanding of developmental variation in the etiology of psychopathology and can be leveraged to identify potential windows of heightened developmental plasticity when clinical interventions might be maximally efficacious.
To determine whether structural and individual forms of stigma are associated with neurodevelopment in children.
Stigma related to gender, race, and Latinx ethnicity was measured at the structural level using objective state-level indicators of social policies and prejudicial attitudes and at the individual level using self-reports of perceived discrimination. Respective associations of stigma with hippocampal volume and amygdala reactivity to threat were examined using data from the Adolescent Brain Cognitive Development (ABCD) Study (N = 11,534, mean age 9.9 years), the first multisite neuroimaging study that provided substantial variability in sociopolitical contexts and that included individual-level measures of stigma among youth.
In a preregistered analysis, Black (B = −58.26, p = .023) and Latinx (B = −40.10, p = .044) youths in higher (vs lower) structural stigma contexts were found to have smaller hippocampal volume, controlling for total intracranial volume, demographics, and family socioeconomic status. This association was also observed at a trend-level among girls (p = .082). The magnitude of the difference in hippocampal volume between high and low structural stigma states was equivalent to the predicted impact of a $20,000 difference in annual family income in this sample. As hypothesized, structural stigma was not associated with hippocampal volume in nonstigmatized youths, providing evidence of specificity. Perceived discrimination was unrelated to hippocampal volume in stigmatized groups. No associations between perceived discrimination or structural stigma and amygdala reactivity to threat were observed.
This study provides novel evidence that an objective measure of structural stigma may be more strongly related to hippocampal volume than subjective perceptions of stigma, suggesting that contextual approaches to stigma could yield new insights into neurodevelopment among marginalized youth.
Over the past decade extensive research has examined the segregation of the human brain into large-scale functional networks. The resulting network maps, i.e. parcellations, are now commonly used for the a priori identification of functional networks. However, the use of these parcellations, particularly in developmental and clinical samples, hinges on four fundamental assumptions: (1) the various parcellations are equally able to recover the networks of interest; (2) adult-derived parcellations well represent the networks in children's brains; (3) network properties, such as within-network connectivity, are reliably measured across parcellations; and (4) parcellation selection does not impact the results with regard to individual differences in given network properties. In the present study we examined these assumptions using eight common parcellation schemes in two independent developmental samples. We found that the parcellations are equally able to capture networks of interest in both children and adults. However, networks bearing the same name across parcellations (e.g., default network) do not produce reliable within-network measures of functional connectivity. Critically, parcellation selection significantly impacted the magnitude of associations of functional connectivity with age, poverty, and cognitive ability, producing meaningful differences in interpretation of individual differences in functional connectivity based on parcellation choice. Our findings suggest that work employing parcellations may benefit from the use of multiple schemes to confirm the robustness and generalizability of results. Furthermore, researchers looking to gain insight into functional networks may benefit from employing more nuanced network identification approaches such as using densely-sampled data to produce individual-derived network parcellations. A transition towards precision neuroscience will provide new avenues in the characterization of functional brain organization across development and within clinical populations.
Objective: Childhood abuse represents one of the most potent risk factors for developing psychopathology, espe- cially in females. Evidence suggests that exposure to early-life adversity may be related to advanced maturation of emotion processing neural circuits. However, it remains unknown whether abuse is related to early circuit matura- tion and whether maturation patterns depend on the pres- ence of psychopathology.
Methods: A multisite sample of 234 girls (ages 8–18 years) completed clinical assessment, maltreatment histories, and high-resolution T1-weighted structural MRI. Girls were stratified by abuse history and internalizing disorder diag- nosis into typically developing (no abuse/no diagnosis), resilient (abuse/no diagnosis), and susceptible (abuse/ current diagnosis) groups. Machine learning models of nor- mative brain development were aggregated in a stacked generalization framework trained to predict chronological age using gray matter volume in whole-brain, emotion, and language circuit parcellations. Brain age gap estima- tions (BrainAGEs; predicted age minus true chronological age) were calculated as indices of relative circuit maturation.
Results: Childhood abuse was related to reduced Brain- AGE (delayed maturation) specific to emotion circuits. Delayed emotion circuit BrainAGE was further related to increased hyperarousal symptoms. Childhood physical neglect was associated with increased whole-brain BrainAGE (advanced maturation). Neural contributors to emotion circuit BrainAGE differed in girls with and with- out an internalizing diagnosis, especially in the lateral prefrontal, parietal, and insular cortices and the hippocampus.
Conclusions: Abuse exposure in girls is associated with a delayed structural maturation pattern specific to emotion circuitry, a potentially adaptive mechanism enhancing threat generalization. Physical neglect, on the other hand, is associated with a broader brain-wide pattern of advanced structural maturation. The differential influence of fronto- parietal cortices and the hippocampus on emotion circuit maturity in resilient girls may represent neurodeve- lopmental markers of reduced psychiatric risk following abuse.
The volume of subcortical structures represents a reliable, quantitative, and objective phenotype that captures genetic effects, environmental effects such as trauma, and disease effects such as posttraumatic stress disorder (PTSD). Trauma and PTSD represent potent exposures that may interact with genetic markers to influence brain structure and function. Genetic variants, associated with subcortical volumes in two large normative discovery samples, were used to compute polygenic scores (PGS) for the volume of seven subcortical structures. These were applied to a target sample enriched for childhood trauma and PTSD. Subcortical volume PGS from the discovery sample were strongly associated in our trauma/PTSD enriched sample (n = 7580) with respective subcortical volumes of the hippocampus (p = 1.10 × 10−20), thalamus (p = 7.46 × 10−10), caudate (p = 1.97 × 10−18), putamen (p = 1.7 × 10−12), and nucleus accumbens (p = 1.99 × 10−7). We found a significant association between the hippocampal volume PGS and hippocampal volume in control subjects from our sample, but was absent in individuals with PTSD (GxE; (beta = −0.10, p = 0.027)). This significant GxE (PGS × PTSD) relationship persisted (p < 1 × 10−19) in four out of five threshold peaks (0.024, 0.133, 0.487, 0.730, and 0.889) used to calculate hippocampal volume PGSs. We detected similar GxE (G × ChildTrauma) relationships in the amygdala for exposure to childhood trauma (rs4702973; p = 2.16 × 10−7) or PTSD (rs10861272; p = 1.78 × 10−6) in the CHST11 gene. The hippocampus and amygdala are pivotal brain structures in mediating PTSD symptomatology. Trauma exposure and PTSD modulate the effect of polygenic markers on hippocampal volume (GxE) and the amygdala volume PGS is associated with PTSD risk, which supports the role of amygdala volume as a risk factor for PTSD.
Children from low-socioeconomic status (SES) households on average exhibit lower academic achievement than their higher-SES peers. We investigated a novel hypothesis that differences in early-developing sensory networks—specifically the ventral visual stream (VVS), which is involved in processing visual stimuli—contribute to SES-related disparities in executive functions (EF) and academic outcomes. We used fMRI to investigate SES-related differences in neural function in children (6–8 years, n = 62) during two attentional tasks involving attention to visual information: cued attention and memory-guided attention. Recruitment of VVS during both tasks was associated with EF and academic achievement, and SES-related differences in VVS activation during cued attention were marginally explained by differences in cognitive stimulation. VVS activation during cued attention mediated SES-related differences in academic achievement. Finally, the link between VVS activation during both tasks and academic achievement was mediated by differences in EF. We extend previous work by highlighting that: (i) early-developing visual processing regions play a role in supporting complex attentional processes, (ii) childhood SES is associated with VVS function, which is explained in part by SES-related differences in cognitive stimulation and (iii) provide preliminary evidence that individual differences in VVS function may play a role in the emergence of the income-achievement gap.