Publications by Year: 2022

2022
Kim, H. H., McLaughlin, K., Chibnik, L. B., Koenen, K. C., & Timelier, H. (2022). Poverty, Cortical Structure, and Psychopathologic Characteristics in Adolescence. JAMA Network Open , 5 (11), 1-12. Publisher's VersionAbstract

IMPORTANCE Childhood poverty has been associated with increased internalizing and externalizing problems in adolescence, a period of peak onset for psychiatric problems. The underlying neural mechanisms remain unclear because longitudinal studies of poverty, brain structure, and changes in psychiatric symptoms are lacking.

OBJECTIVE To examine whether structural differences in cortical regions mediate the association between household poverty and change in psychiatric symptoms in early adolescence.

DESIGN, SETTING, AND PARTICIPANTS This longitudinal cohort study used baseline and 1-year follow-up data from the Adolescent Brain Cognitive Development Study. Children aged 9 to 10 years in the US were enrolled between September 1, 2016, and October 15, 2018. Data analysis was performed from August 13, 2021, to September 30, 2022.

EXPOSURES Household poverty as measured by income-to-needs ratio, which incorporates family income and adjusts for family size as a percentage of the federal poverty level.

MAIN OUTCOMES AND MEASURES Mediators were children’s cortical surface area, thickness, and

volume, obtained usingmagnetic resonance imaging. Internalizing and externalizing problems at

1-year follow-up were outcomes measured by maternal report using the Child Behavior Checklist. Analyses were adjusted for baseline psychiatric problems and sociodemographic variables, including sex, race and ethnicity, parental educational level, and study site.

RESULTS Of the 7569 children (mean [SD] age, 9.91 [0.62] years; 3970 boys [52.5%]) included in the analysis, 1042 children (13.8%) lived below the poverty threshold between 2016 and 2018. Poverty was associated with increased externalizing symptoms score at 1-year follow-up (b = 1.57; 95%CI, 1.14-1.99), even after adjustment for baseline externalizing symptoms (b = 0.35; 95%CI, 0.06-0.64). The longitudinal associations of poverty with increases in externalizing problems over time were mediated by reductions in surface area in multiple cortical regions that support executive functioning (middle frontal gyrus), decision-making (lateral orbitofrontal cortex), visual processing (fusiform gyrus), auditory processing (transverse temporal gyrus), and emotion and language processing (superior temporal gyrus).

CONCLUSIONS AND RELEVANCE The findings of this study suggest that childhood poverty is associated with increases in externalizing problems, but not internalizing problems, over time in early adolescence. This association is mediated by reductions in cortical surface area across numerous brain regions. These findings highlight potential neurobiological mechanisms underlying the link between poverty and the emergence of externalizing problems during early adolescence.

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Berman, I., McLaughlin, K., Tottenham, N., Godfrey, K., Seeman, T., Loucks, E., Soumi, S., et al. (2022). Measuring early life adversity: A dimensional approach . Development and Psychopathology , 34 (2), 499 - 511. Publisher's VersionAbstract

Exposure to adversity in childhood is associated with elevations in numerous physical and mental health outcomes across the life course. The biological embedding of early experience during periods of developmental plasticity is one pathway that contributes to these associations. Dimensional models specify mechanistic pathways linking different dimensions of adversity to health and well-being outcomes later in life. While findings from existing studies testing these dimensions have provided promising preliminary support for these models, less agreement exists about how to measure the experiences that comprise each dimension. Here, we review existing approaches to measuring two dimensions of adversity: threat and deprivation. We recommend specific measures for measuring these constructs and, when possible, document when the same measure can be used by different reporters and across the lifespan to maximize the utility with which these recommendations can be applied. Through this approach, we hope to stimulate progress in understanding how particular dimensions of early environmental experience contribute to lifelong health.

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Sheridan, M., Mukerji, C., Wade, M., Humphreys, K., Garrisi, K., Goel, S., Patel, K., et al. (2022). Early deprivation alters structural brain developmentfrom middle childhood to adolescence. Science Advances , 1-13. Publisher's VersionAbstract

Hypotheses concerning the biologic embedding of early adversity via developmental neuroplasticity mechanisms have been proposed on the basis of experimental studies in animals. However, no studies have demonstrated a causal link between early adversity and neural development in humans. Here, we present evidence from a randomized controlled trial linking psychosocial deprivation in early childhood to changes in cortical development from childhood to adolescence using longitudinal data from the Bucharest Early Intervention Project. Changes in cortical structure due to randomization to foster care were most pronounced in the lateral and medial prefrontal cortex and in white matter tracts connecting the prefrontal and parietal cortex. Demonstrating the causal impact of exposure to deprivation on the development of neural structure highlights the importance of early placement into family-based care to mitigate lasting neurodevelopmental consequences associated with early-life deprivation.

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Humphreys, K., King, L., Guyon-Harris, K., Sheridan, M., McLaughlin, K., Radulescu, A., Nelson, C., et al. (2022). Foster care leads to sustained cognitive gains following severeearly deprivation. Proceedings of the National Academy of Sciences , 119 (38), 1-6. Publisher's VersionAbstract

This study examined longitudinal data from the Bucharest Early Intervention Project, a randomized controlled trial of foster care as an alternative to institutional care following exposure to severe psychosocial deprivation. We report data from 135 participants assessed in early adulthood (age 18 y). We find that 16 y after randomization occurred, those who had been randomized to high-quality foster care had significantly higher IQ scores (9 points, 0.6 SD) than those randomized to care as usual. Mediation analyses provide evidence that the causal effect of the intervention on cognitive ability in early adulthood could be explained, in part, by higher-quality caregiving and attachment security. These findings indicate that early investment in family care as an alternative to institutional care leads to sustained gains in cognitive ability. Fostering caregiving relationships is a likely mechanism of the intervention. In addition, exploratory analyses indicate that stable placements throughout childhood are associated with the greatest long-term gains in cognitive ability. Whether early interventions for infants and young children lead to lasting change has significant implications for decisions to invest in programs aimed at improving children’s developmental outcomes.

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Wade, M., Parsons, J., Humphreys, K., McLaughlin, K., Sheridan, M., Zeanah, C., Nelson, C., et al. (2022). The Bucharest Early Intervention Project: Adolescent mental health and adaptation following early deprivation. Child Development Perspectives , 154 - 164. Publisher's VersionAbstract

 

Over the last 20 years, we have learned much about the extent to which early-life deprivation affects the mental health of children and adolescents. This body of evidence comes predominantly from studies of children raised in institutional care. The Bucharest Early Intervention Project (BEIP) is the only randomized controlled trial designed to evaluate whether the transition to family-based foster care early in development can ameliorate the long-term impact of institutional deprivation on psychopathology during vulnerable developmental windows such as adolescence. In this review, we detail the extent to which early deprivation affects mental health during this period, the capacity of family-based care to facilitate recovery from early deprivation, and the mechanisms underpinning these effects spanning social–emotional, cognitive, stress, and neurobiological domains. We end by discussing the implications and directions for the BEIP and other studies of youth raised in institutions.

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McLaughlin, K., Rosen, M., Kasparek, S., & Rodman, A. (2022). Stress-related psychopathology during the COVID-19 pandemic. Behaviour Research and Therapy , 154, 1-11. Publisher's VersionAbstract
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.
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Maihofer, A. X., & et. al,. (2022). Enhancing discovery of genetic variants for posttraumatic stress disorder through integration of quantitative phenotypes and trauma exposure information. Biological Psychiatry , 91 (7), 626 - 636. Publisher's VersionAbstract

Background

Posttraumatic stress disorder (PTSD) is heritable and a potential consequence of exposure to traumatic stress. Evidence suggests that a quantitative approach to PTSD phenotype measurement and incorporation of lifetime trauma exposure (LTE) information could enhance the discovery power of PTSD genome-wide association studies (GWASs).

Methods

A GWAS on PTSD symptoms was performed in 51 cohorts followed by a fixed-effects meta-analysis (N = 182,199 European ancestry participants). A GWAS of LTE burden was performed in the UK Biobank cohort (N = 132,988). Genetic correlations were evaluated with linkage disequilibrium score regression. Multivariate analysis was performed using Multi-Trait Analysis of GWAS. Functional mapping and annotation of leading loci was performed with FUMA. Replication was evaluated using the Million Veteran Program GWAS of PTSD total symptoms.

Results

GWASs of PTSD symptoms and LTE burden identified 5 and 6 independent genome-wide significant loci, respectively. There was a 72% genetic correlation between PTSD and LTE. PTSD and LTE showed largely similar patterns of genetic correlation with other traits, albeit with some distinctions. Adjusting PTSD for LTE reduced PTSD heritability by 31%. Multivariate analysis of PTSD and LTE increased the effective sample size of the PTSD GWAS by 20% and identified 4 additional loci. Four of these 9 PTSD loci were independently replicated in the Million Veteran Program.

Conclusions

Through using a quantitative trait measure of PTSD, we identified novel risk loci not previously identified using prior case-control analyses. PTSD and LTE have a high genetic overlap that can be leveraged to increase discovery power through multivariate methods.

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Tang, A., McLaughlin, K. A., Sheridan, M., Nelson, C. A., & Zeanah, C. H. (2022). Autonomic reactivity to social rejection, peer difficulties, and the buffering effects of adolescent friendships following early psychosocial deprivation . Emotion , 22 (3), 318 - 330. Publisher's VersionAbstract
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)
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Reid-Russell, A., Cvencek, D., Meltzoff, A. N., & McLaughlin, K. A. (2022). Lower implicit self-esteem as a pathway linking childhood abuse to depression and suicidal ideation. Development and Psychopathology , 34, 1272–1286. Publisher's VersionAbstract
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.
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Luby, J., Rogers, C., & McLaughlin, K. A. (2022). Environmental conditions to promote healthy childhood brain/behavioral development: Informing early preventive interventions for delivery in routine care. Biological Psychiatry , 2 (3), 233-241. Publisher's VersionAbstract

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.

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Gee, D. G., DeYoung, K. A., Mclaughlin, K. A., Tillman, R. M., Barch, D. M., Forbes, E. E., Krueger, R. F., et al. (2022). Training the Next Generation of Clinical Psychological Scientists: A Data-Driven Call to Action. Annual Review of Clinical Psychology , 18, 43-70. Publisher's VersionAbstract
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.
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Colich, N. L., & McLaughlin, K. A. (2022). Accelerated pubertal development as a mechanism linking trauma exposure with depression and anxiety in adolescenceAuthor links open overlay panel. Current Opinion in Psychology , 46, 1-6. Publisher's VersionAbstract
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.
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Sumner, J. A., Gambazza, S., Gao, X., Baccarelli, A. A., Uddin, M., & McLaughlin, K. A. (2022). Epigenetics of early-life adversity in youth: cross-sectional and longitudinal associations. Clinical Epigenetics , 14 (48), 1-12. Publisher's VersionAbstract

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

 

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DeCross, S. N., Sambrook, K. A., Sheridan, M. A., Tottenham, N., & McLaughlin, K. A. (2022). Dynamic alterations in neural networks supporting aversive learning in children exposed to trauma: neural mechanisms underlying psychopathology. Biological Psychiatry , 91 (7), 667-675. Publisher's VersionAbstract
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.
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Romeo, R. R., Flournoy, J. C., McLaughlin, K. A., & Lengua, L. J. (2022). Language development as a mechanism linking socioeconomic status to executive functioning development in preschool. Developmental Science , 1 - 12. Publisher's VersionAbstract
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.
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McLaughlin, K. A., & Gabard-Durnam, L. J. (2022). Experience-Driven Plasticity and the Emergence of Psychopathology: A Mechanistic Framework Integrating Development and the Environment into the Research Domain Criteria (RDoC) Model. Journal of Abnormal Psychology , 575 - 587. Publisher's VersionAbstract
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.
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Hatzenbuehler, M. L., Weissman, D. G., McKetta, S., Lattanner, M. R., Ford, J. V., Barch, D. M., & McLaughlin, K. A. (2022). Smaller Hippocampal Volume Among Black and Latinx Youth Living in High-Stigma Contexts. Journal of the American Academy of Child & Adolescent Psychiatry , 61 (6), 809 - 819. Publisher's VersionAbstract

Objective

To determine whether structural and individual forms of stigma are associated with neurodevelopment in children.

Method

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.

Results

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.

Conclusion

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.

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