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Previously institutionalized adolescents show increased risk for psychopathology, though placement into high-quality foster care can partially mitigate this risk. White matter (WM) structure is associated with early institutional rearing and psychopathology in youth. Here we investigate associations between WM structure and psychopathology in previously institutionalized youth. Adolescent psychopathology data were collected using the MacArthur Health and Behavior Questionnaire. Participants underwent diffusion MRI, and data were processed using fixel-based analyses. General linear models investigated interactions between institutionalization groups and psychopathology on fixel metrics. Supplementary analyses also examined the main effects of psychopathology and institutionalization group on fixel metrics. Ever-Institutionalized children included 41 randomized to foster care (Mage=16.6), and 40 to care-as-usual (Mage=16.7)). In addition, 33 participants without a history of institutionalization were included as a reference group (Mage=16.9). Ever-Institutionalized adolescents displayed altered general psychopathology-fixel associations within the cerebellar peduncles, inferior longitudinal fasciculi, corticospinal tract, and corpus callosum, and altered externalizing-fixel associations within the cingulum and fornix. Our findings indicate brain-behavior associations reported in the literature may not be generalizable to all populations. Previously institutionalized youth may develop differential brain development, which in turn leads to altered neural correlates of psychopathology that are still apparent in adolescence.

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BACKGROUND: Early adversity, broadly defined as a set of negative exposures during childhood, is extremely common and increases risk for psychopathology across the life span. Previous research suggests that separate dimensions of adversity increase risk through developmental plasticity mechanisms shaping unique neurobiological pathways. Specifically, research suggests that deprivation is associated with deficits in higher order cognition, while threat is associated with atypicality in fear learning and emotion dysregulation. However, most of this research has been conducted in adolescent and adult samples, long after exposure to adversity occurs and far from periods of peak developmental plasticity. OBJECTIVE: The Wellness Health and Life Experiences (WHALE) study examines the neurobiological and behavioral mechanisms by which deprivation, threat, and unpredictability increase risk for psychopathology in early childhood (age 4-7 years) directly following periods of peak developmental plasticity. The objective of this study is to describe the study rationale and aims, the research design and procedures, and the analytical plan to test the study hypotheses. METHODS: This is a retrospective cohort study that examines associations between exposure to deprivation and threat and their hypothesized neurobiological mechanisms, how these neurobiological mechanisms link early adversity and psychopathology, and associations between unpredictability, reward learning, and psychopathology. The sample was a convenience sample of children (aged 4-7 years) and their families, identified through flyers, email blasts to listserves, school-based advertising, and involvement in community events. Data were collected during a home visit, a subsequent laboratory visit, and a final neuroimaging visit. Planned analyses include linear regression, path analyses, and functional magnetic resonance imaging analyses to explore the role of neural function in the association between early adversity and psychopathology. RESULTS: Participants (N=301) have been recruited into the study, and data collection has commenced. The expected results will be available in 2024. CONCLUSIONS: The findings of this study will help elucidate the neurobiological mechanisms by which early adversity increases risk for psychopathology in early childhood. This study represents the earliest test of an influential theory of biological embedding of early adversity. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/59636.

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BACKGROUND: Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth. METHODS: The sample includes 170 youths aged 10-13 years (M = 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later. RESULTS: Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS-) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms. CONCLUSIONS: Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.

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Stressful life events (SLEs) are tightly coupled with the emergence of anxiety and depression symptoms among adolescents, but the mechanisms underlying this relationship remain poorly understood. We investigated within-person fluctuations in emotion regulation as a mechanism linking SLEs and internalizing psychopathology in an intensive longitudinal study. We examined how monthly fluctuations in SLEs were related to engagement in three emotion regulation strategies-acceptance, reappraisal, and rumination-and whether these strategies were associated with changes in internalizing symptoms in adolescents followed for one year (N = 30; n = 355 monthly observations). Bayesian hierarchical models revealed that on months when adolescents experienced more SLEs than was typical for them, they also engaged in more rumination, which, in turn, was associated with higher anxiety and depression symptoms and mediated the prospective relationship between SLEs and internalizing symptoms. In contrast, greater use of acceptance and reappraisal selectively moderated the association between stressors and internalizing symptoms, resulting in stronger links between SLEs and symptoms. These results suggest that emotion regulation strategies play different roles in the stress-psychopathology relationship. Understanding how changes in emotion regulation contribute to increases in internalizing symptoms following experiences of stress may provide novel targets for interventions aimed at reducing stress-related psychopathology.

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Despite significant historical progress toward gender parity in employment status in the US, women remain more likely to provide domestic labor, creating role competition which may increase depression symptoms. Pro-family employee benefits may minimize the stress of competing roles. We tested whether depressive symptoms were higher among women with vs. without competing roles and whether this effect was greater among women without (vs. with) pro-family benefits. Data included employed women surveyed across 4 waves of the National Longitudinal Survey (2010-2019) (N=9884). Depression symptoms were measured with the Mental Health Inventory (MHI-5). The interaction between competing roles and pro-family employee benefits on depressive symptoms was also compared with non-family-related benefits, using marginal structural models to estimate longitudinal effects in the presence of time-varying confounding. MHI-5 scores were 0.56 points higher (95% CI=0.15, 0.97) among women in competing roles (vs. not). Among women without pro-family benefits, competing roles increased MHI-5 scores by 6.1-points (95% CI=1.14, 11.1). In contrast, there was no association between competing roles and MHI-5 scores among women with access to these benefits (MHI-5 difference=0.44; 95% CI=-0.2, 1.0). Results were similar for non-family-related benefits. Dual workplace and domestic labor role competition increases women's depression symptoms, though broad availability of workplace benefits may attenuate that risk.

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Consistent evidence documents powerful effects of social inequality on health, well-being and academic achievement. Yet research on whether social inequality may also be linked to brain structure and function has, until recently, been rare. Here we describe three methodological approaches that can be used to study this question-single site, single study; multi-site, single study; and spatial meta-analysis. We review empirical work that, using these approaches, has observed associations between neural outcomes and structural measures of social inequality-including structural stigma, community-level prejudice, gender inequality, neighbourhood disadvantage and the generosity of the social safety net for low-income families. We evaluate the relative strengths and limitations of these approaches, discuss ethical considerations and outline directions for future research. In doing so, we advocate for a paradigm shift in cognitive neuroscience that explicitly incorporates upstream structural and contextual factors, which we argue holds promise for uncovering the neural correlates of social inequality.

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Childhood experiences of low socioeconomic status are associated with alterations in neural function in the frontoparietal network and ventral visual stream, which may drive differences in working memory. However, the specific features of low socioeconomic status environments that contribute to these disparities remain poorly understood. Here, we examined experiences of cognitive deprivation (i.e. decreased variety and complexity of experience), as opposed to experiences of threat (i.e. violence exposure), as a potential mechanism through which family income contributes to alterations in neural activation during working memory. As part of a longitudinal study, 148 youth between aged 10 and 13 years completed a visuospatial working memory fMRI task. Early childhood low income, chronicity of low income in early childhood, and current income-to-needs were associated with task-related activation in the ventral visual stream and frontoparietal network. The association of family income with decreased activation in the lateral occipital cortex and intraparietal sulcus during working memory was mediated by experiences of cognitive deprivation. Surprisingly, however, family income and deprivation were not significantly related to working memory performance, and only deprivation was associated with academic achievement in this sample. Taken together, these findings suggest that early life low income and associated cognitive deprivation are important factors in neural function supporting working memory.

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OBJECTIVE: We evaluated whether respiratory sinus arrhythmia (RSA) reactivity and resting RSA-physiological markers reflecting the increase in heart rate with inspiration and decrease during expiration related to parasympathetic influence on the heart-are modifiable and predict symptom change during youth psychotherapy. Methods: Diverse youth (N = 158; ages 7-15; 48.1% female) received the Modular Approach to Therapy for Children and completed pre-treatment (pre), post-treatment (post), and 18-months postbaseline (18Mo) assessments. We measured resting RSA, RSA reactivity during stress induction, and psychopathology symptoms. Results: Pre-to-post and pre-to-18Mo, reactivity decreased, and resting RSA increased. Changes in reactivity and resting RSA, separately, did not predict reduced psychopathology. Yet, decreased reactivity combined with increased resting RSA predicted reduced psychopathology over time, suggesting that observed RSA changes were beneficial for some. Higher dosage of a module utilizing slow-breathing, muscle-relaxation, and imagery predicted greater pre-to-18Mo changes in reactivity and resting RSA, whereas a similar module with less emphasis on slow-breathing did not. Conclusions: Findings raise the possibility that youth reactivity and resting RSA could be modifiable during cognitive behavioral therapy and contribute to the amelioration of psychopathology. More studies are needed to determine whether resting RSA and RSA reactivity are modifiable indices of symptom change in slow-breathing practices and psychotherapy. CLINICALTRIALS.GOV IDENTIFIER: NCT03153904, registered May 15, 2017.

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PURPOSE: Incarceration rates are highest in rural communities, disproportionately exposing rural children to parental incarceration (PI). Substance use is a pressing public health issue-and a key driver of incarceration-in rural areas, yet limited research has examined PI as a social determinant of health for adolescent alcohol and drug use. This study links exposure to PI with rural adolescent substance use and examines the role of coresidence with parents in these associations. METHODS: Data come from the 2019 Minnesota Student Survey, including 18,820 rural adolescents. Respondents self-reported experiences of PI (current, former, never), whether they lived with the parent at the time of incarceration, and past-year alcohol, marijuana, cocaine, heroin, and methamphetamine use. FINDINGS: Over 22% of rural adolescents experienced PI. In adjusted logistic regression models, current PI was associated with greater past-year alcohol (aOR = 2.20), marijuana (aOR = 4.08), cocaine (aOR = 3.61), heroin (aOR = 4.96), and methamphetamine (aOR = 5.43) use compared to peers who never experienced PI. Current PI was also associated with greater counts of use. Associations between coresidence and substance use were largely nonsignificant. CONCLUSIONS: The elevated risk for substance use in the context of rural PI and its adverse sequelae call for expanded prevention and intervention strategies that support adolescent health alongside targeted decarceration efforts in rural communities that reduce the number of families put in the potentially compromising situation of PI.

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Recent work demonstrating low test-retest reliability of neural activation during fMRI tasks raises questions about the utility of task-based fMRI for the study of individual variation in brain function. Two possible sources of the instability in task-based BOLD signal over time are noise or measurement error in the instrument, and meaningful variation across time within-individuals in the construct itself-brain activation elicited during fMRI tasks. Examining the contribution of these two sources of test-retest unreliability in task-evoked brain activity has far-reaching implications for cognitive neuroscience. If test-retest reliability largely reflects measurement error, it suggests that task-based fMRI has little utility in the study of either inter- or intra-individual differences. On the other hand, if task-evoked BOLD signal varies meaningfully over time, it would suggest that this tool may yet be well suited to studying intraindividual variation. We parse these sources of variance in BOLD signal in response to emotional cues over time and within-individuals in a longitudinal sample with 10 monthly fMRI scans. Test-retest reliability was low, reflecting a lack of stability in between-person differences across scans. In contrast, within-person, within-session internal consistency of the BOLD signal was higher, and within-person fluctuations across sessions explained almost half the variance in voxel-level neural responses. Additionally, monthly fluctuations in neural response to emotional cues were associated with intraindividual variation in mood, sleep, and exposure to stressors. Rather than reflecting trait-like differences across people, neural responses to emotional cues may be more reflective of intraindividual variation over time. These patterns suggest that task-based fMRI may be able to contribute to the study of individual variation in brain function if more attention is given to within-individual variation approaches, psychometrics-beginning with improving reliability beyond the modest estimates observed here, and the validity of task fMRI beyond the suggestive associations reported here.

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Conversational turn-taking is a complex communicative skill that requires both linguistic and executive functioning (EF) skills, including processing input while simultaneously forming and inhibiting responses until one's turn. Adult-child turn-taking predicts children's linguistic, cognitive, and socioemotional development. However, little is understood about how disruptions to temporal contingency in turn-taking, such as interruptions and overlapping speech, relate to cognitive outcomes, and how these relationships may vary across developmental contexts. In a longitudinal sample of 275 socioeconomically diverse mother-child dyads (children 50% male, 65% White), we conducted pre-registered examinations of whether the frequency of dyads' conversational disruption during free play when children were 3 years old related to children's executive functioning (EF; 9 months later), self-regulation skills (18 months later), and externalizing psychopathology in early adolescence (age 10-12 years). Contrary to hypotheses, more conversational disruptions significantly predicted higher inhibition skills, controlling for sex, age, income-to-needs (ITN), and language ability. Results were driven by maternal disruptions of the child's speech, and could not be explained by measures of overall talkativeness or interactiveness. Exploratory analyses revealed that ITN moderated these relationships, such that the positive effect of disruptions on inhibition was strongest for children from lower ITN backgrounds. We discuss how adult-driven "cooperative overlap" may serve as a form of engaged participation that supports cognition and behavior in certain cultural contexts.

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OBJECTIVE: Ample evidence demonstrates that structural stigma - defined as societal-level conditions, cultural norms, and institutional policies and practices that constrain opportunities, resources, and well-being of stigmatized populations - is associated with psychopathology in adults from marginalized groups. Yet there is limited research on whether structural stigma is similarly associated with internalizing and externalizing symptoms among youth. METHOD: Structural stigma related to sex, sexual orientation, race, and Latinx ethnicity was measured using indicators of state-level policy and aggregated attitudes. Using data from the Adolescent Brain Cognitive Development (ABCD) Study (N = 10,414; M age = 12 years, SD = 0.66; 48% female, 6.8% lesbian, gay, and bisexual (LGB), 13.4% Black, 20% Latinx), we examined associations of structural stigma with internalizing and externalizing symptoms among female, LGB, Black, and Latinx youth. RESULTS: LGB youth living in higher (vs. lower) structural stigma states had elevated levels of internalizing and externalizing symptoms. In lower structural stigma states, there were no differences in externalizing symptoms between LGB and heterosexual youth. Similarly, Latinx youth and females living in higher (vs. lower) structural stigma states had elevated levels of externalizing symptoms. In lower structural stigma states, there were no differences in externalizing symptoms between Latinx youth and non-Latinx White youth. Structural stigma related to race was unrelated to internalizing or externalizing symptoms for Black youth. CONCLUSIONS: This study provides novel evidence that macro-level social environments, in the form of structural stigma, contribute to adverse mental health outcomes for marginalized youth and partly explain disparities in externalizing symptoms.

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Childhood adversity is a common, powerful risk factor for future mental and physical health problems. Appropriately aggregating and categorizing discrete adverse experiences into cumulative indices remains an active area of research and debate in the field of developmental psychopathology. In a recent article by Sisitsky et al. (2013), they report using confirmatory factor analysis and latent profile analysis to categorize participants into "profiles" of childhood adversity. In this commentary, we argue that categorizing dimensions or profiles of childhood adversity based on the tendency of adversities to co-occur is misaligned with dimensional models of adversity, which derive underlying dimensions from their tendency to cumulatively predict certain outcomes rather than adversity co-occurrence. We summarize the history of theories and methods of operationalizing childhood adversity that led to the development of the dimensional model of adversity and psychopathology. We then explain why latent variable approaches, which simply reflect the tendency of adverse experiences to co-occur, are inappropriate for validating any given approach.

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Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10-15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity.

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The COVID-19 pandemic has presented unprecedented challenges for youths and families, dramatically increasing exposure to stressors and stress-related psychopathology. Increasing work has leveraged pre-pandemic neuroimaging data to predict adolescent psychopathology and stress responses during the pandemic, with a particular focus on internalizing symptoms. We review this recent literature on pre-pandemic brain structure and function and adolescent internalizing psychopathology during the pandemic. At present, existing studies have not consistently identified specific alterations in brain structure and function that predict anxiety or depressive symptoms during the pandemic. In contrast, exposure to stress and adversity before and during the pandemic as well as access to peer and family support have emerged as consistent and reliable predictors of youth mental health during the pandemic.

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Socioeconomic status (SES) is associated with children's brain and behavioral development. Several theories propose that early experiences of adversity or low SES can alter the pace of neurodevelopment during childhood and adolescence. These theories make contrasting predictions about whether adverse experiences and low SES are associated with accelerated or delayed neurodevelopment. We contextualize these predictions within the context of normative development of cortical and subcortical structure and review existing evidence on SES and structural brain development to adjudicate between competing hypotheses. Although none of these theories are fully consistent with observed SES-related differences in brain development, existing evidence suggests that low SES is associated with brain structure trajectories more consistent with a delayed or simply different developmental pattern than an acceleration in neurodevelopment.

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

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

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