Fluctuations in emotion regulation as a mechanism linking stress and internalizing psychopathology among adolescents: An intensive longitudinal study.

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.

Bringing home the benefits: Do pro-family employee benefits mitigate the risk of depression from competing workplace and domestic labor roles?

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.

A research agenda for understanding how social inequality is linked to brain structure and function.

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.

Is respiratory sinus arrhythmia a modifiable index of symptom change in cognitive behavioral therapy for youth? A pooled-data analysis of a randomized trial.

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.

Cognitive stimulation as a mechanism linking socioeconomic status and neural function supporting working memory: a longitudinal fMRI study.

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.

A precision neuroscience approach to estimating reliability of neural responses during emotion processing: Implications for task-fMRI.

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.

Conversation disruptions in early childhood predict executive functioning development: A longitudinal study.

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.

Associations Between Structural Stigma and Psychopathology Among Early Adolescents.

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.

Does reward processing moderate or mediate the link between childhood adversity and psychopathology: A longitudinal study.

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.

Challenges with Latent Variable Approaches to Operationalizing Dimensions of Childhood adversity - a Commentary on Sisitsky et al. (2023).

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.

Pre-pandemic brain structure and function and adolescent psychopathology during the COVID-19 pandemic.

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.

State-level macro-economic factors moderate the association of low income with brain structure and mental health in U.S. children.

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.

Childhood socioeconomic status and the pace of structural neurodevelopment: accelerated, delayed, or simply different?

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.

Differentiating Between Us & Them: Reduced In-Group Bias as a Novel Mechanism Linking Childhood Violence Exposure with Internalizing Psychopathology.

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.

Resilient phenotypes among bereaved youth: a comparison of trajectory, relative, and cross-domain approaches.

BACKGROUND: Bereavement is a common traumatic event associated with adverse health outcomes across the life course. Despite these risks, not all bereaved individuals experience these negative effects. Limited scientific consensus exists on how to define resilience in individuals who have experienced the death of a loved one. METHODS: Using a sample of N = 3766 youth from the Avon Longitudinal Study of Parents and Children birth cohort, we identified bereavement of a family member between ages 7 and 8.5. We derived and compared three different approaches to assess resilience among bereaved youth. Trajectory-based psychological resilience identified sub-groups with similar psychological symptom profiles between ages 6 and 16 using latent growth mixture models. Relative psychological resilience at age 16 leveraged standardized residuals from a model regressing psychological symptoms on bereavement to determine better-than-expected psychological functioning relative to bereavement status. Relative cross-domain resilience around age 16 was a sum score of the residuals approach applied to eight unique domains of health. Predictive validity of each approach was assessed using depressive symptoms at age 17.5 RESULTS: Overall, N = 877 (23%) youth were bereaved of a family member between ages 7 and 8.5. Using latent growth mixture models, a three-class solution described 84% of bereaved youth with low and stable psychological symptoms over time, 8% with worsening symptoms, and 8% with improving yet elevated symptoms. Each relative resilience score was largely concordant with the trajectory-based approach in identifying individuals as resilient or not, though relative psychological resilience demonstrated a stronger degree of concordance than the cross-domain score. Relative psychological and cross-domain resilience exhibited moderate to low correlation, depending on the domains included (r = 0.14-0.43). For each approach, resilience significantly predicted lower depressive symptoms at age 17.5, highlighting predictive validity of these measures. CONCLUSIONS: Psychological symptom trajectories among bereaved youth aligned with those previously identified among bereaved adults. The residual-based approach to defining resilience exhibited limited utility in the context of bereavement. When identifying risk and resilience after bereavement, researchers and clinicians must address the interplay across psychosocial and physical health domains, as bereaved youth considered resilient from a mental health perspective may benefit from intervention in other domains.

Stressful life events and accelerated biological aging over time in youths.

Experiencing adversity in childhood and adolescence, including stressful life events (SLEs), may accelerate the pace of development, leading to adverse mental and physical health. However, most research on adverse early experiences and biological aging (BA) in youths relies on cross-sectional designs. In 171 youths followed for approximately 2 years, we examined if SLEs over follow-up predicted rate of change in two BA metrics: epigenetic age and Tanner stage. We also investigated if rate of change in BA was associated with changes in depressive symptoms over time. Youths aged 8-16 years at baseline self-reported Tanner stage and depressive symptoms at baseline and follow-up and provided saliva samples for DNA at both assessments. Horvath epigenetic age estimates were derived from DNA methylation data measured with the Illumina EPIC array. At follow-up, contextual threat interviews were administered to youths and caregivers to assess youths' experiences of past-year SLEs. Interviews were objectively coded by an independent rating team to generate a SLE impact score, reflecting the severity of all SLEs occurring over the prior year. Rate of change in BA metrics was operationalized as change in epigenetic age or Tanner stage as a function of time between assessments. Higher objective SLE impact scores over follow-up were related to a greater rate of change in epigenetic age (ß = 0.21, p = .043). Additionally, among youths with lower-but not higher-Tanner stage at baseline, there was a positive association of SLE impact scores with rate of change in Tanner stage (Baseline Tanner Stage × SLE Impact Score interaction: ß = - 0.21, p = .011). A greater rate of change in epigenetic age was also associated with higher depressive symptom levels at follow-up, adjusting for baseline symptoms (ß = 0.15, p = .043). Associations with epigenetic age were similar, although slightly attenuated, when adjusting for epithelial (buccal) cell proportions. Whereas much research in youths has focused on severe experiences of early adversity, we demonstrate that more commonly experienced SLEs during adolescence may also contribute to accelerated BA. Further research is needed to understand the long-term consequences of changes in BA metrics for health.

Childhood trauma, earlier pubertal timing, and psychopathology in adolescence: The role of corticolimbic development.

Earlier pubertal development appears to be one pathway through which childhood trauma contributes to psychopathology in adolescence. Puberty-related changes in neural networks involved in emotion processing, namely the amygdala-medial prefrontal (mPFC) circuit, may be a potential mechanism linking trauma and adolescent psychopathology. Our participants were 227 youth between 10 and 13 years of age who completed assessments of threat and deprivation-related experiences of adversity, pubertal stage, and internalizing and externalizing symptoms. A subset (n = 149) also underwent a functional MRI scan while passively viewing fearful and calm faces. Potential mechanisms linking childhood trauma with psychopathology, encompassing earlier pubertal timing and neural response to aversive stimuli were explored. Earlier pubertal development was associated with childhood trauma as well as increased externalizing symptoms in boys only. Earlier pubertal timing in males and females was negatively associated with activation in bilateral amygdala, hippocampal, and fusiform regions when comparing fearful and calm faces. However, amygdala-mPFC connectivity showed no association with pubertal timing or psychopathology symptoms. These findings do not support accelerated amygdala-mPFC development as a mechanism linking childhood trauma and psychopathology, but instead provide support for the role of pubertal development in normative decreases in limbic activation across development.