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Exposure to social adversity has been associated with cortisol dysregulation during pregnancy and in later childhood; less is known about how prenatal exposure to social stressors affects postnatal cortisol of infants. In a secondary analysis of data from a longitudinal study, we tested whether a pregnant woman's reports of social adversity during the third trimester were associated with their infant's resting cortisol at 1, 6, and 12 months postnatal. Our hypothesis was that prenatal exposure to social adversity would be associated with elevation of infants' cortisol. Measures included prenatal survey reports of social stressors and economic hardship, and resting cortisol levels determined from infant saliva samples acquired at each postnatal timepoint. Data were analyzed using linear mixed effects models. The final sample included 189 women and their infants (46.56% assigned female sex at birth). Prenatal economic hardship was significantly associated with infant cortisol at 6 months postnatal; reports of social stressors were not significantly associated with cortisol at any time point. Factors associated with hardship, such as psychological distress or nutritional deficiencies, may alter fetal HPA axis development, resulting in elevated infant cortisol levels. Developmental changes unique to 6 months of age may explain effects at this timepoint. More work is needed to better comprehend the complex pre- and post-natal physiologic and behavioral factors that affect infant HPA axis development and function, and the modifying role of environmental exposures.

Research exploring developmental explanations for sexual and/or gender minority (i.e. SGM) mental health disparities often rely on adults' retrospectively reported childhood adversity, leaving gaps in understanding how childhood adversity affects SGM mental health disparities during critical developmental periods and/or in contemporary youth. We tested the association between 459 12- to 17-year-old Canadian adolescents' SGM status and mental health (i.e. life satisfaction, internalizing symptoms) and whether this was explained by indirect effects of peer and family adversity. Additionally, we examined developmental differences between early and middle adolescence. SGM status significantly predicted worse mental health. In an adjusted model, indirect effects through peer and family adversity were significant; the previously detected total effect of SGM status on life satisfaction disappeared and the effect on internalizing symptoms lessened. No significant developmental differences were detected. This suggests that mental health disparities are present in contemporary SGM youth and concurrent adverse experiences may underlie these disparities. [ABSTRACT FROM AUTHOR]

The nature versus nurture debate has intrigued scientific circles for decades. Although extensive research has established a clear relationship between genetics and disease development, recent evidence has highlighted the insufficiency of attributing adverse health outcomes to genetic factors alone. In fact, it has been suggested that environmental influences, such as socioeconomic position (SEP), may play a much larger role in the development of disease than previously thought, with extensive research suggesting that low SEP is associated with adverse health conditions. In relation to oral health, a higher prevalence of caries (tooth decay) exists among those of low SEP. Although little is known about the biological mechanisms underlying this relationship, epigenetic modifications resulting from environmental influences have been suggested to play an important role. This review explores the intersection of health inequalities and epigenetics, the role of early-life social adversity and its long-term epigenetic impacts, and how those living within the lower hierarchies of the socioeconomic pyramid are indeed at higher risk of developing diseases, particularly in relation to oral health. A deeper understanding of these mechanisms could lead to the development of targeted interventions for individuals of low SEP to improve oral health or identify those who are at higher risk of developing oral disease. [ABSTRACT FROM AUTHOR]

AbstractExposure to social adversity has been associated with cortisol dysregulation during pregnancy and in later childhood; less is known about how prenatal exposure to social stressors affects postnatal cortisol of infants. In a secondary analysis of data from a longitudinal study, we tested whether a pregnant woman’s reports of social adversity during the third trimester were associated with their infant’s resting cortisol at 1, 6, and 12 months postnatal. Our hypothesis was that prenatal exposure to social adversity would be associated with elevation of infants’ cortisol. Measures included prenatal survey reports of social stressors and economic hardship, and resting cortisol levels determined from infant saliva samples acquired at each postnatal timepoint. Data were analyzed using linear mixed effects models. The final sample included 189 women and their infants (46.56% assigned female sex at birth). Prenatal economic hardship was significantly associated with infant cortisol at 6 months postnatal; reports of social stressors were not significantly associated with cortisol at any time point. Factors associated with hardship, such as psychological distress or nutritional deficiencies, may alter fetal HPA axis development, resulting in elevated infant cortisol levels. Developmental changes unique to 6 months of age may explain effects at this timepoint. More work is needed to better comprehend the complex pre- and post-natal physiologic and behavioral factors that affect infant HPA axis development and function, and the modifying role of environmental exposures.

We describe the language ability of children at age 9.5 years who were born to women with an opioid use disorder and examine the associations between prenatal opioid exposure, sex, social adversity, caregiver psychological factors, and child language. Data were drawn from the regional prospective longitudinal Canterbury Methadone in Pregnancy study. At the 9.5-year wave, 80 children who were born to mothers in Methadone Maintenance Treatment and their caregivers, and 98 non-exposed comparison children were assessed using a comprehensive standardized measure of language. Information related to social adversity and caregiver psychological factors was obtained from comprehensive caregiver interviews. At age 9.5 years, opioid-exposed children had lower language scores than the non-exposed children, however their group average was within the normal range on the CELF-4 norms. A series of multivariate hierarchical regression models predicting low language at 9.5 years showed sex and opioid-exposure status predicted low language in the first step. The addition of social adversity factors significantly improved the model. The further addition of caregiver psychological factors did not improve prediction. Only sex was a significant predictor throughout. In this sample, children prenatally exposed to opioids were at higher risk of low language outcomes. However, the child being male and social adversity were important influencing factors. This suggests early language support services are indicated for opioid-exposed children, particularly boys and those in socially adverse circumstances. [ABSTRACT FROM AUTHOR]

Contemporary health services are primarily designed around single diseases. People with multimorbidity (multiple long‐term health conditions) often become burdened by accumulated treatments. Through multimodal fieldwork in a socially disadvantaged London borough, we explore how people living with multimorbidity navigate conditions of 'chronic crisis', encompassing ill‐health, overmedicalisation, polypharmacy and social exclusion. Participants in our study frequently experience 'existential stuckness', exacerbated by processes of social exclusion. We argue that diagnoses and treatments should account for people's unique aetiologies, and prioritise the notion of 'flourishing' over 'cure' as the absence of disease is not always achievable. To foster this emphasis on flourishing, we advocate for a dialogical turn in diagnostic processes that better support patients' existential needs in the context of long‐term illness. [ABSTRACT FROM AUTHOR]

Increasing age is associated with dysregulated immune function and increased inflammation—patterns that are also observed in individuals exposed to chronic social adversity. Yet we still know little about how social adversity impacts the immune system and how it might promote age-related diseases. Here, we investigated how immune cell diversity varied with age, sex and social adversity (operationalized as low social status) in free-ranging rhesus macaques. We found age-related signatures of immunosenescence, including lower proportions of CD20 + B cells, CD20 + /CD3 + ratio, and CD4 + /CD8 + T cell ratio – all signs of diminished antibody production. Age was associated with higher proportions of CD3 + /CD8 + Cytotoxic T cells, CD16 + /CD3- Natural Killer cells, CD3 + /CD4 + /CD25 + and CD3 + /CD8 + /CD25 + T cells, and CD14 + /CD16 + /HLA-DR + intermediate monocytes, and lower levels of CD14 + /CD16-/HLA-DR + classical monocytes, indicating greater amounts of inflammation and immune dysregulation. We also found a sex-dependent effect of exposure to social adversity (i.e., low social status). High-status males, relative to females, had higher CD20 + /CD3 + ratios and CD16 + /CD3 Natural Killer cell proportions, and lower proportions of CD8 + Cytotoxic T cells. Further, low-status females had higher proportions of cytotoxic T cells than high-status females, while the opposite was observed in males. High-status males had higher CD20 + /CD3 + ratios than low-status males. Together, our study identifies the strong age and sex-dependent effects of social adversity on immune cell proportions in a human-relevant primate model. Thus, these results provide novel insights into the combined effects of demography and social adversity on immunity and their potential contribution to age-related diseases in humans and other animals. [ABSTRACT FROM AUTHOR]

The identification of human violence determinants has sparked multiple questions from different academic fields. Innovative methodological assessments of the weight and interaction of multiple determinants are still required. Here, we examine multiple features potentially associated with confessed acts of violence in ex-members of illegal armed groups in Colombia (N = 26,349) through deep learning and feature-derived machine learning. We assessed 162 social-contextual and individual mental health potential predictors of historical data regarding consequentialist, appetitive, retaliative, and reactive domains of violence. Deep learning yields high accuracy using the full set of determinants. Progressive feature elimination revealed that contextual factors were more important than individual factors. Combined social network adversities, membership identification, and normalization of violence were among the more accurate social-contextual factors. To a lesser extent the best individual factors were personality traits (borderline, paranoid, and antisocial) and psychiatric symptoms. The results provide a population-based computational classification regarding historical assessments of violence in vulnerable populations.

Individuals face discrimination based on characteristics including race/ethnicity, gender, age, and disability. Discriminatory experiences (DE) are associated with poor psychological health in the general population and with worse outcomes among individuals at clinical high risk for psychosis (CHR). Though the brain is sensitive to stress, and brain structural change is a well-documented precursor to psychosis, potential relationships between DE and brain structure among CHR or healthy individuals are not known. This report assessed whether lifetime DE are associated with cortical thinning and clinical outcomes across time, after controlling for discrimination-related demographic factors among CHR individuals who ultimately do (N = 57) and do not convert to psychosis (N = 451), and healthy comparison (N = 208) participants in the North American Prodrome Longitudinal Study 2. Results indicate that DE are associated with thinner cortex across time in several cortical areas. Thickness in several right hemisphere regions partially mediates associations between DE and subsequent anxiety symptoms, but not attenuated positive symptoms of psychosis. This report provides the first evidence to date of an association between DE and brain structure in both CHR and healthy comparison individuals. Results also suggest that thinner cortex across time in areas linked with DE may partially explain associations between DE and cross-diagnostic indicators of psychological distress.

Purpose: Shorter breast cancer (BC) survival outcomes persist by neighborhood disadvantage independent of patient, tumor, and treatment characteristics. This suggests unaccounted mechanisms by which neighborhood disadvantage "gets under the skin" to impact BC survival outcomes. Here, we evaluate the relationship between neighborhood disadvantage and clinical and neuroendocrine markers of stress in BC patients. Methods: Women with stage 0–III BC were enrolled 2–10 weeks post-surgery and before initiating adjuvant treatment in a study examining stress and stress management processes. Women provided an afternoon-evening (PM) serum cortisol sample and were administered the Hamilton Anxiety Rating Scale (HAM-A). Home addresses were used to determine the Area Deprivation Index (ADI), a validated measure of neighborhood disadvantage. Multiple regression assessed the relationship between ADI and PM serum cortisol and the presence of elevated HAM-A symptoms. Results: Our sample (n = 225) was predominately middle-aged (M = 50.4 years; range 23–70 years), non-Hispanic White (64.3%), with stage I (38.1%), or II (38.6%) disease. The majority (n = 175) lived in advantaged neighborhoods (ADI 1–3). After controlling for age, stage, and surgery type, women from high ADI (4–10) (vs low ADI) neighborhoods had higher PM cortisol levels (β = 0.19, 95% CI [0.24, 5.00], p = 0.031) and were nearly two times as likely to report the presence of elevated anxiety symptoms (OR = 1.96, 95% CI [1.00, 3.86], p = 0.050). Conclusion: Neighborhood disadvantage is significantly associated with higher levels of PM cortisol and elevated anxiety symptoms suggesting stress pathways could potentially contribute to relationships between neighborhood disadvantage and BC survival. [ABSTRACT FROM AUTHOR]

Background: Social scientists generally agree that health disparities are produced, at least in part, by adverse social experiences, especially during childhood and adolescence. Building on this research, we use an innovative method to measure early adversity while drawing upon a biopsychosocial perspective on health to formulate a model that specifies indirect pathways whereby childhood and adolescent adversity become biologically embedded and influence adult health. Method: Using nearly 20 years of longitudinal data from 382 Black Americans, we use repeated-measures latent class analysis (RMLCA) to construct measures of childhood/adolescent adversities and their trajectories. Then, we employ structural equation modeling to examine the direct and indirect effects of childhood/adolescent adversity on health outcomes in adulthood through psychosocial maladjustment. Results: RMLCA identified two classes for each component of childhood/adolescent adversity across the ages of 10 to 18, suggesting that childhood/adolescent social adversities exhibit a prolonged heterogeneous developmental trajectory. The models controlled for early and adult mental health, sociodemographic and health-related covariates. Psychosocial maladjustment, measured by low self-esteem, depressive and anxiety symptoms, and lack of self-control, mediated the relationship between childhood/adolescent adversity, especially parental hostility, racial discrimination, and socioeconomic class, and both self-reported illness and blood-based accelerated biological aging (with proportion mediation ranging from 8.22% to 79.03%). Conclusion: The results support a biopsychosocial model of health and provide further evidence that, among Black Americans, early life social environmental experiences, especially parenting, financial stress, and racial discrimination, are associated with adult health profiles, and furthermore, psychosocial mechanisms mediate this association. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate if social adversity is associated with mother reported emotional dysregulation behaviors and trajectories during infancy and early childhood. A secondary data analysis from the Durham Child Health and Development study study included 206 child-mother dyads. Three models were used to explore the relationship between social adversity and mother reported emotional dysregulation during infancy (Infant Behavior Questionnaire-Revised) and early childhood (Child Behavior Checklist - Dysregulation Profile). Linear mixed effects models were adopted to investigate if social adversity was associated with mother reported emotional dysregulation longitudinally. Regression analysis was conducted to explore if social adversity was associated with maternal reported emotional dysregulation trajectory slope scores and maternal reported emotional dysregulation trajectory class. Maternal psychological distress and the child's sex assigned at birth were included as covariates in each analysis. Infants with greater social adversity scores had significantly higher maternal reported fear responses across the first year of life. Social adversity was associated with maternal reported distress to limitations trajectory, dysregulated recovery class, and dysregulated distress to limitations class. During early childhood social adversity was significantly associated with maternal reported emotional dysregulation but not trajectories which showed little variability. Our results indicate that social adversity is associated with maternal reported emotional dysregulation during infancy and early childhood. Nursing and other professionals can participate in early screening to determine risk and provide intervention. • Social adversity was related to infant and child emotional dysregulation behaviors. • Social adversity was related to infant fear, distress, and recovery subscales. • Social adversity was not related to childhood emotional dysregulation trajectories. • Childhood emotional trajectories were stable across 18–84 months. • Nurses can screen and intervene on children susceptible to emotional dysregulation. [ABSTRACT FROM AUTHOR]

Maternal infection during pregnancy and childhood social trauma have been associated with neurodevelopmental and affective disorders, such as schizophrenia, autism spectrum disorders, bipolar disorder and depression. These disorders are characterized by changes in microglial cells, which play a notable role in synaptic pruning, and synaptic deficits. Here, we investigated the effect of prenatal infection and social adversity during adolescence – either alone or in combination – on behavior, microglia, and synaptic density. Male offspring of pregnant rats injected with poly I:C, mimicking prenatal infection, were exposed to repeated social defeat during adolescence. We found that maternal infection during pregnancy prevented the reduction in social behavior and increase in anxiety induced by social adversity during adolescence. Furthermore, maternal infection and social adversity, alone or in combination, induced hyperlocomotion in adulthood. Longitudinal in vivo imaging with [11C]PBR28 positron emission tomography revealed that prenatal infection alone and social adversity during adolescence alone induced a transient increase in translocator protein TSPO density, an indicator of glial reactivity, whereas their combination induced a long-lasting increase that remained until adulthood. Furthermore, only the combination of prenatal infection and social adversity during adolescence induced an increase in microglial cell density in the frontal cortex. Prenatal infection increased proinflammatory cytokine IL-1β protein levels in hippocampus and social adversity reduced anti-inflammatory cytokine IL-10 protein levels in hippocampus during adulthood. This reduction in IL-10 was prevented if rats were previously exposed to prenatal infection. Adult offspring exposed to prenatal infection or adolescent social adversity had a higher synaptic density in the frontal cortex, but not hippocampus, as evaluated by synaptophysin density. Interestingly, such an increase in synaptic density was not observed in rats exposed to the combination of prenatal infection and social adversity, perhaps due to the long-lasting increase in microglial density, which may lead to an increase in microglial synaptic pruning. These findings suggest that changes in microglia activity and cytokine release induced by prenatal infection and social adversity during adolescence may be related to a reduced synaptic pruning, resulting in a higher synaptic density and behavioral changes in adulthood.

This study tested whether multiple domains of social adversity, including neighborhood opportunity/deprivation and life stress, moderate genetic (A), common environmental (C), and unique environmental (E) influences on externalizing behaviors in 760 same-sex twin pairs (332 monozygotic; 428 dizygotic) ages 10–11 from the ABCD Study. Proportion of C influences on externalizing behavior increased at higher neighborhood adversity (lower overall opportunity). A decreased and C and E increased at lower levels of educational opportunity. A increased at lower health-environment and social-economic opportunity levels. For life stress, A decreased and E increased with number of experienced events. Results for educational opportunity and stressful life experiences suggest a bioecological gene-environment interaction pattern such that environmental influences predominate at higher levels of adversity, whereas limited access to healthcare, housing, and employment stability may potentiate genetic liability for externalizing behavior via a diathesis-stress mechanism. More detailed operationalization of social adversity in gene-environment interaction studies is needed. [ABSTRACT FROM AUTHOR]

BackgroundMaternal social environmental stressors during pregnancy are associated with adverse birth and child developmental outcomes, and epigenetics has been proposed as a possible mechanism for such relationships.MethodsIn a Mexican-American birth cohort of 241 maternal-infant pairs, cord blood samples were measured for repeat element DNA methylation (LINE-1 and Alu). Linear mixed effects regression was used to model associations between indicators of the social environment (low household income and education, neighborhood-level characteristics) and repeat element methylation. Results from a dietary questionnaire were also used to assess the interaction between maternal diet quality and the social environment on markers of repeat element DNA methylation.ResultsAfter adjusting for confounders, living in the most impoverished neighborhoods was associated with higher cord blood LINE-1 methylation (β = 0.78, 95%CI 0.06, 1.50, p = 0.03). No other neighborhood-, household-, or individual-level socioeconomic indicators were significantly associated with repeat element methylation. We observed a statistical trend showing that positive association between neighborhood poverty and LINE-1 methylation was strongest in cord blood of infants whose mothers reported better diet quality during pregnancy (pinteraction = 0.12).ConclusionOur findings indicate a small yet unexpected positive association between neighborhood-level poverty during pregnancy and methylation of repetitive element DNA in infant cord blood and that this association is possibly modified by diet quality during pregnancy. However, our null findings for other adverse SES indicators do not provide strong evidence for an adverse association between early-life socioeconomic environment and repeat element DNA methylation in infants.

Summary: We propose a model for obesity development that traces a considerable part of its origins to the social domain (mainly different forms of prolonged social adversity), both within and across generations, working in tandem with a genetic predisposition. To facilitate overview of social pathways, we place particular focus on three areas that form a cascading sequence: (A) social adversity within the family (parents having a low education, a low social position, poverty and financial insecurity; offspring being exposed to gestational stress, unmet social and emotional needs, abuse, maltreatment and other negative life events, social deprivation and relationship discord); (B) increasing levels of insecurity, negative emotions, chronic stress, and a disruption of energy homeostasis; and (C) weight gain and obesity, eliciting further social stress and weight stigma in both generations. Social adversity, when combined with genetic predisposition, thereby substantially contributes to highly effective transmission of obesity from parents to offspring, as well as to obesity development within current generations. Prevention efforts may benefit from mitigating multiple types of social adversity in individuals, families, and communities, notably poverty and financial strain, and by improving education levels. [ABSTRACT FROM AUTHOR]

Background: Vitamin D insufficiency and child antisocial behavior are public health concerns. It is unknown whether vitamin D plays a role in antisocial outcomes. This study examines whether higher levels of vitamin D can act as a protective factor against antisocial behavior for children who are exposed to early social adversity. Methods: In a community sample of 300 children aged 11–12 years (151 females, 149 males), serum concentrations of 25-hydroxyvitamin D [25(OH)D] were assessed alongside early social adversity, and both parent and child-reported antisocial behavior. Results: Vitamin D moderated the association between early social adversity and multiple antisocial outcomes. Higher social adversity was associated with greater antisocial behavior among vitamin D-insufficient [25(OH)D < 30 ng/mL], but not vitamin D-sufficient children [25(OH)D ⩾ 30 ng/mL], after adjusting for other variables. Results from child reports of antisocial behavior were replicated with parent reports, providing support for the robustness of the findings. At serum 25(OH)D concentrations above 27.16–30.69 ng/mL (close to 30 ng/mL, the recommended optimal vitamin D level for pediatric populations), the effect of social adversity on antisocial behavior outcomes was nullified. Conclusions: To our knowledge, this study is the first to document that a nutritional factor, vitamin D, can potentially confer resilience to antisocial behavior. Our findings in a pediatric population suggest a possible role of vitamin D supplementation in interventions to reduce antisocial behavior, which may be further investigated in future randomized controlled trials. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic is extraordinary, but many ordinary events have contributed to its becoming and persistence. Here, we argue that the emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, which has radically altered day-to-day life for people across the globe, was an inevitability of contemporary human ecology, presaged by spillovers past. We show the ways in which the emergence of this virus reiterates other infectious disease crises, from its origin via habitat encroachment and animal use by humans to its evolution of troublesome features, and we spotlight a long-running crisis of inequitable infectious disease incidence and death. We conclude by describing aspects of SARS-CoV-2 and the COVID-19 pandemic that present opportunities for disease control: spaces for intervention in infection and recovery that reduce transmission and impact. There are no more "before times"; therefore, we encourage embracing a future using old mitigation tactics and government support for ongoing disease control. [ABSTRACT FROM AUTHOR]

Background: Maternal social environmental stressors during pregnancy are associated with adverse birth and child developmental outcomes, and epigenetics has been proposed as a possible mechanism for such relationships. Methods: In a Mexican-American birth cohort of 241 maternal-infant pairs, cord blood samples were measured for repeat element DNA methylation (LINE-1 and Alu). Linear mixed effects regression was used to model associations between indicators of the social environment (low household income and education, neighborhood-level characteristics) and repeat element methylation. Results from a dietary questionnaire were also used to assess the interaction between maternal diet quality and the social environment on markers of repeat element DNA methylation. Results: After adjusting for confounders, living in the most impoverished neighborhoods was associated with higher cord blood LINE-1 methylation (β = 0.78, 95%CI 0.06, 1.50, p = 0.03). No other neighborhood-, household-, or individual-level socioeconomic indicators were significantly associated with repeat element methylation. We observed a statistical trend showing that positive association between neighborhood poverty and LINE-1 methylation was strongest in cord blood of infants whose mothers reported better diet quality during pregnancy (pinteraction = 0.12). Conclusion: Our findings indicate a small yet unexpected positive association between neighborhood-level poverty during pregnancy and methylation of repetitive element DNA in infant cord blood and that this association is possibly modified by diet quality during pregnancy. However, our null findings for other adverse SES indicators do not provide strong evidence for an adverse association between early-life socioeconomic environment and repeat element DNA methylation in infants.

Individuals considered resilient can overcome adversity, achieving normal physical and psychological development, while those deemed vulnerable may not. Adversity promotes structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus. Moreover, activity-dependent synaptic plasticity is intricately linked to neuronal shaping resulting from experiences. We hypothesize that this plasticity plays a crucial role in resilience processes. However, there is a notable absence of studies investigating this plasticity and behavioral changes following social adversity at different life stages. Consequently, we evaluated the impact of social adversity during early postnatal development (maternal separation [MS]), adulthood (social defeat [SD]), and a combined exposure (MS + SD) on behavioral outcomes (anxiety, motivation, anhedonia, and social interaction). We also examined cFos expression induced by social interaction in mPFC and hippocampus of adult male rats. Behavioral analyses revealed that SD-induced anhedonia, whereas MS + SD increased social interaction and mitigated SD-induced anhedonia. cFos evaluation showed that social interaction heightened plasticity in the prelimbic (PrL) and infralimbic (IL) cortices, dentate gyrus (DG), CA3, and CA1. Social interaction-associated plasticity was compromised in IL and PrL cortices of the MS and SD groups. Interestingly, social interaction-induced plasticity was restored in the MS + SD group. Furthermore, plasticity was impaired in DG by all social stressors, and in CA3 was impaired by SD. Our findings suggest in male rats (i) two adverse social experiences during development foster resilience; (ii) activity-dependent plasticity in the mPFC is a foundation for resilience to social adversity; (iii) plasticity in DG is highly susceptible to social adversity., (© 2024 The Author(s). Journal of Neuroscience Research published by Wiley Periodicals LLC.)

It has been hypothesized that even 'perfect' polygenic scores (PGSs) composed of only causal variants may not be fully portable between different social groups owing to gene-by-environment interactions modifying the expression of relevant variants. The impacts of such interactions involving two forms of social adversity (low socioeconomic status [SES] and discrimination) are examined in relation to the expressivity of a PGS for educational attainment composed of putatively causal variants in a large, representatively sampled and genotyped cohort of US children. A relatively small-magnitude Scarr-Rowe effect is present (SES × PGSEDU predicting General Cognitive Ability [GCA]; sR = .02, 95% CI [.00, .04]), as is a distinct discrimination × PGSEDU interaction predicting GCA (sR = -.02, 95% CI [-.05, 00]). Both are independent of the confounding main effects of 10 ancestral principal components, PGSEDU, SES, discrimination and interactions among these factors. No sex differences were found. These interactions were examined in relation to phenotypic and genotypic data on height, a prospectively more socially neutral trait. They were absent in both cases. The discrimination × PGSEDU interaction is a co-moderator of the differences posited in modern versions of Spearman's hypothesis (along with shared environmentality), lending support to certain environmental explanations of those differences. Behavior-genetic analysis of self-reported discrimination indicates that it is nonsignificantly heritable (h2 = .027, 95% CI [-.05, .10]), meaning that it is not merely proxying some underlying source of heritable phenotypic variability. This suggests that experiences of discrimination might stem instead from the action of purely social forces. [ABSTRACT FROM AUTHOR]

Adolescence may be a window of opportunity to attenuate the effects of early social adversity, which impedes cognitive, emotional, and social development, and increases risk of psychopathology into adulthood. We ran a pragmatic randomized controlled trial to assess the impact of a brief intervention designed to facilitate life skills for psychosocial competence. Socially disadvantaged young people living in South India who had experienced early adversity (N = 645; age range = 17–22 years) participated in the intervention or were assigned to a wait-list control group. The intervention led to large differences in life skills between the two groups. This brief, scalable intervention can be made available to address the impact of early social adversity on young people's development. [ABSTRACT FROM AUTHOR]

Background: A growing body of evidence from high-income contexts suggests a strong association between sexual violence victimisation and self-harm and eventual suicide. However, both sexual violence and self-harm among adolescents are still less researched in sub-Saharan African countries, including Ghana.Objectives: To estimate the 12-month prevalence of self-harm, and to describe the associated factors and reported reasons for self-harm among school-going adolescent survivors of sexual violence victimisation during the previous 12 months in urban Ghana.Methods: Analytic data came from a regional-based representative cross-sectional survey including in-school youth (N = 1,723) conducted in 2017 within the Greater Accra Region of Ghana. Of these, 297 (17.2%) self-reported sexual violence victimisation in the previous 12 months; this proportion of the participants (n = 297) was the focus of the current study. Items measuring sexual violence victimisation, self-harm, and correlates were adopted from the 2012 Ghana WHO–Global School-based Student Health Survey and the Child and Adolescent Self-harm in Europe Study. Data analysis involved multivariable logistic regression models.Results: The estimate of self-harm ideation during the previous 12 months was 45.8% (95% CI: 40–52), whereas the estimate of self-harm behaviour was 38.7% (95% CI: 33–44). About two in five of the participants who reported self-harm wanted to die by their last episode of the behaviour. While bullying victimisation was associated with increased odds of self-harm ideation (aOR = 1.97, 95% CI 1.17, 3.31, p = 0.010) and behaviour (aOR = 2.76, 95% CI 1.59, 4.80, p < 0.001), weekly alcohol use (aOR = 2.56, 95% CI 1.32, 4.93, p = 0.005), conflict with parents (aOR = 2.30, 95% CI 1.28, 4.12, p = 0.005), and physical abuse victimisation (aOR = 1.80, 95% CI 1.03, 3.15, p = 0.037) showed strong associations with increased odds of self-harm behaviour in the past 12 months.Conclusions: The evidence underscores the need for both universal and targeted multi-level intervention and prevention programmes to mitigate the offence of sexual violence and reduce the chances of self-harm among adolescent survivors of sexual violence in urban Ghana.

Summary: The identification of human violence determinants has sparked multiple questions from different academic fields. Innovative methodological assessments of the weight and interaction of multiple determinants are still required. Here, we examine multiple features potentially associated with confessed acts of violence in ex-members of illegal armed groups in Colombia (N = 26,349) through deep learning and feature-derived machine learning. We assessed 162 social-contextual and individual mental health potential predictors of historical data regarding consequentialist, appetitive, retaliative, and reactive domains of violence. Deep learning yields high accuracy using the full set of determinants. Progressive feature elimination revealed that contextual factors were more important than individual factors. Combined social network adversities, membership identification, and normalization of violence were among the more accurate social-contextual factors. To a lesser extent the best individual factors were personality traits (borderline, paranoid, and antisocial) and psychiatric symptoms. The results provide a population-based computational classification regarding historical assessments of violence in vulnerable populations. The bigger picture: We assessed a comprehensive group of social-contextual and individual mental health factors to classify confessed acts of violence committed in the past among a large sample of Colombian ex-members of illegal armed groups (N = 26,349). We used a novel data-driven approach to classify subjects based on four confessed domains of violence (DoVs) and including two groups, (1) ex-members who admitted violent acts and (2) ex-members who denied violence in each DoV, matched by sex, age, and education stage. We found that accurate classification required both social-contextual and individual mental health factors, although the social-contextual factors were the most relevant. Our study provides population-based evidence on the factors associated with historical assessments of violence and describes a powerful analytical approach. This study opens up a new agenda for developing computational approaches for situated, multidimensional, and evidence-based assessments of violence.

Individuals face discrimination based on characteristics including race/ethnicity, gender, age, and disability. Discriminatory experiences (DE) are associated with poor psychological health in the general population and with worse outcomes among individuals at clinical high risk for psychosis (CHR). Though the brain is sensitive to stress, and brain structural change is a well-documented precursor to psychosis, potential relationships between DE and brain structure among CHR or healthy individuals are not known. This report assessed whether lifetime DE are associated with cortical thinning and clinical outcomes across time, after controlling for discrimination-related demographic factors among CHR individuals who ultimately do (N = 57) and do not convert to psychosis (N = 451), and healthy comparison (N = 208) participants in the North American Prodrome Longitudinal Study 2. Results indicate that DE are associated with thinner cortex across time in several cortical areas. Thickness in several right hemisphere regions partially mediates associations between DE and subsequent anxiety symptoms, but not attenuated positive symptoms of psychosis. This report provides the first evidence to date of an association between DE and brain structure in both CHR and healthy comparison individuals. Results also suggest that thinner cortex across time in areas linked with DE may partially explain associations between DE and cross-diagnostic indicators of psychological distress.

BackgroundSeveral studies suggest significant relationships between migration and autism spectrum disorder (ASD) but there are discrepant results. Given that no studies to date have included a pathological control group, the specificity of the results in ASD can be questioned.AimsTo compare the migration experience (premigration, migratory trip, postmigration) in ASD and non-ASD pathological control groups, and study the relationships between migration and autism severity.MethodParents’ and grandparents’ migrant status was compared in 30 prepubertal boys with ASD and 30 prepubertal boys without ASD but with language disorders, using a questionnaire including Human Development Index (HDI)/Inequality-adjusted Human Development Index (IHDI) of native countries. Autism severity was assessed using the Child Autism Rating Scale, Autism Diagnostic Observation Schedule and Autism Diagnostic Interview-Revised scales.ResultsThe parents’ and grandparents’ migrant status frequency did not differ between ASD and control groups and was not associated with autism severity. The HDI/IHDI values of native countries were significantly lower for parents and grandparents of children with ASD compared with the controls, especially for paternal grandparents. Furthermore, HDI/IDHI levels from the paternal line (father and especially paternal grandparents) were significantly negatively correlated with autism severity, particularly for social interaction impairments.ConclusionsIn this study, parents’ and/or grandparents’ migrant status did not discriminate ASD and pathological control groups and did not contribute either to autism severity. However, the HDI/IHDI results suggest that social adversity-related stress experienced in native countries, especially by paternal grandparents, is potentially a traumatic experience that may play a role in ASD development. A ‘premigration theory of autism’ is then proposed.

Abstract Background Maternal social environmental stressors during pregnancy are associated with adverse birth and child developmental outcomes, and epigenetics has been proposed as a possible mechanism for such relationships. Methods In a Mexican-American birth cohort of 241 maternal-infant pairs, cord blood samples were measured for repeat element DNA methylation (LINE-1 and Alu). Linear mixed effects regression was used to model associations between indicators of the social environment (low household income and education, neighborhood-level characteristics) and repeat element methylation. Results from a dietary questionnaire were also used to assess the interaction between maternal diet quality and the social environment on markers of repeat element DNA methylation. Results After adjusting for confounders, living in the most impoverished neighborhoods was associated with higher cord blood LINE-1 methylation (β = 0.78, 95%CI 0.06, 1.50, p = 0.03). No other neighborhood-, household-, or individual-level socioeconomic indicators were significantly associated with repeat element methylation. We observed a statistical trend showing that positive association between neighborhood poverty and LINE-1 methylation was strongest in cord blood of infants whose mothers reported better diet quality during pregnancy (p interaction = 0.12). Conclusion Our findings indicate a small yet unexpected positive association between neighborhood-level poverty during pregnancy and methylation of repetitive element DNA in infant cord blood and that this association is possibly modified by diet quality during pregnancy. However, our null findings for other adverse SES indicators do not provide strong evidence for an adverse association between early-life socioeconomic environment and repeat element DNA methylation in infants.

Social experience is an important predictor of disease susceptibility and survival in humans and other social mammals. Chronic social stress is thought to generate a proinflammatory state characterized by elevated antibacterial defenses and reduced investment in antiviral defense. Here we manipulated long-term social status in female rhesus macaques to show that social subordination alters the gene expression response to ex vivo bacterial and viral challenge. As predicted by current models, bacterial lipopolysaccharide polarizes the immune response such that low status corresponds to higher expression of genes in NF-κB–dependent proinflammatory pathways and lower expression of genes involved in the antiviral response and type I IFN signaling. Counter to predictions, however, low status drives more exaggerated expression of both NF-κB– and IFN-associated genes after cells are exposed to the viral mimic Gardiquimod. Status-driven gene expression patterns are linked not only to social status at the time of sampling, but also to social history (i.e., past social status), especially in unstimulated cells. However, for a subset of genes, we observed interaction effects in which females who fell in rank were more strongly affected by current social status than those who climbed the social hierarchy. Taken together, our results indicate that the effects of social status on immune cell gene expression depend on pathogen exposure, pathogen type, and social history—in support of social experience-mediated biological embedding in adulthood, even in the conventionally memory-less innate immune system. [ABSTRACT FROM AUTHOR]

Trauma is associated with the appearance of the concept of 'accident' as a social and legal entity, as well as with the successive discoveries of surgery, psychiatrics, and psychoanalysis. Today, epigenetics has redefined trauma as an extreme form of social adversity. Because of the exceptional nature of the events studied and also the social and political significance of its results, the social epigenetics of historical trauma has received undeniable public success. The present article investigates the general dynamics of this research front, as well as the forms and consequences of its public circulation. We highlight the specificity of the circulation modes associated with social epigenetics and the myriad ways it has been used socially and politically. This study addresses four registers of action in particular: to attest, to repair, to intervene, and to text. The social circulation of the epigenetics of trauma is as influenced by the public's willingness to see it as socially and politically relevant as it is by the ability of researchers to prepare this collective appropriation through different forms of public engagement. Finally this study allows us to refute the dichotomic conception of the genetics/epigenetics relationship, which is too frequently the foundation for making epigenetics academically acceptable in the social sciences. [ABSTRACT FROM AUTHOR]

Schizotypy is a personality-organisation related to schizophrenia-liability as well as the emergence of psychotic symptoms and psychotic-like experiences (PLEs) in non-schizophrenic individuals. It has been suggested that some non-schizophrenic individuals may exhibit PLEs frequently, but in a fashion that is not distressing but life-enhancing ("benign schizotypy"). In schizophrenia and at-risk individuals, however, psychotic symptoms are not only distressing, but also triggered stress. To further investigate questions of causality and examine how PLEs may present as distressing symptoms in some individuals and as benign experiences in others, we explored how schizotypy-facets moderated PLEs-variability under experimentally induced social stress.We performed a standardised social stress-paradigm in 107 healthy adults (77 female, 30 male; average age 22,5 years), measuring changes in psychometrically assessed PLEs and the moderation of changes under stress through positive, negative and disorganised schizotypy. Results suggest two discrete effects: On the one hand, individuals high in disorganised and negative schizotypy showed stress-dependent increases in PLEs; without added effects of positive schizotypy. On the other, individuals low in negative and disorganised schizotypy showed higher levels of PLEs solely as a function of positive schizotypy but not stress. We discuss these findings in light of the fully-dimensional model of schizotypy and hypothesize that PLEs in individuals high in schizotypy-facets suggested to convey risk-for-schizophrenia (negative and disorganised) may reflect qualitatively different entities than PLEs in individuals with low values in these facets, but high expressions of positive schizotypy ("happy schizotypes"). Additionally, we emphasize the importance of not overlooking the disorganised schizotypy-facet in related research. [ABSTRACT FROM AUTHOR]

As mental health services are increasingly embracing the recovery model, we conducted a study to better understand how social adversity impacts recovery. We also examined how associations between social adversity and recovery are influenced (moderated or mediated) by symptom severity. Data on seven social adversity measures, eight recovery measures, and symptom severity were collected from 300 English-speaking participants, ages 18–65 years, with a diagnosis of a psychotic or mood disorder, from five community mental health agencies in diverse neighborhoods in Washington, D.C. We employed standard correlation, exploratory factor analyses, analysis of variance, and hierarchic regression procedures. Diagnostic category and gender impacted Home Environment Adversities (e.g., food insecurity, perceived neighborhood disorder), the diagnostic category-by-gender interaction influenced Social and Economic Adversities (e.g., years of education and income), and gender affected Recovery. Controlling for diagnostic category and gender, Social and Economic Adversities accounted for 1.7% of variance in Recovery, while Home Environment Adversities accounted for 8.6% (their joint influence was 3.4%). Although symptom severity did not moderate these associations, it partially mediated the effect of Social and Economic Adversities on Recovery, and substantially mediated the effect of Home Environment Adversities on Recovery. The extent to which patients with serious mental illnesses experience recovery may be meaningfully influenced not only by symptoms, but by their social and environmental circumstances. [ABSTRACT FROM AUTHOR]

Hair cortisol has the potential to provide insight into young children's long‐term stress response to social adversity. This study investigated associations between children's exposure to adversity from pregnancy to 2 years of age and their hair cortisol at 2 years, using a longitudinal cohort of children enriched for adversity risk, whose mothers were recruited during pregnancy through the "right@home" trial. Exposures were 18 maternal socioeconomic and psychosocial indicators of adversity, examined as concurrent, cumulative, and longitudinal exposure from pregnancy to 2 years. Hair samples were analyzed from 319/603 (53%) children participating at 2 years. Multivariable regression analyses for concurrent exposure showed three indicators of adversity were associated with higher hair cortisol (housing tenure of public rental, paying board or living rent free; not living in a safe place; higher maternal stress symptoms), one with lower hair cortisol (housing problems), and 14 indicators with no evidence of association. There was no evidence of association for the cumulative adversity count. Longitudinal exposure showed "intermittent" and "persistent" high maternal stress symptoms were associated with higher hair cortisol. The small number of associations identified suggests that hair cortisol is limited as a measure of stress response to social adversity in children at 2 years. [ABSTRACT FROM AUTHOR]

Intimate partner violence (IPV) is associated with an increased risk of poorer child development. Existing research has focused on physical abuse with less known about the associations with emotional IPV. To describe the period prevalence of mother's experiences of emotional IPV during children's preschool years and associations with child mental, physical, social, and cognitive development. Secondary analysis of control group data (n = 194) from an Australian randomised trial (right@home), which recruited pregnant women experiencing social adversity from antenatal clinics in 2013–14. Women reported emotional abuse (Composite Abuse Scale) at child ages 3–5 years. Measures of child development at 5 years included: Strengths and Difficulties Questionnaire, Social Skills Improvement System, Pediatric Quality of Life Inventory, Clinical Evaluation of Language Fundamentals, School Entry Alphabetic and Phonological Awareness Readiness Test, NIH executive function subtests, sleep and health. The prevalence of emotional IPV from 3 to 5 years was estimated. Regression models compared developmental outcomes according to emotional IPV exposure, adjusted for child age, child gender, and maternal education. Missing data were accounted for using multiple imputation. From 3-5 years, emotional IPV was experienced by 57% of women. Emotional IPV exposure was consistently associated with poorer child developmental outcomes. Differences were most apparent for SDQ internalising (mean difference 1.2, 95% CI 0.2 to 2.1) and externalising difficulties (1.2, 95% CI −0.1 to 2.4). Emotional IPV was highly prevalent amongst families experiencing social adversity. Developing acceptable and effective identification processes and interventions that prioritise families experiencing co-occurring social adversities should be a public health priority. • Emotional IPV was highly prevalent (57%) in a cohort of women and young children experiencing social adversity. • Children raised in families experiencing social adversity had poorer developmental outcomes compared to population cohorts. • Outcomes were poorer when exposed to emotional IPV and were most apparent for internalising and externalising difficulties. • Assessing social adversity more broadly may help identify families at risk of emotional IPV. [ABSTRACT FROM AUTHOR]

Social experiences are strongly associated with individuals' health, aging, and survival in many mammalian taxa, including humans. Despite their role as models of many other physiological and developmental bases of health and aging, biomedical model organisms (particularly lab mice) remain an underutilized tool in resolving outstanding questions regarding social determinants of health and aging, including causality, context-dependence, reversibility, and effective interventions. This status is largely due to the constraints of standard laboratory conditions on animals' social lives. Even when kept in social housing, lab animals rarely experience social and physical environments that approach the richness, variability, and complexity they have evolved to navigate and benefit from. Here we argue that studying biomedical model organisms outside under complex, semi-natural social environments ("re-wilding") allows researchers to capture the methodological benefits of both field studies of wild animals and laboratory studies of model organisms. We review recent efforts to re-wild mice and highlight discoveries that have only been made possible by researchers studying mice under complex, manipulable social environments. [ABSTRACT FROM AUTHOR]

Background Sound evidence has linked the experience of adversity with depression. Less is known about this association over time. Aim The aim of this study is to determine whether or not social adversity experienced by pregnant women is associated with their patterns of depressive symptoms over their reproductive life course. Methods Data were obtained from a cohort of women collected at their first obstetrical clinic visit of an index pregnancy (time-point 1) and at a further six time-points to 27 years following the birth. Latent Class Growth Modelling was used to estimate trajectories of women’s depressive symptoms over this time period. Logistic regression modelling determined the prospective association between measures of adversity in pregnancy and 27-year postpartum depression trajectories, controlling for potential confounders. Findings Experiencing financial problems, housing problems, serious disagreements with partners and with others, and experiencing serious health problems in pregnancy were associated with membership of high and middle depression trajectories over the 27 years. Having someone close die or have a serious illness was associated with the high depression trajectory only. Younger maternal age and low family-income at first clinic visit were also associated with an increased risk of women’s membership of both high and middle depression trajectories. Conclusions Experiencing adversity during pregnancy predicts subsequent patterns of maternal depression over an extended period of women’s reproductive life course. It is not clear whether women’s experiences of adversity during pregnancy were causally associated with subsequent depression or whether there are other explanations of the observed association. [ABSTRACT FROM AUTHOR]

The display of antisocial behaviors in children and adolescents has been of interest to criminologists and developmental psychologists for years. Exposure to social adversity is a well-documented predictor of antisocial behavior. Additionally, measures of autonomic nervous system (ANS) activity, including heart rate variability (HRV), pre-ejection period (PEP), and heart rate, have been associated with antisocial behaviors including rule-breaking and aggression. Social neuroscience research has begun to investigate how neurobiological underpinnings affect the relationship between social adversity and antisocial/psychopathic behavior in children and adolescents. This study investigated the potential mediating effects of ANS activity on the relationship between social adversity and antisocial behavior in a group of 7- to 10-year-old children from the community (N = 339; 48.2% male). Moderated multiple mediation analyses revealed that low resting heart rate, but not PEP or HRV, mediated the relationship between social adversity and antisocial behavior in males only. Social adversity but not ANS measures were associated with antisocial behavior in females. Findings have implications for understanding the neural influences that underlie antisocial behavior, illustrate the importance of the social environment regarding the expression of these behaviors, and highlight essential gender differences. [ABSTRACT FROM AUTHOR]

Background The causal role of childhood trauma for psychosis is well established, but the mechanisms that link trauma to psychosis are largely unknown. Since childhood trauma is known to cause difficulties in emotion regulation (ER) and patients with psychosis show impaired ER, we hypothesize that impaired ER explains why people with a background of trauma are prone to psychotic experiences. Methods The study used a longitudinal cohort design based on a community sample ( N = 562) from Germany, Indonesia, and the United States. Childhood trauma was assessed at baseline. ER and psychotic experiences (defined as positive symptom frequency and related distress) were measured repeatedly at a 4-, 8-, and 12-month follow-up. Cross-lagged panel and longitudinal mediation analyses with structural equation modeling were used to test the predictive value of ER on psychotic experiences and its mediating role in the association of childhood trauma and psychotic experiences. Results The cross-lagged paths from impaired ER to symptom distress (but not frequency) were significant. However, there was also evidence for the reverse causation from symptom frequency and distress to impaired ER. ER partially mediated the significant prospective paths from childhood trauma to symptom distress. Conclusion The findings demonstrate that ER plays a role in translating childhood trauma into distressing psychotic experiences in later life. Moreover, the findings point to a maintenance mechanism in which difficulties in ER and symptom distress exacerbate each other. Thus, ER could be a promising target for interventions aimed at prevention of psychosis. [ABSTRACT FROM AUTHOR]

BackgroundA growing body of evidence suggests that indicators of social disadvantage are associated with an increased risk of psychosis. However, only a few studies have specifically looked at cumulative effects and long-term associations. The aims of this study are: To compare the prevalence of specific indicators of social disadvantage at, and prior to, first contact with psychiatric services in patients suffering their first episode of psychosis and in a control sample. To explore long-term associations, cumulative effects, and direction of effects.MethodWe collected information on social disadvantage from 332 patients and from 301 controls recruited from the local population in South London. Three indicators of social disadvantage in childhood and six indicators of social disadvantage in adulthood were analysed.ResultsAcross all the domains considered, cases were more likely to report social disadvantage than were controls. Compared with controls, cases were approximately two times more likely to have had a parent die and approximately three times more likely to have experienced a long-term separation from one parent before the age of 17 years. Cases were also more likely than controls to report two or more indicators of adult social disadvantage, not only at first contact with psychiatric services [odds ratio (OR) 9.5], but also at onset of psychosis (OR 8.5), 1 year pre-onset (OR 4.5), and 5 years pre-onset (OR 2.9).ConclusionsGreater numbers of indicators of current and long-term exposure are associated with progressively greater odds of psychosis. There is some evidence that social disadvantage tends to cluster and accumulate. [ABSTRACT FROM PUBLISHER]

Summary: Background: A number of studies have found associations between multiple aspects of social adversity and obesity in childhood, yet this research has largely been limited to cross‐sectional data. Objectives: This study aimed to address this limitation by using life course trajectory methods to determine whether multiple aspects of social adversity in early childhood are associated with changes in body mass index (BMI) throughout childhood. Methods: Associations between multiple measures of social adversity from birth to 4 years and subsequent BMI trajectories to age 17 were examined in 7021 children in the Avon Longitudinal Study of Parents and Children. Results: Higher BMI throughout ages 12–17 were observed for children whose parents had separated, were exposed to frequent residential mobility or who experienced moderate or great household financial difficulty in early childhood. After adjustment for confounding variables, associations were attenuated but remained for both moderate (two moves) and high (≥3 moves) residential mobility (mean % difference in BMI at age 17 for children experiencing moderate and high residential mobility before age 4 compared with those experiencing no moves: 2.3; 95% CI: 0.5–4.2; P = 0.015 and 4.2; 95% CI: 1.4–7.0; P = 0.004, respectively). Conclusions: Associations between BMI and social adversity in childhood are present but largely explained by background socioeconomic position. However, there remain small but important differences between the BMI of children who are exposed to frequent residential mobility in early childhood after adjustment for socioeconomic and other confounders. [ABSTRACT FROM AUTHOR]

Abnormal parasympathetic nervous system (PNS)-related cardiac activity has been linked to aggression. However, little is known about how it interacts with psychosocial adversity in predisposing to reactive-proactive aggression. In the current study, 84 male and female college students self-reported reactive and proactive aggression, and were assessed for respiratory sinus arrhythmia (RSA), a measure of PNS-related cardiac activity, during rest and when they contemplated an emotion-evoking decision-making task. Regression analyses showed that (a) resting RSA was positively linked to reactive aggression in conditions of high social adversity, and (b) RSA reactivity was positively associated with reactive but negatively associated with proactive aggression, in conditions of low social adversity. Main effects were not found for psychophysiological functioning or psychosocial adversity, suggesting the importance of their interaction. Findings support a biosocial basis for aggression and add additional support for the distinctions between reactive and proactive aggression. [ABSTRACT FROM AUTHOR]

Psychiatric disorders in adolescence are linked to social adversity, family dysfunction and abuse. In Mexico City, up to 68% of the adolescents have experienced at least one chronic adversity. Mental health problems, such as depression and attention deficit hyperactivity disorder, are frequent and cause academic problems. The social and economic differences between students in public and private secondary is well known. However, it has not been established what the differences between social adversity and psychiatric disorders are among these populations. The aim of this investigation was to determine and compare, in a clinical two-step procedure, these features in secondary students from southern Mexico City. Method Agreement for convenience with seven secondary schools from southern Mexico City, four public and three private, was carried out. Prior parental consent and adolescent assent, a clinical screening that evaluated internalized and externalized symptoms was applied to 1 474 students. Positive screening for probable psychopathology was found in 419 students. Of these, 319 accepted a clinical interview and 177 were interviewed. Results Of the 117 adolescents interviewed, 83.8% were cases. There were more public school students than private school students: 64 (91%) vs. 34 (71%) (χ2=7.85, P=0.005), respectively. The average age was 13.39 years (SD=0.98). Family dysfunction was found in 57 (48.71%) of the 117 adolescents. The overall performance was assessed by the GAF; the mean score of all students was 65.48 (SD=11.68). Major depressive disorder and attention deficit hyperactivity disorder were the most frequent diagnoses, with 48.7% and 59.8%, respectively. The psychological and physical abuse, family dysfunction and major depressive disorder occurred significantly in more students from public schools. Conclusions Social adversity and depression were present and more associated in students from public than private secondary schools. This represents a challenge for educational and mental health services for the early recognition and prompt attention as there is a link between social welfare and mental health. [ABSTRACT FROM AUTHOR]