Socioeconomic changes predict genome-wide DNA methylation in childhood.

Childhood socioeconomic position (SEP) is a major determinant of health and well-being across the entire life course. To effectively prevent and reduce health risks related to SEP, it is critical to better understand when and under what circumstances socioeconomic adversity shapes biological processes. DNA methylation (DNAm) is one such mechanism for how early life adversity 'gets under the skin'. In this study, we evaluated the dynamic relationship between SEP and DNAm across childhood using data from 946 mother-child pairs in the Avon Longitudinal Study of Parents and Children. We assessed six SEP indicators spanning financial, occupational and residential domains during very early childhood (ages 0-2), early childhood (ages 3-5) and middle childhood (ages 6-7). Epigenome-wide DNAm was measured at 412 956 cytosine-guanines (CpGs) from peripheral blood at age 7. Using an innovative two-stage structured life-course modeling approach, we tested three life-course hypotheses for how SEP shapes DNAm profiles-accumulation, sensitive period and mobility. We showed that changes in the socioeconomic environment were associated with the greatest differences in DNAm, and that middle childhood may be a potential sensitive period when socioeconomic instability is especially important in shaping DNAm. Top SEP-related DNAm CpGs were overrepresented in genes involved in pathways important for neural development, immune function and metabolic processes. Our findings highlight the importance of socioeconomic stability during childhood and if replicated, may emphasize the need for public programs to help children and families experiencing socioeconomic instability and other forms of socioeconomic adversity.

DNA methylation as a possible causal mechanism linking childhood adversity and health: Results from two-sample mendelian randomization study.

Childhood adversity is an important risk factor for adverse health across the life course. Epigenetic modifications, such as DNA methylation (DNAm), are one hypothesized mechanism linking adversity to disease susceptibility. Yet, few studies have determined whether adversity-related DNAm alterations are causally related to future health outcomes or if their developmental timing plays a role in these relationships. Here, we used two-sample Mendelian Randomization to obtain stronger causal inferences about the association between adversity-associated DNAm loci across development (i.e., birth; childhood; adolescence; young adulthood) and 24 mental, physical, and behavioral health outcomes. We identified particularly strong associations between adversity-associated DNAm and ADHD, depression, obsessive-compulsive disorder, suicide attempts, asthma, coronary artery disease, and chronic kidney disease. A greater number of associations were identified for birth and childhood DNAm, while adolescent and young adulthood DNAm were more closely linked to mental health. Childhood DNAm loci also showed primarily risk suppressing relationships with health outcomes, suggesting that DNAm might reflect compensatory or buffering mechanisms against childhood adversity, rather than acting solely as an indicator of disease risk. Together, our results suggest adversity-related DNAm alterations are linked to both physical and mental health outcomes, with particularly strong impacts of DNAm differences emerging earlier in development.

Depressive symptoms in adolescence and adult educational and employment outcomes: a structured life course analysis.

BACKGROUND: Depression is a common mental health disorder that often starts during adolescence, with potentially important future consequences including 'Not in Education, Employment or Training' (NEET) status. METHODS: We took a structured life course modeling approach to examine how depressive symptoms during adolescence might be associated with later NEET status, using a high-quality longitudinal data resource. We considered four plausible life course models: (1) an early adolescent sensitive period model where depressive symptoms in early adolescence are more associated with later NEET status relative to exposure at other stages; (2) a mid adolescent sensitive period model where depressive symptoms during the transition from compulsory education to adult life might be more deleterious regarding NEET status; (3) a late adolescent sensitive period model, meaning that depressive symptoms around the time when most adults have completed their education and started their careers are the most strongly associated with NEET status; and (4) an accumulation of risk model which highlights the importance of chronicity of symptoms. RESULTS: Our analysis sample included participants with full information on NEET status (N = 3951), and the results supported the accumulation of risk model, showing that the odds of NEET increase by 1.015 (95% CI 1.012-1.019) for an increase of 1 unit in depression at any age between 11 and 24 years. CONCLUSIONS: Given the adverse implications of NEET status, our results emphasize the importance of supporting mental health during adolescence and early adulthood, as well as considering specific needs of young people with re-occurring depressed mood.

The Prevalence, Predictors, and Health Consequences of Disagreement in Reports of Child Maltreatment Exposure.

The purpose of this study was to examine the prevalence, predictors, and consequences of disagreement between prospective caregiver and retrospective child reports of childhood physical and emotional maltreatment. The design was a secondary analysis of data from the Avon Longitudinal Study of Parents and Children, a three-decade long UK-based birth cohort. Prospective caregiver reports were in poor to fair agreement with retrospective child reports for physical and emotional maltreatment exposure, with caregivers tending to underreport exposure. Disagreement between reporters was associated with increased risk of depressive symptoms and substance use severity, but decreased risk for mental health diagnoses. Screening measures of childhood maltreatment exposure should take caution against using measures from different reporters interchangeably (i.e., from mother versus child). Disagreement in reports may indicate unmet need for mental health evaluation.

Testing lifecourse theories characterising associations between maternal depression and offspring depression in emerging adulthood: the Avon Longitudinal Study of Parents and Children.

BACKGROUND: Maternal depression is a major determinant of offspring mental health. Yet, little is understood about how the duration and timing of maternal depression shapes youth risk for depressive symptoms, which if understood could inform when best to intervene. This study aimed to determine how the timing and duration of maternal depression was related to offspring depression in emerging adulthood, and if these associations varied by sex. METHODS: We analysed data from the Avon Longitudinal Study of Parents and Children (a prenatal cohort in the Avon area of England, 1991-2003), n = 3,301. We applied the structured lifecourse modelling approach to maternal depression (assessed at 13 points from prenatal period to adolescence) and emerging adult depressive symptoms (age 21). Lifecourse models assessed were accumulation (sum of timepoints when maternal depression was reported), sensitive periods (each period assessed as one during which maternal depression has a stronger effect) and instability (frequent fluctuations in maternal depression). RESULTS: Female adolescents (n = 2,132) had higher SMFQ scores (mean = 6.15, SD = 5.90) than males (n = 1,169, mean = 4.87, SD = 4.82). Maternal depression was most common in the infancy period (21.2% males; 21.4% females). For males, accumulation was the most appropriate lifecourse model; for each additional period of maternal depression, depressive symptoms in emerging adulthood increased by 0.11 (95% CI: 0.07, 0.15, one-sided p value ≤ .001). For females, exposure to maternal depression was associated with increasing depressive symptoms in emerging adulthood, with the largest effect in mid-childhood (increase of 0.27 units, 95% CI 0.03-0.50, p = .015 for difference between mid-childhood and other time-periods) and a smaller, equal effect at all other time-periods (increase of 0.07 units per time-period, 95% CI: 0.03-0.12, p = .002). CONCLUSIONS: This study highlights the importance of ongoing maternal depression for the development of depression in offspring through to emerging adulthood. Because long-term exposure to maternal depression was particularly important, early interventions are warranted.

Autosomal sex-associated co-methylated regions predict biological sex from DNA methylation.

Sex is a modulator of health that has been historically overlooked in biomedical research. Recognizing this knowledge gap, funding agencies now mandate the inclusion of sex as a biological variable with the goal of stimulating efforts to illuminate the molecular underpinnings of sex biases in health and disease. DNA methylation (DNAm) is a strong molecular candidate for mediating such sex biases; however, a robust and well characterized annotation of sex differences in DNAm is yet to emerge. Beginning with a large (n = 3795) dataset of DNAm profiles from normative adult whole blood samples, we identified, validated and characterized autosomal sex-associated co-methylated genomic regions (sCMRs). Strikingly, sCMRs showed consistent sex differences in DNAm over the life course and a subset were also consistent across cell, tissue and cancer types. sCMRs included sites with known sex differences in DNAm and links to health conditions with sex biased effects. The robustness of sCMRs enabled the generation of an autosomal DNAm-based predictor of sex with 96% accuracy. Testing this tool on blood DNAm profiles from individuals with sex chromosome aneuploidies (Klinefelter [47,XXY], Turner [45,X] and 47,XXX syndrome) revealed an intimate relationship between sex chromosomes and sex-biased autosomal DNAm.

Early-life trauma endophenotypes and brain circuit-gene expression relationships in functional neurological (conversion) disorder.

Functional neurological (conversion) disorder (FND) is a neuropsychiatric condition whereby individuals present with sensorimotor symptoms incompatible with other neurological disorders. Early-life maltreatment (ELM) is a risk factor for developing FND, yet few studies have investigated brain network-trauma relationships in this population. In this neuroimaging-gene expression study, we used two graph theory approaches to elucidate ELM subtype effects on resting-state functional connectivity architecture in 30 patients with motor FND. Twenty-one individuals with comparable depression, anxiety, and ELM scores were used as psychiatric controls. Thereafter, we compared trauma endophenotypes in FND with regional differences in transcriptional gene expression as measured by the Allen Human Brain Atlas (AHBA). In FND patients only, we found that early-life physical abuse severity, and to a lesser extent physical neglect, correlated with corticolimbic weighted-degree functional connectivity. Connectivity profiles influenced by physical abuse occurred in limbic (amygdalar-hippocampal), paralimbic (cingulo-insular and ventromedial prefrontal), and cognitive control (ventrolateral prefrontal) areas, as well as in sensorimotor and visual cortices. These findings held adjusting for individual differences in depression/anxiety, PTSD, and motor phenotypes. In FND, physical abuse also correlated with amygdala and insula coupling to motor cortices. In exploratory analyses, physical abuse correlated connectivity maps overlapped with the AHBA spatial expression of three gene clusters: (i) neuronal morphogenesis and synaptic transmission genes in limbic/paralimbic areas; (ii) locomotory behavior and neuronal generation genes in left-lateralized structures; and (iii) nervous system development and cell motility genes in right-lateralized structures. These circuit-specific architectural profiles related to individual differences in childhood physical abuse burden advance our understanding of the pathophysiology of FND.

Master-planned communities in the United States as novel contexts for individual and population-level research.

It has long been known that social and physical environments can shape individual and population health, for better or worse. Master-planned communities (MPCs) in the US are custom-designed residential neighborhoods with defined boundaries planned and developed under a single, private owner or entity from their inception. Across the US, these vary greatly in scale ranging from 100 to over 50,000 homes, but broadly all provide residents with housing, infrastructure, landscaping, and purpose-built facilities to support socialization. Current research in the urban planning literature suggests that MPCs can influence the health of their residents. However, few studies have examined the use of MPCs as settings to conduct individual or population health research. In this paper, we examine the potential of MPCs as context for observational or intervention studies aimed at understanding individual and population-level health and well-being. We first summarize links between built and social environment and individual and population health research. Next, we describe the history of planned communities in the US. Then, we review specific features of MPCs related to governance, development, design, and social structure. We end by exploring how those specific features may lead to potential opportunities and challenges when using MPCs in health research. Through this discussion, we highlight MPCs as overlooked settings that may offer potential for collaborative, innovative, and socially engaged health research.

Exposure to early childhood maltreatment and its effect over time on social cognition.

Social cognitive deficits can have many negative consequences, spanning social withdrawal to psychopathology. Prior work has shown that child maltreatment may associate with poorer social cognitive skills in later life. However, no studies have examined this association from early childhood into adolescence. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 4,438), we examined the association between maltreatment (caregiver physical or emotional abuse; sexual or physical abuse), assessed repeatedly (every 1-3 years) from birth to age 9, and social cognitive skills at ages 7.5, 10.5, and 14 years. We evaluated the role of both the developmental timing (defined by age at exposure) and accumulation of maltreatment (defined as the number of occasions exposed) using a least angle regression variable selection procedure, followed by structural equation modeling. Among females, accumulation of maltreatment explained the most variation in social cognitive skills. For males, no significant associations were found. These findings underscore the importance of early intervention to minimize the accumulation of maltreatment and showcase the importance of prospective studies to understand the development of social cognition over time.

Associations Between Childhood Trauma Characteristics and Theory of Mind in Adults: Results From a Large, Diverse Sample.

Theory of mind (ToM) is an essential social cognitive process encompassing abilities to represent and understand others' mental states. Although previous reports linked childhood trauma to social cognitive deficits, how characteristics of trauma exposure, such as subtype or timing, affect ToM remains unaddressed. Using data from a diverse adult sample (n = 2200), we tested whether exposure type and first exposure timing of common childhood trauma associated with ToM. Neither interpersonal loss (ß = - 0.25, p = 0.170, [- 0.61, 0.10]) nor child maltreatment (ß = - 0.21, p = 0.369, [- 0.66, 0.25]) was associated with lower ToM. There was no effect of timing of age at which trauma was experienced (F = 2.19, p = 0.087). While we did not identify age-dependent effects, future studies should examine links between timing or chronicity of prospectively reported childhood trauma and social cognition. Understanding of how childhood experiences shape ToM could reveal mechanisms underlying social cognition development and inform prevention efforts.

A Structured Approach to Evaluating Life-Course Hypotheses: Moving Beyond Analyses of Exposed Versus Unexposed in the -Omics Context.

The structured life-course modeling approach (SLCMA) is a theory-driven analytical method that empirically compares multiple prespecified life-course hypotheses characterizing time-dependent exposure-outcome relationships to determine which theory best fits the observed data. In this study, we performed simulations and empirical analyses to evaluate the performance of the SLCMA when applied to genomewide DNA methylation (DNAm). Using simulations (n = 700), we compared 5 statistical inference tests used with SLCMA, assessing the familywise error rate, statistical power, and confidence interval coverage to determine whether inference based on these tests was valid in the presence of substantial multiple testing and small effects-2 hallmark challenges of inference from -omics data. In the empirical analyses (n = 703), we evaluated the time-dependent relationship between childhood abuse and genomewide DNAm. In simulations, selective inference and the max-|t|-test performed best: Both controlled the familywise error rate and yielded moderate statistical power. Empirical analyses using SLCMA revealed time-dependent effects of childhood abuse on DNAm. Our findings show that SLCMA, applied and interpreted appropriately, can be used in high-throughput settings to examine time-dependent effects underlying exposure-outcome relationships over the life course. We provide recommendations for applying the SLCMA in -omics settings and encourage researchers to move beyond analyses of exposed versus unexposed individuals.

Measures of adult psychological resilience following early-life adversity: how congruent are different measures?

BACKGROUND: Psychological resilience - positive psychological adaptation in the context of adversity - is defined and measured in multiple ways across disciplines. However, little is known about whether definitions capture the same underlying construct and/or share similar correlates. This study examined the congruence of different resilience measures and associations with sociodemographic factors and body mass index (BMI), a key health indicator. METHODS: In a cross-sectional sample of 1429 African American adults exposed to child maltreatment, we derived four resilience measures: a self-report scale assessing resiliency (perceived trait resilience); a binary variable defining resilience as low depression and posttraumatic stress (absence of distress); a binary variable defining resilience as low distress and high positive affect (absence of distress plus positive functioning); and a continuous variable reflecting individuals' deviation from distress levels predicted by maltreatment severity (relative resilience). Associations between resilience measures, sociodemographic factors, and BMI were assessed using correlations and regressions. RESULTS: Resilience measures were weakly-to-moderately correlated (0.27-0.69), though similarly patterned across sociodemographic factors. Women showed higher relative resilience, but lower perceived trait resilience than men. Only measures incorporating positive affect or resiliency perceptions were associated with BMI: individuals classified as resilient by absence of distress plus positive functioning had lower BMI than non-resilient (ß = -2.10, p = 0.026), as did those with higher perceived trait resilience (ß = -0.63, p = 0.046). CONCLUSION: Relatively low congruence between resilience measures suggests studies will yield divergent findings about predictors, prevalence, and consequences of resilience. Efforts to clearly define resilience are needed to better understand resilience and inform intervention and prevention efforts.

Genetic liability to schizophrenia is associated with exposure to traumatic events in childhood.

BACKGROUND: There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene-environment correlation. METHODS: The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0-17 years; ALSPAC) and at age 8 years (MoBa). RESULTS: Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure. CONCLUSIONS: Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment.

Genome-wide gene-environment analyses of major depressive disorder and reported lifetime traumatic experiences in UK Biobank.

Depression is more frequent among individuals exposed to traumatic events. Both trauma exposure and depression are heritable. However, the relationship between these traits, including the role of genetic risk factors, is complex and poorly understood. When modelling trauma exposure as an environmental influence on depression, both gene-environment correlations and gene-environment interactions have been observed. The UK Biobank concurrently assessed Major Depressive Disorder (MDD) and self-reported lifetime exposure to traumatic events in 126,522 genotyped individuals of European ancestry. We contrasted genetic influences on MDD stratified by reported trauma exposure (final sample size range: 24,094-92,957). The SNP-based heritability of MDD with reported trauma exposure (24%) was greater than MDD without reported trauma exposure (12%). Simulations showed that this is not confounded by the strong, positive genetic correlation observed between MDD and reported trauma exposure. We also observed that the genetic correlation between MDD and waist circumference was only significant in individuals reporting trauma exposure (rg = 0.24, p = 1.8 × 10-7 versus rg = -0.05, p = 0.39 in individuals not reporting trauma exposure, difference p = 2.3 × 10-4). Our results suggest that the genetic contribution to MDD is greater when reported trauma is present, and that a complex relationship exists between reported trauma exposure, body composition, and MDD.

Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence.

BACKGROUND: Early-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. METHODS: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures. RESULTS: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. CONCLUSIONS: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns.

Individual Differences in the Stability and Change of Childhood Depression: A Growth Mixture Model With Structured Residuals.

Studies of developmental trajectories of depression are important for understanding depression etiology. Existing studies have been limited by short time frames and no studies have explored a key factor: differential patterns of responding to life events. This article introduces a novel analytic technique, growth mixture modeling with structured residuals, to examine the course of youth depression in a large, prospective cohort (N = 11,641, ages 4-16.5, 96% White). Age-specific critical points were identified at ages 8 and 13 where depression symptoms spiked for a minority of children. Most depression risk was due to dynamic responses to environmental events, drawn not from a small pool of persistently depressed children, but a larger pool of children who varied across higher and lower symptom levels.

The mental health effects of pet death during childhood: is it better to have loved and lost than never to have loved at all?

Pet ownership is common. Growing evidence suggests children form deep emotional attachments to their pets. Yet, little is known about children's emotional reactions to a pet's death. The goal of this study was to describe the relationship between experiences of pet death and risk of childhood psychopathology and determine if it was "better to have loved and lost than never to have loved at all". Data came from the Avon Longitudinal Study of Parents and Children, a UK-based prospective birth cohort (n = 6260). Children were characterized based on their exposure to pet ownership and pet death from birth to age 7 (never loved; loved without loss; loved with loss). Psychopathology symptoms at age 8 were compared across groups using multivariable linear regression. Psychopathology symptoms were higher among children who had loved with loss compared to those who had loved without loss (ß = 0.35, p = 0.013; 95% CI = 0.07, 0.63), even after adjustment for other adversities. This group effect was more pronounced in males than in females. There was no difference in psychopathology symptoms between children who had loved with loss and those who had never loved (ß = 0.20, p = 0.31, 95% CI = -0.18-0.58). The developmental timing, recency, or accumulation of pet death was unassociated with psychopathology symptoms. Pet death may be traumatic for children and associated with subsequent mental health difficulties. Where childhood pet ownership and pet bereavement is concerned, Tennyson's pronouncement may not apply to children's grief responses: it may not be "better to have loved and lost than never to have loved at all".

Genomics and psychological resilience: a research agenda.

Although exposure to adversity increases risk for poor mental health outcomes, many people exposed to adversity do not develop such outcomes. Psychological resilience, defined broadly as positive emotional and/or behavioral adaptation to adversity, may be influenced by genetic factors that have remained largely unexplored in the era of large-scale genome-wide studies. In this perspective, we provide an integrative framework for studying human genome-wide variation underlying resilience. We first outline three complementary working definitions of psychological resilience-as a capacity, process, and outcome. For each definition, we review emerging empirical evidence, including findings from positive psychology, to illustrate how a resilience-based framework can guide novel and fruitful directions for the field of psychiatric genomics, distinct from the ongoing study of psychiatric risk and related traits. Finally, we provide practical recommendations for future genomic research on resilience, highlighting a need to augment cross-sectional findings with prospective designs that include detailed measurement of adversities and outcomes. A research framework that explicitly addresses resilience could help us to probe biological mechanisms of stress adaptation, identify individuals who may benefit the most from prevention and early intervention, and ascertain modifiable protective factors that mitigate negative outcomes even for those at high genetic risk.

Physical activity offsets genetic risk for incident depression assessed via electronic health records in a biobank cohort study.

BACKGROUND: Physical activity is increasingly recognized as an important modifiable factor for depression. However, the extent to which individuals with stable risk factors for depression, such as high genetic vulnerability, can benefit from the protective effects of physical activity, remains unknown. Using a longitudinal biobank cohort integrating genomic data from 7,968 individuals of European ancestry with high-dimensional electronic health records and lifestyle survey responses, we examined whether physical activity was prospectively associated with reduced risk for incident depression in the context of genetic vulnerability. METHODS: We identified individuals with incident episodes of depression, based on two or more diagnostic billing codes for a depressive disorder within 2 years following their lifestyle survey, and no such codes in the year prior. Polygenic risk scores were derived based on large-scale genome-wide association results for major depression. We tested main effects of physical activity and polygenic risk scores on incident depression, and effects of physical activity within stratified groups of polygenic risk. RESULTS: Polygenic risk was associated with increased odds of incident depression, and physical activity showed a protective effect of similar but opposite magnitude, even after adjusting for BMI, employment status, educational attainment, and prior depression. Higher levels of physical activity were associated with reduced odds of incident depression across all levels of genetic vulnerability, even among individuals at highest polygenic risk. CONCLUSIONS: Real-world data from a large healthcare system suggest that individuals with high genetic vulnerability are more likely to avoid incident episodes of depression if they are physically active.

Features of Childhood Maltreatment and Resilience Capacity in Adulthood: Results from a Large Community-Based Sample.

Childhood maltreatment is consistently associated with poor outcomes. However, few epidemiological studies have examined the association between childhood maltreatment and adult resilience capacity, defined as one's perceived ability to cope successfully with challenges. This study aimed to determine associations between adult resilience capacity and specific types and features of childhood maltreatment. Participants were African American adults recruited from a public urban hospital in Atlanta, GA (N = 1,962) between 2005 and 2013. Childhood maltreatment, including witnessing domestic violence or physical, emotional, and sexual abuse, was assessed retrospectively using the Traumatic Events Inventory. Perceived resilience capacity was assessed using the Connor-Davidson Resilience Scale. Linear regressions were performed assessing the association between resilience capacity and childhood maltreatment exposure in general, as well as specific dimensions of exposure, including type, co-occurrence, and developmental timing, adjusting for covariates. Participants exposed to any maltreatment reported lower resilience capacity than unexposed peers, B = -0.38, SE = 0.04, p < .001. All maltreatment types were negatively associated with resilience capacity, even after adjusting for other lifetime trauma exposure. Only emotional abuse remained significantly associated with resilience capacity after accounting for current psychological distress, B = -0.11, SE = 0.05, p = .022. Maltreatment co-occurrence followed an inverse dose-response relationship with resilience capacity: For each additional maltreatment type, scores decreased by 0.18 units (SD = 0.02), p < .001. Finally, the developmental timing of maltreatment did not reveal any differential influences on resilience capacity. The results suggest that childhood emotional abuse and co-occurrence of maltreatment types may be particularly deleterious to adult resilience capacity.