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.

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".

What life course theoretical models best explain the relationship between exposure to childhood adversity and psychopathology symptoms: recency, accumulation, or sensitive periods?

BACKGROUND: Although childhood adversity is a potent determinant of psychopathology, relatively little is known about how the characteristics of adversity exposure, including its developmental timing or duration, influence subsequent mental health outcomes. This study compared three models from life course theory (recency, accumulation, sensitive period) to determine which one(s) best explained this relationship. METHODS: Prospective data came from the Avon Longitudinal Study of Parents and Children (n = 7476). Four adversities commonly linked to psychopathology (caregiver physical/emotional abuse; sexual/physical abuse; financial stress; parent legal problems) were measured repeatedly from birth to age 8. Using a statistical modeling approach grounded in least angle regression, we determined the theoretical model(s) explaining the most variability (r2) in psychopathology symptoms measured at age 8 using the Strengths and Difficulties Questionnaire and evaluated the magnitude of each association. RESULTS: Recency was the best fitting theoretical model for the effect of physical/sexual abuse (girls r2 = 2.35%; boys r2 = 1.68%). Both recency (girls r2 = 1.55%) and accumulation (boys r2 = 1.71%) were the best fitting models for caregiver physical/emotional abuse. Sensitive period models were chosen alone (parent legal problems in boys r2 = 0.29%) and with accumulation (financial stress in girls r2 = 3.08%) more rarely. Substantial effect sizes were observed (standardized mean differences = 0.22-1.18). CONCLUSIONS: Child psychopathology symptoms are primarily explained by recency and accumulation models. Evidence for sensitive periods did not emerge strongly in these data. These findings underscore the need to measure the characteristics of adversity, which can aid in understanding disease mechanisms and determining how best to reduce the consequences of exposure to adversity.

Exposure to childhood adversity and deficits in emotion recognition: results from a large, population-based sample.

BACKGROUND: Emotion recognition skills are essential for social communication. Deficits in these skills have been implicated in mental disorders. Prior studies of clinical and high-risk samples have consistently shown that children exposed to adversity are more likely than their unexposed peers to have emotion recognition skills deficits. However, only one population-based study has examined this association. METHODS: We analyzed data from children participating in the Avon Longitudinal Study of Parents and Children, a prospective birth cohort (n = 6,506). We examined the association between eight adversities, assessed repeatedly from birth to age 8 (caregiver physical or emotional abuse; sexual or physical abuse; maternal psychopathology; one adult in the household; family instability; financial stress; parent legal problems; neighborhood disadvantage) and the ability to recognize facial displays of emotion measured using the faces subtest of the Diagnostic Assessment of Non-Verbal Accuracy (DANVA) at age 8.5 years. In addition to examining the role of exposure (vs. nonexposure) to each type of adversity, we also evaluated the role of the timing, duration, and recency of each adversity using a Least Angle Regression variable selection procedure. RESULTS: Over three-quarters of the sample experienced at least one adversity. We found no evidence to support an association between emotion recognition deficits and previous exposure to adversity, either in terms of total lifetime exposure, timing, duration, or recency, or when stratifying by sex. CONCLUSIONS: Results from the largest population-based sample suggest that even extreme forms of adversity are unrelated to emotion recognition deficits as measured by the DANVA, suggesting the possible immutability of emotion recognition in the general population. These findings emphasize the importance of population-based studies to generate generalizable results.

Sensitive period-regulating genetic pathways and exposure to adversity shape risk for depression.

Animal and human studies have documented the existence of developmental windows (or sensitive periods) when experience can have lasting effects on brain structure or function, behavior, and disease. Although sensitive periods for depression likely arise through a complex interplay of genes and experience, this possibility has not yet been explored in humans. We examined the effect of genetic pathways regulating sensitive periods, alone and in interaction with common childhood adversities, on depression risk. Guided by a translational approach, we: (1) performed association analyses of three gene sets (60 genes) shown in animal studies to regulate sensitive periods using summary data from a genome-wide association study of depression (n = 807,553); (2) evaluated the developmental expression patterns of these genes using data from BrainSpan (n = 31), a transcriptional atlas of postmortem brain samples; and (3) tested gene-by-development interplay (dGxE) by analyzing the combined effect of common variants in sensitive period genes and time-varying exposure to two types of childhood adversity within a population-based birth cohort (n = 6254). The gene set regulating sensitive period opening associated with increased depression risk. Notably, 6 of the 15 genes in this set showed developmentally regulated gene-level expression. We also identified a statistical interaction between caregiver physical or emotional abuse during ages 1-5 years and genetic risk for depression conferred by the opening genes. Genes involved in regulating sensitive periods are differentially expressed across the life course and may be implicated in depression vulnerability. Our findings about gene-by-development interplay motivate further research in large, more diverse samples to further unravel the complexity of depression etiology through a sensitive period lens.

Comparison of Genetic and Self-Identified Ancestry in Modeling Intracerebral Hemorrhage Risk.

Background: We sought to determine whether a small pool of ancestry-informative DNA markers (AIMs) improves modeling of intracerebral hemorrhage (ICH) risk in heterogeneous populations, compared with self-identified race/ethnicity (SIRE) alone. Methods: We genotyped 15 preselected AIMs to perform principal component (PC) analysis in the ERICH study (a multi-center case-control study of ICH in whites, blacks, and Hispanics). We used multivariate logistic regression and tests for independent samples to compare associations for genetic ancestry and SIRE with ICH-associated vascular risk factors (VRFs). We then compared the performance of models for ICH risk that included AIMs and SIRE alone. Results: Among 4,935 subjects, 34.7% were non-Hispanic black, 35.1% non-Hispanic white, and 30.2% Hispanic by SIRE. In stratified analysis of these SIRE groups, AIM-defined ancestry was strongly associated with seven of the eight VRFs analyzed (p < 0.001). Within each SIRE group, regression of AIM-derived PCs against VRFs confirmed independent associations of AIMs across at least two race/ethnic groups for seven VRFs. Akaike information criterion (AIC) (6,294 vs. 6,286) and likelihood ratio test (p < 0.001) showed that genetic ancestry defined by AIMs achieved a better ICH risk modeling compared to SIRE alone. Conclusion: Genetically-defined ancestry provides valuable risk exposure information that is not captured by SIRE alone. Particularly among Hispanics and blacks, inclusion of AIMs adds value over self-reported ancestry in controlling for genetic and environmental exposures that influence risk of ICH. While differences are small, this modeling approach may be superior in highly heterogeneous clinical poulations. Additional studies across other ancestries and risk exposures are needed to confirm and extend these findings.