Predicting the accuracy of facial affect recognition: The interaction of child maltreatment and intellectual functioning

Previous research demonstrates that both child maltreatment and intellectual performance contribute uniquely to the accurate identification of facial affect by children and adolescents. The purpose of this study was to extend this research by examining whether child maltreatment affects the accuracy of facial recognition differently at varying levels of intellectual functioning. A sample of maltreated (n = 50) and nonmaltreated (n = 56) adolescent females, 14 to 19 years of age, was recruited to participate in this study. Participants completed demographic and study-related questionnaires and interviews to control for potential psychological and psychiatric confounds such as symptoms of posttraumatic stress disorder, negative affect, and difficulties in emotion regulation. Participants also completed an experimental paradigm that recorded responses to facial affect displays starting in a neutral expression and changing into a full expression of one of six emotions: happiness, sadness, anger, disgust, fear, or surprise. Hierarchical multiple regression assessed the incremental advantage of evaluating the interaction between child maltreatment and intellectual functioning. Results indicated that the interaction term accounted for a significant amount of additional variance in the accurate identification of facial affect after controlling for relevant covariates and main effects. Specifically, maltreated females with lower levels of intellectual functioning were least accurate in identifying facial affect displays, whereas those with higher levels of intellectual functioning performed as well as nonmaltreated females. These results suggest that maltreatment and intellectual functioning interact to predict the recognition of facial affect, with potential long-term consequences for the interpersonal functioning of maltreated females

A longitudinal study of several potential mediators of the relationship between child maltreatment and posttraumatic stress disorder symptoms

Child maltreatment is a reliable predictor of post-traumatic stress disorder (PTSD) symptoms. However, not all maltreated children develop PTSD symptoms, suggesting that additional mediating variables explain how certain maltreated children develop PTSD symptoms when others do not. The current study tested three potential mediators of the relationship between child maltreatment and subsequent PTSD symptoms: 1) respiratory sinus arrhythmia reactivity, 2) cortisol reactivity, and 3) experiential avoidance, or the unwillingness to experience painful private events such as thoughts and memories. Maltreated (n = 51) and non-maltreated groups (n = 59) completed a stressor paradigm, a measure of experiential avoidance, and a semi-structured interview of PTSD symptoms. One year later, participants were re-administered the PTSD symptoms interview. Results of a multiple mediator model showed the set of potential mediators mediated the relationship between child maltreatment and subsequent PTSD symptoms. However, experiential avoidance was the only significant specific indirect effect, demonstrating that maltreated children avoiding painful private events after the abuse were more likely to develop a range of PTSD symptoms one year later. These results highlight the importance of experiential avoidance in the development of PTSD symptoms for maltreated children and implications for secondary prevention and clinical intervention models are discussed

Introduction to the Special Issue: The Physical Health Consequences of Childhood Maltreatment-Implications for Public Health

Childhood maltreatment, including physical and sexual abuse as well as child neglect, is highly prevalent with recent estimates from the Department of Health & Human Services This special issue emphasizes state of the art methodologies and focuses on the explication of potential mechanisms that might help explain the connection between childhood maltreatment and physical health outcomes. Examples of methodological advances included in this special issue are: meta-analysis, longitudinal prospective study, mediational modeling, extensive statistical control for potential confounds, inclusion of substantiated/confirmed childhood maltreatment victims, and one-to-one demographic matching of subjects in control conditions. The compiled papers also include inquiry into multiple levels of human functioning including psychopathology, immune function, brain activity, neurocognitive function, autonomic nervous system activity, and gene  environment interactions. In addition to identifying the potential for deleterious effects of childhood maltreatment, several articles introduce and test models of physiologic protective factors that might serve to buffer the effects of childhood maltreatment on the development of psychopathology in pediatric samples. Hence, this special issue is an opportunity to bring together and synthesize rigorous research in order to bolster strong inference and to function as a key resource aimed at improving pediatric care for victims of childhood maltreatment. Special Issue There are two broad sections to this special issue: (a) documenting the relationships between childhood maltreatment and general physical health outcomes across a wide range of conditions and complaints, and (b) examining the impact of childhood maltreatment on a number of biological systems that may have long-term implications for overall physiologic functioning and quality of life. The first section, focused on general health outcomes, includes several articles documenting the relationship between childhood maltreatment and several distinct health outcomes. Irish, Kobayashi, and Delahanty (2010) bring together 31 studies in a comprehensive meta-analysis examining the long-term physical health effects attributable to childhood sexual abuse. The meta-analysis include

Epigenetic age acceleration as a biomarker for impaired cognitive abilities in adulthood following early life adversity and psychiatric disorders

Background: Early life adversity and psychiatric disorders are associated with earlier declines in neurocognitive abilities during adulthood. These declines may be preceded by changes in biological aging, specifically epigenetic age acceleration, providing an opportunity to uncover genome-wide biomarkers that identify individuals most likely to benefit from early screening and prevention. Methods: Five unique epigenetic age acceleration clocks derived from peripheral blood were examined in relation to latent variables of general and speeded cognitive abilities across two independent cohorts: 1) the Female Growth and Development Study (FGDS; n = 86), a 30-year prospective cohort study of substantiated child sexual abuse and non-abused controls, and 2) the Biological Classification of Mental Disorders study (BeCOME; n = 313), an adult community cohort established based on psychiatric disorders. Results: A faster pace of biological aging (DunedinPoAm) was associated with lower general cognitive abilities in both cohorts and slower speeded abilities in the BeCOME cohort. Acceleration in the Horvath clock was significantly associated with slower speeded abilities in the BeCOME cohort but not the FGDS. Acceleration in the Hannum clock and the GrimAge clock were not significantly associated with either cognitive ability. Accelerated PhenoAge was associated with slower speeded abilities in the FGDS but not the BeCOME cohort. Conclusions: The present results suggest that epigenetic age acceleration has the potential to serve as a biomarker for neurocognitive decline in adults with a history of early life adversity or psychiatric disorders. Estimates of epigenetic aging may identify adults at risk of cognitive decline that could benefit from early neurocognitive screening

Histogram distributions of continuous variables of interest, before and after winsorization (gray and blue distributions, respectively).

A datapoint was winsorized if it fell outside the range of (Q1-1.5IQR) to (Q3+1.5IQR) for its respective cohort-tissue distribution of data points, where Q1 and Q3 are lower and upper quartiles respectively, and the IQR is the interquartile ratio. Outlier values were winsorized to the boundary values of this range. 375/6673 (5.6%) datapoints were winsorized across the study. (PDF)</p