Emotion regulation as mediator between childhood adversity and psychopathology: A meta-analysis.

Childhood adversity is a major risk factor for multiple forms of psychopathology, and recent efforts have focused on understanding the underlying psychological mechanisms. One outstanding candidate is emotion regulation, which has been associated with both childhood adversity, and psychopathology. Based on the available evidence, the present meta-analysis set out to investigate the mechanistic involvement of emotion regulation in the relation between childhood adversity and psychopathology. Systematic searches in three databases (PubMed; PsycINFO; Web of Science) identified 215 eligible studies. Using meta-analytic structural equation modeling, we fitted a partial mediation model to the available data across studies, in which childhood adversity was related to psychopathology both directly and through emotion regulation. Multiple emotion regulation dimensions were analyzed, including emotion regulation difficulties and the habitual use of rumination, distraction, reappraisal, and suppression. Measures of psychopathology included a wide range of internalizing and externalizing symptoms in both clinical and non-clinical samples. The results indicated that childhood adversity was positively associated with emotion regulation difficulties, as well as with the habitual use of rumination and suppression. In turn, these measures of emotion regulation were positively associated with psychopathology. Habitual reappraisal use showed negative relations with both childhood adversity and psychopathology. All these emotion regulation measures were supported as mediators in the relation between childhood adversity and psychopathology. In contrast, distraction was not related to childhood adversity or psychopathology, and its mediator role was not supported. These results suggest that altered emotion regulation is a consistent marker of childhood adversity and contributes to risk of psychopathology.

Childhood trauma and emotion regulation: The moderator role of BDNF Val66Met.

Emotion regulation difficulties have been involved in multiple forms of psychopathology and may represent an important focus for current efforts to understand the biological mechanisms underlying transdiagnostic symptoms. The present study investigated a gene-environment interaction (G × E) in reappraisal, a form of emotion regulation that has been extensively linked to psychopathology. In light of recent meta-analytic evidence of its consistent role in depression and anxiety disorders, this study focused on the Val66Met (rs6265) single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene and examined its moderator role in the relation between childhood trauma and reappraisal. A sample of N = 266 participants were genotyped for BDNF Val66Met, filled in a self-report measure of childhood trauma, and underwent a cognitive task designed to assess reappraisal ability. The results indicated that, as expected, BDNF Val66Met was a significant moderator in the relation between childhood trauma and reappraisal. There was a negative relation between the number of childhood traumatic events and reappraisal ability in BDNF Met carriers, but not Val homozygotes. This finding suggests that BDNF Val66Met contributes to susceptibility to childhood stress, with long term impact on emotion regulation.

Early-life adversity and cortisol response to social stress: a meta-analysis.

Early-life adversity has been associated with a life-long increased risk for psychopathology and chronic health problems. These long-term negative effects have been explained through stress sensitization, which may involve dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis through either increased or decreased reactivity. The present meta-analysis assessed for the first time the effect of early-life adversity on cortisol response to social stress. Thirty data sets were included in the meta-analysis, in which early-life adversity and salivary cortisol response to social stress were assessed in 4292 individuals of different ages. Results indicated a moderate effect size (g = -0.39) in overall cortisol levels across studies. Separate analyses of cortisol at different stages of response showed large effect sizes at peak and recovery, and a moderate effect at baseline. Heterogeneity was large in this sample of studies and several moderators were identified. The effect size was larger in studies that focused on maltreatment compared to those that included other adversities, and in adults compared to children and adolescents. Percent of women in each sample and methodological quality were positive predictors of the effect size. Publication bias may be present, but the analysis was hampered by the high heterogeneity. Therefore, these results support the association between early-life adversity and blunted cortisol response to social stress, and they suggest that the long-term negative effects of early-life adversity may reach maximum levels in adults.