In: Child abuse & neglect: the international journal ; official journal of the International Society for the Prevention of Child Abuse and Neglect, Band 44, S. 26-35
In: Child abuse & neglect: the international journal ; official journal of the International Society for the Prevention of Child Abuse and Neglect, Band 38, Heft 10, S. 1590-1598
In: Child abuse & neglect: the international journal ; official journal of the International Society for the Prevention of Child Abuse and Neglect, Band 58, S. 111-118
In: Child abuse & neglect: the international journal ; official journal of the International Society for the Prevention of Child Abuse and Neglect, Band 118, S. 105139
Parenting behavior is key to understanding transmission of intergenerational trauma-related risk. Emotion dysregulation (ED) and psychological symptoms are associated with negative parenting behaviors, although their unique roles remain unclear. The current study examined associations of ED dimensions, depression, PTSD, and substance use with parenting behaviors in African American mothers. Participants included 98 mother-child dyads recruited from an urban hospital setting. Trauma exposure, ED, depression, substance use, and parenting behaviors (overreactivity, laxness, demandingness, warmth, corporal punishment) were assessed using self-report measures. PTSD was assessed using a semi-structured interview. Correlational results showed significant positive associations between ED and dysfunctional parenting behavior ( p < .001), overreactivity ( p < .001), and laxness ( p < .01) and negative associations with warmth ( p < .01). These associations varied across the dimensions of ED examined. Regression analyses were run to examine the unique effects of ED (separate models for overall and specific dimensions) and psychological symptoms; overall ED and its dimensions accounted for significant variance in parental behaviors ( R2 = .10–.24, p's < .01), while additional model steps including psychological symptoms were not significant except for the association between depression and lower warmth. In efforts to reduce the intergenerational effects of trauma, parenting interventions that include a direct focus on certain dimensions of ED may be critical.
In: Child abuse & neglect: the international journal ; official journal of the International Society for the Prevention of Child Abuse and Neglect, Band 51, S. 212-222
Genetic factors appear to be highly relevant to predicting differential risk for the development of post-traumatic stress disorder (PTSD). In a discovery sample, we conducted a genome-wide association study (GWAS) for PTSD using a small military cohort (Systems Biology PTSD Biomarkers Consortium; SBPBC, N = 147) that was designed as a case-controlled sample of highly exposed, recently returning veterans with and without combat-related PTSD. A genome-wide significant single nucleotide polymorphism (SNP), rs717947, at chromosome 4p15 (N = 147, β = 31.34, P = 1.28×10−8) was found to associate with the gold-standard diagnostic measure for PTSD (the Clinician Administered PTSD Scale). We conducted replication and follow-up studies in an external sample, a larger urban community cohort (Grady Trauma Project, GTP, N = 2006), to determine the robustness and putative functionality of this risk variant. In the GTP replication sample, SNP rs717947 associated with PTSD diagnosis in females (N = 2006, P = 0.005), but not males. SNP rs717947 was also found to be a methylation quantitative trait locus (meQTL) in the GTP replication sample (N = 157, P = 0.002). Further, the risk allele of rs717947 was associated with decreased medial and dorsolateral cortical activation to fearful faces (N = 53, P < 0.05) in the GTP replication sample. These data identify a genome-wide significant polymorphism conferring risk for PTSD, which was associated with differential epigenetic regulation and with differential cortical responses to fear in a replication sample. These results may provide new insight into understanding genetic and epigenetic regulation of PTSD and intermediate phenotypes that contribute to this disorder.