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Published on: November 30, 2015
Epigenetic Age Acceleration and Risk for Posttraumatic Stress Disorder following Exposure to Substantiated Child
Chad E Shenk1,2, Kieran J O'Donnell3,4, Irina Pokhvisneva3
1Department of Human Development and Family Studies, The Pennsylvania State University.
Insights
Epigenetic age acceleration, a biomarker of stress, helps explain why some children develop posttraumatic stress disorder (PTSD) after maltreatment, while others do not. This finding may lead to new prevention and treatment strategies for pediatric PTSD.
Area of Science:
- Psychiatry
- Genetics
- Developmental Psychology
Background:
- Child maltreatment is a significant risk factor for posttraumatic stress disorder (PTSD).
- However, not all maltreated children develop PTSD, indicating other contributing factors.
- Epigenetic age acceleration, a measure of biological aging influenced by stress, is a potential explanatory factor.
Purpose of the Study:
- To investigate if epigenetic age acceleration explains variations in PTSD diagnostic status among children exposed to maltreatment.
- To explore the relationship between epigenetic age acceleration and PTSD symptom severity.
Main Methods:
- A case-control study involving 70 children and adolescents (8-15 years) with recent substantiated child maltreatment.
- Buccal swabs were used to measure epigenetic age acceleration.
- PTSD diagnosis was assessed using the Child PTSD Symptoms Scale.
Main Results:
- Epigenetic age acceleration significantly predicted PTSD status (OR=2.35), even after adjusting for demographics, genetic risk, and other adversities.
- Higher epigenetic age acceleration was associated with increased PTSD arousal symptoms (r=0.29, p=0.015).
- No differences were found based on child maltreatment subtype.
Conclusions:
- Epigenetic age acceleration may represent the biological impact of child maltreatment, explaining differing PTSD risk.
- This biomarker offers a novel approach for identifying at-risk children and developing targeted interventions for pediatric PTSD.
Objective:
Child maltreatment is among the strongest predictors of posttraumatic stress disorder (PTSD). However, less than 40% of children who have been maltreated are ever diagnosed with PTSD, suggesting that exposure to child maltreatment alone is insufficient to explain this risk. This study examined whether epigenetic age acceleration, a stress-sensitive biomarker derived from DNA methylation, explains variation in PTSD diagnostic status subsequent to child maltreatment.
Method:
Children and adolescents (N = 70; 65.7% female), 8-15 years of age (M = 12.00, SD = 2.37) and exposed to substantiated child maltreatment within the 12 months prior to study entry, were enrolled. Participants provided epithelial cheek cells via buccal swab for genotyping and quantification of epigenetic age acceleration within a case-control design. PTSD diagnostic status was determined using the Child PTSD Symptoms Scale according to the DSM-IV-TR algorithm.
Results:
Epigenetic age acceleration predicted current PTSD status, revealing an effect size magnitude in the moderate range, OR = 2.35, 95% CI: 1.22- 4.51, after adjusting for sample demographics, polygenic risk for PTSD, and lifetime exposure to other childhood adversities. Supplemental analyses demonstrated that epigenetic age acceleration was related to a greater severity of PTSD arousal symptoms (r =.29, p =.015). There were no differential effects for child maltreatment subtype on epigenetic age acceleration or PTSD status.
Conclusions:
The biological embedding of child maltreatment may explain variation in PTSD diagnostic status and serve as a novel approach for informing selective prevention or precision-based therapeutics for those at risk for PTSD.
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