The relevance of epigenetics to PTSD: Implications for the DSM‐V
Open accessAbstract
Epigenetic modifications, such as DNA methylation, can occur in response to environmental influences to alter the functional expression of genes in an enduring and potentially, intergenerationally transmissible manner. As such, they may explain interindividual variation, as well as the long‐lasting effects of trauma exposure. Although there are currently no findings that suggest epigenetic modifications that are specific to posttraumatic stress disorder (PTSD) or PTSD risk, many recent observations are compatible with epigenetic explanations. These include recent findings of stress‐related gene expression, in utero contributions to infant biology, the association of PTSD risk with maternal PTSD, and the relevance of childhood adversity to the development of PTSD. The relevance of epigenetic mechanisms to formulations of PTSD for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM‐V) is described.
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Animal models have demonstrated that stress exposure can result in epigenetic alterations in the next generation.
“Animal models have demonstrated that stress exposure can result in epigenetic alterations in the next generation, and such mechanisms have been hypothesized to underpin vulnerability to symptoms in offspring of trauma survivors (6)(7)(8)(9).”
From Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation (2016) · cites this paper as [7]
The section “Cytosine Methylation in Response to Variations in Maternal Care: A Behavioral Model” (page unavailable) reports altered DNA methylation in rat pups receiving different levels of maternal care and says associated biological effects were transmitted to a third generation. It does not clearly demonstrate that stress exposure in one generation caused epigenetic alterations in the next; the animal model described is one of variation in maternal care. (LLM, conf=0.82)
Experimental — accuracy not yet measuredEnduring changes in the transcriptome may facilitate the response to early developmental challenges and play a central role in the long-term (and sometimes transgenerational) biological trajectories of stress-related disease through programming effects for stress reactivity after ELS/CT exposure.
“Taken together, enduring changes in the transcriptome may facilitate the response to early developmental challenges and thus play a central role in the long-term (and sometimes transgenerational) biological trajectories of stress-related disease through programming effects for stress reactivity after ELS/CT exposure (104, 413, 414).”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [413]
Previous studies have associated differential DNAm patterns with diseases, such as post-traumatic stress disorder, which can be triggered by the experience of a single stressful life event.
“However, previous studies have associated differential DNAm patterns with diseases, such as post-traumatic stress disorder, which can be triggered by the experience of a single stressful life event [42].”
From Dynamic DNA methylation changes in the COMT gene promoter region in response to mental stress and its modulation by transcranial direct current stimulation (2021) · cites this paper as [42]
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“Taken together, enduring changes in the transcriptome may facilitate the response to early developmental challenges and thus play a central role in the long-term (and sometimes transgenerational) biological trajectories of stress-related disease through programming effects for stress reactivity after ELS/CT exposure (…”
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- Authors
- Yehuda, R., & Bierer, L. M.
- Affiliations
- James J. Peters VA Medical Center (US)
- Corresponding author
- Yehuda, Rachel
- ORCID
- Yehuda, Rachel
- Venue
- Journal of Traumatic Stress
- Publisher
- Wiley
- Published
- 2009-10
- Volume
- 22
- Issue
- 5
- Pages
- 427-434
- ISSN
- 0894-9867 (ISSN-L)
- 1573-6598
- PMC
- PMC2891396
- OpenAlex
- W2022768282
- Cited by
- 229
- References
- 61
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 14 · 2023: 7 · 2022: 6 · 2021: 12 · 2020: 15 · 2019: 16 · 2018: 15 · 2017: 11 · 2016: 16 · 2015: 19 · 2014: 15 · 2013: 18 · 2012: 12
- FWCI
- 14.48
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Traumatic Stress (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R56MH077321)
- National Center for Research Resources (M01RR000071)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Keywords
- epigenetics, post-traumatic stress disorder, DNA methylation, intergenerational transmission, trauma exposure, stress-responsive gene expression, intrauterine environment, maternal PTSD, childhood adversity, PTSD risk, DSM-5 diagnostic criteria
- MeSH terms
- Animals, Disease Models, Animal, Female, Humans, Infant, Models, Psychological, Mother-Child Relations, Pregnancy, Prenatal Exposure Delayed Effects, Stress Disorders, Post-Traumatic, Child of Impaired Parents, DNA Methylation, Diagnostic and Statistical Manual of Mental Disorders, Epigenesis, Genetic, Rats
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