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Accelerated Epigenetic Aging in Veterans Exposed to Blast
Sarah L Martindale1, Kyle J Bourassa, Nathan A Kimbrel
1Author Affiliations: VISN 6 Mid-Atlantic Mental Illness, Research Education and Clinical Center (MIRECC), Durham, North Carolina (Dr Martindale, Dr Bourassa, Dr Kimbrel, Dr Beckham, Dr Rowland); Salisbury VA Healthcare System, Salisbury, North Carolina (Dr Martindale, Dr Rowland); Department of Translational Neuroscience, Wake Forest School of Medicine, Winston-Salem, North Carolina (Dr Martindale, Dr Rowland); Durham VA Health Care System, Durham, North Carolina (Dr Bourassa, Dr Kimbrel, Dr Beckham); Department of Psychology, Georgetown University, Washington, District of Columbia (Dr Bourassa); Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, North Carolina (Dr Kimbrel, Dr Beckham); Health Services Research and Development ADAPT Center of Innovation, Durham, North Carolina (Dr Kimbrel); and Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina (Garrett, Dr Ashley-Koch).
Objective:
To determine whether lifetime blast exposure severity is independently associated with accelerated biological aging among post-9/11 Veterans.
Setting:
Veterans Affairs medical centers in the southeastern United States.
Participants:
In total, 114 post-9/11 combat Veterans (43.0 ± 9.6 years; 88.6% male) who completed detailed clinical interviews and provided whole-blood DNA samples were included.
Design:
Cross-sectional analysis of participants enrolled in 2 coordinated VA research protocols: the Chronic Effects of Neurotrauma Consortium Study 34 and the Post-Deployment Mental Health Study.
Main Measures:
Lifetime blast exposure severity (Salisbury Blast Interview), posttraumatic stress disorder (PTSD) diagnosis (Clinician-Administered PTSD Scale for DSM-5), and mild traumatic brain injury (TBI) history (Mid-Atlantic MIRECC Assessment of TBI) were assessed with clinical interviews. Biological aging was measured using DunedinPACE , an epigenetic biomarker of the pace of aging derived from whole-blood DNA methylation data. Hierarchical linear regression tested additive and interactive effects of blast exposure, PTSD, and TBI, adjusting for demographic and technical covariates.
Results:
Greater blast exposure severity was significantly associated with faster DunedinPACE scores (B = 0.12; P = .042), indicating accelerated biological aging. Mild TBI history was also independently associated with faster aging (B = 0.50; P = .036), whereas PTSD diagnosis was not (B = 0.01; P = .970). No significant interaction effects were observed. Exploratory analyses suggested that higher-intensity and more frequent blast exposures contributed to faster accelerated aging.
Conclusions:
Lifetime blast exposure severity was independently associated with accelerated epigenetic aging in post-9/11 Veterans, even after accounting for PTSD and TBI. These findings suggest that blast exposure may promote biological aging processes contributing to long-term health decline. Accelerated biological aging may represent a pathway linking blast exposure to increased vulnerability for age-related disease and could inform early identification of at-risk Veterans through biomarkers such as DunedinPACE .
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