Accelerated Epigenetic Aging in Veterans Exposed to Blast

Scritto il 18/03/2026
da Sarah L Martindale

J Head Trauma Rehabil. 2026 Mar 18. doi: 10.1097/HTR.0000000000001159. Online ahead of print.

ABSTRACT

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.

PMID:41849738 | DOI:10.1097/HTR.0000000000001159