The Journal of head trauma rehabilitation · 2026
Accelerated Epigenetic Aging in Veterans Exposed to Blast.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Martindale Sarah L, Bourassa Kyle J, Kimbrel Nathan A, Beckham Jean C, Garrett Melanie E, Ashley-Koch Allison E, Rowland Jared A, Mid-Atlantic MIRECC Workgroup
Аннотация
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 .
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 .