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Published on: November 29, 2024
Traumatic Brain Injury and Accelerated Epigenetic Aging Among Post-9/11 Veterans
Kyle J Bourassa1, Sarah L Martindale, Melanie E Garrett
1Author Affiliations: VISN 6 Mid-Atlantic Mental Illness, Research Education and Clinical Center (MIRECC), Durham, North Carolina (Dr Bourassa, Dr Martindale, MIRECC Workgroup, Dr Beckham, Dr Kimbrel, and Dr Rowland); Durham VA Health Care System, Durham, North Carolina (Dr Bourassa); Department of Psychology, Georgetown University, Washington, District of Columbia (Dr Bourassa); Salisbury VA Health Care System, Salisbury, North Carolina (Dr Martindale and Dr Rowland); Department of Translational Neuroscience, Wake Forest School of Medicine, Winston-Salem, North Carolina (Dr Martindale and Dr Rowland); Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina (Ms Garrett and Dr Ashley-Koch); Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, North Carolina (Dr Beckham and Dr Kimbrel); and Health Services Research and Development ADAPT Center of Innovation, Durham, North Carolina (Dr Kimbrel).
Objective:
Military service over the last several decades has been associated with an increased risk of injuries, including traumatic brain injury (TBI). Veterans with a history of TBI often experience poor health outcomes and have higher rates of premature mortality. In this study, we examined whether accelerated biological aging could help explain negative health outcomes following TBI.
Setting, Participants, And Design:
We evaluated the association between TBI and rate of epigenetic aging (assessed using DunedinPACE) using data from post-9/11 veterans ( N = 1152) enrolled in the VA Mid-Atlantic (VISN 6) MIRECC Post-Deployment Mental Health cohort study.
Main Measures:
TBI was assessed using self-report during a clinical interview categorized into three TBI groups (none, 1, 2 +), epigenetic aging was assessed using DunedinPACE derived from DNA methylation data.
Results:
Veterans who reported more lifetime TBI (β = 0.07, 95% CI [0.01, 0.14], P = .029) or deployment-related TBI (β = 0.09, 95% CI [0.01, 0.18], P = .046) had faster epigenetic aging. TBI during and after military service was more strongly associated with accelerated aging than TBI prior to military service, and deployment-related TBI was more strongly associated with accelerated aging for women veterans. Overall, associations were small to moderate in size.
Conclusion:
These findings show TBI could increase risk for accelerated aging and underscores its potential utility in identifying veterans who may face aging-related health issues. Early identification of TBI-related accelerated aging could inform interventions that mitigate long-term health risks as post-9/11 veterans transition into middle and older age.
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