创伤后应激
表观遗传学
复制(统计)
细胞老化
肥胖
临床心理学
心理学
医学
老年学
精神科
内科学
生物
遗传学
病毒学
端粒
基因
作者
Kyle J. Bourassa,Melanie E. Garrett,Allison E. Ashley‐Koch,Jean C. Beckham,Nathan A. Kimbrel
标识
DOI:10.1097/psy.0000000000001397
摘要
Posttraumatic stress disorder (PTSD) is associated with poor health, and prior research suggests that accelerated epigenetic aging could help explain this association. A recent study found that veterans with both PTSD and obesity had greater risk for accelerated epigenetic aging compared to those with either PTSD or obesity individually, or neither condition. The objective of this study was to conduct a replication and extension of this prior work. This study included models approximating the recent study's analytic approach in a sample of 1,828 post-9/11 veterans. Our extension also included additional aging measures (PC-GrimAge and DunedinPACE), a more diverse sample, additional covariates (chronological age, smoking), and use of continuous measures of PTSD, obesity, and accelerated aging. In contrast with the original report, we did not find evidence that obesity moderated the association of PTSD and aging, indicating that veterans with both conditions had greater risk for accelerated aging. Although several significant interactions were observed, they were in the opposite direction of the original study findings (i.e., PTSD was more strongly associated with aging scores among veterans with less body mass). Our results instead demonstrated that PTSD was associated with accelerated aging across all continuously measured aging scores (0.08 ≤all βs ≤0.10), and that obesity was associated with faster DunedinPACE aging scores (β=0.36, 95% CI [0.28, 0.44]). Our findings provide additional evidence that PTSD and obesity may be useful targets for interventions aiming to slow aging and improve health.
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