National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States.
National Center for PTSD at VA Boston Healthcare System, United States.
Psychoneuroendocrinology. 2018 Jun;92:123-134. doi: 10.1016/j.psyneuen.2017.12.007. Epub 2017 Dec 27.
Recent studies examining the association between posttraumatic stress disorder (PTSD) and accelerated aging, as defined by DNA methylation-based estimates of cellular age that exceed chronological age, have yielded mixed results.
We conducted a meta-analysis of trauma exposure and PTSD diagnosis and symptom severity in association with accelerated DNA methylation age using data from 9 cohorts contributing to the Psychiatric Genomics Consortium PTSD Epigenetics Workgroup (combined N = 2186). Associations between demographic and cellular variables and accelerated DNA methylation age were also examined, as was the moderating influence of demographic variables.
Meta-analysis of regression coefficients from contributing cohorts revealed that childhood trauma exposure (when measured with the Childhood Trauma Questionnaire) and lifetime PTSD severity evidenced significant, albeit small, meta-analytic associations with accelerated DNA methylation age (ps = 0.028 and 0.016, respectively). Sex, CD4T cell proportions, and natural killer cell proportions were also significantly associated with accelerated DNA methylation age (all ps < 0.02). PTSD diagnosis and lifetime trauma exposure were not associated with advanced DNA methylation age. There was no evidence of moderation of the trauma or PTSD variables by demographic factors.
Results suggest that traumatic stress is associated with advanced epigenetic age and raise the possibility that cells integral to immune system maintenance and responsivity play a role in this. This study highlights the need for additional research into the biological mechanisms linking traumatic stress to accelerated DNA methylation age and the importance of furthering our understanding of the neurobiological and health consequences of PTSD.
最近的研究检查了创伤后应激障碍(PTSD)与加速衰老之间的关联,加速衰老通过基于 DNA 甲基化的细胞年龄估计值超过实际年龄来定义。这些研究结果不一。
我们使用来自参与精神疾病基因组学联盟 PTSD 表观遗传学工作组的 9 个队列的数据(合并 N=2186)进行了荟萃分析,分析了创伤暴露、PTSD 诊断和症状严重程度与加速 DNA 甲基化年龄之间的关系。还检查了人口统计学和细胞变量与加速 DNA 甲基化年龄之间的关联,以及人口统计学变量的调节作用。
来自参与队列的回归系数的荟萃分析显示,童年创伤暴露(用童年创伤问卷测量)和终生 PTSD 严重程度与加速 DNA 甲基化年龄有显著的、尽管很小的荟萃分析关联(ps=0.028 和 0.016)。性别、CD4T 细胞比例和自然杀伤细胞比例也与加速 DNA 甲基化年龄显著相关(所有 ps<0.02)。PTSD 诊断和终生创伤暴露与先进的 DNA 甲基化年龄无关。人口统计学因素对创伤或 PTSD 变量没有调节作用。
结果表明,创伤应激与加速的表观遗传年龄有关,并提出了免疫系统维持和反应性所必需的细胞可能在这方面发挥作用的可能性。这项研究强调了需要进一步研究将创伤应激与加速的 DNA 甲基化年龄联系起来的生物学机制,以及进一步了解 PTSD 的神经生物学和健康后果的重要性。