Wolf Erika J, Schnurr Paula P
Clinical Research Psychologist; National Center for PTSD at VA Boston Healthcare System; Assistant Professor; Boston University School of Medicine, Department of Psychiatry.
Executive Director; National Center for PTSD, White River Junction, Vermont; Research Professor of Psychiatry; Geisel School of Medicine at Dartmouth.
Psychiatr Ann. 2016;46:527-532. doi: 10.3928/00485713-20160729-01.
We reviewed the literature from 2010 to 2016 on the relationship between posttraumatic stress disorder (PTSD) and cardiometabolic health conditions, including metabolic syndrome, coronary artery disease, stroke, and myocardial infarction, among others. Collectively, PTSD was associated with increased risk of cardiometabolic health problems, with pre-clinical and clinical studies offering evidence of behavioral (e.g., poor sleep, cigarette use, poor diet and insufficient exercise) and biological (e.g., autonomic reactivity, inflammation) mediators of these associations. We discuss the possibility that these behavioral and biological mechanisms lead to accelerated cellular aging, as regulated in the epigenome, which contributes to premature cardiometabolic health decline. This has implications for the assessment, prevention, and treatment of cardiometabolic conditions among those with PTSD. It also highlights the need to better understand the mechanisms linking PTSD to accelerated aging and to develop interventions to attenuate or reverse this phenomenon.
我们回顾了2010年至2016年期间关于创伤后应激障碍（PTSD）与心脏代谢健康状况之间关系的文献，这些状况包括代谢综合征、冠状动脉疾病、中风和心肌梗死等。总体而言，PTSD与心脏代谢健康问题风险增加相关，临床前和临床研究提供了这些关联的行为（如睡眠不佳、吸烟、饮食不良和运动不足）和生物学（如自主反应性、炎症）介导因素的证据。我们讨论了这些行为和生物学机制导致细胞衰老加速的可能性，这种加速在表观基因组中受到调控，进而导致心脏代谢健康过早衰退。这对PTSD患者心脏代谢状况的评估、预防和治疗具有启示意义。它还凸显了更好地理解将PTSD与加速衰老联系起来的机制以及开发干预措施以减轻或逆转这一现象的必要性。
