Blessing Esther M, Reus Victor, Mellon Synthia H, Wolkowitz Owen M, Flory Janine D, Bierer Linda, Lindqvist Daniel, Dhabhar Firdaus, Li Meng, Qian Meng, Abu-Amara Duna, Galatzer-Levy Isaac, Yehuda Rachel, Marmar Charles R
Steven and Alexandra Cohen Veterans Center for Posttraumatic Stress and Traumatic Brain Injury, Department of Psychiatry, New York University Langone Medical Center, United States.
Department of Psychiatry, University of California, San Francisco (UCSF), School of Medicine, San Francisco, CA, United States.
Psychoneuroendocrinology. 2017 Aug;82:91-97. doi: 10.1016/j.psyneuen.2017.04.016. Epub 2017 May 1.
Posttraumatic stress disorder (PTSD) is associated with increased risk for Type 2 diabetes and cardiovascular disease (cardiometabolic disease), warranting research into targeted prevention strategies. In the present case-control study of 160 young (mean age 32.7 years) male military veterans, we aimed to assess whether PTSD status predicted increased markers of cardiometabolic risk in otherwise healthy individuals, and further, to explore biological pathways between PTSD and these increased markers of cardiometabolic risk. Toward these aims, we compared measures of cardiometabolic risk, namely insulin resistance (IR) (HOMA-IR), metabolic syndrome (MetS) and prediabetes, between 80 PTSD cases and 80 controls without PTSD. We then determined whether PTSD-associated increases in HOMA-IR were correlated with select biological variables from pathways previously hypothesized to link PTSD with cardiometabolic risk, including systemic inflammation (increased C-reactive protein, interleukin-6, and tumor necrosis factor α), sympathetic over-activity (increased resting heart rate), and neuroendocrine dysregulation (increased plasma cortisol or serum brain-derived neurotrophic factor (BDNF)). We found PTSD diagnosis was associated with substantially higher HOMA-IR (cases 4.3±4.3 vs controls 2.4±2.0; p<0.001), and a higher frequency of MetS (cases 21.3% vs controls 2.5%; p<0.001), but not prediabetes (cases 20.0% vs controls 18.8%; p>0.05). Cases also had increased pro-inflammatory cytokines (p<0.01), heart rate (p<0.001), and BDNF (p<0.001), which together predicted increased HOMA-IR (adjusted R=0.68, p<0.001). Results show PTSD diagnosis in young male military veterans without cardiometabolic disease is associated with increased IR, predicted by biological alterations previously hypothesized to link PTSD to increased cardiometabolic risk. Findings support further research into early, targeted prevention of cardiometabolic disease in individuals with PTSD.
创伤后应激障碍（PTSD）与2型糖尿病和心血管疾病（心脏代谢疾病）的风险增加相关，因此有必要对针对性的预防策略进行研究。在这项针对160名年轻（平均年龄32.7岁）男性退伍军人的病例对照研究中，我们旨在评估PTSD状态是否能预测在其他方面健康的个体中心脏代谢风险标志物的增加，并且进一步探索PTSD与这些增加的心脏代谢风险标志物之间的生物学途径。为了实现这些目标，我们比较了80例PTSD患者和80例无PTSD的对照者的心脏代谢风险指标，即胰岛素抵抗（IR）（稳态模型评估胰岛素抵抗指数）、代谢综合征（MetS）和糖尿病前期。然后，我们确定PTSD相关的稳态模型评估胰岛素抵抗指数增加是否与先前假设将PTSD与心脏代谢风险联系起来的途径中的特定生物学变量相关，包括全身炎症（C反应蛋白、白细胞介素-6和肿瘤坏死因子α增加）、交感神经过度活跃（静息心率增加）和神经内分泌失调（血浆皮质醇或血清脑源性神经营养因子（BDNF）增加）。我们发现PTSD诊断与显著更高的稳态模型评估胰岛素抵抗指数相关（患者4.3±4.3 vs对照2.4±2.0；p<0.001），以及更高的代谢综合征发生率（患者21.3% vs对照2.5%；p<0.001），但与糖尿病前期无关（患者20.0% vs对照18.8%；p>0.05）。患者还出现促炎细胞因子增加（p<0.01）、心率增加（p<0.001）和脑源性神经营养因子增加（p<0.001），这些因素共同预测了稳态模型评估胰岛素抵抗指数的增加（调整后R=0.68，p<0.001）。结果表明，在无心脏代谢疾病的年轻男性退伍军人中，PTSD诊断与胰岛素抵抗增加相关，这是由先前假设将PTSD与增加的心脏代谢风险联系起来的生物学改变所预测的。研究结果支持进一步研究对PTSD个体进行早期、针对性的心脏代谢疾病预防。
