Post-traumatic stress disorder and cardiometabolic disease: improving causal inference to inform practice.
Post-traumatic stress disorder and cardiometabolic disease: improving causal inference to inform practice.
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DOI：
10.1017/s0033291716002294
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发表时间：
2017-01
影响因子：
6.9
通讯作者：
Kubzansky, L. D.
中科院分区：
文献类型：
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作者：
Koenen, K. C.;Sumner, J. A.;Gilsanz, P.;Glymour, M. M.;Ratanatharathorn, A.;Rimm, E. B.;Roberts, A. L.;Winning, A.;Kubzansky, L. D.
有证据表明，创伤后应激障碍（PTSD）会导致一系列身体健康问题，因此它被宣布为“无期徒刑”。一些强有力的实证研究——在方法和发现方面——已经表明，创伤后应激障碍预示着更高的心脏代谢疾病风险，特别是心血管疾病（CVD）和2型糖尿病（T2D）。尽管有越来越多的证据，PTSD目前还没有被心血管或内分泌医学认为是一个危险因素。如果没有令人信服的证据表明创伤后应激障碍会导致心脏代谢疾病，这种观点不太可能改变。这篇综述表明，随着流行病学研究方法的发展以及对PTSD的行为和生物学影响的迅速了解，该领域准备为因果关系问题提供更明确的答案。首先，我们讨论了利用创伤后应激障碍和健康研究中最常用的观察数据来改进因果推理的方法，特别是关于暂时性和混淆的问题。其次，我们考虑了最近将PTSD与特定行为和生物过程联系起来的工作，并评估这些是否可能合理地作为PTSD导致心脏代谢疾病的机制。第三，我们评估了如何更全面地研究PTSD表型，以了解PTSD现象学的特定方面是否与心脏代谢疾病特别相关。最后，我们讨论了新的研究领域，这些领域是可行的，可以增强对创伤后应激障碍与心脏代谢关系的理解，例如测试创伤后应激障碍的治疗是否可以停止甚至逆转与CVD和T2D相关的心脏代谢危险因素。
Posttraumatic stress disorder (PTSD) has been declared “a life sentence” based on evidence that the disorder leads to a host of physical health problems. Some of the strongest empirical research—in terms of methodology and findings—has shown that PTSD predicts higher risk of cardiometabolic diseases, specifically cardiovascular disease (CVD) and type 2 diabetes (T2D). Despite mounting evidence, PTSD is not currently acknowledged as a risk factor by cardiovascular or endocrinological medicine. This view is unlikely to change absent compelling evidence that PTSD causally contributes to cardiometabolic disease. This review suggests that with developments in methods for epidemiologic research and the rapidly expanding knowledge of the behavioral and biological effects of PTSD the field is poised to provide more definitive answers to questions of causality. First, we discuss methods to improve causal inference using the observational data most often used in studies of PTSD and health, with particular reference to issues of temporality and confounding. Second, we consider recent work linking PTSD with specific behaviors and biological processes, and evaluate whether these may plausibly serve as mechanisms by which PTSD leads to cardiometabolic disease. Third, we evaluate how looking more comprehensively into the PTSD phenotype provides insight into whether specific aspects of PTSD phenomenology are particularly relevant to cardiometabolic disease. Finally, we discuss new areas of research that are feasible and could enhance understanding of the PTSD-cardiometabolic relation, such as testing whether treatment of PTSD can halt or even reverse the cardiometabolic risk factors causally related to CVD and T2D.