Posttraumatic Stress Disorder as a Catalyst for the Association Between Metabolic Syndrome and Reduced Cortical Thickness.
Posttraumatic Stress Disorder as a Catalyst for the Association Between Metabolic Syndrome and Reduced Cortical Thickness.
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DOI：
10.1016/j.biopsych.2015.11.023
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发表时间：
2016-09-01
影响因子：
10.6
通讯作者：
Miller MW
中科院分区：
文献类型：
--
作者：
Wolf EJ;Sadeh N;Leritz EC;Logue MW;Stoop TB;McGlinchey R;Milberg W;Miller MW
代谢综合征（MetS）由一系列心脏代谢病理学定义，在退伍军人中非常普遍，特别是那些患有创伤后应激障碍（PTSD）的退伍军人，并对不良健康结果构成重大风险，包括神经变性和死亡率。鉴于此，我们评估了：（a）MetS和神经完整性之间的关联，以皮质厚度为指标;（B）PTSD和MetS之间的关系;（c）PTSD是否通过MetS间接与皮质厚度相关。样本包括346名美国退伍军人（89.3%男性; 71.4%白色）谁部署到伊拉克和/或阿富汗。274名参与者的神经影像学数据可用。在全脑分析中，MetS与2个左半球和4个右半球区域的皮质厚度呈负相关：（a）双侧颞叶，包括颞极、梭状回和颞叶，并延伸到枕叶皮质（左半球）和眶额皮质（右半球）;（B）双侧楔前叶、后扣带回、距状核和枕顶叶皮质;（c）右喙前扣带皮层和中央沟/中央后回。路径模型显示，PTSD预测MetS（β = 0.19，p <0.001），而MetS又与皮质厚度的减少相关（βs从-0.29到-0.43，所有p <0.001）。来自这个年轻退伍军人样本的结果提供了证据，证明PTSD赋予心脏代谢病理学和神经退行性变的风险，并引起了人们的担忧，即这个队列可能是老年前期，并有严重的医疗和认知能力下降的风险。这突出了需要确定PTSD与MetS之间的分子机制，并采取有效干预措施减少PTSD相关的健康共病。
Metabolic syndrome (MetS), defined by a constellation of cardiometabolic pathologies, is highly prevalent among veterans, especially those with posttraumatic stress disorder (PTSD), and poses a major risk for adverse health outcomes, including neurodegeneration and mortality. Given this, we evaluated: (a) the association between MetS and neural integrity, indexed by cortical thickness; (b) the relationship between PTSD and MetS; and (c) if PTSD was associated with cortical thickness indirectly through MetS. The sample consisted of 346 US military veterans (89.3% male; 71.4% white) who deployed to Iraq and/or Afghanistan. Neuroimaging data were available for 274 participants. In whole-brain analyses, MetS was negatively associated with cortical thickness in 2 left and 4 right hemisphere regions: (a) bilateral temporal lobe, including temporal pole, fusiform gyrus, and insula, and extending into occipital cortex (left hemisphere) and orbitofrontal cortex (right hemisphere); (b) bilateral precuneus, posterior cingulate, calcarine, and occipital-parietal cortex; and (c) right rostral anterior cingulate cortex and central sulcus/postcentral gyrus. Path models showed that PTSD predicted MetS (β = .19, p < .001), which, in turn, was associated with reduced cortical thickness (βs from −.29 to – .43, all p <.001). Results from this young veteran sample provide evidence that PTSD confers risk for cardiometabolic pathology and neurodegeneration and raise concern that this cohort may be aging pre-maturely and at risk for substantial medical and cognitive decline. This highlights the need to identify the molecular mechanisms linking PTSD to MetS and for effective interventions to reduce PTSD-related health comorbidities.