DIABETES, DEPRESSION, & CORONARY HEART DISEASE

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 糖尿病和抑郁症都独立地增加了女性患冠心病（CHD）的风险。 因此，更好地了解这些风险因素如何相互作用对我们了解女性心脏病至关重要。 抑郁症-糖尿病-CHD关系的一个假设机制是下丘脑-肾上腺-肾上腺（HPA）轴和皮质醇的产生。 目前，还没有数据公布，看看这些变量在音乐会。 因此，尚不清楚它们是否各自传递一个单独的风险，当它们结合在一起时会变成累加的风险，或者它们是否相互作用以传递倍增的风险。 这项研究是一项关于女性抑郁症、糖尿病和冠心病风险的横断面研究。 研究设计为2 × 2析因设计。 样本将由80名年龄匹配的绝经后女性组成。 自变量为1）是否存在抑郁症病史（是或否）和2）T2 DM状态（是或否）。 因变量为唾液皮质醇水平、脂质（总胆固醇、HDL亚组分和甘油三酯）、腰臀比、肱动脉血流介导的扩张、止血指标（vWF）、炎症标志物（c-反应蛋白）、微量白蛋白尿和血压。将控制的变量包括BMI（骨量指数）、降脂药、β受体阻滞剂、ACE抑制剂、降压药以及吸烟、体力活动和饮酒史。 将检验三个假设：1）对糖尿病有主效应，糖尿病受试者的WHR、血压、vWf、C-反应蛋白（CRP）、血脂异常、微量白蛋白尿和内皮依赖性肱动脉反应性（EDBR）受损程度高于非糖尿病受试者; 2）抑郁症史将有主效应，使得具有阳性病史的参与者将显示更高的WHR、血压、vWf、CRP、微量白蛋白尿、更多受损的EDBR，抑郁症病史与糖尿病之间存在交互作用，即抑郁症病史与糖尿病病史同时存在的受试者，其WHR、血压、vWf、CRP和EDBR受损程度均高于抑郁症或糖尿病病史者。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Diabetes and depression both independently put women at increased risk for coronary heart disease (CHD). Thus, a better understanding of how these risk factors interact is crucial to our understanding of heart disease in women. One hypothesized mechanism for the depression-diabetes-CHD relationship is the Hypothalamic-Pituitary-Adrenal (HPA) axis and cortisol production. Currently, no data have been published that look at these variables in concert. Thus, it is unclear if they each convey an individual risk that becomes additive when combined, or if they interact to convey multiplicative risk. The study being proposed is a cross sectional study of depression, diabetes, and CHD risk in women. The research design is a 2X2 factorial design. The sample will consist of 80 age-matched postmenopausal women. The independent variables are 1) presence of a history of depression (yes or no), and 2) T2DM status (yes or no). The dependent variables are salivary cortisol levels, lipids (total cholesterol, HDL subfractions, and triglycerides), waist-to-hip ratio, brachial artery flow mediated dilation, hemostatic indicator (vWF), inflammatory marker (c-reactive protein), microalbuminuria, and blood pressure. Variables that will be controlled for include BMI (Bone Mass Index), lipid lowering agents, beta blockers, ACE inhibitors, antihypertensive agents, and history of smoking, physical activity, and alcohol use. Three hypotheses will be tested: 1) There will be a main effect for diabetes, such that participants with diabetes will show higher WHR, blood pressure, vWf, C-Reactive Protein (CRP), dyslipidemia, microalbuminuria, and more impaired endothelium dependent brachial reactivity (EDBR) than those without diabetes; 2) There will be a main effect for history of depression, such that participants a positive history will show higher WHR, blood pressure, vWf, CRP, microalbuminuria, more impaired EDBR, and a flatter cortisol pulsatile circadian rhythm than those with a negative history; 3) there will be an interaction between history of depression and diabetes, such that participants with both diabetes and positive history of depression will show higher WHR, blood pressure, vWf, CRP, and more impaired EDBR, than those with only history of depression or diabetes.