DIABETES, DEPRESSION, & CORONARY HEART DISEASE

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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.