Abstract # 2208 Event # 88:

Scheduled for Friday, June 22, 2007 11:30 AM-11:50 AM: Session 8 (North Main Hall C/D) Symposium


C. A. Shively, T. C. Register, M. R. Adams, D. L. Golden, S. L. Willard and T. B. Clarkson
Wake Forest University School of Medicine, Comparative Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1040, USA
     Depression is associated with increased coronary heart disease (CHD), and it is thought that depression may cause CHD. While CHD develops over several decades, little is known about the relationship between depression and subclinical coronary artery atherosclerosis (CAA), the underlying cause. Adult female cynomolgus monkeys, an established model of both atherogenesis and depression, were studied. Thirty-six adult females housed in small social groups of 4 females each, consumed an atherogenic diet (0.28 mg cholesterol/Cal, ~human consumption of 500 mg/day, and 42% of calories as fat) for 52 mos. Time spent in depressed behavior (defined as a slumped or collapsed body posture accompanied by a lack of responsiveness to environmental stimuli to which other monkeys are attending, and open eyes) was recorded in weekly 15 minute focal samples. CHD risk factors were measured annually. Time spent in depressed behavior was significantly correlated [a=0.05] with CHD risk factors: reduced cortisol response to corticotrophin releasing hormone, increased telemetered overnight heart rate, increased total plasma cholesterol, and a decrease in mean peak luteal phase progesterone. CAA extent, measured as coronary artery plaque area, was highly correlated with the percent of time spent depressed. Thus, in primates, depression is associated with adverse perturbations in multiple CHD risk factors and accelerated early atherogenesis. This work was supported by MH56881.