Professor Emeritus in Psychiatry and Behavioral Sciences
Education & Training
Ph.D., McGill University (Canada) 1972
Ph.D., McGill University (Canada)
B.A., Earlham College
The second major focus of our research program is to evaluate whether the apparent differential relationship between the personality construct of hostility and glucose metabolism in blacks and whites might contribute to the racial disparity in the prevalence of 2 diabetes. African-Americans are at increased risk for developing type 2 diabetes, but the reasons for this racial disparity are poorly understood. We are exploring our previous finding of a differential relationship of hostility to glucose metabolism in African-Americans and Caucasians and determine the underlying behavioral and/or physiologic mechanisms of these relationships. Two studies are being undertaken. First, we are assessing the multi-factorial nature of hostility in 100 African American men, 100 African American women, 100 Caucasian men, and 100 Caucasian women. These measures will be examined in relation to fasting and two-hour post-prandial glucose and insulin and hemoglobin A1c (HbA1c) on all subjects. This study should allow us to further understand the personality variables most directly related to glucose metabolism and to investigate the possibility that race and sex interact in determining this relationship. We also plan to further explore our preliminary findings that hostility is related to insulin sensitivity and elevated insulin levels in Caucasians and to fasting glucose in African-Americans. We will assess glucose-stimulated insulin release, glucose disposal, hepatic glucose production and glucose effectiveness utilizing an intravenous glucose tolerance test with labeled glucose in a subset of our sample. In addition, three sets of mediators will be examined: measures of hypothalamic-pituitary-adrenal (HPA) axis activity, measures of body mass and fat distribution, and measures caloric intake and exercise habits. It is hypothesized that hostility is related to diminished insulin sensitivity, but not to a defect in insulin secretion in Caucasians and that this relationship is mediated by BMI and the behavioral variables that impact on BMI. Furthermore, we hypothesize that hostility is related to increased hepatic glucose production and diminished insulin secretion in African-Americans and these relationships are mediated by neuroendocrine factors, but not by BMI. Confirmation of this hypothesis would confirm that African-Americans are more vulnerable to the metabolic effects of hostility and could partially explain the racial disparity in diabetes prevalence.
Finally, our laboratory continues to work on defining the mechanisms by which the C57BL/6J (B6) mouse develops diet-induced obesity and diabetes. This mouse will remain lean and euglycemic if it is raised on a low fat diet. However, when allowed access to a high fat diet, the B6 mouse will become obese and develop an analog of type 2 diabetes, even if caloric intake is matched to that of mice reared on a low fat diet.