Disparities exist in the U.S. between the health status of African American and Hispanic individuals and the health status of non-Hispanic Caucasian individuals across all age groups. Those minority individuals age 55 and over are more likely to suffer from specific health disparities in areas such as diabetes, heart disease, and cancer than their white majority counterparts. Among the most common chronic disorders experienced within this age group are obesity, type II diabetes and cardiovascular disease, all three of which collectively form what has recently become known as metabolic syndrome. As of 2004, metabolic syndrome is diagnosable once criteria are clinically significant for a variety of different risk factors designated by the World Health Organization. However, like many syndromes these criteria are not stable across individuals, and leaves variability between individuals being diagnosed. It has been seen that each of the above mentioned racial/ethnic groups experience the individual risk factors at disproportionate rates, making it plausible that metabolic syndrome could be experienced in distinctly different ways depending upon racial/ethnic background. Using two nationally representative data sets, it is first largely evident that African American and Hispanic individuals are reaching higher peak rates of diabetes and cardiovascular disease much earlier in age than are non-Hispanic Caucasian individuals. The study goes on to reveals that the metabolic syndrome appears to follow one underlying progressive syndrome that begins with obesity and progresses towards heart disease. Each of the racial/ethnic groups experience significantly different progressions of the syndrome across time. Behavioral analysis found significant differences in health behaviors across the three groups; however a more pervasive lack of initiative in practicing preventive health behaviors is also present. The study achieved a higher understanding of individual differences within metabolic syndrome and insight into how and at what time in the lifespan health services can be most beneficial in providing preventive services to culturally diverse populations.

Indiana University-Purdue University Indianapolis (IUPUI) / Prospective epidemiologic evidence indicates that both stressful life events (SLEs) and depression are associated with an increased risk of subclinical atherosclerosis and cardiovascular disease (CVD) events. Even though stressful life events (SLEs) and depression co-occur and may act together to influence cardiovascular disease (CVD) risk, these psychosocial factors have been mainly examined in isolation. For instance, depression may moderate the relationship between SLEs and CVD outcomes. I hypothesized that depressive symptoms would potentiate the deleterious effect of SLEs on subclinical atherosclerosis. This hypothesis is plausible, given that depressed adults exhibit exaggerated and prolonged sympathetic nervous system, hypothalamic-pituitary-adrenal (HPA) axis, and inflammatory responses to stress, which in turn could promote atherosclerosis. As compared to their nondepressed counterparts, depressed individuals may also be more likely to engage in maladaptive methods to cope with SLEs (e.g., increased tobacco use, alcohol use, and consumption of low-nutrient, energy dense foods), which could also promote atherosclerosis. I examined cross-sectional data from 274 to 279 (depending on the outcome measure) older, African American adults (mean age = 66 years, 67% female) with no evidence of clinical CVD or dementia who participated in the St. Louis African American Health-Heart study (2009–2011). Number of SLEs was assessed using the Life Events Calendar, a structured interview. From this interview, a continuous SLEs variable was computed (number of adult SLEs: 0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11+). Severity of depression symptoms was measured using the 17-item Hamilton Rating Scale for Depression (HAM-D). Two measures of subclinical atherosclerosis were obtained: carotid intima-media thickness (CIMT; assessed by ultrasonography) and coronary artery calcification (CAC; assessed by multi-detector computerized tomography). I conducted linear (CIMT) and logistic (CAC) regression models, first adjusted for demographics (age, sex, education) and then fully-adjusted (demographics; mean arterial pressure; low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C); hemoglobin A1c; BMI; tobacco use; diabetes diagnosis; and use of antihypertensitve, lipid lowering, antidiabetic, and antidepressant medications). No main effects of SLEs or HAM-D were found for CIMT or CAC. There were also no SLEs by HAM-D interactions for CIMT or CAC. Because the current results are largely inconsistent with prior literature and there is a paucity of studies utilizing African American samples, future research is needed to examine the independent and interactive associations of SLEs and depressive symptoms with measures of subclinical atherosclerosis. If the present results are replicated, it may suggest that SLEs, depressive symptoms, and their interactive effect are not cardiotoxic among African American adults.