Type 2 diabetes mellitus (T2DM) afflicts some 21 million US adults, with annual attributable costs exceeding $132 billion. A disproportionate burden of T2DM is borne by US minority populations. Black and Hispanic Americans have higher prevalence of T2DM, achieve poorer disease control, and have greater prevalence of T2DM complications than do their white counterparts. The confluence of local environmental disadvantages, lack of access to adequate health care, behavioral risk factors, and other influences likely contribute to these increased burdens in a synergistic fashion. This application responds to NIH program announcement PA-07-027 ("Health Disparities in NIDDK Diseases") by investigating "upstream," antecedent factors contributing to "downstream" disparities in T2DM risk. It is specifically intended to measure the relative contributions of multilevel social, environmental, behavioral, and biophysiologic factors to racial and ethnic heterogeneity in the prevalence of prediabetes. Prediabetes will be defined either as impaired fasting glucose, or the prevalence of the metabolic syndrome. This project will obtain data on 3000 subjects from a unique and newly available population-based cohort - the NIDDK supported Boston Area Community Health (BACH) sample (DK 56842;principal investigator: John McKinlay, PhD). It will therefore cost-effectively capitalize on our previous work in obtaining this large, randomly-chosen, and representative population. The BACH cohort - 5,506 community- dwelling subjects - is socio-demographically diverse, consisting of 2,301 men and 3,205 women (1,780 black, 1,858 Hispanic, and 1,868 white) across a broad age-range (30-79 years). This cohort exhibits the wide variability in overall health status, current life circumstances and access to health care that is required for the planned study. Importantly, use of this sample will permit the study of health and disease among subjects who typically go unobserved in a clinical setting. Extensive preliminary studies support the feasibility of this effort. The upstream focus on prediabetes represents a unique opportunity to examine the influence of the multilevel contributors to health differences antecedent to T2DM diagnosis, when targeted interventions might achieve tremendous impact in preventing transition to T2DM. The measurement of multilevel contributors is motivated by their potential to inform such interventions, either at the social and the environmental levels (healthy public policy and community action), or the behavioral and biophysiologic levels (primary and secondary prevention). The multi-level, interdisciplinary approach builds upon existing literature and permits balanced estimation of the independent and relative contribution of different factors. The inclusion of well justified measures at each level will facilitate understanding of disease pathways within their social and environmental contexts, thus adding to the armamentarium of both clinical providers and policy makers, and enhancing their ability to prevent and treat T2DM.
This project will obtain data on 3000 subjects, a sample equally divided by gender and race/ethnicity (black, Hispanic, and white men and women), in order to understand the reasons that among black and Hispanic Americans, type 2 diabetes is more common, and more severe, than among their white compatriots. To do so, the study team will examine physiologic influences and health conditions that often occur before diabetes is diagnosed, to determine if they are different across race and ethnicity, and if so, what explanatory factors (such as environment, family history, or socioeconomic status) contribute to those differences. If successful, this project will identify ways that the excess risk of type 2 diabetes observed among vulnerable populations can be reduced.
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|Piccolo, Rebecca S; Pearce, Neil; Araujo, Andre B et al. (2014) The contribution of biogeographical ancestry and socioeconomic status to racial/ethnic disparities in type 2 diabetes mellitus: results from the Boston Area Community Health Survey. Ann Epidemiol 24:648-54, 654.e1|