Bridging the Gap: Biologic, Behavioral, and Environmental Contributions to the Development of Type 2 Diabetes

Social Epidemiology;Diabetes;Public Health;Health Sciences;Epidemiological Science PhD

Christine, PaulSmith, Jennifer Ann ;

University of Michigan

关键词: Social Epidemiology;    Diabetes;    Public Health;    Health Sciences;    Epidemiological Science PhD;   

Others  :  https://deepblue.lib.umich.edu/bitstream/handle/2027.42/137022/pjchris_1.pdf?sequence=1&isAllowed=y

瑞士|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

Type 2 diabetes is an important cause of death and disability worldwide. Causes of the growing epidemic have been primarily attributed to obesity, unhealthy diets, and physical inactivity. Prevention of diabetes, therefore, has focused largely on individual behavioral modification. However, the recognition that health behaviors are structured by social conditions and environmental resources has highlighted the importance of thinking about the multi-level causes of diabetes. With continued increases in diabetes prevalence and incidence, population-based prevention strategies that account for both individual and environmental causes of disease are necessary. In this dissertation, we used a large, multi-ethnic, prospective cohort, to examine the social and environmental contributions to the development of diabetes. Our goal was to understand: (1) if neighborhood environments, including the availability of physical resources to support healthy diets and physical activity and social resources to promote safety and social cohesion, are related to diabetes incidence; (2) how neighborhood environments interact with and shape individual genetic susceptibility to diabetes; and (3) the utility of including individual and area-level social information in public health and clinical decision-making using risk prediction models. In the first study, we found that long-term exposure to neighborhoods with greater availability of healthy food and physical activity resources was associated with a lower incidence of diabetes over 10 years. Neighborhood social environments were largely unrelated to diabetes risk. Our second study found that individual genetic susceptibility to diabetes was modified by the availability of healthy food and physical activity resources. High genetic risk was most harmful for individuals living in neighborhoods with few healthy food and physical activity resources, but was considerably less harmful for individuals living in neighborhoods with more health- promoting resources. In the third study, we found that including social information in risk prediction models helped correct the systematic misestimation of risk for individuals at high and low levels of social disadvantage. The results all support the notion that social and environmental factors play an important role in the development of diabetes, and that altering neighborhood environments may represent a viable, population-based approach to diabetes prevention.