Date of Award


Document Type

Open Access Dissertation




College of Arts and Sciences

First Advisor

Dawn K. Wilson


Obesity research in the area of prevention has become a national priority given the increasingly high prevalence rate of this condition among US adults, and subsequent health risks that are associated. The etiology of obesity is complex, so a more comprehensive understanding of the interaction between genetic predisposition and the social environment in regards to obesity in adults would advance our knowledge for future public health and prevention efforts. This study’s aim was to assess the impact of a gene by neighborhood social environment interactions on weight-related (i.e., waist circumference) and stress-related (i.e. cortisol) outcomes in underserved African-American adults. A bioecological framework was used in the present study to integrate factors, including social environmental factors (i.e. perceptions of safety from crime, neighborhood satisfaction, neighborhood social life, and collective efficacy) and genetic risk (Sympathetic Nervous System and Hypothalamic-Pituitary-Adrenal axis related genes) to better understand the gene by environment interactions on weigh-related and stress-related outcomes in adults. This study utilized participants from the Positive Action for Today’s Health (PATH) trial. Based on a dual risk model, it is hypothesized that those with the highest genetic risk and who experienced negative neighborhood environment conditions would have the worst outcomes (i.e. highest waist circumference and highest cortisol levels). There were no significant three-way interactions with gene by environment interactions predicting change over time. However, results did indicate three significant gene by environment interactions on weight related outcomes, all within the SNS pathway. These significant results included two interactions that support the dual risk model, which were the SNS genetic risk by neighborhood social life interaction (b=-0.108, t(618)=-2.018, p=0.04), and SNS genetic risk by informal social control (collective efficacy) interaction (b=-0.510, t(618)=-1.95, p=0.05) on waist circumference outcomes. Further, there was a significant SNS genetic risk by neighborhood satisfaction interaction (b=1.481, t(618)=2.233, p=0.02) on waist circumference outcomes, which did not match the dual risk hypothesis. For the secondary aims, however, there was only one SNS by social cohesion and trust interaction (b=0.59, p=0.02) on cortisol in the unexpected direction for the linear regression. Implications of these findings, limitations of the study and future directions are discussed.