Despite 50 years since the passage of the Fair Housing Act of 1968, the majority of black Americans continue to live in highly segregated communities. Differing exposure to obesogenic environments in segregated neighborhoods may contribute to racial disparities in obesity prevalence.
We used prospective data from the Coronary Artery Risk Development in Young Adults (CARDIA) study to examine associations between levels of neighborhood-level racial residential segregation and incident obesity in black men and women. Obesity, determined by measured anthropometry, and residential segregation, measured using the local Gi*statistic, were recorded at baseline and follow-up at years 7, 10, 15, 20, and 25. We used marginal structural survival models to account for time-dependent confounding and for loss to follow-up.
Black women living in highly segregated neighborhoods at the prior exam were 30% more likely to become obese during the follow-up period as compared with women living in neighborhoods with low levels of segregation after adjustment for sociodemographic and cardiovascular risk covariates (hazard ratio = 1.3 [95% confidence interval = 1.0, 1.7]). Cumulatively high exposure to segregation averaged across time points was associated with 50% higher hazard of obesity (hazard ratio = 1.5 [95% confidence interval = 1.0, 2.3]) among women. We observed few differences in obesity incidence among men by segregation levels.
Fewer health-promoting resources, stressful neighborhood context, and social norms that are less stigmatizing of obesity may contribute to these findings, but more research on specific pathways leading from segregation to obesity is needed to understand differing patterns between men and women.
From the aDepartment of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL; bDepartment of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO; cDepartment of Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC; and dDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC.
Submitted December 16, 2016; accepted December 19, 2017.
Statement of replication: The data are available for replication through approval and oversight by the CARDIA Coordinating Center. Further information on accessing CARDIA data and computing code to produce these results is available in the eAppendix (http://links.lww.com/EDE/B302).
The Coronary Artery Risk Development in Young Adults Study (CARDIA) is supported by contracts HHSN268201300025C, HHSN268201300026C, HHSN268201300027C, HHSN268201300028C, HHSN268201300029C, and HHSN268200900041C from the National Heart, Lung, and Blood Institute (NHLBI), the Intramural Research Program of the National Institute on Aging (NIA), and an intra-agency agreement between NIA and NHLBI (AG0005).
The authors report no conflicts of interest.
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Correspondence: Lindsay R. Pool, Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, 680 North Lake Shore, Suite 1400, Chicago, IL 60611. E-mail: firstname.lastname@example.org.