Search

Objective: The aim of this study was to examine relationships between the food environment and obesity by community type. Methods: Using electronic health record data from the US Veterans Administration Diabetes Risk (VADR) cohort, we examined associations between the percentage of supermarkets and fast‐food restaurants with obesity prevalence from 2008 to 2018. We constructed multivariable logistic regression models with random effects and interaction terms for year and food environment variables. We stratified models by community type. Results: Mean age at baseline was 59.8 (SD = 16.1) years; 93.3% identified as men; and 2,102,542 (41.8%) were classified as having obesity. The association between the percentage of fast‐food restaurants and obesity was positive in high‐density urban areas (odds ratio [OR] = 1.033; 95% CI: 1.028–1.037), with no interaction by time (p = 0.83). The interaction with year was significant in other community types (p < 0.001), with increasing odds of obesity in each follow‐up year. The associations between the percentage of supermarkets and obesity were null in high‐density and low‐density urban areas and positive in suburban (OR = 1.033; 95% CI: 1.027–1.039) and rural (OR = 1.007; 95% CI: 1.002–1.012) areas, with no interactions by time. Conclusions: Many healthy eating policies have been passed in urban areas; our results suggest such policies might also mitigate obesity risk in nonurban areas. [ABSTRACT FROM AUTHOR]

Exposure to particulate matter ≤2.5 μm in diameter (PM 2.5) and ozone (O 3) has been linked to numerous harmful health outcomes. While epidemiologic evidence has suggested a positive association with type 2 diabetes (T2D), there is heterogeneity in findings. We evaluated exposures to PM 2.5 and O 3 across three large samples in the US using a harmonized approach for exposure assignment and covariate adjustment. Data were obtained from the Veterans Administration Diabetes Risk (VADR) cohort (electronic health records [EHRs]), the Reasons for Geographic and Racial Disparities in Stroke (REGARDS) cohort (primary data collection), and the Geisinger health system (EHRs), and reflect the years 2003–2016 (REGARDS) and 2008–2016 (VADR and Geisinger). New onset T2D was ascertained using EHR information on medication orders, laboratory results, and T2D diagnoses (VADR and Geisinger) or report of T2D medication or diagnosis and/or elevated blood glucose levels (REGARDS). Exposure was assigned using pollutant annual averages from the Downscaler model. Models stratified by community type (higher density urban, lower density urban, suburban/small town, or rural census tracts) evaluated likelihood of new onset T2D in each study sample in single- and two-pollutant models of PM 2.5 and O 3. In two pollutant models, associations of PM 2.5 , and new onset T2D were null in the REGARDS cohort except for in suburban/small town community types in models that also adjusted for NSEE, with an odds ratio (95% CI) of 1.51 (1.01, 2.25) per 5 μg/m3 of PM 2.5. Results in the Geisinger sample were null. VADR sample results evidenced nonlinear associations for both pollutants; the shape of the association was dependent on community type. Associations between PM 2.5 , O 3 and new onset T2D differed across three large study samples in the US. None of the results from any of the three study populations found strong and clear positive associations. • PM 2.5 and O 3 were minimally associated with new onset type 2 diabetes (T2D) in three large study samples in the United States. • Results did not substantially differ between single and two pollutant models. • Associations of PM 2.5 and O 3 with new onset T2D were impacted by adjustment for neighborhood socio-economic disadvantage. [ABSTRACT FROM AUTHOR]