Geospatial analysis of food environment demonstrates associations with gestational diabetes.

BACKGROUND: Gestational diabetes mellitus (GDM) is one of most common complications of pregnancy, with incidence rates varying by maternal age, race/ethnicity, obesity, parity, and family history. Given its increasing prevalence in recent decades, covariant environmental and sociodemographic factors may be additional determinants of GDM occurrence. OBJECTIVE: We hypothesized that environmental risk factors, in particular measures of the food environment, may be a diabetes contributor. We employed geospatial modeling in a populous US county to characterize the association of the relative availability of fast food restaurants and supermarkets to GDM. STUDY DESIGN: Utilizing a perinatal database with >4900 encoded antenatal and outcome variables inclusive of ZIP code data, 8912 consecutive pregnancies were analyzed for correlations between GDM and food environment based on countywide food permit registration data. Linkage between pregnancies and food environment was achieved on the basis of validated 5-digit ZIP code data. The prevalence of supermarkets and fast food restaurants per 100,000 inhabitants for each ZIP code were gathered from publicly available food permit sources. To independently authenticate our findings with objective data, we measured hemoglobin A1c levels as a function of geospatial distribution of food environment in a matched subset (n = 80). RESULTS: Residence in neighborhoods with a high prevalence of fast food restaurants (fourth quartile) was significantly associated with an increased risk of developing GDM (relative to first quartile: adjusted odds ratio, 1.63; 95% confidence interval, 1.21-2.19). In multivariate analysis, this association held true after controlling for potential confounders (P = .002). Measurement of hemoglobin A1c levels in a matched subset were significantly increased in association with residence in a ZIP code with a higher fast food/supermarket ratio (n = 80, r = 0.251 P < .05). CONCLUSION: As demonstrated by geospatial analysis, a relationship of food environment and risk for gestational diabetes was identified.

Heritable IUGR and adult metabolic syndrome are reversible and associated with alterations in the metabolome following dietary supplementation of 1-carbon intermediates.

Metabolic syndrome (MetS), following intrauterine growth restriction (IUGR), is epigenetically heritable. Recently, we abrogated the F2 adult phenotype with essential nutrient supplementation (ENS) of intermediates along the 1-carbon pathway. With the use of the same grandparental uterine artery ligation model, we profiled the F2 serum metabolome at weaning [postnatal day (d)21; n = 76] and adulthood (d160; n = 12) to test if MetS is preceded by alterations in the metabolome. Indicative of developmentally programmed MetS, adult F2, formerly IUGR rats, were obese (621 vs. 461 g; P < 0.0001), dyslipidemic (133 vs. 67 mg/dl; P < 0.001), and glucose intolerant (26 vs. 15 mg/kg/min; P < 0.01). Unbiased gas chromatography-mass spectrometry (GC-MS) profiling revealed 34 peaks corresponding to 12 nonredundant metabolites and 9 unknowns to be changing at weaning [false discovery rate (FDR) < 0.05]. Markers of later-in-life MetS included citric acid, glucosamine, myoinositol, and proline (P < 0.03). Hierarchical clustering revealed grouping by IUGR lineage and supplementation at d21 and d160. Weanlings grouped distinctly for ENS and IUGR by partial least-squares discriminate analysis (PLS-DA; P < 0.01), whereas paternal and maternal IUGR (IUGR(pat)/IUGR(mat), respectively) control-fed rats, destined for MetS, had a distinct metabolome at weaning (randomForest analysis; class error < 0.1) and adulthood (PLS-DA; P < 0.05). In sum, we have found that alterations in the metabolome accompany heritable IUGR, precede adult-onset MetS, and are partially amenable to dietary intervention.