Introduction and Objective: Postpartum diabetes increases cardiometabolic risk and may occur among individuals with and without gestational diabetes (GDM). The association of racial/ethnic residential segregation with postpartum diabetes is unclear. Methods: This cohort study followed 431,104 pregnant individuals for up to 10 years (mean ± SD 5.2 ± 3.4) at Kaiser Permanente Northern California. Cox regression estimated adjusted hazard ratio (aHR) of postpartum diabetes by prenatal racial/ethnic segregation via the Getis-Ord Gi* statistic. Results: Postpartum diabetes incidence was 2.5% in Asian/Pacific Islander (API), 2.6% in Black, 2.6% in Hispanic, and 0.8% in White. Black segregation was associated with a higher risk of postpartum diabetes in Black (aHR 1.37 [95% CI 1.08, 1.74]), Hispanic (1.12 [1.01, 1.24]), and White (1.20 [1.01, 1.42]) (Figure). Hispanic segregation was associated with a higher risk of postpartum diabetes in API (1.27 [1.12, 1.44]) and Hispanic (1.13 [1.01, 1.26]), while White segregation was associated with a lower risk. Associations were stronger in individuals without vs. with GDM. Conclusion: The higher risk of postpartum diabetes in Black and Hispanic segregated neighborhoods and lower risk in White segregated neighborhoods may inform structural targets for advancing maternal health equity. The stronger associations in individuals without GDM need investigation. R.F. Chehab: None. A. Ferrara: None. L. Chen: None. A. Ngo: None. M. Greenberg: None. Y. Zhu: None. NICHD (K99HD115836); NIMHD (R01MD018459)
Introduction and Objective: Both in utero exposure to GDM and prenatal depression have been shown to increase childhood obesity risk, but their combined effect is unknown. We assessed the combined effect of GDM and prenatal depression on childhood obesity. Methods: At Kaiser Permanente, pregnant individuals were universally screened for GDM and prenatal depression (2011-2019). Their children had height and weight recorded in the medical records. Obesity was defined as a sex and age-specific BMI-z-score≥95th percentile based on CDC metrics. Children ages 5-7 years (N=116,398) and ages 8-10 years (N=44,894) were analyzed separately. Adjusted Poisson regression with robust standard errors assessed the association between GDM and childhood obesity, stratified by prenatal depression status. Results: Pregnant individuals were on average 31±5 years at delivery, had pre-pregnancy overweight (BMI 26±6 kg/m²), and were racially/ethnically diverse (27% Asian/Pacific Islander, 6% Black, 26% Hispanic, 36% White). Both GDM and prenatal depression were individually significantly associated with childhood obesity. In models stratifying individuals by prenatal depression status and adjusting for maternal age, race/ethnicity, neighborhood deprivation index, parity, and smoking and alcohol use during pregnancy, in utero exposure to GDM was significantly associated with higher obesity risk at ages 5-7 (depression: RR 1.07 [95% CI 1.05, 1.09]; no depression: 1.06 [1.05, 1.07]) and ages 8-10 (depression: 1.07 [1.04, 1.11]; no depression: 1.06 [1.05, 1.08]). When additionally adjusting for pre-pregnancy BMI, associations were slightly attenuated but remained significant (ages 5-7: depression: 1.03 [1.01, 1.05]; no depression: 1.03 [1.02, 1.03]; ages 8-10: depression: 1.03 [1.00, 1.07]; no depression: 1.02 [1.01, 1.03]). Conclusion: In a large and diverse population, in utero exposure to GDM was associated with an increased risk of childhood obesity, with similar risk levels observed in children regardless of prenatal depression exposure. A.K. Peterson: None. L. Avalos: None. Y. Zhu: None. M. Craft: None. M. Greenberg: None. A. Ngo: None. C. Quesenberry: None. A. Ferrara: None. Kaiser Permanente, Community Health (RNG212851)
Introduction and Objective: Managing carbohydrate intake and physical activity (PA) are recommended for individuals with pregnancy hyperglycemia, but the concurrent impact of these behaviors and meal timing on postprandial glucose levels has not been explored. Methods: Fourteen participants with gestational glucose intolerance (GGI) and 2 with GDM from the Time to Move Randomized Crossover Trial (ClinicalTrials.gov #NCT06125704) wore blinded Dexcom G6 Pro continuous glucose monitoring devices; completed timestamped photo-upload assisted, 24-hr dietary recalls; and wore Actigraph CentrePoint Insight Watch PA monitoring devices in the third trimester. This analysis explored differences in mean 2-hr postprandial glucose following breakfast (between 5-9am) compared to dinner (between 4-8pm), across 3 observation-days. Estimates from Proc Mixed in SAS v9.4 were adjusted for meal-specific carbohydrate intake (dichotomized at the 75th percentile) and postprandial PA (i.e., completion of trial assigned, moderate intensity walking or stepping, within 30-40 minutes of the meal). Results: After adjusting for meal-specific carbohydrate intake and postprandial PA, mean 2-hr postprandial glucose was 105.87 mg/dl (SE 5.78) for breakfast compared to 108.73 mg/dl (SE 5.77) for dinner (p =.41). Adjusted mean 2-hr postprandial glucose was 103.95 mg/dl (SE 5.72) after meals with carbohydrate in the lower quartiles compared to 110.65 mg/dl (SE 5.90) after high carbohydrate meals (p=.08), and 106.10 mg/dl (SE 6.02) for postprandial PA compared to 108.49 mg/dl (SE 5.60) for no PA (p =.52). Conclusion: Additional data are pending and will improve the precision of estimated differences, but this preliminary analysis does not support an independent association between meal timing and mean 2-hr postprandial glucose levels in free-living individuals with GDM or GGI. Disclosure J.E. Lewis: None. B.R. Hallenbeck: None. H. Raynor: None. S.E. Crouter: None. J.I. Miller: None. S. Yousefi: None. N. Zite: Research Support; Merck & Co., Inc. W. Schoutko: None. K.B. Fortner: Other Relationship; Pfizer Inc. J.M. Maples: None. S.F. Ehrlich: None. Funding American Diabetes Association (11-22-ICTSN-29)
Introduction and Objective: Medical nutrition therapy (MNT) is the first line of treatment for gestational diabetes mellitus (GDM); failing this, pharmacologic treatment is recommended. Racial/ethnic disparities in diagnosis of GDM and progression to T2D exist, but little is known about disparities in progression to medication. We conducted a time-to-event analysis of progression to any GDM medication by race/ethnicity. Methods: We identified GDM singleton pregnancies (2008-2023) among patients ≥18 years, with no prior diabetes and medical coverage from 1 year before pregnancy in an integrated health care delivery system. We assessed self-reported race/ethnicity, and the outcome was progression to medication (insulin, glyburide, metformin) after GDM diagnosis using medication fills as a proxy. We ran Cox proportional hazard regressions, adjusted for maternal characteristics and highest quartile of screening glucose (binary proxy for GDM severity; fasting glucose used if screening was missing), with White individuals (as historically advantaged) as the reference group. Results: Among 27,310 patients with GDM, 41% were Asian, 4% were Black, 28% were Hispanic, 1% were Pacific Islander (PI) and 23% were White. The mean age was 32.7 (SD: 4.8) and mean pre-pregnancy BMI was 29.5 (SD: 7.0). Asian (41%) and PI (40%) individuals had lower proportions of medication use compared to Black (48%) and White (45%) individuals. Median time to progression was lowest among White (27 days) and highest among Asian (32 days) individuals. Relative to White individuals, PI (0.80, 95% CI 0.68-0.95) and Hispanic (0.94, 95% CI 0.89-0.99) individuals had lower adjusted hazards; all other groups had non-significant hazard ratios. Conclusion: The proportion who progresses, time to progression, and hazard of progression to medication after GDM diagnosis vary by racial/ethnic groups. Medication fills are an imperfect proxy for prescribing information; however these data suggest that the efficacy of MNT may vary by racial/ethnic subgroups. S.S. Bane: Employee; Malama Health. E.F. Liu: None. M. Greenberg: None. R. Neugebauer: None. M.M. Hedderson: None. National Institutes of Health (DK138135-02)
Introduction and Objective: General obesity scaled by body mass index (BMI) is a risk factor for diabetes. Despite recognized limitations of BMI in assessing obesity, little is known about the role of central obesity in GDM and postpartum preDM/DM, or whether certain central obesity indices are stronger predictors. Methods: We examined associations between central obesity and GDM (n=304) and postpartum preDM/DM (n=743) from electronic health records in the PETALS cohort (n=3,055), with up to 9.9 years (mean 4.8; SD 2.7) follow-up. We used height, waist circumference (WC), and hip circumference at 10-13 weeks gestation to calculate body roundness index (BRI), waist-to-height ratio (WHtR), and waist-to-hip ratio (WHR). We used modified Poisson regression for GDM and Cox regression for postpartum preDM/DM, with adjustment for confounders and testing for effect modification by pre-pregnancy BMI (ppBMI). Results: The highest (>5.9) vs. lowest (≤3.3) quartile of BRI had an increased risk of GDM (relative risk [RR] 7.5, 95% CI 4.1-13.5) and postpartum preDM/DM (hazard ratio [HR] 3.0, 2.0-4.4). The highest (≥0.63) vs. lowest (<0.5, no central obesity) group of WHtR had a similar increased risk of GDM (RR 7.1, 3.9-13.2) and postpartum preDM/DM (HR 2.9, 2.0-4.3). Among people with ppBMI≥25, BRI and WHtR above vs. below the median had increased risks of GDM (RR for both 2.8, 1.7-4.4) and preDM/DM (HR for both 1.6, 1.3-2.1). When ppBMI<25, the association of BRI and WHtR persisted with preDM/DM (HR for both 1.7, 1.0-2.7) but not GDM. WC and WHR were also associated with GDM and postpartum preDM/DM, with smaller effect sizes. Conclusion: Central obesity indices, especially BRI and WHtR, are independent risk factors for GDM and postpartum preDM/DM beyond general obesity, with the potential to inform clinical screening/prevention strategies. In practice, WHtR may be preferrable to BRI given its ease of calculation and interpretation. A.K. Rosen Vollmar: None. A. Ferrara: None. M.M. Hedderson: None. A. Ngo: None. R.F. Chehab: None. A.K. Peterson: None. M. Greenberg: None. Y. Zhu: None. National Institute of Environmental Health Sciences (R01ES019196), National Institute on Minority Health and Health Disparities (R01MD018459), Kaiser Permanente Center for Upstream Prevention of Adiposity and Diabetes Mellitus (UPSTREAM), Kaiser Permanente Translational Research Fellowship
