Key result
Prepregnancy obesity is linked to ~4.1-fold higher postpartum diabetes risk vs normal weight.
Why the study?
Adverse pregnancy outcomes rarely occur in isolation, and previous studies often focused on isolated events or surrogate markers rather than confirmed clinical endpoints. The nature of distinct adverse pregnancy outcome patterns and their specific mediating role in the pathway from prepregnancy obesity to clinical cardiometabolic outcomes remained poorly defined.
Does prepregnancy obesity increase the risk of early postpartum diabetes mellitus, cardiometabolic comorbidities, and stage-4 cardiovascular-kidney-metabolic syndrome through distinct adverse pregnancy outcome patterns compared to normal weight?
Cohort (n=555,591)
Does prepregnancy obesity increase the risk of early postpartum diabetes mellitus, cardiometabolic comorbidities, and stage-4 cardiovascular-kidney-metabolic syndrome through distinct adverse pregnancy outcome patterns compared to normal weight?
Prepregnancy obesity increases early postpartum risk of diabetes, cardiometabolic comorbidities, and stage-4 CKM syndrome through divergent adverse pregnancy outcome pathways, with gestational diabetes predominantly mediating future diabetes and hypertensive disorders of pregnancy predominantly mediating stage-4 CKM.
Background Prepregnancy obesity is a well-established risk factor for adverse pregnancy outcomes (APOs) and future cardiovascular metabolic disease. However, previous studies often focused on isolated APOs or surrogate markers rather than confirmed clinical endpoints. Furthermore, APOs rarely occur in isolation but manifest as complex clinical clusters. The nature of these distinct APO patterns and their specific mediating role in the pathway from obesity to clinical outcomes remain poorly defined. We aimed to quantify these associations and determine the mediating contribution of distinct APO patterns versus individual APOs. Methods This retrospective study analyzed data from a Medical Data Platform (2015-2023). Participants were categorized by prepregnancy body mass index (BMI) levels into underweight (BMI<18.5 kg/m2), normal weight (18.5≤BMI<24 kg/m2), overweight (24≤BMI<28 kg/m2), and obese (BMI≥28 kg/m2). The outcomes including diabetes mellitus (DM), cardiometabolic comorbidities (CMC, composite of DM, hypertension, and dyslipidemia) and stage-4 cardiovascular-kidney-metabolic (CKM) syndrome. Missing data were handled via multiple imputation. Latent Class Analysis (LCA) identified APO patterns based on mediators including gestational diabetes mellitus (GDM), hypertensive disorders of pregnancy (HDP), preterm, small for gestational age (SGA), large for gestational age (LGA), pregnancy loss, antepartum infection. Cox proportional hazards models and causal mediation analyses were employed to estimate hazard ratios (HR) and the proportion mediated (PM). Results Among 555,591 individuals (mean age 29.5 years), 5.8% were obese and 18.3% were overweight. During a median follow-up of 5.8 years, incidence rate were 1.3% for DM, 4.9% for CMC and 3.1% for stage-4 CKM. LCA identified five distinct APO patterns: low burden (85.3%), term non-SGA (4.6%, characterized by GDM/LGA), Term SGA (6.8%), preterm non-SGA (2.5%), and high-burden (0.8%, characterized by HDP/preterm/SGA). Compared with normal weight, obesity significantly increased the risk of DM (HR 4.10, 95%CI 3.83-4.32), CMC (HR 2.36, 95%CI 2.29-2.47) and stage-4 CKM (HR 1.19, 95%CI 1.12-1.27). Mediation analysis revealed distinct pathways: the identified APO patterns mediated 27.3% of the association with DM, 15.9% with CMC, and 16.6% with stage-4 CKM. Component-specific analysis further highlighted mechanism divergence: GDM was the dominant mediator for DM (PM 30.6% vs. HDP 7.2%), whereas HDP was the dominant mediator for stage-4 CKM (PM 22.5% vs. GDM 8.4%). Conclusion The early postpartum health risks of prepregnancy obesity are mediated through divergent APO patterns. We identified a metabolic trajectory driving future DM and a separate vascular/high-burden trajectory predisposing to stage-4 CKM. Recognizing these distinct pathways is crucial for moving beyond generic postpartum advice toward precision prevention strategies tailored to specific APOs.Abstract graph-01Abstract graph-02
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Zuo et al. (2026) conducted a cohort in Prepregnancy obesity and early postpartum cardiometabolic risk (n=555,591). Prepregnancy obesity (BMI ≥28 kg/m2) mediated by adverse pregnancy outcome (APO) patterns vs. Normal prepregnancy weight (18.5 ≤ BMI < 24 kg/m2) was evaluated on Diabetes mellitus (DM), cardiometabolic comorbidities (CMC: composite of DM, hypertension, and dyslipidemia), and stage-4 cardiovascular-kidney-metabolic (CKM) syndrome (HR 4.10, 95% CI 3.83-4.32). Prepregnancy obesity vs normal weight increased postpartum risk of DM (HR 4.10; 95% CI 3.83-4.32), CMC (HR 2.36), and stage-4 CKM (HR 1.19), mediated 15.9-27.3% by APO patterns.
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