Key result
Higher BMI polygenic risk scores linked to ~14-fold greater childhood obesity odds with maternal GDM.
Why the study?
Gestational diabetes mellitus and polygenic risk scores of BMI both associate with childhood obesity, but their interaction on childhood obesity risk is unclear.
Does the interaction between maternal gestational diabetes mellitus and BMI polygenic risk score increase the risk of childhood obesity?
Cohort (n=1,040)
Does the interaction between maternal gestational diabetes mellitus and BMI polygenic risk score increase the risk of childhood obesity?
Odds Ratio: 13.8 (95% CI 5.41–43.3)
There is a strong interaction between maternal gestational diabetes and child BMI polygenic risk score, with GDM exposure markedly amplifying the risk of childhood obesity in those with high genetic risk.
Should not yet change practice; supports hypothesis-generating gene-environment interaction between maternal GDM and BMI PRS.
Introduction and Objective: Gestational diabetes mellitus (GDM) and polygenetic risk scores (PRS) of body mass index (BMI) are both associated with childhood obesity. However, the interaction between GDM and PRS of BMI on childhood obesity is unclear. Methods: A total of 1,040 mother-child pairs were included from Tianjin GDM longitudinal observational study. Genome-Wide Association Study (GWAS) studies were performed using DNA extracted from whole blood collected during clinical visits. PRS of BMI was generated by associations between BMI at age of 3-9 and SNPs from GWAS and children were grouped into three PRS tiers. Odds ratios for childhood obesity according to PRS tertiles and GDM status were estimated by logistic regression. Results: Among 1,040 children (mean age 5.87 years, 52.2% male, 50.2% with maternal GDM), 13.3% developed childhood obesity. In interaction analyses stratified by GDM status and PRS categories, a clear dose-response relationship of childhood obesity risk across PRS tertiles was observed in both GDM and non-GDM groups. Across both non-GDM and GDM strata, higher PRS categories were associated with progressively higher odds of the outcome. Relative to the low risk PRS reference T1, Model 1 showed an OR of 1.70 (95% CI, 0.57 to 5.66) for T2 and 10.4 (4.33 to 30.9) for T3, and these estimates were similar after additional adjustment in Model 2 with ORs of 1.59 (0.50 to 5.56) for T2 and 10.7 (4.19 to 33.7) for T3. In the GDM group, compared with T1, Model 1 yielded ORs of 1.16 (0.34 to 4.13) for T2 and 17.0 7.21 to 50.2) for T3, while Model 2 produced ORs of 1.11 (0.31 to 4.18) for T2 and 13.8 (5.41 to 43.3) for T3. Conclusion: This study demonstrated a clear interaction between GDM and BMI-related PRS on childhood obesity, with increasing odds across PRS tertiles and stronger associations among children exposed to GDM. Notably, GDM exposure was not associated with increased obesity risk among children with low genetic risk. Disclosure G. Xu: None. Y. Shen: None. W. Cao: None. H. Sun: None. G. Hu: None.
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徐谷峰 et al. (2026) conducted a cohort in Childhood obesity (n=1,040). Gestational diabetes mellitus and high BMI polygenic risk score vs. Non-GDM and low BMI polygenic risk score (T1) was evaluated on Childhood obesity (OR 13.8, 95% CI 5.41-43.3). Higher BMI polygenic risk scores were associated with increased odds of childhood obesity, with the strongest association observed among children exposed to maternal GDM (OR 13.8; 95% CI 5.41-43.3).
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