Background: Maternal obesity is associated with altered polyunsaturated fatty acid (PUFA) status during pregnancy and may programme offspring adiposity, yet the contribution of specific n-3 and n-6 PUFAs across gestation and in cord blood to childhood body composition remains incompletely understood. We investigated these associations between maternal PUFA status during pregnancy and offspring obesity-related outcomes at 8.5 years. Methods: Here, we analysed data of 172 mother–child pairs from the PREOBE cohort, grouped by maternal pregestational body mass index (BMI) as normal weight (NW, n = 84), overweight (OW, n = 47), or obese (OB, n = 41). Plasma phospholipid PUFAs were quantified at 24, 34, and 40 weeks of gestation and in cord blood. At 8.5 years, children underwent anthropometry and body-composition assessment by skinfolds and bioelectrical impedance, remaining 104 mother–child pairs with valid data. Associations analyses included ANOVA/ANCOVA adjusted by confounders variables, unadjusted bivariate Spearman rank correlations with Benjamini–Hochberg False Discovery Rate (FDR) correction, and pooled robust linear regression. Results: Compared with NW mothers, OW and OB mothers showed lower α-linolenic acid (ALA) and docosahexaenoic acid (DHA) and higher n-6 PUFAs and n-6/n-3 ratios during pregnancy. Cord γ-linolenic acid (GLA) was inversely associated with several adiposity measures in the NW and OW groups after FDR correction. No correlation in the OB group met the FDR threshold; the inverse cord GLA–fat-free mass index (FFMI) association was nominal only (ρ = −0.52, p = 0.016, q = 0.688). In pooled regression models, cord GLA was inversely associated with BMI-for-age z-score, waist circumference z-score, waist-to-height ratio, body fat mass percentage, and fat mass index (FMI), whereas maternal GLA at 40 weeks was positively associated with body fat mass percentage and FMI. These pooled estimates do not establish group-specific effects. Conclusions: Maternal and cord-blood PUFA profiles were associated with childhood body composition, with patterns that varied descriptively by sampling time and maternal BMI group. These observational findings do not establish causality, protection, or differences between groups in the strength of association. Mechanistic and interventional research is required before individualised long-chain PUFA monitoring or supplementation can be recommended for obesity prevention.
No takes yet. Share an insight, caveat, or question.
Escudero-Marín et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: