Background: Maternal polyunsaturated fatty acid (PUFA) concentrations during pregnancy may have persistent effects on growth and adiposity in the offspring. A suboptimal maternal diet during pregnancy might lead to fetal cardiometabolic adaptations with persistent consequences in the offspring. Objective: We examined the associations of maternal PUFA concentrations during pregnancy with childhood general and abdominal fat–distribution measures. Design: In a population-based, prospective cohort study of 4830 mothers and their children, we measured maternal second-trimester plasma n–3 (ω-3) and n–6 (ω-6) PUFA concentrations. At the median age of 6.0 y (95% range: 5.6, 7.9 y), we measured childhood body mass index (BMI), the fat mass percentage, and the android:gynoid fat ratio with the use of dual-energy X-ray absorptiometry and measured the preperitoneal abdominal fat area with the use of ultrasound. Analyses were adjusted for maternal and childhood sociodemographic- and lifestyle-related characteristics. Results: We observed that higher maternal total n–3 PUFA concentrations, and specifically those of eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid, were associated with a lower childhood total-body fat percentage and a lower android:gynoid fat mass ratio (P < 0.05) but not with childhood BMI and the abdominal preperitoneal fat mass area. Higher maternal total n–6 PUFA concentrations, and specifically those of dihomo-γ-linolenic acid, were associated with a higher childhood total-body fat percentage, android:gynoid fat mass ratio, and abdominal preperitoneal fat mass area (P < 0.05) but not with childhood BMI. In line with these findings, a higher maternal n–6:n–3 PUFA ratio was associated with higher childhood total-body and abdominal fat mass. Conclusions: Lower maternal n–3 PUFA concentrations and higher n–6 PUFA concentrations during pregnancy are associated with higher body fat and abdominal fat in childhood. Additional studies are needed to replicate these observations and to explore the causality, the underlying pathways, and the long-term cardiometabolic consequences.
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