Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, China.
MOE Key Laboratory of Population Health Across Life Cycle, Hefei, China.
Eur J Nutr. 2024 Nov 26;64(1):25. doi: 10.1007/s00394-024-03531-7.
Our aim was to assess the risk of higher insulinemic, inflammatory, and hyperglycemia potential in the diet during pregnancy with child neurodevelopmental delay.
We enrolled 7,438 pregnant women participating in a prospective cohort study. The food frequency questionnaire was used to evaluate the empirical dietary index for hyperinsulinemia (EDIH), empirical dietary inflammatory pattern (EDIP), glycemic index (GI), and glycemic load (GL) during mid-pregnancy. Child neurodevelopmental assessment was conducted at 6-36 months postpartum using the Denver Developmental Screening Test-II (DDST-II) scale, and the Gesell Developmental Diagnosis Scale (GDDS) was administered to assess children who did not meet the criteria for passing the DDST-II screening.
We documented 540 incident child neurodevelopmental delay cases over 7,438 pregnant women (median follow-up: 2 years). Pregnant women exhibiting the high levels of hyperinsulinemic or proinflammatory components, or GI encountered an elevated risk of child neurodevelopmental delay; HRs (95% CI) comparing highest to lowest dietary index quintiles were EDIH 1.48 (1.07,2.04; P = 0.017), EDIP 1.39 (1.05,1.84; P = 0.019) and GI 1.36 (1.02,1.81; P = 0.038). In sex-stratified analyses, these results remained significant only in boys (P = 0.018 for EDIH, P = 0.028 for EDIP, P = 0.029 for GI). The performance of combined model of EDIH and EDIP for boys is comparable to that of the combined model of EDIH, EDIP, and GI to assess the risk of neurodevelopmental delay (AUC [area under curve] 0.801 vs. AUC 0.830). Both values are higher than the AUC values achieved by models using either set of indicators individually.
Our findings suggest that maternal consumption of diets with high insulinemic, inflammatory, or glycemic index properties may be associated with neurodevelopmental delays in children, particularly in boys. Higher insulinemic and inflammatory potentials in maternal diet may forecast neurodevelopmental delay in boys.
我们旨在评估妊娠期间饮食中胰岛素水平升高、炎症反应和高血糖潜在风险与儿童神经发育迟缓的关系。
我们纳入了 7438 名参与前瞻性队列研究的孕妇。采用食物频率问卷评估妊娠中期经验性胰岛素生成指数（EDIH）、经验性炎症饮食模式（EDIP）、血糖指数（GI）和血糖负荷（GL）的饮食经验指数。产后 6-36 个月采用丹佛发育筛查试验-II（DDST-II）量表评估儿童神经发育情况，对未通过 DDST-II 筛查的儿童采用盖塞尔发育诊断量表（GDDS）进行评估。
在 7438 名孕妇中，我们共记录了 540 例儿童神经发育迟缓事件（中位随访时间：2 年）。表现出高胰岛素或促炎成分或高 GI 的孕妇，其儿童神经发育迟缓的风险增加；与饮食指数五分位最低组相比，最高组的 HR（95%CI）分别为 EDIH 1.48（1.07，2.04；P = 0.017）、EDIP 1.39（1.05，1.84；P = 0.019）和 GI 1.36（1.02，1.81；P = 0.038）。在性别分层分析中，这些结果仅在男孩中具有统计学意义（EDIH：P = 0.018；EDIP：P = 0.028；GI：P = 0.029）。EDIH 和 EDIP 联合模型对男孩神经发育迟缓风险的评估效能与 EDIH、EDIP 和 GI 联合模型相当（AUC [曲线下面积]：0.801 比 0.830）。这两个值均高于仅使用一组指标的模型的 AUC 值。
本研究结果提示，母亲摄入高胰岛素、高炎症或高血糖指数的饮食可能与儿童神经发育迟缓有关，尤其是男孩。母亲饮食中的高胰岛素和高炎症潜能可能预示着男孩的神经发育迟缓。
