Department of Maternal, Child & 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 Child Adolesc Psychiatry. 2024 Jun;33(6):1771-1781. doi: 10.1007/s00787-023-02267-9. Epub 2023 Aug 18.
Maternal inflammation has been proposed as a possible pathway connecting prenatal environmental adversity (PEA), which includes maternal overweightness or obesity, diabetes, hypertensive disorders, and mood or anxiety disorders, to child neurodevelopmental delay. However, effective preventive measures have not yet been reported. Herein, we aimed to investigate whether a maternal anti-inflammatory diet reduced the risk of PEA-induced neurodevelopmental delay, by inhibiting inflammation. This prospective study included 7438 mother-child pairs. Maternal overweightness or obesity, diabetes, and hypertensive disorders were diagnosed before 28 week gestation. Maternal depression disorders were identified using the Edinburgh postnatal depression survey (EPDS) during mid-pregnancy. During mid- and late pregnancy, maternal high-sensitivity C-reactive protein (hs-CRP) levels were measured to evaluate systemic inflammation. The inflammatory potential of the diet was evaluated using the food-based empirical dietary inflammatory pattern (EDIP) score during mid-pregnancy. Pregnant women were classified into high- or low-score groups based on the median EDIP score. The outcomes of neurodevelopmental delay at 6-36 month postpartum were extracted from the Register of Child Healthcare. Among the 7438 mother-child pairs, 2937 (39.5%) were exposed to PEA, and neurodevelopmental delay occurred in 540 (7.3%). Children exposed to PEA had a higher risk of neurodevelopmental delay than those not exposed. PEA exposure was associated with increased hs-CRP during pregnancy in a PEA monotonic manner, an interquartile range increase in hs-CRP in mid- and late pregnancy was associated with an increased risk of child neurodevelopmental delay. Higher maternal persistent inflammation partially mediated the effect of PEA exposure on child neurodevelopmental delay by 17.19%. An increased risk of PEA-related neurodevelopmental delay was observed only in the children of mothers with high-EDIP rather than low-EDIP. These results suggest that increased systemic inflammation through mid- and late pregnancy mediates the association between PEA and child neurodevelopmental delay. A maternal anti-inflammatory diet may improve PEA-induced neurodevelopmental delay, by inhibiting inflammation.
母体炎症被认为是将产前环境逆境（PEA）连接起来的一种可能途径，PEA 包括母体超重或肥胖、糖尿病、高血压疾病以及情绪或焦虑障碍，与儿童神经发育迟缓有关。然而，目前尚未报道有效的预防措施。在此，我们旨在通过抑制炎症，研究母体抗炎饮食是否可以降低 PEA 引起的神经发育迟缓的风险。本前瞻性研究纳入了 7438 对母婴。在 28 孕周前诊断母体超重或肥胖、糖尿病和高血压疾病。在妊娠中期使用爱丁堡产后抑郁量表（EPDS）确定母体抑郁障碍。在妊娠中期和晚期，测量母体高敏 C 反应蛋白（hs-CRP）水平以评估全身炎症。在妊娠中期使用基于食物的经验性饮食炎症模式（EDIP）评分评估饮食的炎症潜能。根据 EDIP 评分中位数将孕妇分为高分组或低分组。从儿童保健登记处提取产后 6-36 个月神经发育迟缓的结局。在 7438 对母婴中，有 2937（39.5%）暴露于 PEA，540（7.3%）发生神经发育迟缓。与未暴露的儿童相比，暴露于 PEA 的儿童发生神经发育迟缓的风险更高。PEA 暴露与妊娠期间 hs-CRP 的增加呈 PEA 单调趋势相关，妊娠中期和晚期 hs-CRP 的一个四分位距增加与儿童神经发育迟缓的风险增加相关。母体持续性炎症的增加部分通过 17.19%介导了 PEA 暴露对儿童神经发育迟缓的影响。仅在母亲 EDIP 高而非低的儿童中观察到与 PEA 相关的神经发育迟缓风险增加。这些结果表明，通过妊娠中期和晚期，全身性炎症增加介导了 PEA 与儿童神经发育迟缓之间的关联。母体抗炎饮食可能通过抑制炎症来改善 PEA 引起的神经发育迟缓。
