Prenatal environmental adversity and child neurodevelopmental delay: the role of maternal low-grade systemic inflammation and maternal anti-inflammatory diet

Authors：Wang H, Yin W, Ma S, Wang P, Zhang L, Li P, Shao Z, Chen X, Zhu P.

Source：Eur Child Adolesc Psychiatry. 2023 Aug 18.

DOI: 10.1007/s00787-023-02267-9.

Abstract：

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.

Keywords: Anti-inflammation diet; Empirical dietary inflammatory pattern; Inflammation; Neurodevelopmental delay; Prenatal environmental adversity.

中文摘要：

母体炎症被认为是连接产前环境逆境(PEA)与儿童神经发育迟缓的可能途径，产前环境逆境包括母体超重或肥胖、糖尿病、高血压疾病、情绪或焦虑障碍。然而，尚未报告有效的预防措施。在此，我们旨在研究母体抗炎饮食是否通过抑制炎症来降低PEA诱导的神经发育迟缓的风险。这项前瞻性研究包括7438对母子。孕妇超重或肥胖、糖尿病和高血压疾病在妊娠28周前被诊断。在怀孕中期使用爱丁堡产后抑郁症调查(EPDS)来确定产妇抑郁症。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。使用基于食物的经验性饮食炎症模式(EDIP)评分评估妊娠中期饮食的炎症潜力。根据EDIP中位数评分，将孕妇分为高分组和低分组。产后6-36个月神经发育迟缓的结果从儿童保健登记册中提取。在7438对母子中，2937对(39.5%)暴露于PEA, 540对(7.3%)出现神经发育迟缓。暴露于PEA的儿童比未暴露于PEA的儿童有更高的神经发育迟缓风险。PEA暴露与妊娠期间hs-CRP单调升高有关，妊娠中后期hs-CRP升高的四分位数范围与儿童神经发育迟缓的风险增加有关。母亲较高的持续性炎症部分介导了PEA暴露对儿童神经发育迟缓的影响(17.19%)。仅在高EPDS母亲的孩子中观察到PEA相关神经发育迟缓的风险增加，而不是低EPDS母亲的孩子。这些结果表明，妊娠中后期全身性炎症的增加介导了PEA与儿童神经发育迟缓之间的关联。母体抗炎饮食可通过抑制炎症改善pea诱导的神经发育迟缓。

关键词：抗炎饮食;经验性饮食炎症模式；炎症;神经发育延迟；产前环境逆境。