One carbon metabolism (OCM) is critical for early development, as it provides one carbon (1C) units for the biosynthesis of DNA, proteins, and lipids and epigenetic modification of the genome. Epigenetic marks established early in life can be maintained and exert lasting impacts on gene expression and functions later in life. Animal and human studies have increasingly demonstrated that prenatal 1C nutrient deficiencies impair fetal growth, neurodevelopment, and cardiometabolic parameters in childhood, while sufficient maternal 1C nutrient intake is protective against these detrimental outcomes. However, recent studies also highlight the potential risk of maternal 1C nutrient excess or imbalance in disrupting early development. Further studies are needed to delineate the dose–response relationship among prenatal 1C nutrient exposure, epigenetic modifications, and developmental outcomes.

一碳代谢 (OCM) 对于早期发育至关重要，因为它为 DNA、蛋白质和脂质的生物合成以及基因组的表观遗传修饰提供了一个碳 (1C) 单位。生命早期建立的表观遗传标记可以维持，并对生命后期的基因表达和功能产生持久影响。动物和人体研究越来越多地表明，产前 1C 营养素缺乏会损害儿童期的胎儿生长、神经发育和心脏代谢参数，而母亲摄入足够的 1C 营养素可以防止这些有害结果。然而，最近的研究也强调了母体 1C 营养过剩或不平衡在破坏早期发育方面的潜在风险。需要进一步的研究来描述产前 1C 营养素暴露之间的剂量反应关系，