Psychosocial maternal stress experienced during different vulnerable periods throughout gestation is thought to increase the individual’s risk to develop neuropsychiatric, cardiovascular and metabolic disease in later life. Cortisol has generally been identified as the major mediator of maternal stress transfer to the fetus. Its lipophilic nature allows a trans-placental passage and thus excessive maternal cortisol could persistently impair the development of the fetal hypothalamic-pituitary-adrenal axis (HPAA). However, cortisol alone cannot fully explain all effects of maternal stress especially during early to mid pregnancy before maturation of the fetal HPAA has even begun and expression of fetal glucocorticoid receptors is limited. This review focuses on mediators of maternal fetal stress transfer that in addition to cortisol have been proposed as transmitters of maternal stress: catecholamines, cytokines, serotonin/tryptophan, reactive-oxygen-species and the maternal microbiota. We propose that the effects of psychosocial maternal stress on fetal development and health and disease in later life are not a consequence of a single pathway but are mediated by multiple stress-transfer mechanisms acting together in a synergistic manner.

在整个妊娠期间的不同脆弱时期经历的社会心理产妇压力被认为增加了个体在以后生活中发展神经精神病，心血管疾病和新陈代谢疾病的风险。皮质醇通常被认为是母体压力转移至胎儿的主要介质。它的亲脂性质允许经胎盘通过，因此母体皮质醇过多会持续损害胎儿下丘脑-垂体-肾上腺轴（HPAA）的发育。然而，仅皮质醇不能完全解释母体压力的所有影响，尤其是在胎儿HPAA尚未开始成熟且胎儿糖皮质激素受体的表达受到限制之前，特别是在怀孕初期至中期。这篇综述的重点是母体胎儿压力转移的介体，除皮质醇外，还被认为是母体压力的传递者：儿茶酚胺，细胞因子，5-羟色胺/色氨酸，活性氧物种和母体微生物群。我们提出心理社会孕产妇应激对胎儿发育，健康和疾病的影响不是单一途径的结果，而是由多种以协同方式协同作用的应激转移机制介导的。