Ethanol exposure during gestation is an early life stressor that profoundly dysregulates structure and functions of the embryonal nervous system, altering the cognitive and behavioral development. Such dysregulation is also achieved by epigenetic mechanisms, which, altering the chromatin structure, redraw the entire pattern of gene expression. In parallel, an oxidative stress response at the cellular level and a global upregulation of neuroendocrine stress response, regulated by the HPA axis, exist and persist in adulthood. This neurobehavioral framework matches those observed in other psychiatric diseases such as mood diseases, depression, autism; those early life stressing events, although probably triggered by specific and different epigenetic mechanisms, give rise to largely overlapping neurobehavioral phenotypes. An early diagnosis of prenatal alcohol exposure, using reliable markers of ethanol intake, together with a deeper understanding of the pathogenic mechanisms, some of them reversible by their nature, can offer a temporal “window” of intervention. Supplementing a mother’s diet with protective and antioxidant substances in addition to supportive psychological therapies can protect newborns from being affected.

妊娠期间暴露于乙醇是一种早期的生活压力源，它极大地失调了胚胎神经系统的结构和功能，从而改变了认知和行为发育。这种异常调节也可以通过表观遗传机制实现，表观遗传机制改变了染色质的结构，重绘了基因表达的整个模式。同时，由HPA轴调节的细胞水平的氧化应激反应和神经内分泌应激反应的整体上调存在并持续到成年。这种神经行为框架与其他精神疾病（如情绪疾病，抑郁症，自闭症）中观察到的相匹配；这些早期生活压力事件虽然可能是由特定的和不同的表观遗传机制触发的，但会引起很大程度上重叠的神经行为表型。使用可靠的乙醇摄入量标记物，对产前酒精暴露进行早期诊断，以及对致病机制的更深入理解（其中一些因其性质可逆），可以提供暂时的干预“窗口”。除了支持性心理疗法外，在母亲饮食中补充保护性和抗氧化剂，可以保护新生儿免于感染。