文章基本信息

标题：Perinatal Maternal Mental Health, Fetal Programming and Child Development
本地全文：下载
作者：Andrew J. Lewis ; Emma Austin ; Rebecca Knapp 等
期刊名称：Healthcare
电子版ISSN：2227-9032
出版年度：2015
卷号：3
期号：4
页码：1212-1227
DOI：10.3390/healthcare3041212
出版社：MDPI Publishing
摘要：Maternal mental disorders over pregnancy show a clear influence on child development. This review is focused on the possible mechanisms by which maternal mental disorders influence fetal development via programming effects. This field is complex since mental health symptoms during pregnancy vary in type, timing and severity and maternal psychological distress is often accompanied by higher rates of smoking, alcohol use, poor diet and lifestyle. Studies are now beginning to examine fetal programming mechanisms, originally identified within the DOHaD framework, to examine how maternal mental disorders impact fetal development. Such mechanisms include hormonal priming effects such as elevated maternal glucocorticoids, alteration of placental function and perfusion, and epigenetic mechanisms. To date, mostly high prevalence mental disorders such as depression and anxiety have been investigated, but few studies employ diagnostic measures, and there is very little research examining the impact of maternal mental disorders such as schizophrenia, bipolar disorder, eating disorders and personality disorders on fetal development. The next wave of longitudinal studies need to focus on specific hypotheses driven by plausible biological mechanisms for fetal programming and follow children for a sufficient period in order to examine the early manifestations of developmental vulnerability. Intervention studies can then be targeted to altering these mechanisms of intergenerational transmission once identified.
关键词：fetal programming; perinatal depression and anxiety; mental health in pregnancy; child temperament; growth; cortisol; placenta; epigenetics fetal programming ; perinatal depression and anxiety ; mental health in pregnancy ; child temperament ; growth ; cortisol ; placenta ; epigenetics