Women's and Children's Center, Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia 30322, USA.
Acta Obstet Gynecol Scand. 2011 Dec;90(12):1307-16. doi: 10.1111/j.1600-0412.2011.01136.x. Epub 2011 May 20.
We reviewed the evidence for three theories of how preconceptional psychosocial stress could act as a contributing determinant of excess preterm birth risk among African American women: early life developmental plasticity and epigenetic programming of adult neuroendocrine systems; blunting, weathering, or dysfunction of neuroendocrine and immune function in response to chronic stress activation through the life course; individuals' adoption of risky behaviors such as smoking as a response to stressful stimuli.
Basic science, clinical, and epidemiologic studies indexed in MEDLINE and Web of Science databases on preconceptional psychosocial stress, preterm birth and race were reviewed.
Mixed evidence leans towards modest associations between preconceptional chronic stress and preterm birth (for example common odds ratios of 1.2-1.4), particularly in African American women, but it is unclear whether this association is causal or explains a substantial portion of the Black-White racial disparity in preterm birth. The stress-preterm birth association may be mediated by hypothalamic-pituitary-adrenal axis dysfunction and susceptibility to bacterial vaginosis, although these mechanisms are incompletely understood. Evidence for the role of epigenetic or early life programming as a determinant of racial disparities in preterm birth risk is more circumstantial.
Preconceptional stress, directly or in interaction with host genetic susceptibility or infection, remains an important hypothesized risk factor for understanding and reducing racial disparities in preterm birth. Future studies that integrate adequately sized epidemiologic samples with measures of stress, infection, and gene expression, will advance our knowledge and allow development of targeted interventions.
我们回顾了三种理论的证据,这些理论解释了孕前心理社会压力如何成为非裔美国女性早产风险过高的一个促成因素:早期发育的可塑性和成年神经内分泌系统的表观遗传编程;通过整个生命周期中对慢性应激激活的神经内分泌和免疫功能的迟钝、适应或功能障碍;个体采用吸烟等危险行为作为对应激刺激的反应。
在 MEDLINE 和 Web of Science 数据库中对孕前心理社会压力、早产和种族进行了索引的基础科学、临床和流行病学研究进行了回顾。
混合证据倾向于表明孕前慢性应激与早产之间存在适度关联(例如常见的比值比为 1.2-1.4),尤其是在非裔美国女性中,但尚不清楚这种关联是否是因果关系,或者是否解释了早产的黑人和白人之间种族差异的很大一部分。应激-早产关联可能通过下丘脑-垂体-肾上腺轴功能障碍和对细菌性阴道病的易感性来介导,尽管这些机制尚不完全清楚。关于表观遗传或早期生活编程作为早产风险种族差异决定因素的作用的证据更多是间接的。
孕前应激,无论是直接作用还是与宿主遗传易感性或感染相互作用,仍然是非裔美国女性早产风险种族差异的一个重要假设风险因素。未来的研究将充分整合具有应激、感染和基因表达测量的大型流行病学样本,将增进我们的知识并允许开发有针对性的干预措施。