Abel E L, Hannigan J H
Department of Obstetrics & Gynecology, Wayne State University School of Medicine, C. S. Mott Center for Human Growth and Development, Detroit, MI 48201, USA.
Neurotoxicol Teratol. 1995 Jul-Aug;17(4):445-62. doi: 10.1016/0892-0362(95)98055-6.
We present an hypothesis integrating epidemiological, clinical case, and basic biomedical research to explain why only relatively few women who drink alcohol during pregnancy give birth to children with alcohol-related birth defects (ARBDs), in particular, Fetal Alcohol Syndrome (FAS). We argue that specific sociobehavioral risk factors, e.g., low socioeconomic status, are permissive for FAS in that they provide the context for increased vulnerability. We illustrate how these permissive factors are related to biological factors, e.g., decreased antioxidant status, which in conjunction with alcohol, provoke FAS/ARBDs in vulnerable fetuses. We propose an integrative heuristic model hypothesizing that these permissive and provocative factors increase the likelihood of FAS/ARBDs because they potentiate two related mechanisms of alcohol-induced teratogenesis, specifically, maternal/fetal hypoxia and free radical formation.
我们提出了一个整合流行病学、临床病例和基础生物医学研究的假说，以解释为何孕期饮酒的女性中只有相对少数会生出患有酒精相关出生缺陷（ARBDs）的孩子，特别是胎儿酒精综合征（FAS）。我们认为，特定的社会行为风险因素，如社会经济地位低下，对FAS具有促成作用，因为它们为易感性增加提供了背景。我们阐述了这些促成因素如何与生物因素相关联，例如抗氧化状态降低，这些生物因素与酒精共同作用，在易损胎儿中引发FAS/ARBDs。我们提出了一个综合启发式模型，假设这些促成因素和激发因素会增加FAS/ARBDs的可能性，因为它们增强了酒精诱导致畸的两个相关机制，具体而言，即母体/胎儿缺氧和自由基形成。
