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进食障碍的产前和围产期因素:描述性综述。

Prenatal and perinatal factors in eating disorders: a descriptive review.

机构信息

Department of Public Health, Hjelt Institute, University of Helsinki, Finland; Child Psychiatry Research Center, Institute of Clinical Medicine, University of Turku, Turku, Finland; Department of Adolescent Psychiatry, Helsinki University Central Hospital, Helsinki, Finland; Department of Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland.

出版信息

Int J Eat Disord. 2014 Nov;47(7):676-85. doi: 10.1002/eat.22323. Epub 2014 Jun 19.

Abstract

OBJECTIVE

The objective of this descriptive review is to summarize the current scientific evidence on various prenatal and perinatal exposures affecting later development of eating disorders among offspring.

METHOD

Studies were searched from PubMed database with the following keywords: eating disorders and disordered eating and anorexia nervosa and bulimia nervosa and binge eating disorder and prenatal exposure delayed effects and maternal exposure and perinatology. A comprehensive manual search, including search from the reference list of included articles, was also performed.

RESULTS

The attributable risk for prenatal and perinatal factors in anorexia nervosa (AN) is 3.6%. Numerous prenatal and perinatal factors have been associated with offspring AN, but only prematurity has been replicated in different samples. The risk of bulimia nervosa (BN) in offspring has attracted less study, and despite varying positive associations, there are no replicated findings. Higher prenatal testosterone may protect against the development of a range of disordered eating symptoms, although studies are not consistent.

DISCUSSION

Evidence in support of an effect of prenatal and perinatal factors on eating disorders or disordered eating in offspring is conflicting. If present, the overall effect appears to be relatively small, and it is likely that the early risk factors operate in conjunction with other biological, genetic, and/or environmental risk factors to bring on eating pathology. Genetically sensitive designs, such as sibling and twin studies, are needed to disentangle the different types of risk factors and ensure that prenatal/perinatal effects are "causal" rather than indications of genetic risk.

摘要

目的

本描述性综述的目的是总结目前关于各种产前和围产期暴露因素对后代进食障碍发展的影响的科学证据。

方法

使用以下关键词在 PubMed 数据库中搜索研究:进食障碍和饮食障碍和神经性厌食症和神经性贪食症和暴食障碍和产前暴露延迟效应和母婴暴露和围产医学。还进行了全面的手动搜索,包括从纳入文章的参考文献列表中进行搜索。

结果

产前和围产期因素导致神经性厌食症(AN)的归因风险为 3.6%。许多产前和围产期因素与后代 AN 有关,但只有早产在不同样本中得到了复制。对后代神经性贪食症(BN)的风险研究较少,尽管存在不同的正相关,但没有发现可重复的结果。较高的产前睾酮可能有助于预防一系列饮食失调症状,但研究并不一致。

讨论

支持产前和围产期因素对后代进食障碍或饮食障碍的影响的证据相互矛盾。如果存在,总体影响似乎相对较小,并且早期风险因素可能与其他生物、遗传和/或环境风险因素一起作用,导致进食障碍。需要进行遗传敏感设计,如兄弟姐妹和双胞胎研究,以理清不同类型的风险因素,并确保产前/围产期的影响是“因果关系”,而不是遗传风险的迹象。

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