Prenatal and Perinatal Factors in Eating Disorders: A Descriptive Review

被引:22
|
作者
Raevuori, Anu [1 ,2 ,3 ,4 ]
Linna, Milla S. [1 ]
Keski-Rahkonen, Anna [1 ]
机构
[1] Univ Helsinki, Dept Publ Hlth, Hjelt Inst, Helsinki, Finland
[2] Univ Turku, Inst Clin Med, Child Psychiat Res Ctr, Turku, Finland
[3] Univ Helsinki, Cent Hosp, Dept Adolescent Psychiat, Helsinki, Finland
[4] Natl Inst Hlth & Welf, Dept Mental Hlth & Subst Abuse Serv, Helsinki, Finland
基金
芬兰科学院;
关键词
eating disorders; prenatal exposure delayed effects; maternal exposure; perinatology; review; disordered eating; anorexia nervosa; bulimia nervosa; binge eating disorder; OPPOSITE-SEX TWINS; ANOREXIA-NERVOSA; RISK-FACTORS; BULIMIA-NERVOSA; BIRTH BIAS; SAME-SEX; DIABETES-MELLITUS; GONADAL-HORMONES; YOUNG-ADULTS; TESTOSTERONE;
D O I
10.1002/eat.22323
中图分类号
B849 [应用心理学];
学科分类号
040203 ;
摘要
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. (C) 2014 Wiley Periodicals, Inc.
引用
收藏
页码:676 / 685
页数:10
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