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A comprehensive manual search, including search from the reference list of included articles, was also performed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>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 \u201ccausal\u201d rather than indications of genetic risk. \u00a9 2014 Wiley Periodicals, Inc. 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