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Prenatal and perinatal factors in eating disorders: a descriptive review
Anu Raevuori1, Milla S Linna, Anna Keski-Rahkonen
1Department 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.
Insights
Prenatal and perinatal exposures show conflicting evidence for causing eating disorders in offspring. If effects exist, they are small and likely interact with other genetic and environmental factors.
Area of Science:
- Reproductive Health
- Developmental Psychology
- Psychiatry
Background:
- Eating disorders (EDs) are complex conditions with multifactorial etiologies.
- Understanding early-life influences, including prenatal and perinatal exposures, is crucial for ED prevention and treatment.
Purpose of the Study:
- To review and synthesize current scientific evidence on the impact of prenatal and perinatal exposures on the development of eating disorders in offspring.
Main Methods:
- A systematic literature search was conducted using PubMed and manual searches of reference lists.
- Keywords included "eating disorders," "prenatal exposure," and "perinatal factors."
Main Results:
- Prenatal/perinatal factors account for 3.6% of anorexia nervosa (AN) risk; prematurity is the only replicated finding.
- Evidence for bulimia nervosa (BN) and other disordered eating is inconsistent, with no replicated risk factors identified.
- Higher prenatal testosterone may offer some protection, but findings are not uniform.
Conclusions:
- The evidence linking prenatal/perinatal factors to EDs is conflicting and suggests a small overall effect.
- Early risk factors likely interact with genetic and environmental influences to contribute to eating pathology.
- Further research using genetically sensitive designs (e.g., twin studies) is needed to establish causality.
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.
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