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Cited by 630

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

The developmental origins of adult disease (Barker) hypothesis

DE BOO, Hendrina A., HARDING, Jane E.·2006·Australian and New Zealand Journal of Obstetrics and Gynaecology

Abstract

Many studies have provided evidence for the hypothesis that size at birth is related to the risk of developing disease in later life. In particular, links are well established between reduced birthweight and increased risk of coronary heart disease, diabetes, hypertension and stroke in adulthood. These relationships are modified by patterns of postnatal growth. The most widely accepted mechanisms thought to underlie these relationships are those of fetal programming by nutritional stimuli or excess fetal glucocorticoid exposure. It is suggested that the fetus makes physiological adaptations in response to changes in its environment to prepare itself for postnatal life. These changes may include epigenetic modification of gene expression. Less clear at this time are the relevance of fetal programming phenomena to twins and preterm babies, and whether any of these effects can be reversed after birth. Much current active research in this field will be of direct relevance to future obstetric practice.

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Crossref · 10.1111/j.1479-828x.2006.00506.x

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Metadata

Authors
DE BOO, H. A., & HARDING, J. E.
Venue
Australian and New Zealand Journal of Obstetrics and Gynaecology
Publisher
Wiley
Published
2006-01-25
Volume
46
Issue
1
Pages
4-14
ISSN
  • 0004-8666 (ISSN-L)
  • 1479-828X
OpenAlex
W2161265633
Cited by
630
References
9
FWCI
14.64
Type
journal article
Language
en
Open access
closed

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This page
CoChat. (2026). Citation check: The developmental origins of adult disease (Barker) hypothesis. https://app.cochat.ai/papers/10.1111/j.1479-828x.2006.00506.x
The paper
DE BOO, H. A., & HARDING, J. E. (2006). The developmental origins of adult disease (Barker) hypothesis. Australian and New Zealand Journal of Obstetrics and Gynaecology. https://doi.org/10.1111/j.1479-828x.2006.00506.x

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.