The developmental origins of adult disease (Barker) hypothesis
Article first published online: 25 JAN 2006
Australian and New Zealand Journal of Obstetrics and Gynaecology
Volume 46, Issue 1, pages 4–14, February 2006
How to Cite
DE BOO, H. A. and HARDING, J. E. (2006), The developmental origins of adult disease (Barker) hypothesis. Australian and New Zealand Journal of Obstetrics and Gynaecology, 46: 4–14. doi: 10.1111/j.1479-828X.2006.00506.x
- Issue published online: 25 JAN 2006
- Article first published online: 25 JAN 2006
- Received 11 October 2005; accepted 24 October 2005.
- coronary heart disease;
- developmental origins of adult disease;
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.