Document Detail


The developmental origins of adult disease (Barker) hypothesis.
MedLine Citation:
PMID:  16441686     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Hendrina A de Boo; Jane E Harding
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The Australian & New Zealand journal of obstetrics & gynaecology     Volume:  46     ISSN:  0004-8666     ISO Abbreviation:  Aust N Z J Obstet Gynaecol     Publication Date:  2006 Feb 
Date Detail:
Created Date:  2006-01-30     Completed Date:  2008-01-16     Revised Date:  2009-11-11    
Medline Journal Info:
Nlm Unique ID:  0001027     Medline TA:  Aust N Z J Obstet Gynaecol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  4-14     Citation Subset:  IM    
Affiliation:
Liggins Institute, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
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MeSH Terms
Descriptor/Qualifier:
Adult
Birth Weight*
Cardiovascular Diseases / etiology*
Coronary Disease / etiology
Developmental Biology
Diabetes Mellitus / etiology*
Epigenesis, Genetic
Female
Humans
Hypertension / etiology
Infant, Low Birth Weight*
Infant, Newborn
Male
Pregnancy
Prenatal Nutritional Physiological Phenomena*
Stroke / etiology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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