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Fetal origins of cardiovascular disease

Name: Fetal origins of cardiovascular disease
Creator: David J.P. Barker
Keywords: 0301 basic medicine, Adult, Male, 2. Zero hunger, Infant, Newborn, Coronary Disease, Placental Insufficiency, 3. Good health, 03 medical and health sciences, 0302 clinical medicine

descriptionPublicationkeyboard_double_arrow_right Article 01 Jan 1999Publisher:Informa UK LimitedJournal:Annals of Medicine, volume 31, pages 3-6 (issn: 0785-3890, eissn: 1365-2060,

Authors: David J.P. Barker;

doi: 10.1080/07853890.1999.11904392

pmid: 10342493 , 28850284

Fetal origins of cardiovascular disease

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Abstract

Low birthweight, thinness and short body length at birth are now known to be associated with increased rates of cardiovascular disease and non-insulin dependent diabetes in adult life. The fetal origins hypothesis proposes that these diseases originate through adaptations which the fetus makes when it is undernourished. These adaptations may be cardiovascular, metabolic or endocrine. They permanently change the structure and function of the body. Prevention of the diseases may depend on prevention of imbalances in fetal growth or imbalances between prenatal and postnatal growth, or imbalances in nutrient supply to the fetus.

Related Organizations

University of Southampton
United Kingdom

Keywords

Adult, Male, Infant, Newborn, Coronary Disease, Placental Insufficiency, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Pregnancy, Animals, Birth Weight, Humans, Female

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	citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	361
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	influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	Top 1%
	impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.	Top 1%