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(Circulation. 2009;119:1459-1462.)
© 2009 American Heart Association, Inc.
Editorial |
From the Department of Medicine, University of California San Diego, La Jolla.
Correspondence to Wulf Palinski, University of California San Diego, Department of Medicine 0682, 9500 Gilman Dr, La Jolla, CA 92093-0682. E-mail wpalinski@ucsd.edu
Key Words: Editorials pathogenesis pregnancy risk factors stroke
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Much progress has been made since Barker and colleagues first proposed that conditions in utero influence the susceptibility to disease later in life.1 The association between fetal growth retardation and adult hypertension, cardiovascular disease and diabetes mellitus has been established by extensive epidemiology.2,3 It has also been recognized that in order to prevent pathogenic programming we need to identify and target specific maternal factors or conditions, and that maternal overnutrition, rather than undernutrition, is prevalent in the Western world. Several such factors have already been established (eg, maternal hypercholesterolemia,4–6 smoking,7 and diabetes mellitus8) and experimental models have been developed in which mechanisms and causal relationships of developmental programming can be investigated. Finally, the influence of maternal or environmental factors on adult disease is now widely accepted, and the expectation of a wave of cardiovascular disease in children of obese, hyperlipidemic, and diabetic mothers has led the US Congress and the National Institutes of Health to place great emphasis on the elucidation of specific risk factors (eg, in the National Childrens Study9). Animal models are key to identifying the mechanisms involved and finding preventive approaches that go beyond simple avoidance of risk during pregnancy or treatment of maternal dysmetabolic conditions.
Article p 1501
In this regard, hypertension and stroke lag far behind. Although hypertension is a major risk factor of cardiovascular disease in adults, and fetal exposure to high salt concentrations promotes hypertension in offspring in both salt-sensitive and resistant rat strains,10,11 most of what we know about in
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