Human growth and cardiovascular disease
Human growth and cardiovascular disease
Low birthweight is now known to be associated with increased rates of coronary heart disease (CHD) and the related disorders, stroke, hypertension and type 2 diabetes. Associations between low birthweight and later disease have been extensively replicated in studies in different countries. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. CHD and the disorders related to it arise through a series of interactions between environmental influences and the pathways of growth and development that precede them.
birth, preschool, weight, maternal nutrition physiology, growth, cardiovascular disease, premature, prenatal care, child, hypertension, stroke, infant, health, humans, cardiovascular-disease, physiology, prenatal nutrition physiology, cardiovascular diseases, heart, developmental plasticity, male, diabetes, cardiovascular, pregnancy, environmental, review, premature birth, etiology, newborn, genotype, consequences, childhood, child nutrition physiology, coronary heart disease, epidemiology, child development, growth & development, female, human, disease, development, low birth weight, weight gain
21-38
Barker, D.
4da1905f-11d2-4673-b261-1895f6455e2b
2008
Barker, D.
4da1905f-11d2-4673-b261-1895f6455e2b
Barker, D.
(2008)
Human growth and cardiovascular disease.
Barker, D.J.P., Bergmann, R.L. and Ogra, P.L.
(eds.)
In The Window of Opportunity: Pre-Pregnancy to 24 Months of Age.
vol. 61,
Karger.
.
(doi:10.1159/000113163).
Record type:
Conference or Workshop Item
(Paper)
Abstract
Low birthweight is now known to be associated with increased rates of coronary heart disease (CHD) and the related disorders, stroke, hypertension and type 2 diabetes. Associations between low birthweight and later disease have been extensively replicated in studies in different countries. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. CHD and the disorders related to it arise through a series of interactions between environmental influences and the pathways of growth and development that precede them.
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More information
Published date: 2008
Additional Information:
ISSN 1661-6677
Venue - Dates:
61st Nestlé Nutrition Workshop, Pediatric Program: Environmental Factors and the Development of Human Health, Bali, Indonesia, 2007-04-01 - 2007-04-01
Keywords:
birth, preschool, weight, maternal nutrition physiology, growth, cardiovascular disease, premature, prenatal care, child, hypertension, stroke, infant, health, humans, cardiovascular-disease, physiology, prenatal nutrition physiology, cardiovascular diseases, heart, developmental plasticity, male, diabetes, cardiovascular, pregnancy, environmental, review, premature birth, etiology, newborn, genotype, consequences, childhood, child nutrition physiology, coronary heart disease, epidemiology, child development, growth & development, female, human, disease, development, low birth weight, weight gain
Identifiers
Local EPrints ID: 60890
URI: http://eprints.soton.ac.uk/id/eprint/60890
PURE UUID: 341bbd0c-4b23-4f2a-b67d-6d5eab033dfe
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Date deposited: 26 Sep 2008
Last modified: 15 Mar 2024 11:21
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Contributors
Author:
D. Barker
Editor:
D.J.P. Barker
Editor:
R.L. Bergmann
Editor:
P.L. Ogra
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