Long-term consequences of intrauterine growth retardation
Long-term consequences of intrauterine growth retardation
Recent studies in Europe, North America and the developing world have shown that low birth weight or other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of raised blood pressure, non-insulin-dependent diabetes and cardiovascular disease in late adult life. These findings have led to the 'fetal origins' hypothesis which proposes that fetal adaptations to an adverse intrauterine environment programme persistent physiological and metabolic changes which predispose to these diseases. The mechanisms are unknown, but evidence from animal studies and preliminary evidence in humans suggest that impaired fetal nutrient supply permanently alters neuroendocrine development in the offspring resulting in longterm changes in the set point of adrenocortical and sympathoadrenal hormonal activity.
Birth weight, Cardiovascular disease, Fetal growth, Hypertension, Programming, Type-2 (non-insulin-dependent) diabetes
28-31
Reynolds, R. M.
9586d7af-f506-48ad-be71-59ac6c6f2bb0
Phillips, D. I.W.
29b73be7-2ff9-4fff-ae42-d59842df4cc6
15 August 1998
Reynolds, R. M.
9586d7af-f506-48ad-be71-59ac6c6f2bb0
Phillips, D. I.W.
29b73be7-2ff9-4fff-ae42-d59842df4cc6
Reynolds, R. M. and Phillips, D. I.W.
(1998)
Long-term consequences of intrauterine growth retardation.
Hormone Research, 49 (SUPPL. 2), .
(doi:10.1159/000053084).
Abstract
Recent studies in Europe, North America and the developing world have shown that low birth weight or other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of raised blood pressure, non-insulin-dependent diabetes and cardiovascular disease in late adult life. These findings have led to the 'fetal origins' hypothesis which proposes that fetal adaptations to an adverse intrauterine environment programme persistent physiological and metabolic changes which predispose to these diseases. The mechanisms are unknown, but evidence from animal studies and preliminary evidence in humans suggest that impaired fetal nutrient supply permanently alters neuroendocrine development in the offspring resulting in longterm changes in the set point of adrenocortical and sympathoadrenal hormonal activity.
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Published date: 15 August 1998
Keywords:
Birth weight, Cardiovascular disease, Fetal growth, Hypertension, Programming, Type-2 (non-insulin-dependent) diabetes
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Local EPrints ID: 480393
URI: http://eprints.soton.ac.uk/id/eprint/480393
ISSN: 0301-0163
PURE UUID: 4dd18e5e-df0c-4dab-8cf4-9028265312bd
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Date deposited: 01 Aug 2023 21:40
Last modified: 17 Mar 2024 00:43
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Author:
D. I.W. Phillips
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