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Consequences of fetal growth restriction during childhood and adult life

Consequences of fetal growth restriction during childhood and adult life
Consequences of fetal growth restriction during childhood and adult life
Over the last decade, a series of epidemiological studies has begun to change the way in which we think about fetal growth restriction. Whereas previous attention was mainly focused on timing and mode of delivery, evidence now exists that this may represent one facet of a much broader spectrum of care.
The ‘Fetal Origins of Adult Disease’ or ‘Barker’ hypothesis postulates that perturbed growth in utero may cause permanent physiological changes (programming) within the fetus. This is thought to increase susceptibility to chronic disease during adult life, such as hypertension, coronary heart disease and type 2 diabetes. In essence, a fetus subjected to adverse conditions in utero undergoes a series of adaptations. These prime it for a postnatal life in which similar adverse conditions, such as scarcity of food, are anticipated. For those born into societies with calorie-rich diets, food is abundant rather than scarce, and adaptations made to anticipate harsh conditions now become a burden. The term ‘programming’ is used to describe the mechanisms which determine fetal adaptation. Such changes are thought to follow gene–environment interaction during specific periods of fetal development.
This review outlines the evidence for the Barker hypothesis, summarizing possible long-term consequences of the influence of the intra-uterine environment for both children and adults.
fetal programming, fetal origins, intra-uterine growth restriction, fetal growth, type 2 diabetes, hypertension, coronary heart disease
0957-5847
212-217
Cunningham, Simon
5a0c7b72-ab72-4a6e-924c-4f533bc773ab
Cameron, Iain T.
f7595539-efa6-4687-b161-e1e93ff710f2
Cunningham, Simon
5a0c7b72-ab72-4a6e-924c-4f533bc773ab
Cameron, Iain T.
f7595539-efa6-4687-b161-e1e93ff710f2

Cunningham, Simon and Cameron, Iain T. (2003) Consequences of fetal growth restriction during childhood and adult life. Current Obstetrics & Gynaecology, 13 (4), 212-217. (doi:10.1016/S0957-5847(03)00039-8).

Record type: Article

Abstract

Over the last decade, a series of epidemiological studies has begun to change the way in which we think about fetal growth restriction. Whereas previous attention was mainly focused on timing and mode of delivery, evidence now exists that this may represent one facet of a much broader spectrum of care.
The ‘Fetal Origins of Adult Disease’ or ‘Barker’ hypothesis postulates that perturbed growth in utero may cause permanent physiological changes (programming) within the fetus. This is thought to increase susceptibility to chronic disease during adult life, such as hypertension, coronary heart disease and type 2 diabetes. In essence, a fetus subjected to adverse conditions in utero undergoes a series of adaptations. These prime it for a postnatal life in which similar adverse conditions, such as scarcity of food, are anticipated. For those born into societies with calorie-rich diets, food is abundant rather than scarce, and adaptations made to anticipate harsh conditions now become a burden. The term ‘programming’ is used to describe the mechanisms which determine fetal adaptation. Such changes are thought to follow gene–environment interaction during specific periods of fetal development.
This review outlines the evidence for the Barker hypothesis, summarizing possible long-term consequences of the influence of the intra-uterine environment for both children and adults.

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More information

Published date: 2003
Keywords: fetal programming, fetal origins, intra-uterine growth restriction, fetal growth, type 2 diabetes, hypertension, coronary heart disease

Identifiers

Local EPrints ID: 25390
URI: http://eprints.soton.ac.uk/id/eprint/25390
ISSN: 0957-5847
PURE UUID: 414ae01c-5672-474d-beb0-a54331cd832f
ORCID for Iain T. Cameron: ORCID iD orcid.org/0000-0002-4875-267X

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Date deposited: 07 Apr 2006
Last modified: 16 Mar 2024 03:00

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Contributors

Author: Simon Cunningham
Author: Iain T. Cameron ORCID iD

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