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Developmental mismatch: consequences for later cardiorespiratory health

Developmental mismatch: consequences for later cardiorespiratory health
Developmental mismatch: consequences for later cardiorespiratory health
Clinical and epidemiological studies have established that people who were small at birth and had poor infant growth have an increased risk of adult cardiovascular and respiratory disease, particularly if their restricted early growth is followed by accelerated childhood weight gain. This relationship extends across the normal range of infant size in a graded manner. The 'mismatch hypothesis' proposes that ill health in later life originates through developmental plastic responses made by the fetus and infant; these responses increase the risk of adult disease if the environment in childhood and adult life differs from that predicted during early development.
cardiovascular disease, epigenetic, fetal growth, maternal nutrition, respiratory disease
1470-0328
149-157
Pike, K.C.
10be90c8-73de-416e-a2d0-0bb7e7276bd3
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Godfrey, K.M.
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Pike, K.C.
10be90c8-73de-416e-a2d0-0bb7e7276bd3
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Godfrey, K.M.
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd

Pike, K.C., Hanson, M.A. and Godfrey, K.M. (2008) Developmental mismatch: consequences for later cardiorespiratory health. BJOG: An International Journal of Obstetrics & Gynaecology, 115 (2), 149-157. (doi:10.1111/j.1471-0528.2007.01603.x).

Record type: Article

Abstract

Clinical and epidemiological studies have established that people who were small at birth and had poor infant growth have an increased risk of adult cardiovascular and respiratory disease, particularly if their restricted early growth is followed by accelerated childhood weight gain. This relationship extends across the normal range of infant size in a graded manner. The 'mismatch hypothesis' proposes that ill health in later life originates through developmental plastic responses made by the fetus and infant; these responses increase the risk of adult disease if the environment in childhood and adult life differs from that predicted during early development.

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More information

e-pub ahead of print date: 7 December 2007
Published date: January 2008
Keywords: cardiovascular disease, epigenetic, fetal growth, maternal nutrition, respiratory disease

Identifiers

Local EPrints ID: 145175
URI: http://eprints.soton.ac.uk/id/eprint/145175
ISSN: 1470-0328
PURE UUID: cc918d6b-8eb6-4bfe-bc37-7e06190ee228
ORCID for M.A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X
ORCID for K.M. Godfrey: ORCID iD orcid.org/0000-0002-4643-0618

Catalogue record

Date deposited: 19 Apr 2010 13:49
Last modified: 14 Mar 2024 02:44

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Contributors

Author: K.C. Pike
Author: M.A. Hanson ORCID iD
Author: K.M. Godfrey ORCID iD

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