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Report on the 2nd World Congress on Fetal Origins of Adult Disease, Brighton, U.K., June 7-10, 2003

Report on the 2nd World Congress on Fetal Origins of Adult Disease, Brighton, U.K., June 7-10, 2003
Report on the 2nd World Congress on Fetal Origins of Adult Disease, Brighton, U.K., June 7-10, 2003
In 1989, reports suggested that the fetal environment, as reflected in birth size, was related to the risk of noncommunicable diseases in adult life. This association was first described for coronary heart disease but rapidly extended to include type 2 diabetes, osteoporosis, and metabolic and endocrine homeostasis. This led to the development of the fetal origins of adult disease paradigm, which resulted in a refocusing of research effort over the next 10 y to consider the lifelong consequences of perinatal influences on chronic diseases. Previously, perinatal influences had largely been seen in terms of teratogenic effects or acute birth injury rather than whether trajectories and responses made during early development had lifelong consequences. Indeed, in developmental biology, it is widely recognized that adaptive plastic responses during early development often have consequences for function in later adulthood. Although the relative importance of this newly recognized set of phenomena to the burden of human disease has been controversial, the research precipitated by those early observations has confirmed their robustness and started to provide a mechanistic basis to this biology. Two world congresses have been held to review progress in this research. Both have been characterized by a unique multidisciplinary attendance ranging from molecular, experimental, and developmental biologists to epidemiologists and health economists.
0031-3998
894-897
Hanson, Mark
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Gluckman, Peter
b7a84049-7ad3-4227-aaed-5803367f77b2
Bier, Dennis
5db54c9f-81b0-48c8-90ea-a42b0d1dd333
Challis, John
b520d39b-26bf-4c61-9c54-fe69f9b9b43a
Fleming, Tom
02c80456-6298-46f8-a640-e20e58658598
Forrester, Terrence
f8b4e72f-5d91-4627-9b8b-2e1316d5b961
Godfrey, Keith
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Nestel, Penelope
c9188991-01f8-4b74-94b0-990ab89adf86
Yajnik, Chittaranjan
f5962976-1322-4c7e-860e-455a29396b4e
Hanson, Mark
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Gluckman, Peter
b7a84049-7ad3-4227-aaed-5803367f77b2
Bier, Dennis
5db54c9f-81b0-48c8-90ea-a42b0d1dd333
Challis, John
b520d39b-26bf-4c61-9c54-fe69f9b9b43a
Fleming, Tom
02c80456-6298-46f8-a640-e20e58658598
Forrester, Terrence
f8b4e72f-5d91-4627-9b8b-2e1316d5b961
Godfrey, Keith
0931701e-fe2c-44b5-8f0d-ec5c7477a6fd
Nestel, Penelope
c9188991-01f8-4b74-94b0-990ab89adf86
Yajnik, Chittaranjan
f5962976-1322-4c7e-860e-455a29396b4e

Hanson, Mark, Gluckman, Peter, Bier, Dennis, Challis, John, Fleming, Tom, Forrester, Terrence, Godfrey, Keith, Nestel, Penelope and Yajnik, Chittaranjan (2004) Report on the 2nd World Congress on Fetal Origins of Adult Disease, Brighton, U.K., June 7-10, 2003. Pediatric Research, 55 (5), 894-897. (doi:10.1203/01.PDR.0000115682.23617.03).

Record type: Article

Abstract

In 1989, reports suggested that the fetal environment, as reflected in birth size, was related to the risk of noncommunicable diseases in adult life. This association was first described for coronary heart disease but rapidly extended to include type 2 diabetes, osteoporosis, and metabolic and endocrine homeostasis. This led to the development of the fetal origins of adult disease paradigm, which resulted in a refocusing of research effort over the next 10 y to consider the lifelong consequences of perinatal influences on chronic diseases. Previously, perinatal influences had largely been seen in terms of teratogenic effects or acute birth injury rather than whether trajectories and responses made during early development had lifelong consequences. Indeed, in developmental biology, it is widely recognized that adaptive plastic responses during early development often have consequences for function in later adulthood. Although the relative importance of this newly recognized set of phenomena to the burden of human disease has been controversial, the research precipitated by those early observations has confirmed their robustness and started to provide a mechanistic basis to this biology. Two world congresses have been held to review progress in this research. Both have been characterized by a unique multidisciplinary attendance ranging from molecular, experimental, and developmental biologists to epidemiologists and health economists.

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Published date: 2004
Additional Information: Meeting Report

Identifiers

Local EPrints ID: 25584
URI: http://eprints.soton.ac.uk/id/eprint/25584
ISSN: 0031-3998
PURE UUID: ea71c050-53c9-4427-a365-056a30cb9073
ORCID for Mark Hanson: ORCID iD orcid.org/0000-0002-6907-613X
ORCID for Keith Godfrey: ORCID iD orcid.org/0000-0002-4643-0618

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Date deposited: 11 Apr 2006
Last modified: 16 Mar 2024 03:17

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Contributors

Author: Mark Hanson ORCID iD
Author: Peter Gluckman
Author: Dennis Bier
Author: John Challis
Author: Tom Fleming
Author: Terrence Forrester
Author: Keith Godfrey ORCID iD
Author: Penelope Nestel
Author: Chittaranjan Yajnik

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