The fetal origins hypothesis proposes that adult cardiovascular and metabolic disease originate through developmental plasticity and fetal adaptations arising from failure of the materno-placental supple of nutrients to match fetal requirements. The hypothesis is supported by experimental data in animals indicating that maternal nutrition can programme long term effects on the offspring without neccssarily affecting size at birth. There is now evidence linking body composition in pregnant women and the balance of nutrient intake during pregnancy with raised levels of cardiovascular risk factors in the offspring. Maternal body composition and diet are thought to affect fetal development and programming as I result of both direct effects oil substrate availability to the fetus and indirectly through changes in placental function and structure. Alterations in placental growth and vascular resistance, altered nutrient and hormone metabolism in the placenta, and changes in nutrient transfer and partitioning between mother, placenta and fetus all have important effects on the fetal adaptations thought to be central to programming. Future interventions to improve placental function are likely to have lifelong health benefits for the offspring. (C) 2002 IFPA and Elsevier Science Ltd.
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Thame, M
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Osmond, C
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Wilks, RJ
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Wilks, RJ
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Bennett, FI
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Bennett, FI
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McFarlane-Anderson, N
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
McFarlane-Anderson, N
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Forrester, TE
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Thame, M
;
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Osmond, C
;
Wilks, RJ
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Wilks, RJ
;
Bennett, FI
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
Bennett, FI
;
McFarlane-Anderson, N
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England
McFarlane-Anderson, N
;
Forrester, TE
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Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, EnglandUniv Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton, Hants, England