Indexed on: 30 Apr '02Published on: 30 Apr '02Published in: Placenta
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 supply 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 necessarily 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 a result of both direct effects on 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.