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Maternal carbohydrate intake and pregnancy outcome

Published online by Cambridge University Press:  28 February 2007

James F. Clapp III*
Departments of Obstetrics and Gynecology and Reproductive Biology, and the Schwartz Center for Metabolism and Nutrition, Case Western Reserve University, MetroHealth Medical Campus, Cleveland, Ohio 44109, USA
Corresponding author: Dr J. F. Clapp III, fax +1 216 778 8847, email JFCLAPP@METROHEALTH.ORG
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Experimental evidence indicates that the primary maternal environmental factor that regulates feto–placental growth is substrate delivery to the placental site, which is the product of maternal substrate levels and the rate of placental-bed blood flow. Thus, maternal factors which change either substrate level or flow alter feto–placental growth rate. The best-studied substrate in human pregnancy is glucose, and there is a direct relationship between maternal blood glucose levels and size at birth. Altering the type of carbohydrate eaten (high- v. low-glycaemic sources) changes postprandial glucose and insulin responses in both pregnant and non-pregnant women, and a consistent change in the type of carbohydrate eaten during pregnancy influences both the rate of feto–placental growth and maternal weight gain. Eating primarily high-glycaemic carbohydrate results in feto–placental overgrowth and excessive maternal weight gain, while intake of low-glycaemic carbohydrate produces infants with birth weights between the 25th and the 50th percentile and normal maternal weight gain. The calculated difference in energy retention with similar total energy intakes is of the order of 80 000 kJ. Preliminary information from subsequent metabolic studies indicates that the mechanisms involved include changes in: daily digestible energy requirements (i.e. metabolic efficiency), substrate utilization (glucose oxidation v. lipid oxidation), and insulin resistance and sensitivity. Thus, altering the source of maternal dietary carbohydrate may prove to be a valuable tool in the management of pregnancies at risk for anomalous feto–placental growth and for the prevention and/or treatment of obesity and insulin resistance in the non-pregnant state.

Plenary Lecture
Copyright © The Nutrition Society 2002


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