Abstract
BackgroundDuring pregnancy, the demand for folic acid increases since the fetus requires this nutrient for its rapid growth and cell proliferation. The placenta concentrates folic acid into the fetal circulation; as a result the fetal levels are 2 to 4 times higher than the maternal level. Animal and in vitro studies have suggested that alcohol may impair transport of folic acid across the placenta by decreasing expression of transport proteins. We aim to determine if folate transfer to the fetus is altered in human pregnancies with chronic alcohol consumption.Methodology/Principal FindingsSerum folate was measured in maternal blood and umbilical cord blood at the time of delivery in pregnancies with chronic and heavy alcohol exposure (n = 23) and in non-drinking controls (n = 24). In the alcohol-exposed pairs, the fetal∶maternal serum folate ratio was ≤1.0 in over half (n = 14), whereas all but one of the controls were >1.0. Mean folate in cord samples was lower in the alcohol-exposed group than in the controls (33.15±19.89 vs 45.91±20.73, p = 0.04).Conclusions/SignificanceOur results demonstrate that chronic and heavy alcohol use in pregnancy impairs folate transport to the fetus. Altered folate concentrations within the placenta and in the fetus may in part contribute to the deficits observed in the fetal alcohol spectrum disorders.
Highlights
The demand for folic acid increases since this nutrient is critically important for DNA synthesis and cell proliferation
Women consuming heavy amounts throughout the pregnancy were included in this study and are the women most at risk of having a child affected by fetal alcohol syndrome (FAS)
As part of this study, the infants were offered follow up care and diagnostic testing for the fetal alcohol spectrum disorders (FASD)
Summary
The demand for folic acid increases since this nutrient is critically important for DNA synthesis and cell proliferation. Other transporters including the reduced folate carrier (RFC) and the proton-coupled folate transporter (PCFT) are important for the placental uptake of folate [15,16]. This results in a high intervillous blood concentration of folate within the placenta where it can be transported to the fetus by passive diffusion and by the RFC [11,12]. This mechanism of transport is established early in pregnancy (within the first trimester [13]) as folate is vital to the proper development of the fetus. We aim to determine if folate transfer to the fetus is altered in human pregnancies with chronic alcohol consumption
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