December 2009

Document Type


Degree Name



Oregon Health & Science University


Previous studies have demonstrated low vitamin E concentrations in infants at birth, and deficient levels in preterm and low birth weight newborns. Low vitamin E has been associated with an increased risk of hemolytic anemia, detrimental fibroplasias, bronchopulmonary dysplasia, and thrombocytosis. It was suggested to supplement pregnant women with vitamin E in order to increase fetal stores, but studies have found that while supplementation during pregnancy increases maternal plasma concentrations, it does not increase the fetal vitamin E concentrations. Thus, the transfer of vitamin E across the placenta is limited. Studies of placental tissue demonstrate that the placenta expresses cytochrome P450 enzymes that are involved in vitamin E metabolism, suggesting that it might actively metabolize this nutrient, and thus prevent vitamin E accumulation in the fetal tissues. The purpose of this study was to 1) determine vitamin E metabolites, carboxyethyl hydroxychromans (α- and γ-CEHC), in umbilical cord plasma and maternal plasma, 2) to investigate possible correlations with α- and γ-tocopherol, 3) to evaluate associations with dietary parameters. The overall goal was to use indirect measures to assess whether the placenta actively metabolizes vitamin E. A total of 15 maternal - cord blood pairs were analyzed for this sub-study. Healthy, pregnant women were enrolled from Oregon Health and Science University’s obstetric clinic and at least one fasting blood sample was collected during their pregnancy. Umbilical cord blood samples were obtained from full-term, uncomplicated deliveries. Maternal and cord plasma samples were analyzed for α-tocopherol, γ-tocopherol, α-CEHC, and γ-CEHC concentrations. Total blood lipids were also measured to assess tocopherol/total lipids ratio between maternal and cord plasma. Dietary and demographic information was analyzed for associations with biochemical parameters. Statistical differences were assessed using paired t-test and Pearson’s correlation analysis. Cord blood α- and γ-CEHC concentrations were 33.4 ± 29.4 nmol/L and 115.8 ± 55.8 nmol/L, and were not significantly different from maternal α- and γ-CEHC concentrations (p = 0.07 and p = 0.08, respectively). The metabolite to tocopherol ratio was significantly higher in cord blood. Cord blood α- and γ-tocopherol concentrations were significantly lower than maternal concentrations (6.8 ± 1.7 μmol/L vs. 34.2 ± 6.6 μmol/L α-tocopherol; and 0.4 ± 0.2 μmol/L vs. 1.9 ± 0.8 μmol/L γ-tocopherol; p <0.001). Tocopherol/total lipids ratios were also significantly lower in cord blood for both forms, α and γ (p < 0.001 and p < 0.05, respectively). Of the tocopherols, only α-tocopherol/total lipids ratio was significantly correlated between maternal and cord concentrations (r = 0.56, p <0.05). Furthermore, the higher dietary intake of vitamin E from prenatal vitamins was associated with the higher α-CEHC concentration in fetal circulation (r = 0.66, p <0.05). The present study did not find significant differences in vitamin E metabolite concentrations between maternal and cord plasma. However, higher dietary intake of vitamin E by the mother correlated with increased vitamin E metabolite concentration in the fetal circulation. This might imply that the higher level of supplemented vitamin E intake results in an increased metabolism of the vitamin, possibly by the placenta. Further insight into placental transfer of vitamin E is important to determine the safety and efficacy of administering supplemented vitamin E during pregnancy and its affect on the fetus.




Graduate Programs in Human Nutrition


School of Medicine



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