Evidence that biotin status is impaired in human pregnancy

Abstract

Marginal biotin deficiency is teratogenic in some mammals, raising concern that biotin deficiency can cause human birth defects. Our previous studies have shown that about one‐half of pregnant women become deficient, but indicators of biotin status depended on renal function, which is altered by pregnancy per se. We have validated lymphocyte activity of the biotin‐dependent enzyme propionyl‐CoA carboxylase (PCC) as a measure of biotin status. We used PCC activity to test whether women develop marginal biotin deficiency during pregnancy. Both early and late in pregnancy, PCC activity was less (p < 0.0002) than non‐pregnant controls. In a pilot study, PCC response to biotin supplementation at 10x RDA (300 µg/d for 2 wks) was measured in 8 pregnant women with low PCC activities. Activity of PCC was determined before and at the end of the supplement period. PCC activity increased for each woman; the mean± SD increase was 103% ± 59% (p < 0.001). These results provide evidence that marginal biotin deficiency is common in pregnancy and suggests that supplementation effectively repletes biotin status. Supported by AR tobacco settlement funds, NIH R37 DK 36823, and UAMS CRC M01RR14288.