Fifteen women who used combined estrogen-progestogen oral contraceptives and nine control women were given a vitamin B6-deficient diet for 4 weeks and the same diet supplemented with 0.8, 2.0, or 20.0 mg of pyridoxine hydrochloride for an additional 4 weeks. At weekly intervals a variety of indices of vitamin B6 nutrition were measured to determine rates of depletion and repletion. The tryptophan load test (2.0 g) was significantly different in the contraceptive users. However, other indices, including urinary cystathionine (3.0 g L-methionine load), urinary 4-pyridoxic acid, plasma phosphate, and erythrocyte alanine and aspartate aminotransferases, were not significantly different. Since altered tryptophan metabolism persisted in contraceptive users even when other indices of vitamin B6 nutrition were normal, we suggest that the use of oral contraceptives specifically affects tryptophan metabolism by some means other than through a vitamin B6 deficiency.
PIP: This study was designed to evaluate the effect of oral contraceptive use on the requirement for Vitamin-B6 and the rate at which such persons became depleted of Vitamin-B6 while ingesting a diet low in this vitamin. The same indices were used to measure the rate at which these persons became repleted when the diet was supplemented by pyridoxine. Before testing, women using estrogen-containing oral contraceptives were shown to excrete increased amounts of tryptophan metabolites after a tryptophan load test as compared with women not taking oral contraceptives. Elevated levels of 3-hydroxyanthranilic acid were also excreted in urines of such subjects. There were 15 young women subjects who had used estrogen-progestogen oral contraceptives for at least 6 months and 9 women who had not used any oral contraceptive. All were given a Vitamin-B6 deficient diet containing only 1.9 mg of pyridoxine equivalent per day for 4 weeks and then the same diet supplemented with .8-20 mg of pyridoxine hydrochloride for 4 more weeks. Weekly indices of Vitamin-B6 nutrition were determined. Only the tryptophan load test was significantly different in contraceptive users. Urinary cystathionine, urinary 4-pyridoxic acid, plasma phosphate, erythrocyte alanine, and aspartate aminotransferases were not significantly changed. The altered tryptophan metabolism persisted in contraceptive users after other indices of Vitamin-B6 nutrition became normal. Therefore, this altered tryptophan metabolism in oral contraceptive users is considered to be due to other factors than Vitamin-B6 deficiency. This effect may be primarily dependent on the activity of tryptophan oxygenase although other enzymes may also be factors. It is suggested that the use of estrogen-containing oral contraceptives may produce a Vitamin-B6 deficiency in some persons but this is not considered consistent or to have been shown by these experiments. The amount of Vitamin-B6, as pyridoxine, needed to maintain normal levels of indices, other than tryptophan, was between .8 and 2 mg/day. Data suggest that any alteration of Vitamin-B6 need by the use of combined estrogen-progestogen preparations is a minor one of doubtful clinical significance in the majority of women taking these steroids.