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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc
to alter anticoagulant status, and there are few data on the extent to which long-term differences in dietary vitamin K intake modulate the response to warfarin. Lubetsky and coworkers (1999) studied a population of 46 patients with an estimated (by food frequency recall) median intake of 179 μg/day of phylloquinone. Patients with intakes greater than 250 μg/day were maintained at the targeted international normalized ratio with 5.8 mg/day warfarin, while patients with an intake of less than 250 μg/day of phylloquinone were maintained on a lower warfarin intake of 4.4 mg/day. These data suggest that alterations in vitamin K intake might influence warfarin dosage. As an effective warfarin dose varies widely within individuals, patients are closely monitored. Once a dose has been established, patients can avoid any complications resulting from variations in vitamin K intake by continuing to follow their normal dietary patterns.
The ability of elevated intakes of vitamin E to antagonize vitamin K action has been clearly established. Woolley (1945) first demonstrated that increased dietary or parenteral α-tocopherol or α-tocopherol quinone could induce a hemorrhagic syndrome in the rat, and vitamin K administration was demonstrated to reverse this response (Rao and Mason, 1975). Studies of the microsomal vitamin K-dependent carboxylase have demonstrated that the enzyme can be inhibited by α-tocopherol and that it is even more sensitive to α-tocopherol quinone (Bettger and Olson, 1982; Dowd and Zheng, 1995).
Increased intakes of vitamin E have not been reported to antagonize vitamin K status in healthy humans. However, in one study, oral supplementation of anticoagulated patients (50 percent plasma prothrombin concentrations) with approximately 360 mg/day (400 IU/day) of α-tocopherol resulted in nonstatistically significant decreases in prothrombin concentrations over a 4-week period, and a statistically significant decrease in the ratio of biologically active prothrombin to prothrombin antigen (Corrigan and Ulfers, 1981). More sensitive measures of vitamin K status are now available and should be used to assess the potential impact of vitamin E supplementation in anticoagulated patients or subjects with low vitamin K intakes.
The metabolic basis for vitamin E antagonism of vitamin K function has not been completely elucidated. Recent data from a study using a rat model have demonstrated an adverse effect of dietary α-