that probably contained less than 10 μg /day of phylloquinone. After 3 weeks, a statistically significant increase in the PT was observed, but it was still within the normal range. In another study, Frick and coworkers (1967) administered a parenteral nutrient solution to a small number of neomycin-treated adults for 4 weeks and observed prolonged PT that responded to the parenteral administration of phylloquinone. They concluded that the minimal daily requirement was between 0.3 and 1.05 μg per kg body weight of phylloquinone. In more recent studies (Allison et al., 1987; Ferland et al., 1993), feeding healthy individuals diets containing 5 to 10 μg/day of phylloquinone for 14- to 16-day periods failed to induce any change in PT measurements.
These limited studies, conducted over a number of years, indicate that the simple restriction of vitamin K intake to levels almost impossible to achieve in any nutritionally adequate, self-selected diet do not impair normal hemostatic control in healthy subjects. Although there is some interference in the hepatic synthesis of the vitamin K-dependent clotting factors that can be measured by sensitive assays, standard clinical measures of procoagulant potential are not changed.
Various indicators have been used to assess vitamin K status in humans (Booth and Suttie, 1998). Of these, only one, prothrombin time (PT), has been associated with adverse clinical effects. All other indicators have been shown to respond to alterations in dietary vitamin K, but the physiological significance of these diet-induced changes is lacking. Therefore, these indicators have been used to assess relative changes in vitamin K status but do not provide, by themselves or collectively, an adequate basis on which to estimate an average requirement for vitamin K.
The classical PT used to measure the procoagulant potential of plasma is not a sensitive indicator of vitamin K status because plasma prothrombin concentration must be decreased by approximately 50 percent before a value is outside of the “normal” range (Suttie, 1992). Furthermore, studies conducted thus far clearly indicate that PT does not respond to a change in dietary vitamin K in healthy