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quinone was consumed with a 400 kcal (27 percent energy from fat) meal, the relative absorption was between five and six times lower from spinach than from a phylloquinone tablet. In this study, phylloquinone absorption from fresh spinach, broccoli, or romaine lettuce did not differ and was highly variable between subjects. It is apparent from these limited studies that until more data are available, the bioavailability of phylloquinone from vegetable sources should not be considered to be more than 20 percent as available as phylloquinone consumed as a supplement.

Approximately 34 percent of phylloquinone in the American diet is consumed from fats and oils (Booth et al., 1995). It might be expected that phylloquinone dissolved in oil would be more available than from a food matrix, but this may not be true. Vitamin K is not well absorbed by patients exhibiting lipid malabsorption syndromes (Savage and Lindenbaum, 1983), and efficient absorption of this fat-soluble vitamin from the digestive tract does require dietary fat. Although direct measures of bioavailabilty have not been reported, a recent study reported no difference in fasting plasma phylloquinone concentrations when 400 μg of phylloquinone as broccoli or as phylloquinone-fortified oil was added to a diet containing 100 μg of phylloquinone (Booth et al., 1999a). Hydrogenated fats contain significant amounts of 2',3'-dihydrophylloquinone formed from phylloquinone during processing. Dietary intake of this form of the vitamin in the United States is estimated to be about 20 percent of phylloquinone (Booth et al., 1999c). Neither the biological activity nor the bioavailability of this form of vitamin K is known. The amount of dietary fat needed for optimal absorption has not been determined.

Drug-Nutrient Interactions

Oral 4-hydroxycoumarin derivatives such as warfarin are widely prescribed anticoagulants for the prevention of thrombotic disorders. These drugs function through the inhibition of a hepatic vitamin K-epoxide reductase. This enzyme reduces the coproduct of the λ-glutamyl carboxylase reaction, the vitamin K 2,3-epoxide, to the hydronaphthoquinone form of the vitamin, which is the substrate for the enzyme. The result is an acquired cellular vitamin K deficiency and a decrease in the synthesis of the vitamin K-dependent plasma clotting factors. Alterations in vitamin K intake can, therefore, influence warfarin efficacy, and numerous case reports of these occurrences have been reviewed (Booth et al., 1997a). Short-term, day-to-day variations in vitamin K intake do not appear

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