Vitamin E and K interactions – a 50-year-old problem

Authors

  • Maret G Traber

    Corresponding author
    1. Linus Pauling Institute, Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, Oregon, USA.
      MG Traber, Linus Pauling Institute, Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, OR 97331, USA. E-mail: maret.traber@oregonstate.edu, Phone: +1-541-737-7977.
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MG Traber, Linus Pauling Institute, Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, OR 97331, USA. E-mail: maret.traber@oregonstate.edu, Phone: +1-541-737-7977.

Abstract

The mechanisms by which vitamin E interferes with vitamin K activity, especially blood clotting, are not known, but hypothetically this interference may involve metabolic pathways. Phylloquinone (K1) must be converted to menaquinone (MK-4, the most potent extrahepatic tissue vitamin K) by truncation of the K1 side chain and replacement with geranylgeranyl. Possible mechanisms for the vitamin E and K interaction include: 1) vitamin E competes for the yet undiscovered enzyme that truncates the K1 side chain; 2) vitamin E competes with K1 for the hypothetical cytochrome P450 enzyme that ω-hydroxylates the K1 side chain, thereby preventing its β-oxidation and its removal for MK-4 formation; or 3) vitamin E increases xenobiotic pathways that increase hepatic metabolism and excretion of all vitamin K forms. Currently, the pathway for K1 conversion to MK-4 is unknown, the process for regulating vitamin K metabolism to urinary excretion products is unknown, and why vitamin E supplements have such a dramatic effect, causing bleeding in some individuals and not in others, remains a mystery.

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