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Vitamin K has a plethora of potential implications, including prevention and treatment of arterial calcifications, coronary heart disease and cancer, improvements in bone strength and reduced risks of fractures as well as improvements in insulin sensitivity.

Vitamin K is a fat-soluble vitamin, important for the function of numerous proteins within the body, such as the coagulation factors (II, VII, IX, X and protein C and protein S), osteocalcin (a bone-forming protein) and matrix-Gla protein (MGP) (an anticalcification protein), to name a few.1–3 Vitamin K exists naturally as vitamin K1 (phylloquinone) and vitamin K2 (menaquinone, MK-4 through MK-10).2–5 Vitamin K1 is mainly found in green leafy vegetables as well as olive oil and soyabean oil, whereas vitamin K2 (menaquinone) is found in small amounts in chicken, butter, egg yolks, cheese and fermented soyabeans (better known as natto).2 6–9

[NOTE ADDED: Kefir has vitamin K but not as high as natto.]

Despite the fact that mammalian bacterial intestinal flora are able to produce vitamin K2, the amount produced is thought to be negligible.2 The adequate intake (AI) for vitamin K has been proposed to be 90 µg/day for women and 120 µg/day for men.2 10 However, it has been speculated that the AI for vitamin K (90–120 µg/day) is not sufficient to induce complete carboxylation of all vitamin K-dependent proteins.2 11 12

Vitamin K1 (5 mg daily) given to 440 postmenopausal women with osteopenia for 2 years in a randomised, placebo-controlled, double-blind trial caused a greater than 50% reduction in clinical fractures (9 vs 20, p=0.04) versus placebo, despite the fact that there was no improvement in bone mineral density.18 Moreover, there was a 75% reduction in cancer incidence with vitamin K1 (3 vs 12, p=0.02). The benefit of vitamin K on bone is thought to be unrelated to increasing BMD but rather increasing bone strength.19

dietary vitamin K1 intake, without vitamin K2, may not be sufficient to suppress arterial calcifications and/or reduce risk for subsequent cardiovascular events and death. The menaquinone form of vitamin K (ie, vitamin K2) has been presumed to be more effective than vitamin K1 at preventing and reversing arterial calcifications.

Low vitamin K status (indicated by undercarboxylated MGP) is associated with increased vascular calcifications, and these levels can be improved by effective vitamin K supplementation28–32

it has also been shown to significantly delay the deterioration of arterial elasticity.37

In a 3-year randomised, double-blind, controlled trial of 355 patients, vitamin K significantly improved insulin sensitivity in men with diabetes.

Vitamin K2 has been shown to inhibit the growth of human cancer cell lines, including hepatoma lines, as well as to treat myelodysplastic syndrome.50–53 Two trials seem to indicate that vitamin K2 45 mg/day reduces the development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis and that vitamin K2 significantly reduces the recurrence of HCC in patients following the curative treatment of HCC with an associated reduction in all-cause mortality in these patients.54–61

data have shown that vitamin K2 may improve bone remodelling in patients with haemodialysis with low serum parathyroid hormone levels.73


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Vitamin K Deficiency

Vitamin K deficiency can contribute to significant bleeding, poor bone development, osteoporosis, and increased risk of cardiovascular disease.

Vitamin K is not transported across the placenta efficiently, and infants are born with low to undetectable concentrations of Vitamin K

Vitamin K deficiency can present with a history of bleeding at venipuncture sites or with minor trauma. The patient may also have a history of antibiotic, anticonvulsant, or other prescription drug use. Additionally, during a physical exam, ecchymosis or petechiae may be found.