Vitamin K, discovered by Danish scientist Henrik Dam in 1929, is well known for its effects on the clotting cascade in blood.1 Also known as phylloquinone, vitamin K is important because it has been found to be involved in many metabolic processes in the body. As recently as 1974, researchers were able to isolate vitamin K’s role in blood coagulation in human beings.2 For such a prominent vitamin, however, its processes, impact, and methods of metabolism in humans remain poorly understood.
Vitamin K is widely known as an antidote or antagonist of warfarin-induced bleeding. It is a key component in the body’s manufacture of prothrombin in the clotting cascade. It has also been a long-standing practice to give newborns an immediate injection of supplemental vitamin K to prevent potentially lethal hemorrhage. This is done because newborns have only 30% to 60% of recommended levels of vitamin K, making them more susceptible to bleeding.3
In addition to its role in hemostasis, vitamin K plays a pivotal role in the metabolism of calcium in the human body. In a cascade similar to that in hemostasis, phylloquinone is converted in the intestinal tract, the endothelium, and in other organs from the plant form, vitamin K1, into the more active form, K2, with subgroups of K4 (menaquinone-4) and K7 (menaquinone-7).4 These forms serve as essential coenzymes that facilitate the incorporation of calcium into hydroxyapatite crystals in the bone, thereby playing a key role in bone structure maintenance.5 A meta-analysis of studies researching vitamin K intake and the incidence of osteoporosis in postmenopausal women reviewed data from trials involving nearly 7000 participants.6 Overall results of pooled data revealed a relative risk reduction of 0.50 in favor of vitamin K supplementation.6
In a study of more than 240 women with known osteoporosis, researchers randomly assigned the participants to either no change in management or diet (control group) or daily supplemental vitamin K27 At the end of the study, participants were examined for new compression fractures and lumbar bone mineral density. The control group, as expected, showed increased fractures and continued loss of lumbar bone density. Some fractures also occurred in the supplemented group; however, there were significantly fewer fractures than in the control group and the supplemented group had a much smaller loss of lumbar bone mineral density.7
The role of vitamin K in bone maintenance is significant, but perhaps the more exciting possibility for vitamin K supplementation is the potential for reversal of atherosclerosis. The mechanism of action of vitamin K and calcium deposition in soft tissues involves the known action of a calcium inhibitory protein that requires vitamin K to function.8 This is seen especially in the arterial endothelium. Increased vitamin K intake has been shown to reduce arterial calcium deposition in humans and, in some animal studies, has been shown to reverse existing plaque.8
This article originally appeared on Clinical Advisor