Along with vitamin D, recent studies put vitamin K2 in the spotlight as a major factor in calcium control in the body. Long considered a passive accompaniment of atherosclerotic plaque growth, calcium deposition in coronary arteries, evidenced by your CT heart scan score, is increasingly looking more like an active component that may be under your control.

Measuring coronary calcium is the basis for CT heart scanning. The heart scan score provides a measure of the volume of calcium in coronary arteries, and thereby yields an indirect index of total plaque volume. This useful insight originated with the observations of Dr. John Rumberger and his Mayo Clinic team, who discovered this relationship in the mid-1990s. Calcium consistently occupies 20% of total plaque volume. Thus, 2 mm³ of calcium translates into 10 mm³ of total plaque—hard, soft, and everything in between.



For years, we’ve therefore viewed calcium as just a convenience, a tool that is easy to visualize, but just a passive marker and not an active participant in the disease. Some have even argued that calcium is nothing more than a remnant of prior “rupture,” a scar from the dangerous activity of a soft plaque. They claim that calcium is, in fact, a reflection of increased stability of a plaque, since the “hard” element is not itself prone to rupture. Thus, some believe that, while it serves a practical purpose, calcium plays no true role in causing atherosclerotic plaque.



Those arguments are being dashed by new observations into phenomena behind vitamin K and its role in causing calcium deposition and coronary plaque.



For several years since its discovery in 1929, vitamin K has been known to play a crucial role in maintaining normal blood clotting. Vitamin K is required by the human liver to manufacture several blood clotting proteins (clotting factors II, VII, IX, X, and proteins S and C). This is the basis for administering the vitamin K-blocking drug, Coumadin (warfarin) to people who have blood clots or risk for blood clot formation, since clot formation is effectively blocked by the drug.



Determination of the human need for vitamin K was therefore based on the amount necessary to maintain normal balance between blood clotting and thinning. We don’t want to have our blood excessively “thinned” and prone to bleeding, nor do we want “thick” blood prone to clots. Vitamin K deficiency that disturbs normal clotting is somewhat unusual, often prompted by antibiotics, since bacteria that normally reside in the colon are responsible for producing approximately 75% of the vitamin K needed every day.



Research has uncovered the fact that vitamin K also plays a crucial role in maintaining bone health. It was found that the amount of vitamin K required to halt bone absorption leading to osteoporosis requires much greater intakes than that required for blood clot regulation. Further, it appears that bone and vascular tissue (like coronary arteries) maintain a preference for a different form of vitamin K than that required for blood clotting regulation. Rather than vitamin K1 needed for clotting, vitamin K2 is the form preferred by bones and arteries (Schurgers LJ et al 2001). It appears that much of the information generated over the years for vitamin K focused on the K1 form, ignoring the K2 form necessary for bone and vascular health.



Normal deposition of calcium occurs only in bone and in teeth. Abnormal deposition of calcium in the body occurs in three places: the inner lining of the arteries of the body (the intima) that causes atherosclerotic plaque; the muscle layer of arteries (“medial calcification”); and heart valves. K2 appears to be the form of vitamin K responsible for controlling these phenomena.

How is vitamin K2 involved in coronary atherosclerotic plaque?

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