Vitamin K2 – The Essential Cardiovascular Ingredient

Times are changing; technology and advanced research has given our medical community the tools to better understand the main culprit responsible for Cardiovascular Disease. But can it be treated?


Publication : Calcium as predictor of outcome

A recent review by Time Magazine revealed the findings: “First it was blood cholesterol that could give you an early warning that a heart attack might be around the corner. Then came C – reactive protein. And now that doctors can get a better look at what’s inside your heart and arteries, they are taking a new interest in something they have always known was present in problem vessels: calcium. Hospitals, clinics and even gyms are touting quick and easy scans that can measure the amount of calcium in your coronary arteries in minutes.” Calcium, the ingredient we all know is necessary for healthy bones; an ingredient we are advised to get in our daily diets is actually causing heart disease. It is not so much calcium itself but more misdirected calcium. Yes, we do need calcium for healthy bones and we should consume the recommended daily allowance, but we do not need this calcium in our vessels. If found in the vessels, calcium is not helping our bones but rather creating the “foundation for heart disease.”

The article further says that “Calcium can build up in the vessels and stiffen them, laying the foundation for heart disease. Getting one’s calcium score is simple, either by electron beam computed tomography (EBCT) or by multi detector CT. Studies show that in every age group people with higher vascular calcium levels have a greater risk of heart attack than do people of the same age with lower scores.”


What can be done about it?

Vitamin K is essential for the activation of vitamin K dependent (VKD) proteins which are involved not only in blood coagulation but in bone metabolism and the inhibition of arterial calcification. Although Osteoporosis and arterial calcification were once thought to be unrelated conditions, recent studies indicate that the common factor may be vitamin K deficiency thus leading to inadequate calcium metabolism and utilization. This is called the Calcium Paradox.

This paradox suggests that necessary calcium is not being effectively utilized by the body for building bones and other healthy functions, thus increasing to unhealthy levels in the vascular system and eventually leading to heart disease. Vitamin K is necessary to prevent complications of the calcium paradox.


Several VKD proteins have been discovered during the last 20 years. Among them are MGP (Matrix Gla Proteins), found in bone, cartilage, and vascular smooth muscle cells. Recent studies have shown that MGP plays a key role in the inhibition of tissue calcification. As with all VKD proteins, MGP needs to be carboxylated (activated) to function properly. This carboxylation or activation is done by Vitamin K. Hence, Vitamin K deficiency may be a risk factor for vascular calcification. Until recently, vascular calcification was widely regarded as merely a rare, end stage, passive, degenerative, and inevitable process of aging. Evidence now suggests that it is an active, cell controlled process that shares many similarities to bone metabolism. One of those regulatory proteins is MGP, a potent inhibitor of soft tissue calcification. And the nutrient required to activate MGP is Vitamin K.


A robust study exists, Rotterdam Study [1]. Scientists followed a cohort of 4807 subjects, men and women age of 55 and older, for a period of 10 years. The end points were aortic calcification, cardiovascular mortality and all cause mortality against the vitamin K2 daily consumption. Their findings are that the tertile consuming 45.8 mcg of K2-7 had a 50% reduction of arterial calcification, 50% reduction of cardiovascular death and 25% reduction in all cause mortality.


Proof of Inactive MGP leads to calcification

Schurger et al [3], using a novel technique to determine inactive ucMGP, show that impaired carboxylation of MGP is associated with intimal and medial vascular calcification and suggest the essentiality of the vitamin K modification to the function of MGP as an inhibitor of ectopic calcification.

K1 or K2 to protect against calcification?

It is well known that warfarin induces calcification. In a study where warfarin was used for artery calcification, Price et al [4] demonstrate the inability of vitamin K1 to counteract the effect of warfarin based calcification. Spronk et al [5], in a highly impressive rat model study, conclude that K2 is preventive of arterial media calcification.

Can calcification be regressed?

It is clear from above that vitamin K2 is essential to inhibit and stop progression of arterial calcification. VitaK Institute at the Masstricht University, Netherland, where Rotterdam study was conducted, has presented initial results of a large study, at a conference in the USA, correlating vitamin K2 administration with regression of calcification.


  1. Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC: Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr 2004, 134(11):3100-3105.
  2. Rosenhek R, Binder T, Porenta G, Lang I, Christ G, Schemper M, Maurer G, Baumgartner H: Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med 2000, 343(9):611-617.
  3. Schurgers LJ, Teunissen KJ, Knapen MH, Kwaijtaal M, van Diest R, Appels A, Reutelingsperger CP, Cleutjens JP, Vermeer C: Novel conformation-specific antibodies against matrix gamma-carboxyglutamic acid (Gla) protein: undercarboxylated matrix Gla protein as marker for vascular calcification. Arterioscler Thromb Vasc Biol 2005, 25(8):1629-1633
  4. Price PA, Kaneda Y: Vitamin K counteracts the effect of warfarin in liver but not in bone. Thromb Res 1987, 46(1):121-131
  5. Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C: Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats. J Vasc Res 2003, 40(6):531-537

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