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Vitamin K has been known as the coagulation vitamin, because of its role in the blood-clotting process. However, research over the last few decades has shown that the role of K Vitamins - and natural Vitamin K2, the menaquinones, in particular - has been greatly expanded. Of note, K Vitamins activity outside the liver is required for calcium utilization, the key factor in maintaining both bone and cardiovascular health.\n\nVitamin K2 helps to activate vitamin K-dependent proteins responsible for healthy tissues. In bone, it activates osteocalcin, a protein required to bind calcium to the mineral matrix, thus strengthening the skeleton. In circulation, Vitamin K2 participates in carboxylation of Matrix Gla Protein (MGP), the most potent inhibitor of arterial calcification known, lowering the risk of vascular damage.

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one is considered a likely predictor of the other. This relationship has led to the hypothesis that these conditions share core pathophysiological mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part II, The Vitamin K Connection to Cardiovascular Health, reviews the ways in which vitamin K regulates calcium utlization, preventing vascular and soft tissue calcification while complimenting the bone-building actions of vitamin D, and also discusses vitamin K safety and dosage issues, and the necessity of providing vitamin K and vitamin A along with vitamin D to preclude adverse effects associated with hypervitaminosis D.

Tufts University Confirms That Vitamin A Protects Against Vitamin D Toxicity by Curbing Excess Production of Vitamin K-Dependent Proteins Tufts University confirmed my hypothesis that vitamin A protects against vitamin D's induction of renal calcification (kidney stones) by normalizing the production of vitamin K-dependent proteins in December, 2008, without citing my hypothesis or telling me they had confirmed it. I am, of course, very grateful that they thought it significant enough to investigate.

Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Schurgers LJ, Spronk HM, Soute BA, Schiffers PM, DeMey JG, Vermeer C. Blood. 2007 Apr 1;109(7):2823-31. PMID: 17138823 DOI 10.1182/blood-2006-07-035345. This is the first study in rats demonstrating that AC and the resulting decreased arterial distensibility are reversible by high-VK intake