Discovery of vitamin K-dependent (VKD) post-translational modification of proteins involved not only in coagulation, but also in bone metabolism, vascular calcification, cell growth regulation, and even ATP production has dramatically shifted both the physiological and clinical importance of this enzymatic cofactor.1,2,3 VKD proteins have a nearly ubiquitous presence in diverse cell types, and modification by ?-carboxylation is necessary for biological activity. Dietary intake of vitamin K is often insufficient, and vitamin K is diverted to those enzymes critical to short term survival (e.g. coagulation), leading to suboptimal carboxylation of VKD proteins associated with aging and chronic disease, such as matrix Gla protein, osteocalcin and Gas6.4
Clinically, a lower intake of vitamin K has translated into a greater risk for myocardial infarction and stroke, plaque instability, and most recently, diabetes.5,6 A greater intake of vitamin K, particularly K2, has been associated with lower all-cause mortality, coronary heart disease, aortic calcification, as well as cancer incidence and fatality.7,8 Higher intake of MK-7, which has the longest half-life and the most extra-hepatic distribution, has been associated with lower risk of fracture and greater BMD.
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