![]() ![]() ![]() There is only limited evidence of a benefit of supplemental vitamin K in the prevention of vessel calcification and cardiovascular events. Vitamin K inadequacy may inactivate several VKDPs that inhibit the formation of calcium precipitates in vessels. (More information)Ībnormal mineralization of blood vessels increases with age and is a major risk factor for cardiovascular disease. Overall, intervention trials have been inconclusive regarding the role of supplemental vitamin K (vitamin K 1 or vitamin K 2) in further reducing bone loss in otherwise calcium- and vitamin D- replete adults. Some, but not all, observational studies have found lower vitamin K status to be associated with lower bone mineral density and higher fracture incidence. Vitamin K deficiency may impair the activity of VKDPs and increase the risk of osteoporosis and fractures. The adequate intake ( AI) level for vitamin K is set at 90 μg/day for women and 120 μg/day for men. An injection of vitamin K is recommended to protect all newborns from life-threatening bleeding within the skull. Vitamin K deficiency increases the risk of excessive bleeding ( hemorrhage). Vitamin K is the essential cofactor for the carboxylation of glutamic acid residues in many vitamin K-dependent proteins (VKDPs) that are involved in blood coagulation, bone metabolism, prevention of vessel mineralization, and regulation of various cellular functions. With limited vitamin K storage capacity, the body recycles vitamin K in the vitamin K oxidation- reduction cycle in order to reuse it multiple times. Naturally occurring forms of vitamin K include phylloquinone (vitamin K 1) and a family of molecules called menaquinones (MKs or vitamin K 2). Healthcare Professional Continuing Education.Chlorophyll and Metallo-Chlorophyll Derivatives.
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