Vitamin K is best known as an essential factor for blood clotting. During the last years we have also seen that vitamin K may protect against osteoporosis/fractures, atherosclerosis, hepatocarcinoma development and dementia. Vitamin K acts as a cofactor in an enzymatic reaction that converts glumate residues (glu) into y-carboxyglutamate residues (gla) in vitamin K-dependent proteins. Without the carboxylation-reaction, the proteins do not have any function.
The purpose of this project was to systematically review published papers about the effect of vitamin K2 on bone mineral density/fractures and atherosclerosis – and to assess K2’s role in prevention and treatment of these diseases.
The search included the words: ”vitamin K2”; ”menatetrenone”; “menakinon” in the combination with one of the following: ”atherosclerosis”; ”coronary disease”; ”heart disease”; ”vascular disease”, ”vascular calcification”; ”cardiovascular disease”; ”blood vessel”; ”osteoporosis”; ”bone mass”; ”bone mineral density” and ”fractures”. The search was done in Pubmed, Medline/Ovid and Cochrane until 1. November 2007. Human randomized controlled trials (RCT) that gave the participants only vitamin K2 were included in this project. The studies with BMD or fractures and arterial calcification or coronary heart disease as the main outcome were included. There was not found any RCT about the association between vitamin K2 and calcification/coronary heart disease, thus other study types were included. In total 49 potentially relevant RCT about BMD/fractures were found, but only 15 fulfilled the criteria for inclusion. In total 58 studies were found that concerned calcification/ coronary heart disease, but only 3 were included in this project. The others did not have calcification/ coronary heart disease as endpoint.
Several studies demonstrated that a high vitamin K2 intake, 45 mg pr day, could maintain or increase bone mineral density and a few studies showed reduced risk of fractures in osteoporotic women. It is suggested that vitamin K2 reduces bone loss in osteoporotic women through the vitamin K-dependent protein osteocalcin. Only a few studies, mostly animal studies, are published about vitamin K2 and atherosclerosis. The vitamin K-dependent protein MGP is assumed to inhibit the calcification in arteries. The studies suggested that intake of adequate doses of vitamin K2 may prevent atherosclerosis, but the effect and the role of vitamin K2 in this connection need further investigation.We conclude that vitamin K2 prevents bone loss/fractures in osteoporotic women. Since most of the studies are from Japan using doses of 45 mg K2, we do need more large-scale, randomized clinical trials in Caucasian and Scandinavian women and men also with other doses, to figure out if we should change our osteoporosis treatment or decide on a recommended daily dose of vitamin K2 in Norway. Vitamin K2 may also prevent arterial calcification, but we need more studies in humans, particularly randomized clinical trials with different doses of vitamin K2.