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Vitamin K2 Shown to Reverse Arterial Calcification


Sunday, April 06, 2008
Research


Vitamin K2 Shown to Reverse Arterial Calcification
PL Thomas & Company (PLT) of Morristown, NJ and Natto Pharma, Norway today announced new findings for Vitamin K2 with significant potential benefits for cardiovascular health. In the study, scientists at the Cardiovascular Research Institute (CARIM) and VitaK, Maastricht University, The Netherlands, demonstrated a reversal of induced arterial calcification in an animal model. The study is available on the website of the high ranked journal Blood under the First Edition Papers section. The study will be published in the regular print and online issues of Blood in early 2007.

Arterial calcification is an important independent risk factor for the development of health concerns including atherosclerosis, myocardial infarction, stroke, and renal disease. It is well established that individuals with marked arterial calcification have an unfavorable prognosis compared to those with no or mild calcification. Therefore, the prevention or reversal of arterial calcification is what researchers and doctors aim for because it may lead to improved outcomes.

"The medical community used to believe that calcification passively occurred in the end stages of cardiovascular disease," said lead researcher Leon Schurgers. "However, in the last 10 years we have learned that Vitamin K-dependent proteins are directly involved in the inhibition of vascular calcification, and that Vitamin K2 is necessary to activate these proteins. This study demonstrates a significant potential role for Vitamin K2 in cardiovascular health."

It has been previously shown in the Journal of Nutrition that high Vitamin K2 consumption was linked to lower coronary heart disease, less aortic calcification and lower all cause mortality. In this study, 4,800 elderly subjects with no history of heart disease were followed for 10 years, and it was found that 45 micrograms/day of natural vitamin K2 resulted in 50% decreased arterial calcification and a similarly decreased cardiovascular mortality risk.

Induced arterial calcification has been shown to be inhibited completely by vitamin K2 in vivo. In the new study, the researchers looked at the potential to regress calcification. Arterial calcification was induced in rats by interfering in the vitamin K-metabolism, by adding the vitamin K-antagonist warfarin to their diets. Vitamin K acts directly on matrix Gla-protein which is the strongest inhibitor of arterial calcification presently known. The rats were divided into two groups, a control group with vitamin K added to the diet, and a warfarin treated group to induced calcifications. After six weeks of treatment with warfarin, the rats had developed significant calcifications. At this point, the warfarin treated rats were divided into four groups and fed a standard diet plus 1/ Warfarin, 2/ vitamin K1 at normal dose, 3/ Vitamin K1 at high dose, and 4/ vitamin K2 at high dose.

During the second six week period, the calcifications in the warfarin treated group continued linearly, and remarkably, in the group receiving a normal dose of K1 continued comparably, demonstrating that the normal amount of vitamin K in the diet had no benefit.

In contrast, high vitamin K intake (both K1 and K2) not only blocked the progress of further calcium accumulation, but led to an over 37 % reduction of previously accumulated arterial calcium precipitates within 6 weeks. It is interesting to note that in the high K1 group, the vitamin K1 converted into vitamin K2 to such an extent that tissue concentrations were similar to the K2 supplemented group.

Additionally, the regression of arterial calcification was accompanied by restoration of arterial distensibility, or elasticity, in the high vitamin K groups to a similar level as in the control rats.

According to Schurgers, "The effect of K1 and the conversion rate of K1 to K2 was due to the extremely high dose of K vitamins used in this model. This would be probably less in a normal diet, even with supplemental K1. In contrast, the Rotterdam study showed a significant protective benefit with Natural Vitamin K2 at just 45mcg per day, whereas K1 had no correlation at all."

"Warfarin also inhibits conversion of K1 to K2, " continued Schurgers. "This is of significance as we and others have reported that the use of coumarin-type anticoagulants is associated with increased cardiac valve calcification."




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