2017-05-21 15:36:38 UTC
Animal studies also show that vitamin K2 not only blocks calcification, but also induces a 37 percent regression of arterial calcification. By the way, pharmaceutical drugs designed to reduce cholesterol have never been great at reversing plaque accumulation within the human body.
In fact, newly published research showed that statin drugs are associated with accelerating coronary artery and aortic artery calcification. A study, published August 2012, in the journal Diabetes Care, revealed that statin users with type 2 diabetes and advanced arthrosclerosis had greater artery calcification.
The science about natto is dramatic!
In the new study, the researchers induced arterial hardening in rats by interfering with vitamin K-metabolism, by adding the vitamin K-antagonist warfarin to the diets. Vitamin K is reported to act on a protein called matrix Gla-Protein (MGP), said to be the strongest inhibitor of arterial calcification.
Initially, the rats were divided into two groups, a control group with vitamin K added to the diet, and a warfarin treated group to induce calcification. After six weeks of treatment with warfarin, the researchers report that the rats showed signs of significant arterial hardening.
The warfarin treated rats were then further divided into four groups and assigned to one of four intervention groups for a further six weeks: a standard diet plus warfarin, a standard diet plus vitamin K1 at normal dose (5 micrograms per gram of food, purchased from Sigma), a standard diet plus high-dose vitamin K1 (100 micrograms per gram of food), or the standard diet plus high-dose vitamin K2 (MK-4, 100 micrograms per gram of food, gifted from Eisai, Japan).
Schurgers and his co-workers report that during the second six week period, the calcifications in the warfarin-treated control group continued linearly, as did the calcification in the normal dose vitamin K1 group, indicating that dietary vitamin K1 intake had no effect.
However, in both high-dose groups (K1 and K2) no continued calcification occurred, but the existing hardening was found to be reversed by about 50 percent after six weeks of supplementation.
Arterial calcification (AC) is generally regarded as an independent risk factor for cardiovascular morbidity and mortality. Matrix Gla protein (MGP) is a potent inhibitor of AC, and its activity depends on vitamin K (VK). In rats, inactivation of MGP by treatment with the vitamin K antagonist warfarin leads to rapid calcification of the arteries. Here, we investigated whether preformed AC can be regressed by a VK-rich diet. Rats received a calcification-inducing diet containing both VK and warfarin (W&K). During a second 6-week period, animals were randomly assigned to receive either W&K (3.0 mg/g and 1.5 mg/g, subsequently), a diet containing a normal (5 microg/g) or high (100 microg/g) amount of VK (either K1 or K2). Increased aortic calcium concentration was observed in the group that continued to receive W&K and also in the group changed to the normal dose of VK and AC progressed. Both the VK-rich diets decreased the arterial calcium content by some 50%. In addition, arterial distensibility was restored by the VK-rich diet. Using MGP antibodies, local VK deficiency was demonstrated at sites of calcification. This is the first study in rats demonstrating that AC and the resulting decreased arterial distensibility are reversible by high-VK intake.
L.J. Schurgers, H.M.H. Spronk, B.A.M. Soute, P.M. Schiffers, J.G.R. DeMey, and C. Vermeer. Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Blood. 2007 Apr 1;109(7):2823-31.