NattoPharma

Vitamin K2 and inhibition of arterial calcification

Cardiovascular disease is the most frequent cause of death in the western world, often due to calcification of blood vessels and especially in the coronary arteries of the heart. Calcification is often symptom-free but potentially a dangerous condition that, combined with deposits of fat in the arteries, causes clogging of the blood vessels and leads to myocardial infarction, angina pectoris and thrombosis.

Cardiovascular disease

Atherosclerosis is the most common form of cardiovascular diseases (CVD). It is characterized by calcification of the arteries, a progressive condition that may lead to arterial sclerisis and, subsequently, angina and stroke. Both abnormal calcium and lipid metabolisms play an inportant role in the development of this disease. Today there exist few nutrition alternatives, besiedes pharmaceuticlas, often with side effects, that can reduce the cardiovascular problem. The best positioned nutrition totday is Omega-3, which finally was approved by the FDA in the US. Scientific studies indicate that Vitamin K2 probably reduces the calcium level in the artery walls. By doing this, it has a sgnificant positive effect in reducing cardiowascular disease.

Prothrombin (Factor II)

Factor

MenaQ7 is a proven new solution for the problems disclosed above. MenaQ7 optimizes the calcium binding to the bone structure, reducing the development of osteoporosis and simultaneously reduce the calcification of arteries. Hence calcium + vitamin D + MenaQ7 is the best known formulation that can improve bone health and reduce calcification in arteries.

Recent human research has unequivocally linked the role of vitamin K2 to the vascular calcification. Vitamin K was considered for over a half century only to be important for normal blood clotting, while no other biological effects were linked to the vitamin. With the recent discovery of the vitamin K-dependent protein MGP, K-vitamins have received more attention during the last decade.

It has been shown that it is possible to create vascular calcification in rats by giving them the anticoagulation drug warfarin (belonging to the group of coumarins). This drug blocks the action of vitamin K in the liver where the coagulation factors are activated. Animals get calcium deposits in their arteries after just two weeks treatment 24, pointing to the need of vitamin K2 for normal vascular physiology.

Vitamin K-antagonists like warfarin also cause a doubling of the arterial calcification in humans, as compared to patients not receiving vitamin K-antagonist. Calcification results in an increase of aortic stiffness and hence contributes to systolic hypertension and left ventricular hypertrophy, coronary insufficiency, ischemia and congestive heart failure. Although calcification of the arterial vessel wall commonly increases with age, the presence of these calcifications increases the risk for cardiovascular events independent of age. This is why it is a necessity to prevent the deposition of calcium in arteries, or even to block or lower already present arterial calcifications.

The Rotterdam study from 2004 had followed more than 4800 initially healthy persons (from 55 years old at the start of the study) for over a 10 year period. The study shows that people who consumed most vitamin K2 through vitamin K2 rich foods (mainly fermented foods and meat from animals fed K3), had a 50% reduced risk of arterial calcification and also a 50% risk reduction for cardiovascular events during the study period.

All cause mortality was also reduced by 25%. Effects were only seen in groups consuming more than 32 µg/day of K2 - and not in groups consuming high doses of vitamin K1.

A new published animal study shows regression of arterial calcification when animals were fed high doses of vitamin K2- but not K1. This is rather astonishing as arterial calcification has been thought of as an irreversible biological phenomenon. To the best of our knowledge there is no pharmaceutical therapy available for prevention or regression of arterial calcification.