Arterial Calcification Reduced With Vitamin K2 Intake According to New Study

PL Thomas and NattoPharma are pleased to announce that a new study demonstrated the association of high dietary Vitamin K2 consumption with reduction of coronary calcification in humans. Accepted by the journal Atherosclerosis, this study is now available online.

Researchers at University Medical Center Utrecht, Wageningen University and Erasmus Medical Center Rotterdam investigated whether daily consumption of natural phylloquinone (K1) and menaquinones (K2) might be related to the extent of calcification within the vasculature of 564 healthy post-menopausal women. This study was undertaken to examine the hypothesis that natural vitamin K plays a crucial role in the prevention of heart disease. The study discovered that high consumption of natural vitamin K2, about 45 mcg daily, was associated with 20% decreased coronary calcification as compared with low consumption of K2, of about 18 mcg daily. Preventing arterial calcification is important for a healthy and flexible vasculature. Further, for Vitamin K1 no such correlation was found.

"This study confirms once again that natural Vitamin K2, also called the menaquinones, is clearly linked to the prevention of cardiovascular disease," said Vitamin K expert Leon J Schurgers, senior scientist from VitaK, at the Maastricht University in the Netherlands. "While all K vitamins are important, it seems that especially the natural vitamin K2 intake is essential to cardiovascular health."

Earlier studies suggested the strongly protective effect of K2 on vascular calcium deposition. One such example is the Rotterdam study, published in the Journal of Nutrition in 2004 (

In this study the dietary intake of 4800 healthy adults over a 10 year period was examined, and revealed that increased dietary intake of specifically vitamin K2 significantly reduced the risk of both arterial calcification and cardiovascular mortality by 50% as compared to low intake. Vitamin K1 - even when taken in large quantities - had no influence on excessive calcium accumulation.

Schurgers continued, "Fermented cheese is the primary source of natural vitamin K2 in the Western diet. Isn't it interesting that cheeses may be considered "unhealthy" due to the high unsaturated fat content – yet consumption of cheese may reduce the risk of a heart attack! Recently we have found a possible scientific explanation in experimental animals in which high vitamin K2 could regress arterial calcifications. Since most apparently healthy adults are vitamin K-deficient in their arteries, extra vitamin K2 intake would be necessary to maintain healthy arteries. Fortunately now dietary supplements are available with natural vitamin K2 and foods may be enriched with it as well."

A natural vitamin K2 as a dietary supplement ingredient called MenaQ7 is now currently available. MenaQ7 is extracted from the traditional Japanese food natto, providing the natural Vitamin K2 as menaquinone-7, the long-chained molecule offering superior bioavailability and health effects in low doses, which has been tied to both bone and cardiovascular health.

Background: MGP and arterial calcification

Arterial calcification contributes to the fragility and stiffness of blood vessels, thereby increasing the risk of cardiovascular disease (CVD). Recent studies have confirmed that arterial calcification is a strong indicator of cardiovascular health: the survival rate is associated with the amount of calcification present within the vasculature. Freely translated, a person is as old as their arteries are: a significant calcification "increases the chronological age" and subsequently shortening lifespan; while an older person with little or no calcification can deduct years from his or hers chronological age (Shaw, 2006).

However, to properly perform its preventive function, MGP must be activated by K Vitamins during the activation (= carboxylation) reaction. Thus, vitamin K deficiency results in under-carboxylation of MGP (ucMGP) species and impairs their biological function. Lacking an adequate vitamin K intake, ucMGP accumulates at the sites of calcium deposition but is inactive and thus ineffective in preventing and inhibiting calcification, which then increases the risk of fatal cardiovascular event.

The different effects of vitamin K2 and vitamin K1 probably reflect differences in how the body metabolizes the different forms of vitamin K. K1 is mainly cleared by the liver and used to activate proteins involved in coagulation. Vitamin K2 is available to the liver, but is also transported to tissues outside the liver, such as bone and cardiovascular tissues.

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