Vitamin K2 Shown to Reduce CVD Risk

Globally, cardiovascular diseases (CVD) are responsible for nearly 1 in 3 deaths. CVDs typically develop over decades, characterized by arteries that clog and harden from plaque deposits in which calcium is the main mineral component.

The Matrix Gla Protein (MGP) is recognized as the most potent inhibitor of vascular calcification today – studies show that it can inhibit, and even reverse, induced vascular calcification. But MGP is dependent upon vitamin K2 to fulfill its role.

While it was believed that calcification is an unfortunate and inevitable consequence of aging, recent studies demonstrate that arterial calcification is an actively regulated process. Healthy arterial tissues have been shown to contain 100 times more vitamin K2 than calcified arteries – meaning that one can actively protect their cardiovascular system by obtaining adequate vitamin K2.

Vitamin K2 Shown to Reduce CVD Risk

The Rotterdam Study (2004) showed that high dietary intake of vitamin K2 – but not K1 –  has a strong protective effect on cardiovascular health. This population-based study, which took place over a 10-year period, included 4,807 men and women 55 years of age or older at the start. Findings from the study indicate that eating foods rich in natural vitamin K2 (at least 32 μg per day) reduces the risk of both arterial calcification and cardiovascular disease by as much as 50% – with no undesirable side effects.

The Rotterdam findings were confirmed in 2008 by another Dutch population-based study investigating the protective effect of vitamin K2. The Prospect study by Gast et al included 16,057 women, and after 8 years of follow-up, vitamin K2 was found to decrease the risk of coronary heart disease (CHD) by 9% for every 10 μg vitamin K2 consumed. The scientists found that the strongest correlation was seen in cases of intake of the higher menaquinones (MK-7, MK-8, and MK-9). Vitamin K1 intake was not significantly related to CHD.

Further, a 2012 double-blind, randomized, clinical trial evaluated the results of a 3-year regular intake of a 180 mcg daily dose of vitamin K2 menaquinone-7 (MK-7) by a group of 244 healthy post-menopausal Dutch women, randomly assigned to receive daily either vitamin K2 or placebo capsules. The trial showed substantial benefits in preventing age-related stiffening of arteries resulting in increase of the PWV (pulse wave velocity) in the placebo group, but not in the vitamin K2 group. Most remarkably, the vitamin K2 group showed it not only prevented stiffening, it also resulted in an unprecedented statistically significant improvement of vascular elasticity both measured with ultrasound techniques and PWV.

Vitamin K2 & Blood Thinners

The mechanism by which blood-thinning medications work inhibits vitamin K. Vitamin K1, due to its ability to support healthy blood clotting, may interact or interfere with anti-coagulants such as warfarin. Researchers concluded in one study that vitamin K2 as MK-7 supplementation at doses as low as 10 μg (lower than usual retail dose of 45 μg) significantly influenced anticoagulation sensitivity in some individuals. Thus, the researchers recommended avoiding use of MK-7 supplements if on vitamin K-antagonist therapy.

However, it has been shown that patients on oral anti-coagulant therapy who take up to 50 mcg of MK-7 per day have more complete activation of osteocalcin without interfering with the effect of the blood thinner. In other words, taking a small amount of MK-7 allows one to avoid the side effects of these medications without interfering with their intended benefits.

On the basis of the latest insights and in order to remain on the safe side, it is recommended that patients on conventional blood thinners consult with their doctor before taking a K2 supplement, since taking more than 50 mcg of K2 might interfere with the prescription.


Gast et al. Nutr Metab Cardiovasc Dis. 2009 Sep;19(7):504-10.

Knapen et al. Thromb Haemost. 2015 May;113(5):1135-44.

Theuwissen et al. Thromb Haemost. 2013 Jun;11(6):1085-92.

Schurgers et al. Blood. 2007 Apr 15;109(8):3279-83.


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