Vitamin K2 for Coronary Artery Disease

Vitamin K2 is unproven for coronary artery disease: two trials found it slowed the build-up of calcium in the heart's arteries, other trials found no effect, and none was designed to test heart attacks or deaths. In VitaK-CAC, 180 people with symptomatic coronary artery disease were randomised to 360 mcg of MK-7 or placebo daily for 2 years; coronary calcium scores rose less with MK-7 (median 135 to 184 AU vs 145 to 214 AU, P = .02) (Vossen 2026). In DANCODE, 398 people with severe coronary calcification (a score of 400 AU or more) took 720 mcg of vitamin K2 plus 25 mcg of vitamin D3 or placebo for 24 months, and their scores rose by 196 vs 248 AU (difference -52 AU, 95% CI -79 to -24) (Hasific 2026, DANCODE).

A slower rise in calcium is an imaging result, not a health outcome. Statins, which lower clinical events, also increase the calcium in coronary plaque (Puri 2015), and the VitaK-CAC authors say the meaning of their result for plaque stability remains to be determined (Vossen 2026). Trials in older men (Diederichsen 2022; Hasific 2023), dialysis (Haroon 2023; Levy-Schousboe 2021) and kidney disease (Kurnatowska 2015) found no overall coronary benefit. The 2023 US guideline for chronic coronary disease does not recommend dietary supplements, including vitamins, given their lack of benefit in reducing cardiovascular events (Virani 2023).

Matrix Gla protein (MGP), a vitamin K-dependent protein in vascular smooth muscle, might help reduce abnormal calcification, and vascular calcification is a risk factor for coronary heart disease because it reduces arterial elasticity (NIH ODS). When vitamin K is short, more MGP stays inactive, measured in blood as dp-ucMGP. In cohort studies, people with the highest dp-ucMGP had higher all-cause mortality (HR 1.84) and cardiovascular mortality (HR 1.96) (Chen 2019).

Supplements reliably fix that marker. Across trials, vitamin K lowered dp-ucMGP by 44.7% compared with control (Lees 2019), and in AVADEC, MK-7 with vitamin D lowered it by 212 pmol/L while it rose 45 pmol/L on placebo (P < 0.001) (Diederichsen 2022). In VitaK-CAC, plasma MK-7 rose from a median 0.50 to 6.56 µg/L (Vossen 2026).

The extent and progression of coronary calcium strongly predict heart attack and death (Hasific 2023), but calcium is also part of how plaque changes under treatment. In a pooled analysis of 8 intravascular ultrasound trials in coronary artery disease, high-intensity statins were associated with plaque regression, yet statins increased the plaque's calcium content, which the authors suggest may be one way statins stabilise plaque (Puri 2015). In VitaK-CAC, the rise in calcium score tracked soft (non-calcified) plaques becoming partly calcified (Vossen 2026).

DANCODE looked inside the plaques of 143 participants with CT angiography: total plaque volume grew similarly in both groups, non-calcified plaque volume did not differ, and only calcified plaque volume grew less with K2 and D3 (-8 mm³, 95% CI -13 to -2) (Hasific 2026, DANCODE). In other words, the supplements slowed calcium deposition but not plaque growth, and whether that changes risk is untested. A Danish cohort adds indirect support for the pathway: long-term use of warfarin-type drugs, which block vitamin K, went with faster coronary calcium progression, while direct oral anticoagulants did not (Hasific 2026, anticoagulant study).

VitaK-CAC used 360 mcg of MK-7 a day for 2 years (Vossen 2026). DANCODE used 720 mcg of vitamin K2 with 25 mcg of vitamin D3 a day for 24 months (Hasific 2026, DANCODE), the same daily doses as AVADEC, which used MK-7 (Diederichsen 2022). The dialysis trials used 360 mcg of MK-7 daily or three times a week (Levy-Schousboe 2021; Haroon 2023), and the kidney disease study used 90 mcg with 10 mcg of vitamin D (Kurnatowska 2015). The coronary and dialysis trial doses of 360-720 mcg are 3 to 8 times the adequate intake for all vitamin K, 120 mcg a day for men and 90 mcg for women (NIH ODS); the kidney disease study's 90 mcg is at that level.

No upper limit has been set for vitamin K, because no adverse effects from vitamin K in food or supplements have been reported (NIH ODS). Natto, a fermented soybean food, is the richest food source, at about 850 mcg of MK-7 per 3 ounces (NIH ODS).

VitaK-CAC is the only trial in people with symptomatic coronary artery disease. Among 180 patients in the Netherlands with calcium scores of 50-400 AU, 360 mcg of MK-7 a day for 2 years slowed the rise in calcium score and calcium mass compared with placebo (P = .02, also after adjustment), with no significant adverse effects (Vossen 2026). Data collection stretched from 2012 to 2022, and the abstract does not report heart attacks or deaths (Vossen 2026).

DANCODE, a Danish multicentre trial in 398 people (median age 71, 30% women, median score 903 AU) with severe coronary calcification, found a smaller rise in calcium score over 24 months with 720 mcg of vitamin K2 plus 25 mcg of vitamin D3, consistent across sexes and calcium levels (Hasific 2026, DANCODE). Because it gave the two vitamins together, the effect can't be credited to K2 alone, and its primary end point was the calcium score, not clinical events.

AVADEC, from the same Danish group, gave 365 men with aortic valve calcification (mean age 71) MK-7 with vitamin D for 2 years. Coronary calcium progression did not differ from placebo, and cardiovascular events were equal (10 vs 10) (Diederichsen 2022). In its 304 men without known ischaemic heart disease, the mean rise was 203 vs 254 AU (P = 0.089); the rise was smaller only in men with scores of 400 AU or more (288 vs 380 AU, P = 0.047), and heart attacks, revascularisations and deaths, a safety end point, were fewer (1.9% vs 6.7%, P = 0.048). The authors called these findings hypothesis-generating (Hasific 2023).

In kidney disease, where calcification is common, MK-7 did not slow coronary calcium in 178 haemodialysis patients over 18 months, and major cardiac events and deaths did not differ (HR 0.98, 95% CI 0.50-1.94) (Haroon 2023). It also failed in 48 dialysis patients over 2 years (Levy-Schousboe 2021), and in 42 people with chronic kidney disease K2 with vitamin D did not slow coronary calcium compared with vitamin D alone (58 vs 74 AU, P = 0.7) (Kurnatowska 2015). In an uncontrolled Japanese study, coronary calcium rose 14% in a year in 26 patients taking 45 mg a day of the MK-4 form (Ikari 2016).

A 2023 meta-analysis of 14 trials (1,533 patients) found vitamin K slightly slowed coronary calcium progression (mean difference -17.37 on the calcium score, 95% CI -34.18 to -0.56, P = 0.04) (Li 2023), and a 2019 meta-analysis of 13 trials found a 9.1% reduction in vascular calcification, limited by few, heterogeneous studies (Lees 2019). A 2020 systematic review of 9 trials concluded that vitamin K does not consistently prevent calcification, with possible benefit in people who already have it (Vlasschaert 2020). These analyses predate VitaK-CAC and DANCODE and combine vitamin K1 and K2 trials.

For vitamin K1, a 3-year trial of 500 mcg a day in 388 older adults found no overall difference in coronary calcium; progression was slower only in adherent participants and in those with existing calcification, which the authors called hypothesis-generating (Shea 2009). A 2026 review focused on kidney disease concluded that neither vitamin K1 nor K2 has shown reductions in major cardiovascular events or deaths (Brandenburg 2026). The vitamin K2 for atherosclerosis page covers the wider artery and arterial-stiffness trials.

In the Rotterdam Study of 4,807 adults, those in the top third of menaquinone intake had a lower risk of coronary death (RR 0.43, 95% CI 0.24-0.77) than those in the bottom third (Geleijnse 2004). In 16,057 Dutch women, each extra 10 mcg a day of K2 went with a 9% lower risk of coronary heart disease (HR 0.91, 95% CI 0.85-1.00), mainly from MK-7, MK-8 and MK-9 (Gast 2009), and a meta-analysis put the risk 30% lower with high menaquinone intake, from two studies (Chen 2019). In 564 postmenopausal women, higher intake went with less coronary calcification (RR 0.80) (Beulens 2009).

The pattern is not consistent. In a Norwegian cohort, the link weakened and lost significance after adjusting for other dietary factors (HR 0.58, 95% CI 0.28-1.19) (Haugsgjerd 2020). Among 53,372 Danes, both K1 and K2 intakes went with fewer hospital admissions for atherosclerotic disease (K2: HR 0.86) (Bellinge 2021), while among 112,111 UK Biobank participants the highest K2 intakes went with slightly higher risk (HR 1.07), which the authors suggest may reflect the foods K2 comes from (Dupuy 2026). Meat and dairy foods supply modest amounts of menaquinones (NIH ODS), and diet studies can't separate K2 from the rest of those foods.

MK-7 was well tolerated in the coronary trials: VitaK-CAC saw no significant adverse effects over 2 years (Vossen 2026), and a meta-analysis of 14 trials found no difference in adverse events between vitamin K and control (Li 2023). No upper limit has been set for vitamin K (NIH ODS).

The real risk is with blood thinners that work against vitamin K, such as warfarin, acenocoumarol and phenprocoumon. People taking them need a consistent vitamin K intake, because sudden changes can increase or decrease the anticoagulant effect (NIH ODS). In volunteers on acenocoumarol, as little as 10 mcg of MK-7 a day caused a clinically relevant fall in INR in at least 40% of people, and the authors advise avoiding MK-7 supplements with these drugs (Theuwissen 2013).

Vitamin K antagonists are the one serious interaction. Antibiotics can lower vitamin K status by destroying vitamin K-producing gut bacteria, and bile acid sequestrants such as cholestyramine, used for cholesterol, can reduce vitamin K absorption (NIH ODS). Orlistat can reduce absorption of fat-soluble vitamins and, combined with warfarin, may raise prothrombin time (NIH ODS).