Two randomized trials published in 2026 found that vitamin K2 slowed the build-up of calcium in coronary arteries. A Dutch trial in people with moderate calcium scores reported a 22-unit smaller rise over two years [6]. A Danish trial in people with severe calcification reported a 52-unit smaller rise [3]. Neither result has changed a single cardiology guideline, and no cardiologist is writing vitamin K2 on a prescription pad.
This article explains what those trials measured, why a lower calcium score is not the same as fewer heart attacks, how the trial doses compare with the amount of vitamin K2 in food, and where a nutritional dose of 90 to 120 micrograms fits.
Table of Contents
- What is vitamin K2 and what does it do in arteries?
- Does vitamin K2 reduce coronary artery calcification?
- Why a lower calcium score does not mean fewer heart attacks
- Does treating coronary calcium save lives at all?
- Did vitamin K2 reduce heart attacks in the trials?
- How much vitamin K2 did the trials use, and how does that compare with food?
- What is a sensible vitamin K2 dose?
- References
What is vitamin K2 and what does it do in arteries?
Vitamin K2, also called menaquinone, is found in cheese, egg yolks and the fermented soybean food natto. It differs from vitamin K1, which comes from leafy greens. The adequate intake for total vitamin K set by the United States National Institutes of Health is 120 micrograms a day for men and 90 micrograms for women [1].
Artery walls make a protein called matrix Gla protein. Its job is to stop calcium settling into the wall, and it only works once vitamin K2 switches it on. Without enough vitamin K2 the protein stays inactive. Animal data suggest that a switched-off protein could allow more calcification and a higher risk of coronary heart disease, though that chain has not been proven in people [1].
The interest in vitamin K2 and arteries started with the Rotterdam Study. In the early 1990s researchers recorded the diets of nearly five thousand people aged 55 and over and then followed them for around seven years. People in the top third of vitamin K2 intake, above 32.7 micrograms a day, had 57 percent fewer deaths from coronary heart disease than the bottom third. The middle third had 27 percent fewer [1]. That was an observational study, so it can show a link but cannot prove that the vitamin caused the difference.
Calcium in the coronary arteries does track risk. In the Multi-Ethnic Study of Atherosclerosis, which followed 6,778 people, the faster a person's coronary artery calcium score climbed, the more heart attacks and other coronary events followed [2].
That link is the reason so many people hoped a vitamin that slows calcification would also prevent heart attacks.
Does vitamin K2 reduce coronary artery calcification?
Three randomized trials have now tested this directly, all using the MK-7 form of vitamin K2.
The first was a Danish trial published in 2022. It enrolled 365 men aged 65 to 74 who already had calcium in the aortic valve. Half took 720 micrograms of vitamin K2 plus vitamin D every day for two years and half took a placebo. Vitamin D was included because it has been shown to increase the amount of matrix Gla protein the body makes, while vitamin K2 switches that protein on [3]. The trial's main result was negative. Valve calcium rose by 275 units on vitamin K2 and 292 units on placebo, a difference that was not statistically significant [4].
A closer look at the coronary arteries found a hint. Among men whose coronary calcium score was already above 400, the score rose by 288 units on vitamin K2 versus 380 on placebo. Serious events, meaning heart attacks, stents, bypasses and deaths from any cause, numbered three in the vitamin K2 group and ten in the placebo group [5]. The trial was funded by the Danish Heart Foundation and other non-commercial bodies, with the tablets supplied free by the manufacturer of the vitamin K2 [5].
The second trial, VitaK-CAC, was run in the Netherlands and published in JAMA Cardiology on 10 June 2026. It enrolled 180 adults with a coronary calcium score between 50 and 400, which counts as moderate disease. Half took 360 micrograms of MK-7 a day and half took a placebo. After two years the calcium score had risen 22 units less in the vitamin K2 group, a statistically significant difference [6].
The third, DANCODE, came from the same Danish team whose valve trial had failed. Published in Circulation on 28 August 2026, it enrolled 398 people with a coronary calcium score above 400, the exact group where the earlier trial had hinted at an effect. Half took 720 micrograms of MK-7 plus 1,000 IU of vitamin D, half took a placebo. After two years the calcium score had risen 196 units on vitamin K2 and 248 on placebo, a difference of 52 units [3].
So there are now two dedicated trials, one in moderate disease and one in severe disease, both showing that vitamin K2 slows the rise in coronary calcium score.
Why a lower calcium score does not mean fewer heart attacks
A coronary calcium scan measures the end stage of a plaque, not the beginning.
A plaque starts when cholesterol lodges in the artery wall. Immune cells arrive to clear it, fail, and die there, leaving a soft pool of fat and dead cells under a thin cap. This young plaque is the dangerous kind, because the cap can rupture and trigger a heart attack. Over years the body walls the plaque off with scar tissue and then calcium, much as it hardens a healing bone. A calcified plaque is old, stiff and far less likely to tear.
That is why cardiologists have long held that the plaques that kill are usually the soft ones a calcium scan cannot see. The score predicts risk because people with a lot of calcified scar usually also carry a lot of soft plaque.
Statins illustrate the point. In a pooled analysis of eight ultrasound studies covering around 3,500 people, statins shrank total plaque while making it denser and more calcified. The authors suggested that this shift from soft to calcified plaque may be part of how statins stabilise plaque and lower heart attack risk [7].
That raises an uncomfortable question about vitamin K2. If it slows calcification, is the soft plaque left unstabilised? Less calcium on the scan could sit alongside the same amount of dangerous plaque.
Both 2026 trials looked. In VitaK-CAC, the number of soft, partially calcified and calcified plaques all increased over two years, with no significant difference between the vitamin K2 and placebo groups [6]. In DANCODE, among the 143 participants with usable contrast scans, total plaque volume and non-calcified plaque volume were not significantly different between groups either [3].
Dr Axel Diederichsen, the cardiologist who led both Danish trials, described the worry to TCTMD: one scenario is that patients are left with "more soft plaque, with more of this lipid core, with more lipids in the walls, and then the patient would be at a larger risk" [8].
Does treating coronary calcium save lives at all?
There is a deeper problem. It is not yet proven that finding coronary calcium and treating it saves lives, even with the drugs that have the strongest evidence.
The DANCAVAS II trial in Denmark invited 31,268 men aged 60 to 64 to cardiovascular screening that included a calcium score, with statins and aspirin offered to those with high scores. After a median of seven years, deaths from any cause were not significantly lower in the screened group, and major cardiovascular events were not significantly lower either. Severe bleeding was higher. The authors describe the trial as most likely underpowered so far and plan a ten-year analysis [9].
If treating a known calcium score with statins has not yet proven itself, changing the score with a vitamin has a long way to go.
The editorial that Circulation published beside the DANCODE trial put it plainly: "there remains no direct, prospectively validated evidence that reduced CAC progression reduces cardiovascular events", and vitamin K2 with vitamin D3 "should not be prioritized or substituted for preventive interventions that have a proven beneficial effect on cardiovascular outcomes" [10].
Two positive trials, then, and still no proven link from the number on the scan to the outcome that matters.
Did vitamin K2 reduce heart attacks in the trials?
The 2022 valve trial reported three serious events on vitamin K2 against ten on placebo, and that figure is often quoted as if it settled the question.
The trial's own authors disagree. In their words, the finding was a safety endpoint, the study was not powered for it, and it remains a possible coincidental finding [5].
The numbers explain why. Thirteen events in total across 365 men. In DANCODE there were five events in 398 people, two on vitamin K2 and three on placebo [3]. Counts that small cannot tell anyone whether a treatment prevents heart attacks.
This is why no cardiologist is prescribing vitamin K2 for calcified arteries. Nobody has yet shown whether these doses reduce heart attacks or not.
How much vitamin K2 did the trials use, and how does that compare with food?
The doses that moved a calcium score were 360 to 720 micrograms a day. That is three to eight times the adequate intake of 90 to 120 micrograms, and roughly ten to twenty times what a diet high in vitamin K2 delivers [1].
The Rotterdam Study group with the fewest heart deaths were eating about 33 micrograms of vitamin K2 a day [1]. The 720 microgram trial dose is around twenty times that.
At those amounts vitamin K2 is being used as a drug rather than as a nutrient, and a drug has to prove two things before it is prescribed: that it is safe, and that it reduces the outcome that matters. Medicine has a long record of promising markers that failed that test. Torcetrapib raised HDL cholesterol, the so-called good cholesterol, by 72 percent, and the trial was stopped early because deaths from any cause rose by 58 percent [11].
A marker moved in the right direction and patients died more often. The calcium score has not failed that test yet, but it has not passed it either.
What is a sensible vitamin K2 dose?
The evidence supports the same approach used for any vitamin or mineral: reach the recommended intake, and be cautious about megadosing.
For total vitamin K the adequate intake is 90 to 120 micrograms a day. How much of that should come from K1 versus K2 is unsettled, because the data are thin. Leafy greens supply K1. Cheese, natto and eggs supply K2. For people who eat few of those foods, a low-dose vitamin K2 supplement can fill the gap, with 90 to 120 micrograms as a sensible ceiling.
The clearest evidence for adequate vitamin K intake concerns bone rather than arteries. The European Food Safety Authority has authorised the claim that "a cause and effect relationship has been established between the dietary intake of vitamin K and the maintenance of normal bone" [1]. That is an adequacy claim about dietary intake, not a treatment claim.
From the MicroVitamin range
MicroVitamin contains 90 mcg of vitamin K2 as MK-7, inside the 90 to 120 microgram adequate-intake range, alongside 1,000 IU of vitamin D3. It is formulated to fill a dietary gap, not to deliver the 360 to 720 microgram doses used in the calcification trials. Vitamin K contributes to the maintenance of normal bones. MicroVitamin.
In a three-year trial, 180 micrograms of MK-7 a day slowed the age-related loss of bone density at the lumbar spine and femoral neck in postmenopausal women, though not at the total hip. That trial measured density only. It did not show fewer fractures [12].
One safety point applies to anyone on warfarin. In healthy volunteers, MK-7 at just 10 micrograms a day caused a clinically relevant drop in the INR clotting test in at least 40 percent of people, and at 20 micrograms in at least 60 percent. The study authors advise that MK-7 supplements be avoided by people on vitamin K antagonists such as warfarin [13]. The newer anticoagulants apixaban, rivaroxaban and dabigatran are not affected by vitamin K, and the DANCODE trial allowed people taking them to enrol [3].
The bottom line from two positive trials is more modest than the headlines. Vitamin K2 at drug-level doses slows the calcium score. Whether that helps or harms the heart is unknown. Meeting the daily requirement is well supported. Going far beyond it is not.
References
1. https://ods.od.nih.gov/factsheets/VitaminK-HealthProfessional/
2. https://doi.org/10.1016/j.jacc.2012.12.035
3. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.082363
4. https://doi.org/10.1161/CIRCULATIONAHA.121.057008
5. https://doi.org/10.1016/j.jacadv.2023.100643
6. https://jamanetwork.com/journals/jamacardiology/fullarticle/2850256
7. https://doi.org/10.1016/j.jacc.2015.01.036
8. https://www.tctmd.com/news/vitamin-k-supplementation-may-reduce-coronary-calcification-vitak-cac
9. https://doi.org/10.1093/eurheartj/ehaf704
10. https://doi.org/10.1161/CIRCULATIONAHA.126.082640
11. https://doi.org/10.1056/NEJMoa0706628
