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Most of my patients think of a heart attack as something that happens suddenly, out of nowhere. It usually doesn't. Coronary artery disease builds silently for decades, and one of the clearest windows into that process is a coronary artery calcium (CAC) scan. This simple CT scan measures how much calcified plaque has accumulated in the arteries feeding the heart, producing an Agatston score. The higher the score, the greater the risk of a future heart attack. For years, patients have asked me the same question after getting a high CAC score back: is there anything I can actually do to slow this down? A new two-year, placebo-controlled clinical trial just published in JAMA Cardiology gives us a real answer, and it centers on a nutrient most physicians never mention: vitamin K2, specifically the menaquinone-7 (MK-7) form.
To understand why K2 matters here, you have to understand matrix Gla-protein, or MGP. MGP is the body's primary local inhibitor of vascular calcification. Its job is to physically block calcium from being deposited in the walls of your arteries. But MGP can only do that job after it has been "activated" through a process called carboxylation, and carboxylation depends entirely on vitamin K. Without enough vitamin K reaching the arterial wall, MGP remains in its inactive, dephosphorylated-uncarboxylated form (dp-ucMGP), calcium deposition goes unchecked, and arteries stiffen and calcify over time. This isn't a minor biochemical detail — elevated circulating dp-ucMGP is itself a recognized risk marker for cardiovascular complications. And here's the uncomfortable truth: in most adults, a substantial fraction of circulating MGP sits in this inactive, uncarboxylated state at any given time. Your liver has first claim on the vitamin K you consume, using it to keep clotting factors carboxylated. What's left over trickles out to the artery wall — and for most people, that leftover amount simply isn't enough.
That's exactly what a research team at Maastricht University Medical Center and VieCuri Medical Center in the Netherlands set out to test in the VitaK-CAC trial, a double-blind, placebo-controlled study just published in JAMA Cardiology. The researchers enrolled 180 patients with symptomatic coronary artery disease and an existing CAC score between 50 and 400 Agatston units, then randomized them to either 360 micrograms of MK-7 daily or an identical placebo for two full years, with repeat CT scans at baseline, one year, and two years.
The results favored MK-7. After adjusting for covariates, the yearly increase in CAC score was reduced by 19 Agatston units in the treatment group compared with placebo, a statistically significant difference. Calcium mass — a second, less variable measure of the same process — told the same story: it rose from 26 mg to 38 mg over two years on placebo, versus 25 mg to 32 mg on MK-7. Because both the Agatston score and the calcium mass score pointed the same direction, the investigators expressed real confidence that MK-7 slows the progression of coronary calcification. Plasma MK-7 levels rose more than tenfold in the treatment group, confirming excellent compliance, and dp-ucMGP — the inactive, calcification-permissive form of MGP — rose significantly less in that group as well, moving in exactly the direction the underlying biology predicts.
This new trial didn't come out of nowhere. It builds on a much earlier dose-finding study, also conducted by researchers connected to Maastricht University, in which forty-two healthy adults were randomized to a placebo or one of six doses of MK-7, ranging from 10 to 360 micrograms daily, for twelve weeks. That earlier study established that doses in the range of 90 to 360 micrograms significantly improved carboxylation of MGP and osteocalcin, while lower doses did not, and it confirmed that MK-7 supplementation had no measurable effect on thrombin generation — the marker researchers use to check whether a vitamin K intervention is nudging the clotting system in a dangerous direction. That dose-finding work is what told investigators which dose of MK-7 to use in the two-year coronary calcification trial: 360 micrograms daily, the top dose from the earlier study.
I want to give you the full picture on the new trial, not just the headline. The researchers themselves describe the overall effect as modest, and the proportion of patients classified as "fast progressors" of calcification didn't differ significantly between the two groups. Stenosis severity and the number of affected vessels also progressed similarly in both arms. What MK-7 appeared to specifically slow was the process by which soft, noncalcified plaque converts into partially calcified plaque — the earliest stage of the calcification cascade — rather than reversing calcification that had already occurred. This is a real, biologically coherent, statistically significant finding, but the authors are appropriately candid that we still need a larger outcome trial to know whether slowing this process by this amount translates into fewer heart attacks. That kind of honesty is exactly what you want from good science, and it doesn't change the fact that this is the most convincing clinical trial evidence to date that a nutrient, not a drug, can meaningfully alter the trajectory of coronary calcification.
Why MK-7 specifically, rather than the vitamin K1 (phylloquinone) found in leafy greens? MK-7 has a longer half-life and better bioavailability than K1, allowing it to build to a stable plasma plateau and reach extra-hepatic tissue — bone and artery wall — with enough consistency to drive meaningful carboxylation. Notably, in the VitaK-CAC trial, plasma K1 levels actually fell slightly over the two years in both groups, while MK-7 levels in the treatment group rose from a median of 0.50 to 6.56 micrograms per liter. K1 gets used up by the liver almost immediately; MK-7 has the staying power to do the job everywhere else.
This is where the conversation gets interesting for anyone on a statin, which described roughly 78% of participants in both arms of the VitaK-CAC trial. The study authors themselves raise an important point in their discussion: statins are known to promote calcification of atherosclerotic plaque, likely by inhibiting the body's own synthesis of MK-4, a different form of vitamin K2 — an effect that runs in the opposite direction of what MK-7 supplementation achieved here. To be fair, a recent systematic review and meta-analysis on statins and coronary calcification found the overall evidence base to be, in the authors' own words, controversial, with some studies showing acceleration of CAC under statin therapy and others showing no clear effect. What we can say with more confidence is that no statin trial has demonstrated the kind of measurable slowing of CAC progression that MK-7 just did in a properly controlled, two-year trial. If you're already on a statin for cholesterol management, that medication was not designed to, and has not been shown to, protect against the calcification process itself — which is a separate reason to make sure your vitamin K2 status is adequate rather than assuming the statin already has this covered. Hopefully there will also be future studies on the effect of K2 on the dangerous arterial soft plaque.
One of the biggest misconceptions about vitamin K2 is that it "thickens the blood" or increases the risk of blood clots. Fortunately, this concern has been carefully studied.
Vitamin K is essential for producing several clotting factors made by the liver. However, in healthy adults who consume a normal diet, these clotting factors are typically already fully activated. Research has shown that adding supplemental vitamin K2 does not further increase blood clotting beyond normal physiological levels.
One of the landmark studies by Theuwissen and colleagues evaluated healthy adults who received varying doses of menaquinone-7 (MK-7). While supplementation significantly improved activation of vitamin K-dependent proteins outside the liver—including Matrix Gla Protein (MGP) and osteocalcin—the investigators found no increase in thrombin generation, one of the best laboratory measures of the blood's tendency to clot. In other words, vitamin K2 improved vascular and bone vitamin K status without making the blood more likely to clot.
The recent 2026 JAMA Cardiology trial provides additional reassurance. Participants took 360 micrograms of MK-7 daily for two years, and investigators reported no increase in clotting-related adverse events. Instead, vitamin K2 significantly improved vitamin K status while slowing the progression of coronary artery calcification. These findings support the growing body of evidence that vitamin K2 can safely activate protective proteins involved in calcium metabolism without acting as a procoagulant in healthy individuals.
The important exception is for individuals taking vitamin K antagonist medications such as warfarin. These medications intentionally block the recycling of vitamin K to reduce clotting. Because vitamin K2 can counteract their effect, anyone taking warfarin should only use vitamin K supplements under the supervision of their prescribing physician. For everyone else, current evidence indicates that vitamin K2 supports normal physiology rather than promoting excessive clot formation.
So what does this mean for you? If you have a known CAC score, a family history of heart disease, or you're simply interested in protecting your arteries proactively, I recommend 360 micrograms of MK-7 daily, taken with a meal that contains some fat for absorption — this is the exact dose used in the trial that slowed CAC progression. Food sources of MK-7 are limited mostly to natto and certain aged, fermented cheeses, which is why the vast majority of people need a supplement to reach these levels. The one important exception: if you're on warfarin or another vitamin K antagonist, do not add vitamin K2 without direct coordination with the prescribing physician, since it works through the vitamin K pathway that those medications intentionally suppress. For everyone else, this is an inexpensive, well-tolerated intervention — adverse effects in the trial were rare and no different between groups — with real two-year clinical trial data now behind it.
Coronary artery calcification has long been framed as a one-way street: once the calcium is there, you simply watch and wait. This new trial tells a different story. This is a nutrient deficiency hiding in plain sight, one that conventional medicine still largely ignores, and correcting it appears to meaningfully change the trajectory of one of the most important predictors of heart attack risk we have.
References
Henein, M., Granåsen, G., Wiklund, U., Schmermund, A., Guerci, A., Erbel, R., & Raggi, P. (2015). High dose and long-term statin therapy accelerate coronary artery calcification. International Journal of Cardiology, 184, 581–586. https://doi.org/10.1016/j.ijcard.2015.02.072
Shahraki, M. N., Jouabadi, S. M., Bos, D., Stricker, B. H., & Ahmadizar, F. (2023). Statin use and coronary artery calcification: A systematic review and meta-analysis of observational studies and randomized controlled trials. Current Atherosclerosis Reports, 25(11), 769–784. https://doi.org/10.1007/s11883-023-01151-w
Schurgers, L. J., Teunissen, K. J., Hamulyak, K., Knapen, M. H., Vik, H., & Vermeer, C. (2007). Vitamin K-containing dietary supplements: Comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood, 109(8), 3279–3283. https://doi.org/10.1182/blood-2006-08-040709
Theuwissen, E., Cranenburg, E. C., Knapen, M. H., Magdeleyns, E. J., Teunissen, K. J., Schurgers, L. J., Smit, E., & Vermeer, C. (2012). Low-dose menaquinone-7 supplementation improved extra-hepatic vitamin K status, but had no effect on thrombin generation in healthy subjects. British Journal of Nutrition, 108(9), 1652–1657. https://doi.org/10.1017/S0007114511007185
Vossen, L. M., de Leeuw, P. W., Schurgers, L. J., Heuts, S., Adriaans, B. P., de Haan, C., van Varik, B. J., & Kroon, A. A. (2026). Two years of menaquinone-7 supplementation and coronary artery calcification: A randomized clinical trial. JAMA Cardiology. Advance online publication. https://doi.org/10.1001/jamacardio.2026.1279
