Vitamin K2 (MK-7) Quietly Slowed Artery Calcification — But Nobody Knows Yet If It Saves Lives

A 2-year Dutch randomized trial found that 360 μg/day of vitamin K2 (MK-7) modestly slowed the buildup of coronary artery calcium in patients with established symptomatic heart disease. The effect was statistically real but small, and it did not change how many patients were classed as “fast progressors.”

Calcium in the coronary arteries is one of cardiology’s most reliable warning signs — the more of it you have, and the faster it accumulates, the higher your risk of heart attack. For years, a tantalizing idea has circulated in both clinics and biohacker forums: that vitamin K2, a cheap over-the-counter supplement, might put the brakes on this process. The biology is plausible. Vitamin K activates a protein called matrix Gla protein (MGP), the body’s main built-in inhibitor of soft-tissue calcification. Without enough vitamin K, MGP stays inactive and calcium deposits go unchecked.

Until now, the evidence was a patchwork of trials in kidney-disease and diabetes patients, often muddled by co-administered vitamins and inconsistent results. A team at Maastricht University Medical Center set out to run a cleaner test. They recruited 180 patients with symptomatic coronary disease and moderate existing calcification, randomly assigning them to either MK-7 or an identical placebo for two years, with CT scans at baseline, one year, and two years.

The result: calcium scores climbed in both groups — this is a progressive disease and nobody expected reversal — but climbed measurably slower in the MK-7 group. Placebo patients went from a median score of 145 to 214 Agatston units; MK-7 patients went from 135 to 184. Calcium mass, a more reproducible metric, told the same story. Blood tests confirmed the supplement worked biochemically, with the inactive-MGP marker rising less in treated patients.

Here is the catch, and the authors are admirably blunt about it. The overall effect was modest. The proportion of patients who qualified as “fast progressors” — arguably the more clinically meaningful cut — did not differ between groups. And the trial measured calcium on a scan, not heart attacks, strokes, or deaths. There is even a wrinkle worth remembering: more calcium can sometimes mean more stable plaque, so slowing calcification is not automatically good. The honest verdict is that MK-7 does something real to a surrogate marker, at trivial cost and with no safety signal — but whether that translates into fewer cardiac events remains genuinely unknown.

Actionable Insights

Intervention: MK-7 (menaquinone-7), 360 μg once daily, oral, for 2 years, in adults with existing moderate coronary calcification (CAC 50–400 AU).

Effect size, made concrete:

Think of “calcium score” as a number that tracks how much hardened calcium has built up in the heart’s arteries. A higher number means more buildup, and the score naturally climbs over time as the disease progresses. The question is whether the supplement slowed that climb.

  • Calcium score: Over two years, the placebo group’s score rose by 69 points — a 48% jump from where they started. The MK-7 group rose by only 49 points, a 36% jump. In other words, the supplement spared about 20 points of buildup, roughly a 29% smaller increase than placebo. The statistical models that accounted for other factors put the difference at about 22 points, and were confident the true effect falls somewhere between 13 and 31.
  • Calcium mass: Measured a second way (the actual weight of calcium deposits), the placebo group gained 12 mg and the MK-7 group gained 7 mg — about a 40% smaller gain. The catch: once the analysis adjusted for other variables, the gap shrank to just 2 mg, so the real-world difference here is small.
  • The “fast progressors” — the number that matters most: Beyond the average, the more meaningful question is how many people had their disease advance rapidly. Here the supplement made essentially no difference: 65% of the placebo group were fast progressors versus 58% on MK-7, a gap small enough that it could easily be chance (and the statistics confirmed it wasn’t a reliable difference). So while MK-7 nudged the group average in the right direction, it didn’t meaningfully reduce the share of people whose arteries were getting worse quickly — arguably the outcome you’d most want to change.

Take-home: For someone with documented coronary calcification, MK-7 is inexpensive, well-tolerated, and biologically active on a validated surrogate. It is not demonstrated to prevent events. The signal that efficacy may depend on actual vitamin K deficiency (treated patients’ dp-ucMGP still rose) suggests baseline status — not blanket supplementation — likely determines who benefits.

Source:

  • Paywalled Paper: Two Years of Menaquinone-7 Supplementation and Coronary Artery Calcification
  • Institution: Maastricht University Medical Center + CARIM (Cardiovascular Research Institute Maastricht), with VieCuri MC (Venlo) as the community-hospital site.
  • Country: The Netherlands.
  • Journal: JAMA Cardiology.
  • Impact Evaluation: The impact score of this journal is 14.1 (2025 Journal Impact Factor; 5-year IF 15.6; CiteScore 32.7), evaluated against a typical high-end range of 0–60+ for top general science, therefore this is a High impact journal. (Within its own field, cardiac & cardiovascular systems, it sits at roughly the 97th percentile — effectively elite for a specialty title.)

https://jamanetwork.com/journals/jamacardiology/article-abstract/2850256

This is sadly behind a paywall.

Key Points

Question What is the effect of menaquinone-7 on coronary artery calcification?

Findings In this randomized clinical trial that included 180 adults, menaquinone-7 significantly attenuated coronary artery calcification compared with placebo.

Meaning In this study, menaquinone-7 slowed the progression of coronary artery calcification, but a large, prospective trial with hard clinical outcomes is needed to ascertain whether supplementation with menaquinone-7 is beneficial among patients with coronary artery disease.

Abstract

Importance Vitamin K supplementation can reduce progression of vascular calcification in patients with diabetes or end-stage kidney disease. Presently, it is unknown whether vitamin K is also beneficial in patients with symptomatic atherosclerotic coronary artery disease (CAD).

Objective To evaluate whether supplementation with the vitamin K homologue menaquinone-7 (MK-7) for a period of 2 years attenuates the progression of coronary artery calcification (CAC) compared with placebo.

Design, Setting, and Participants This randomized placebo-controlled clinical trial including symptomatic patients with CAC score between 50 and 400 Agatston units (AU) with 2 years of follow-up (VitaK-CAC study). The study was conducted at 1 university hospital and 1 community-dwelling hospital in the Netherlands. Data were collected from January 2012 through October 2022 with a few interruptions; analyses were performed from January 2023 to April 2024.

Intervention Supplementation with either the vitamin K homologue menaquinone-7 (MK-7) in a daily dose of 360 µg or identical placebo.

Main Outcomes and Measures The primary outcome of the study was the evolution of the CAC score and calcium mass at 1 and 2 years of follow-up, as measured with computed tomography (CT) scanning. Additionally, CT angiography was performed. The incidence of new calcifications was a secondary outcome measure. Data were analyzed using a generalized estimation equations model, adjusted for covariates.

Results Altogether, 180 patients could be randomized (90 patients per group), with 85 patients receiving MK-7 (median [IQR] age, 59 [54-65] years; 36 [42%] female) and 82 receiving placebo (median [IQR] age, 61 [54-65] years; 34 [42%] female). Baseline characteristics were comparable for the 2 groups. Plasma levels of MK-7 rose significantly in the active treatment group (median [IQR], 0.50 [0.32-0.77] µg/L to 6.56 [2.04-10.35] µg/L; P < .001). In the placebo group, CAC scores increased from a median (IQR) of 145 (99-217) AU to 173 (119-297) AU after the first year and to 214 (148-344) AU after the second. In the active treatment group, these values were 135 (89-226), 150 (110-254) and 184 (122-298) AU, respectively. The difference between the groups was significant (P = .02), even after adjustment for covariates. A similar result was seen for calcium mass. The increase in CAC score correlated with the number of noncalcified plaques that became partially calcified during the study (R 2 = 0.17; P = .04). No significant adverse effects were observed.

Conclusions and Relevance The findings of this study suggest that supplementation with MK-7 for 2 years may slow calcification in noncalcified plaques of patients with symptomatic CAD. The clinical significance of this finding in terms of plaque stability remains to be determined.

JH

The menaquinones and in particular menaquinone-7 are some of my favourite molecules. I have been reading up on the mechanism with mk-7 recently and I think that it could be (and there is some evidence for this, but not masses) that it acts particularly to accept electrons from Complex I. Normally CoQ10 would be more efficient, but if there is damage to the mtDNA for Complex I mk-7 could handle the situation better.

Hence if it can act to fix the mitochondria slightly then it will reduce endothelial problems.

It may need CoQ10 to handle complex III, but mk-7 (or another hydrophobic menaquinone mk-n where n>6) to get into the membrane wall.

The underlying question is whether mk-n where n>6 supplementation makes mitochondria more efficient or not. Provisionally I think it does.

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related: Menaquinone-7 (MK-7): An interesting molecule to power up the mitochondria

I commented on this study, but somehow my comment has gotten buried in a blind link :person_shrugging:?