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Vitamin K2 slowed artery calcium in a two-year trial
A JAMA Cardiology randomized trial gave 180 patients with coronary artery disease vitamin K2 or placebo for two years and found calcium buildup progressed more slowly on the supplement.
Based on a peer-reviewed randomized trial in JAMA Cardiology
- The VitaK-CAC trial randomized 180 patients with symptomatic coronary artery disease to 360 micrograms daily of menaquinone-7 (vitamin K2) or placebo for 2 years, in JAMA Cardiology.
- All had existing calcium scores between 50 and 400 Agatston units. Progression was tracked by CT scan at 1 and 2 years.
- Placebo calcium scores rose from a median 145 to 173 to 214 units. On vitamin K2 they rose from 135 to 150 to 184.
- The difference between groups was statistically significant (P = .02), and held after adjustment. Calcium mass showed the same pattern.
- Blood levels confirmed people took it: plasma vitamin K2 rose roughly thirteenfold in the treated group.
- No significant adverse effects were observed over the two years.
- This is a surrogate endpoint. The trial measured calcium on scans, not heart attacks, and the authors say the clinical significance remains to be determined.
Most supplement trials that reach a top cardiology journal do so by failing. This one did not, though what it found needs handling with care.
Researchers in the Netherlands, writing in JAMA Cardiology, gave 180 patients with symptomatic coronary artery disease either vitamin K2 or a placebo for two years and scanned their arteries. Calcium accumulated in both groups. Two years of menaquinone-7 supplementation may slow calcification in noncalcified plaques, the researchers report.
What was already known, and what was not
Vitamin K’s role here is not folklore. It activates proteins that govern where the body puts calcium, and the evidence had already reached specific patient groups: vitamin K supplementation can reduce progression of vascular calcification in patients with diabetes or end-stage kidney disease.
The open question was broader and more commercially relevant. As the authors put it, presently, it is unknown whether vitamin K is also beneficial in patients with symptomatic atherosclerotic coronary artery disease.
The trial
The study was a randomized placebo-controlled clinical trial including symptomatic patients with a calcium score between 50 and 400 Agatston units with 2 years of follow-up, run at one university hospital and one community hospital.
Participants received either menaquinone-7 in a daily dose of 360 micrograms or identical placebo. Altogether, 180 patients could be randomized, with 85 patients receiving menaquinone-7 and 82 receiving placebo, median age around 60 and 42% women in both arms.
Adherence was verified rather than assumed. Plasma levels of vitamin K2 rose significantly in the active treatment group, from a median of 0.50 to 6.56 micrograms per liter.
The numbers
In the placebo group, calcium scores increased from a median of 145 units to 173 after the first year and to 214 after the second.
In the active treatment group, these values were 135, 150 and 184.
Both groups got worse; the supplement group got worse more slowly. The difference between the groups was significant, even after adjustment for other factors, and calcium mass moved the same way.
Why the authors will not celebrate
Here the story turns careful. A calcium score is a surrogate. It predicts cardiovascular risk, but it is not a heart attack.
Worse, calcification is not straightforwardly harmful. Hardened plaque can be steadier than soft plaque, and less likely to rupture. The trial found that the increase in calcium score correlated with the number of non-calcified plaques that became partially calcified during the study, which is arguably the body doing something protective.
So slowing that process might be good, or might not be. The authors say exactly this: the findings suggest supplementation may slow calcification in non-calcified plaques of patients with symptomatic coronary artery disease, and the clinical significance of this finding in terms of plaque stability remains to be determined.
Where that leaves a reader
This is a well-built trial. It is randomized, placebo-controlled and two years long, with objective imaging and verified adherence. No significant adverse effects were observed. That places it far above the observational evidence most supplements rely on.
It is also 180 people, in one country, in a specific clinical group, measuring a marker rather than an outcome. Vitamin K also interferes with warfarin-type blood thinners, which is a real interaction rather than a theoretical one.
The honest summary is that vitamin K2 did something measurable to arteries over two years, and nobody yet knows whether that something is worth wanting.
People also ask
Does this mean vitamin K2 prevents heart attacks?
No, and the authors are careful not to claim it. The trial measured coronary artery calcification on CT scans, which is a surrogate: a marker that tracks with heart risk rather than an event itself. It was not designed or sized to detect differences in heart attacks or deaths. The paper states plainly that the clinical significance of this finding in terms of plaque stability remains to be determined.
Why would vitamin K affect arteries at all?
Vitamin K activates proteins that regulate where calcium is deposited, keeping it in bone and out of soft tissue. When those proteins are under-activated, calcium can settle in artery walls. Earlier work had shown vitamin K supplementation can reduce progression of vascular calcification in patients with diabetes or end-stage kidney disease. What was unknown is whether it also helps people whose problem is symptomatic coronary artery disease.
Is calcium in the arteries actually bad?
It is complicated, which is why the caution matters. A higher calcium score predicts higher cardiovascular risk. But calcification can also steady an existing plaque, making it less likely to rupture. This trial found the rise in calcium score correlated with previously non-calcified plaques becoming partly calcified, so slowing that process is not automatically good. That ambiguity is precisely why the authors withhold a clinical verdict.
Should I start taking vitamin K2?
Nothing here supports that as a general recommendation, and this is information rather than advice. The participants were a specific group: people with symptomatic coronary artery disease and an existing calcium score between 50 and 400. Vitamin K also interacts with warfarin and similar blood thinners, which is a genuine safety issue. Anyone considering it, particularly on heart medication, should ask a doctor or pharmacist first.
How strong is a 180-person trial?
Modest in size but strong in design. It is randomized and placebo-controlled with two years of follow-up and objective imaging, which is far better evidence than the observational studies most supplements rest on. Blood levels confirmed adherence. What 180 people cannot do is detect rare harms or measure clinical events, so it is a well-run early answer rather than a final one.