Supplement Source Podcast
Supplement Source Podcast
Vitamin K2 and Heart Health: What the VITAK-CAC Trial Tells Us
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In this episode of Supplement Source, CRN’s Jeff Ventura speaks with Dr. Leon Schurgers, professor of biochemistry of vascular calcification at Maastricht University, about new research examining vitamin K2 and cardiovascular health.
Dr. Schurgers takes us inside the VITAK-CAC trial, a placebo-controlled, double-blind study examining whether vitamin K2 as MK-7 can influence the progression of coronary artery calcification. He explains why calcification matters, how vitamin K-dependent proteins function in the vessel wall, and what researchers found after two years of supplementation—including a 29% lower increase in calcification in the MK-7 group compared with the control group.
The conversation also explores what the findings do—and do not—tell us about cardiovascular health, important considerations around vitamin K and medications, and the longer-term studies still needed to determine whether slowing calcification ultimately translates into fewer cardiovascular events.
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SPEAKER_03You are listening to Supplement Source, the official publicist of the Council for Responsible Nutrition. And now your host, Jeffin Turba.
SPEAKER_02Hello, and thank you for listening to Supplement Source. My name is Jeff Vinchura, and I am the Vice President of Communications here at the Council for Responsible Nutrition. I am delighted to be joined today by Dr. Leon Schergers, who's a professor of biochemistry of vascular calcification, and he is working with our member Gnosis. He is on the faculty at Maastricht University. I hope I'm pronouncing that right, Doctor. Welcome. Yeah, welcome to the show. Yeah, great. We're so happy to have you here, and we're really interested to learn more about Vita K CAC, this trial that you're working on. Tell me a little bit about it. What uh researchers, what are researchers doing with regard to this investigation?
SPEAKER_01So when working on vitamin K, then you finally have to prove that it also works for humans. And so we work a lot with vitamin K in cells and sometimes in experimental animals. But the exclusive evidence of a nutrient that is good for patients or for people, you have to test it in a human population. And so what we often do is we take patient populations because they are diseased and it's easier to cure diseased people or to rescue diseased people than making healthy people even healthier. So that is something that you start to work on. And so many, many years back, because this trial started in 2012 already, it was funded by the Dutch Hart Foundation, came up with the idea that if you have coronary artery calcification, which is the abbreviation CAC CAC, it's actually the calcification of your coronary artery. In the clinic, people use this score, this CAC score, to say something about the aterosclerotic burden of a patient. So the higher the score, the higher the aterosclerotic burden, the more cardiovascular disease you have. On the other hand, the lower your CAC score, the less cardiovascular disease you have. And that is a good sign. So this CT scan says something about the health of your vessels around the heart. And in the vessels, there is a protein that is called matrix glabrotein. It's a very small protein. And these smooth muscle cells they produce this protein, which is a vitamin K-dependent protein. And we have shown if you give vitamin K, then this protein becomes activated, and then this protein can inhibit calcification initiation, but also the progression, or let's say the growth of calcium phosphate crystals in your vessel wall. And that was actually the start of this Vitac study. We had some evidence, preclinical evidence, in vitro evidence, yet we had to prove it in patients.
SPEAKER_02First of all, on a personal note, I am scheduled to have a scan of my heart and the calcification. So it's it's interesting that this is our topic for today. I think a lot of people immediately understand uh what we're talking about here because they've they've had some sort of touch point uh to this themselves clinically. So very, very interesting. But tell me though, how does this differ from previous research on vitamin K and cardiovascular health?
SPEAKER_01So back in 2012, there were not many clinical trials done with vitamin K in patients or in volunteers. And what we wanted to do is to have a really well-controlled clinical trial, meaning it is placebo controlled, it is double blind. So both the patient and the researchers do not know which supplement a patient gets. This is only, let's say, the code is only given at the very end of the study when all results are there. And we had sufficient number of patients in our trial. There was a lot of data already, and also in the in the in the in the years uh in between, a lot of studies showed results. Some were positive, some did not show the effect that we hoped to see. And that is why this Vita Cack study was really important because it was very well designed, and it is uh it lasted for two years, where patients had to take a daily supplement with a relatively high dose of MK7, vitamin K2. And what we measured is using CT scan, the absolute amount of calcium in the coronary arteries. So often these clinical trials they use surrogate markers, only let's say biomarkers that react, but they don't tell anything of what is really happening in the vessel wall. But in this trial, we had everything. We had the measurement of calcium in the coronary arteries, like it is done in the clinic, also to establish and to prove if somebody has coronary artery disease. And we had also access to these blood samples because we had blood samples for measuring vitamin K, meaning we could measure the absorption of vitamin K, but also this biomarker, MGP, whether or not it was active or not. And that makes this trial, I think, unique, that it was very well designed with also very good statistical um um boundaries so that we know if we find something, then it is also uh uh a good and and and honest finding.
SPEAKER_02That's that's very, very interesting. Um tell me a little bit, uh you touched on this, but I I I think I would love to know more, uh particularly for those who aren't familiar, what what is coronary artery calcification exactly? And why is it such an important marker of cardiovascular health and and and for that matter, vascular aging?
SPEAKER_01Yeah, it's a very good question. So the question, of course, starts with why is there calcium in your vessel wall? And this is often a reaction of the vessel wall because your vessel wall you're born with, and it has to last, let's say, 80, 90 years. And there is a lot of stress on this vessel wall because with each heartbeat, the bolus of blood goes through the vessels and also through these coronary vessels, and there is a lot of pressure on these vessels. So these vessels have to dilate and to contract and to have to push the blood further and also feed all the organs. And over the years, we develop damage, and that can be age-related damage, that can be comorbidities such as hypertension or uh chronic kidney disease, or maybe even that people have hypercholesteremia. So, for example, if you are diabetic or then you have a high uh glucose levels, this is all kind of injury that builds up over the years, and we get damage to our vessel walls. And this damage is very susceptible for calcification. And once this calcification takes place, this means that there is a bone formation in your vessel wall, you get a stiffened vessel wall. And if you have a stiffened vessel wall, it cannot dilate and pulsate and contract. And I always tell people you should envision it as a rubber tire of your car. If there is a small stone in your tire, each time it hits the the road, there will be small ruptures because the rubber is soft and is elastic. The stone is very hard and and and and and will create damage. And this is the same what happens in our in our vessel wall. We have this impurity of calcium phosphate, which is a kind of bone structure, which gives damage to your vessel wall and eventually can lead to a rupture of your atherosclerotic plaque, and then you get a heart infarct, a myocardial infarction.
SPEAKER_02Right, a heart attack. Yes, yeah, yeah. Yeah, that's not good.
SPEAKER_01No.
SPEAKER_02Tell me a little bit about um in your you're again, you're I think you're you're touching on this, but just a little bit more. So, vitamin K, the role that it plays in vascular health. Tell me a little bit more about that and how vitamin K dependent proteins are involved in the calcification process.
SPEAKER_01So, actually, vitamin K-dependent proteins were discovered already many, many years ago, more than over almost 100 years ago, and they play a very important role in blood coagulation. And most people know that we give vitamin K to new burns because they have a high risk on brain bleedings. And if you give vitamin K, this is reduced by a factor thousand. So vitamin K can activate these um coagulation factors, these blood coagulation factors, and thereby activating them. More recently, this is work of the 90s of last century. This protein MGP turned out to be very important for the vessel wall. And actually, in a pre-clinical mouse model, they deleted this protein, and then these mice were born, except they did not have this protein anymore. And these mice were born to term, they were born normal, but all died within eight weeks after birth. And what they found out is was is that this protein, the lack of this protein, resulted in massive calcification of the vessel wall. So they realized this MGP, this matrix glad protein, this vitamin K-dependent protein, is important for inhibiting vascular calcification. Now, this doesn't say anything about the function of the protein because the absence is a complete absence. So if you reduce the function of this protein, and we can see that in patients receiving vitamin K antagonists, and as the name says, as a vitamin K antagonist, inhibits the function of vitamin K, these patients are more susceptible for vascular calcification. So if you reduce the function of this protein by inhibiting vitamin K, you get more calcification. We said, okay, let's work with people from internal medicine in our hospital and give patients vitamin K to maximally activate this MGP and prevent the initiation of calcification and the further growth of calcification.
SPEAKER_02So let's talk about the because I think you're you're getting into that now, let's talk about the clinical meaningfulness with regard to the MK7 control group versus placebo over the course of the two years. What what are we actually talking about in terms of in terms of numbers?
SPEAKER_01Normally we see, and that is something that we that we calculated on forehand, if you have calcification, then the growth is about 25% per year, or 15% per year, let's say 30% over two years. And we said we need an inhibition of this growth of calcification by at least 25% over two years, because then we have a meaningful effect, and so that is what we did is we gave vitamin K and we measured at baseline the calcification score of the coronary arteries after one year and after two years, so at the end of the study. And what we found is that the MK7 active group had 29% less increase in calcification as compared to the control group. So we could significantly inhibit the growth of calcification, and a detailed analysis also showed that we inhibited the formation of new calcifications in our vessel wall.
SPEAKER_02That wasn't all, right? I mean, the study also uh measured the vitamin K status, but the biomarker DPUC MGP.
SPEAKER_01Actually, our primary outcome that was the calcification. And that is, of course, what the clinician wants to see. If I give something, can I see really the result in the vestibular? But we are researchers and we also want to establish and and and come up with biomarkers and prove that it is via a certain mechanism. So when you give vitamin K to these patients, then you want to also see that these patients take their vitamin K supplements and if they are compliant. So what we did is we measured after one year and after two years also the vitamin K concentration in both the placebo group and in the MK7 active group. And what we showed is that the active group had a significant rise in MK7 in the bloodstream, whereas the placebo group, patients in the placebo group, did not show any MK7 increase, which makes sense, of course. Next, we wanted to show if you have an increase of MK7 in the bloodstream, does it also reach the vessel wall and activate this matrix glad protein? Because that was actually our hypothesis. And that is why we also measured the um the activity status of this protein. And what we could conclude is that there was a significant uh increase in activating this MGP. So what we showed is in this trial, we give MK7, it is absorbed and it is also taken by the the uh patients. We know that it reaches the vessel wall because it activates this MGP, that is something we can measure. And finally, we could also see that the endpoint, meaning less increase in coronary artery calcification, was also there.
SPEAKER_02Let's uh let's zoom out for a bit um and take this you know from the lab to the living room, as it were, and talk about the broader context of what this actually means about vitamin K2 and vascular health. How are we to interpret these studies?
SPEAKER_01So for me, this is really nice to see because what we used here were patients, patients which had a baseline and coronary artery scan with a uh a value between 50 and 400, which is that you have significantly visible coronary artery calcification. In this population, the supplementation of MK7 over two years inhibited the progression of calcification. How does that translate? We can treat patients once a disease is there, but what we want to do is to prevent the disease. And since we showed that MK7 supplementation in these patients also inhibited the new formed calcifications in the vessel wall, I could hypothesize that if you start early enough, you might even prevent the initiation of calcification and also inhibit cardiovascular disease significantly.
SPEAKER_02We have to also provide some context, do we not? The study looked at the progression of calcification rather than cardiovascular events themselves. Why is that distinction important when interpreting the results?
SPEAKER_01Because we we do know that the amount of calcium says something about the amount of cardiovascular burden. If we inhibit the growth of calcium, we do not know if this will result in less events, less myocardial attacks, for example. So this is something we should take into account. And I'm absolutely agreeing with you that this is at this moment lacking. But it is also very difficult to come up with a study that is long enough to see that there is less cardiovascular events by simply giving vitamin K. Remind, vitamin K is a nutraceutical, it's it's a vitamin. These kind of trials are not sponsored by the pharmaceutical industry where there is a lot of money and where you can spend uh a lot of money, including thousands of patients, over a period of maybe five, ten years. So that is a little bit the the the the difficulty um that we have to face.
SPEAKER_02Yeah, no not a billion dollars hanging around for uh development of uh of a new molecule per se.
SPEAKER_01I haven't seen it yet.
SPEAKER_02Yeah, you haven't seen that stack of money yet. Um so um what safety considerations are important then when when we're talking about K2? It's not it, you know, there there obviously are parameters here. It's not like everybody should run out and just start gobbling up K2. There are safety considerations, are there not?
SPEAKER_01No, that's a good thing of vitamin K. There is no upper tolerance level set by the World Health Organization. So it's absolutely safe. You can take uh high amounts. I know in Japan they take uh 45 milligrams, which is something like thousandfold the minimal uh required dose. And there has not been reported side effects or negative side effects. So, in that respect, it's very good. I can tell you that um we are now busy also with analyzing the complete cohort because if you give MK7 to patients, some patients react, meaning there is a significant increase in the activation of MGP. But some people, some patients have a lesser effect. We classify or want to classify them as responders versus non-responders. I think that the effect of vitamin K might be even bigger if we only study the responders, meaning the people that really are in need of vitamin K because they were deficient in vitamin K. And this is something that in very uh near future studies we will investigate. And I'm pretty sure that vitamin K will have a greater effect if we only give it or select patients that really are in need of vitamin K. Vitamin K is absolutely safe, so you can give it.
SPEAKER_02But certain medications, does it interact with certain medications?
SPEAKER_01That is a good question. We haven't really dived into. So there is one medication that you should not give vitamin K together with, and that is vitamin K antagonists, because otherwise you're antagonizing the antagonist, which doesn't make sense. But I do but I do fully agree with you that the combination of medication together with MK7 would be a very logic choice. So in a pre-clinical animal model, we have already shown that the combination of a phosphate binder to lower the absorption of phosphate, which is a risk factor to develop cardiovascular calcification, together with MK7 gave the best result. So I'm pretty convinced that we should look at multiple supplements or treatments rather than the one golden bullet.
SPEAKER_02And I think that forward looking, um, you know, sort of looking ahead, uh, you're kind of answering that now, but uh more specifically, uh what questions still remain unanswered in your mind? You know, where where would you like to see the research really go next?
SPEAKER_01I I would really love to see that vitamin K can rescue cardiovascular disease, not only limit the calcification processes in the coronary arteries or in other vessel walls, but also to see that it can really limit or lower cardiovascular disease. And then we need outcome studies, people, survival studies, uh studies that are done over maybe 10, 20 years. And we are looking at this moment uh international grants in the Netherlands because we have some kind of these these grants supported by the Dutch government. And hopefully we uh we will succeed in in getting such a grant.
SPEAKER_02This has been fascinating. I know that I'm gonna go out and buy this buy my K2 uh this evening, um, just based on this conversation. So I I really do uh appreciate uh the insight uh here uh Doctor, and we we just want to thank you again for coming on to Supplement Source. Love to have you back to hear more about uh where your uh where your research takes you.
SPEAKER_01It was a pleasure to uh to have this conversation.
SPEAKER_02Thank you very much.