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Knife Down is a podcast about how to actually invest in your health so you can live longer, stronger, and with less time in doctors’ offices. The core focus is the world’s leading cause of death—cardiovascular disease—and what to do about it before it shows up as a catastrophe.
Hosted by a vascular surgeon on a mission to put herself out of business, the show translates cutting-edge science on prevention, metabolic health, and longevity into real-world strategies you can use in clinic or at your kitchen table. Expect evidence, nuance, and zero wellness hype—plus the occasional dark joke about the state of modern medicine.
Knife Down
Can You Take Too Much Vitamin K2? Vascular Surgeon Explains
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Can you take too much vitamin K2? In this video, I answer the most common follow-up questions about vitamin K2, including dose, safety, testing, interactions, and whether more is actually better.
Here's the original video on the K2 clinical trial: https://youtu.be/ArxAXtzsue4
We’ll cover:
* Whether vitamin K2 toxicity is possible
* Whether using MK7 to slow coronary artery calcification is desirable
* What we know — and do not know — about upper dosing limits
* Who should be especially cautious with vitamin K supplements
* Why warfarin/Coumadin changes the conversation
* Whether vitamin K2 levels can be tested
* The difference between MK-4 and MK-7
* Whether vitamin K2 can “remove” calcium from arteries
* How I think about vitamin K2 in real-world cardiovascular prevention
The bottom line: vitamin K2 looks promising, but “promising” is not the same thing as “take as much as possible and hope your arteries applaud.”
This video is for education only and is not personal medical advice. Do not start, stop, or change supplements or medications based on YouTube — especially if you take warfarin or another medication affected by vitamin K. Talk with your own clinician.
⏰ Chapters
0:00 - More of your vitamin K2 questions
0:22 - Is softer plaque more dangerous than calcified plaque?
2:35 - Should people with high CAC avoid vitamin D3?
4:13 - Didn’t the AVADEC trial already show K2 works?
6:25 - Would a higher dose of K2 work better?
7:33 - Does K2 actively stop calcium from entering plaque?
8:28 - Can too much vitamin K2 cause blood clots?
8:55 - Vitamin K2 and warfarin/Coumadin
9:48 - Is K2 safe with Eliquis or Xarelto?
10:23 - Is 100 mcg enough—or should you take more?
11:16 - Can vitamin K2 remove calcium from arteries?
11:53 - Can you test for vitamin K deficiency?
12:37 - MK-4 vs MK-7: which form is better?
13:25 - Food sources vs K2 supplements
14:33 - Should K2 be taken with vitamin D3?
14:58 - Final takeaways
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🧬 About Dr. Lily Johnston
Dr. Johnston is a double board-certified vascular and general surgeon in San Diego, specializing in metabolic and cardiovascular prevention. She’s the founder of CorSight Health and a passionate advocate for reimagining how medicine approaches chronic disease.
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We are back with more comments and questions from you guys. Thank you for all of the wonderful suggestions from the vitamin K video. Let's get right into it. If you're new here, my name is Dr. Lily Johnston. I am a board-certified vascular surgeon, but I specialize in cardiometabolic prevention. So hopefully you will never need me as a surgeon. Marion Moses writes, ideally, one wants no plaque laid down in the coronary arteries. Yeah, absolutely. But if you do, everyone seems to agree that hard plaques are generally more stable and much to be preferred to the soft plaque, right? Because it's the soft ones that rupture and cause the blood clots leading to heart attacks and strokes. And I agree. That is my understanding as well. And that is really the key piece that was missing in this whole trial, which is okay, great. We have slowed progression of coronary calcification. And at a population level, people who rapidly progress in their calcium scores have more events. So if we slow that down, shouldn't we slow the events down? But we're missing the piece about is it the calcium that's the problem or is it the total plaque burden? Because if you step back and think about it, the people who are progressing out in the wild, right, they're probably progressing because they have poor risk factor control. And most of that is just overall disease progression. So not only are they calcifying plaque, but they're also laying down new, soft, vulnerable, lipid-rich plaque that is ugly and gonna rupture. The converse situation is that you have a stable amount of total plaque volume, but you are converting some of that that's early soft lipid-rich into this more stable calcified plaque. And that is actually a great outcome, right? That is a stabilization. And optimally, then that plaque never ruptures or becomes a problem. We don't know what's happening on the inside for these patients. They didn't measure total plaque volume. They said that they did that on purpose. There was not a big difference in any other plaque measures, but they had a pretty modest way of looking at it, right? They did a semi-quantitative uh involvement of stenosis or segment involved scores when they did the CCTA part of this study. So I don't have a huge amount of confidence that we would see small changes in any soft plaque measures. So all we know is that calcification was modestly decreased, but we have no idea whether that's going to translate into help, harm, or none of the above for these patients. So stay tuned as we get more information. And Dennis LePlant says since vitamin D3 increases calcium absorption into the bloodstream, should people with high CAC scores not supplement with D3, especially if their blood levels of vitamin D are already optimal? Dennis, if your vitamin D levels are already optimal, I would wonder why you're supplementing in the first place anyway. We don't have strong evidence that vitamin D supplementation would be harmful. And in fact, there's a trial we'll talk about here in a little bit where they used D3 and K2 together, and in fact, showed again, in some people there was slowing of calcium progression. In others, there was no change, but there didn't seem to be any signal for harm. And there is another study that looks at using targeted vitamin D supplementation in people who are low. And in fact, that might help reduce cardiac events. So getting people who are low up to a therapeutic or optimal range can be helpful. But I see where you're coming from, but we actually don't have strong evidence that there's any harm associated with it. The other caveat to this, though, is that there is perhaps a signal for calcium supplementation by itself. And this comes out of an older trial, I think a subset of the Women's Health Initiative, actually, where they were given calcium supplements and looked at overall mortality, and there was a small signal for increase in mortality. So I generally don't like calcium supplements by themselves unless people really get none from their diet and really need it for bone protection. But in general, I prefer people not supplement with calcium based on that one finding. And Dennis has a second question. He says, I'm encouraged but also confused by your video. You say there hasn't been previous studies that show a positive outcome for vitamin K2 supplementation and talks about the 2023 Avidek trial that studied vitamin K2 and D3 for a couple of years. And he says that his doctor told him that coronary calcification was significantly slowed and reported fewer composite safety events. Am I not familiar with the study? I am. It's not K2 in isolation. So they studied K2 and D3. And if you look at their overall results, there was not actually any significant difference in coronary calcium between people who took the supplements and people who were on placebo. The primary outcome of the trial was aortic valve calcification. It was not coronary calcification. They did look at that. What they found was that in a subset of the patients who had very elevated coronary calcium scores, over 400 agatson units, there was a slowing of calcification in those particular patients. But that's a subset analysis. And it's encouraging, but we also don't know whether it was K2 or D3 because they didn't do a separate analysis of just each one independently. The reduction in adverse events is interesting, but those were just safety events. This was actually not an outcome trial. They were not powered to detect outcomes, and the number of total events was very low. It was single digits in one arm and maybe 10 in the other arm. So very low rates and not something that I would change my practice on, although I agree it's an interesting signal. Again, I don't think there's a lot of harm associated with taking vitamin K2. This question about whether it might prevent plaque stabilization, we don't have any information about that. In many trials that have studied it, there does not seem to be a signal for harm. So I don't have any objection to people who want to take it. I just think we don't have enough information. And the adit of trial is interesting, but does not speak to K2 all by itself. And it was a null or neutral outcome in the whole population. Larry Wilson says they should have included a dose range to get dose response. Higher doses would likely have had more beneficial effects. Unfortunately, drug companies won't run a trial like this, so it's up to the medical schools, which have little incentive to run a proper study where the doses were increased. So you may remember at the end of the video, we actually went through who funded the study. Part of it was a grant, but all of the medicine, all of the supplements, excuse me, in the trial were provided by the company. And one of the authors is in fact part of that company. So this was indeed, in some part, funded by the supplement manufacturer. I'm sure that they had a vested interest in having the best outcome possible in the trial. So, you know, I don't disagree with you. It would have been nice to show a dose response, but it took them 10 years to enroll enough patients to actually power this study appropriately. If they had had another arm that was a different dose, it could have taken twice that long to get enough people to actually run the study. So I'm not surprised they didn't do it. I agree. It would have been very interesting. But again, um, this was in fact partly funded by the supplement manufacturer. Question from at CMT Way Does vitamin K2 actively inhibit calcium deposition in the coronary plaques, or it's only because more calcium goes to the bones and less becomes available in the blood as a passive process? And I'm still not clear if K2 is a good idea for people with AFib, whether it's prothrombotic or if it interferes in any way with warfarin and the newer DOAX. So stick that one part at a time. Uh, whether it's not specific to coronary plaques. So that matrix GLA protein that we talked about is what gets activated when we have enough vitamin K, and it does encourage calcium to be drawn out of the bloodstream and hopefully go into the bones, but I would say it's more of a passive process. We are certainly not actively sucking calcium out of the artery wall. We are just preventing additional deposition into the coronary plaques or any plaque, really, and helping that calcium go to bone where it belongs. Regarding the prothrombotic effects, there is very little evidence that overdosing on vitamin K2 or K1 or taking too much K in the normal average person will cause any pro clotting effects. So it's very safe, even though it's a fat-soluble vitamin. And in general, we have to be a little more careful with our fat-soluble vitamins because we don't just pee them out if we get too much, they can accumulate in the body. Vitamin K has been shown to be very, very safe, but warfarin in particular, or cumidin, is a vitamin K antagonist drug. It works by inhibiting vitamin K. There are people, this is not medical advice, there are people who will tell you that if you supplement with vitamin K, it is also possible to be on warfarin as long as both your warfarin dose and your vitamin K dose are stable and steady. That in practice almost never happens. And most people who are still on warfarin or cumidin will be told never to take vitamin K, not to eat more green leafy vegetables because everybody's worried that it will impair the function of the warfarin and people will have clots. That is up to you and your physician team. Warfarin specifically is the drug to worry about. And I would certainly not do anything with vitamin K if you are taking warfarin without a very upfront conversation with your clinician about that. The other oral anticoagulants, like Eliquis, which is um a pixaban, or revaxaban, which is Zorelto, they work differently. They do not work through a vitamin K dependent pathway. That means it is possible and safe, we think, to supplement vitamin K and still take those and have them be effective. That's why we don't have to measure the levels of those medicines anymore. You just take your pill twice a day and we get steady state levels in most people most of the time. We don't check. So in those people, vitamin K should be fine. At JR says the supplement I've been using is 100 micrograms, which is about a quarter of the study dose. Considering the trials and toleration, are higher doses appropriate for the general population? We don't know. This is a good question. And everybody asks me, well, if I'm gonna take the K2 with the D3, how much should I take? And I say, I don't know. We don't have an answer. Again, these dose response trials are not super helpful because we don't have outcomes yet. And this is the first trial that we've shown that's been isolated K2, looking at calcification to show anything at all, really. So we just don't know. It is safe at higher doses. We don't have a good way of knowing whether people are deficient in vitamin K. We can talk about that here in a minute. But I think you're safe at that 100 microgram dose. Best we can tell. Whether higher doses are appropriate or helpful, no idea. Michelle S says, I think what bothers me the most about vitamin K2 is so many doctors emphatically declare that this miracle vitamin will remove coronary calcium and put it back in your bones. How, pray tell, can a vitamin remove calcification and miraculously put calcium back into the bones? Michelle, you're so right. It doesn't, it doesn't do that at all. And I agree it would be great if we could all, I don't know, stick to the facts here. But uh, the best we can do is hopefully prevent new calcium from getting deposited in our plaque. And we don't even know if that is helpful. So stay tuned as we continue to study and get more information. All right, Tron says, What specific lab test should we have our doctor run to see if we're low on vitamin K? Which vitamin K is suggested to be taken and what else with it to absorb effectively? And there are some dietary sources like grass-fed beef, pasture-raised eggs. Uh, whole fat dairy is also a good source of vitamin K too, but isn't it more effective to take a supplement if we want vitamin K? All right, so specific lab tests. We don't have one. There is no current FDA-proof test to test for vitamin K levels. There was a whole conversation in the live chat when the video premiered about proxy measures for vitamin K status. Um, that is not prime time. Honestly, it's not something I do for my patients, so we don't know which vitamin K is suggested. Vitamin K2 is what I typically recommend for my patients. MK7, there are multiple versions of it. MK7 is the one that was used in this trial. MK4 has also been studied, and I think it is very reasonable. Some are one or the other, or a combination of both. We're kind of in a data-free zone here. I don't feel strongly about MK4 versus MK7, to be honest. One or the other is probably reasonable. Again, not much harm at higher doses. Maybe it's helpful, not sure. I think if it's helpful, we're talking about the utility of helping calcium deposit in bone, not necessarily to get it away from the arteries, but if that's a significant problem for you, for example, if you have kidney disease or diabetes, maybe, although it's been studied in those populations with not very much impact. Lastly, food sources versus supplements. Obviously, supplements are probably going to be the most efficient in terms of raising blood levels, but we never know whether what else comes with it in the food is helpful. Certainly that seems to be how nature wanted us to absorb it. But when we're thinking of the highest intake of vitamin K2, it tends to be from natto. So that's that fermented soy food that is prevalent in Japan. It also comes with natokinase, it comes with a lot of other active things. And we know that people who have high levels naturally of their vitamin K2 stores have fewer cardiac events. That was where all of this research got started and why it became such an interesting compound. But is it the vitamin K2 specifically, or is it all the stuff that comes with it? We don't know. In general, I am always going to recommend, if we can, to get whole food-based sources of our nutrients in our modern food environment, that can be a challenge. And there are sometimes other undesirable things that come with these nutrients. We just have to balance that and do the best we can. So, again, if we're taking D3, if we're increasing our own body's absorption of calcium, I am personally still recommending some K2 with that for my patients and for myself so that I put it in the bones where it belongs so that I don't get brittle bones later. But we still don't have a great basis for evidence that it's going to be helpful for cardiovascular disease like it would be if it were just naturally high. Thanks for your questions, Tron. Thank you for all the great questions. Please keep them coming until next time. Take really good care.