Try THIS instead of Nattokinase (Surgeon Explains)

The nattokinase video clearly hit a nerve. Your comments were sharp, occasionally feisty, and worth a real answer. So this is the follow-up Q&A: natto the food versus nattokinase the isolated capsule, whether CIMT is a test I actually trust, the dosing argument a lot of you raised, and the supplement many of you asked about instead — lumbrokinase.

The back half is a proper walk through the one randomized trial testing lumbrokinase for secondary stroke prevention. I go through the design, the parts that gave me pause, and the plaque and IMT findings that genuinely caught my attention. My take, for what it's worth with the evidence we have: if you're going to hang your hat on an enzyme, lumbrokinase looks like the safer bet. Watch and decide for yourself.

⏱️ CHAPTERS
0:00 Why I'm answering your nattokinase comments
0:25 Natto the food vs. nattokinase the supplement
1:54 Is nattokinase the same as vitamin K2?
2:46 Do I trust CIMT? Plaque vs. IMT, explained
3:59 The "n=1" critique, Susan, and Dr. Brewer
6:01 The dosing fight: 2,000 vs. 10,800 FU
7:58 Lumbrokinase and serrapeptase: what they actually are
10:22 The 2013 lumbrokinase stroke trial: setup
13:09 Where the trial design gives me pause
15:46 Results: the patients and the open-label problem
17:26 Baseline data and the missing standard meds
20:20 Lab results: fibrinogen, CRP, D-dimer, tPA
22:29 The interesting part: plaque and IMT changes
24:57 Stroke scores, outcomes, and the low event count
27:52 How lumbrokinase differs from nattokinase (and why it's likely safer)
30:15 Bottom line: should you take it?

📚 STUDY DISCUSSED
Cao YJ, Zhang X, Wang WH, et al. Oral fibrinogen-depleting agent lumbrokinase for secondary ischemic stroke prevention: results from a multicenter, randomized, parallel-group and controlled clinical trial. Chin Med J (Engl). 2013;126(21):4060-4065. PMID: 24229674. https://pubmed.ncbi.nlm.nih.gov/24229674/

▶️ WATCH NEXT
"I Stopped Using Nattokinase. Here's Why.":  https://youtu.be/vpenJQ3UJh0
The VitaK-CAC study: https://youtu.be/ArxAXtzsue4
Vit K Comments & Questions: https://youtu.be/uORGxMsedic

⚕️ DISCLAIMER
This channel is for education, not medical advice. I'm a board-certified vascular surgeon, but I'm not your surgeon, and nothing here replaces a conversation with your own physician. Supplements carry real risks, including bleeding. Talk to your doctor before starting, stopping, or changing anything — especially if you take blood thinners or antiplatelet medication.

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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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Transcript

SPEAKER_00 0:00

You all had a lot to say about the Nato kinase video, and I am here to address some of your comments and answer some questions. So stick around for all of your great questions and comments. If you're new here, I'm Dr. Lily Johnston. I'm a board certified vascular surgeon, but I also specialize in cardiometabolic prevention. So hopefully you will never need me as a surgeon. Zuki Design says, Dr. Johnson, what about eating natto? Will I get the same benefits? By the way, thanks to the several of you who pointed out that I did not pronounce that right in the original video, appreciate that. So I really want to highlight the distinction between functional foods like natto and natokinase, which is an isolated enzyme from the bacteria that come from the fermentation process of the natto. So foods are always preferable. And I would always encourage people to eat their functional foods that contain the vitamins, minerals, and other compounds that are beneficial to us. We don't know how much we're getting, but I think it's pretty hard to overdose on functional compounds in foods. And I do think that there is very likely some synergy, right? The natto contains K2 in addition to the enzymes and possibly other things that we don't know about. And certainly the amount of natto consumed in Japan has been associated, not necessarily causally related, but associated with reduced cardiac disease. So I think eating these foods is a great idea if that is something that suits you. The video was really specifically talking about isolated supplement in capsule form and potentially taking at very high doses that you have seen reported in my comment section. So that's really the distinction. I am great with the food. I think the supplement can be useful for some people. I am just encouraging caution. Next question is from M. Brisbane. Isn't natokinase used on vitamin K2 supplements? I wish the presenter had clarified if it's only natokinase to avoid a form of K2 or if K2 is to be avoided. They are actually two separate things. And this goes back to the last question about natto and the foods or the, excuse me, the compounds that we see within it. So K2 is a separate molecule from natokinase, which is an enzyme and works on our clotting system predominantly. So they are totally separate. They are both found in natto, but um we talk about them separately when we're thinking about supplements. So we had the vitamin K videos, we'll link those for you in the description, and then this one, but they are separate things and keep that in mind going forward, even though you might find them together in a functional food like natto. All right, next question is from Chessmaster. She says she does not trust CIMT measurements, but then she stops the treatment as the result of a CIMT. Shouldn't she have used a CT angiogram before and after? So there are actually a couple of points here that I want to address. The first is there are many components to the CIMT. What I was referencing uh is the plaque measurement specifically. CIMT is a great test when it is done well. There are some ways that it can be made more precise and reliable. We don't know whether the imaging lab for that study followed those procedures and protocols. The plaque measurement is different than the IMT measurement. They are all bundled together under the umbrella term, C IMT. But the assessment of plaque is one thing. The assessment of the intimal medial thickness, the IMT, is a separate piece. IMT tends to be much more precise and reliable and repeatable than plaque measurements, which are more irregular. So it's the plaque piece of it that is a little bit suspect for me when we're talking about the measurements that they're making in the artery wall. But overall, I really like C IMT as a test. The next piece that I want to address is can this came up in several other comments that I didn't uh pull out here. You know, I got a lot of flack for doing this all based on an N equals one. And Susan, the example from the video, is the most poignant one that I have. She has the most reliable data. Um, spoiler, she's a family member, so I am very certain that she was taking this reliably on an empty stomach and uh that her diet was dialed in and all of these other things. I had several other patients who have been on nato kinase. I have not seen that by itself do much, but Susan was just the most poignant example, and she was the one who caused me to kind of go back and look at that study a second time. So while, yes, I agree with you, the uh plural of anecdotes is not data, and making decisions based on just one patient in my practice is not something that anybody would take seriously. I totally appreciate that. Um, it's been my experience with many patients who have been on it, that it's not been as effective as we hoped it would be in isolation. And ultimately, I have concerns about the safety. I have concerns about the um reproducibility of the or the consistency of supplement quality. And for those reasons, I have gone to doing other things to help manage soft plaque formation and progression in my patients. That's another video for another day. Many of you will continue to use natokinase. I get it. I'm not objecting to it. I am simply pointing out that for me in my practice, I think that there are some real risks, and I have not seen as much benefit as I had hoped. And several of you mentioned Dr. Brewer. Uh, Dr. Brewer is a friend and we talk a lot. He does many things in his practice besides just give natokinase out. So I think it's important to take the big picture here. But um, overall, CIMT is a good test in the umbrella of CIMT, plaque measurement, less reliable. IMT, pretty reliable as long as you have a good protocol. Okay, we had a couple of questions on dosing. Stephen Fraser says that's strange. 2,000 FU shouldn't it be 12,000? 2,000 is too low, and then deep warm voice. Saying that 2000 FU of nato kinase doesn't work, it's like saying aspirin doesn't work for a headache. Uh basically a long comment to point out that I didn't take into consideration the study using 10,800. That was actually the study we were looking at in the video. So I didn't ignore it, but it's the only study that uses high dose. Okay. Even the 2024 paper that combined nato kinese and red yeast rice, we didn't talk about that in the actual video itself because they didn't have any imaging or outcomes measurements. It was mostly a lipid trial. But some of you pointed out that I should have included that. Uh, nevertheless, that was 3,600 per day. The Chen paper from 2022, we did talk about at length in the original video. They picked 10,800, but I don't know where the number came from. And we don't have any dose escalation trials specifically. They had some patients on 10,800, they had other patients on 3600, a very, very small portion of that study group. We don't know how they picked, we don't know how they were assigned, and it is the only trial that has looked at that higher dose. Um, there was another study, I think, that has used 8,000 in the past, but it was a blood pressure study, if I recall correctly. Don't nail me down to that one. Um, but in general, like the high dosing protocols are all derived from this one paper. And I get it, I it's a reasonable thing to think about. I just have never seen it replicated and I don't know. Just show me the data. I mean, that's all I'll say about it. Um, I appreciate the possibility that higher doses might be more effective. They probably also come with higher bleeding risk. So again, you do you. I'm not saying don't do it. I'm just saying for me personally, it's not something I'm gonna recommend in my practice for most patients going forward if they're willing to consider other alternatives. Okay, lastly, many of you mentioned lumbrokinase and also cereptase. So John Simpson, look into lumbrokinase. Val Peters says, what do you take instead? Kay Farley, I would be interested in any work you have done on lumbrokinase and uh MISOft Tau. Do you know anything about lumbrokyase? So there are a couple of other enzymes that are all talked about in the same family. Natokinase is the first one, obviously, that we were talking about in the last video. Lumbrokinase and serapeptase are the other two that are frequently brought up here. And I was not as familiar with them. We're gonna go through them in a little more detail. Lumbrokinase is actually a family. It sounds like it's one enzyme. It's actually a family of enzymes that are derived from earthworms. They have been used in uh Chinese medicine for thousands of years. And cerepeptase is a separate group of compounds that has been studied for mostly swelling, edema, and postoperative inflammation. My deep uh mini-dive into serapeptase did not really suggest much in the way of treatment for chronic inflammation. It was really used in a postoperative setting to manage swelling. So I'm not really going to talk about serapeptase because I didn't find any evidence, at least at a cursory level, that it was going to show any effect on long-term chronic inflammation, which is what we worry about for heart disease, or that it had any impact on other markers or imaging findings in the artery wall. But lumbrokinase is a very interesting compound. So I think we should take a deep dive into the paper where they actually looked at using lumbrokinase for secondary prevention. Most of the studies on lumbrokinase have been treatment for stroke. And that's in an acute setting, right? Patients come in, they've had a stroke, and especially in China, they have been given lymbrokinase as a treatment modality. But that's a different question than what we're really focusing on here, which is if I take it chronically over the long haul, will it do anything to help reduce my plaque or reduce my chances of having a heart attack or stroke? There is only one paper that I found that speaks to it, and all of the usual caveats about changing your whole practice based on one paper still apply. However, it's an interesting study. Let's get into it. So this trial was published in 2013 and it's titled Oral Fibrinogen Depleting Agent Lumbrokinase for secondary ischemic stroke prevention. Results from a multi-center randomized parallel group and controlled clinical trial. So they're, I'm gonna skip through the abstract here and go through the introduction because it helps us understand a little bit about what they're doing and why they chose lumbokinase. Elevated fibrinogen level is a known risk factor for stroke. Fibrinogen is one of the components of our clotting cascade. So it allows our blood to clot and then form that sticky um blockage. And the presence of more fibrinogen makes our blood a little thicker, a little stickier. And elevated fibrinogen level measured in patients within six hours of stroke onset has been associated with poor functional outcome, meaning less likely to recover movement in the arms or legs or in the face after a stroke. And this is why lumbrokinase has been used for acute stroke treatment. They say lumbrokinase is an effective enzyme extracted by a method modified from a traditional Chinese herb and has been used again for the treatment of acute phase ischemic stroke. But our study was intended to observe the efficacy one year oral lymbrokinase for effectiveness on secondary stroke prevention. So that means for patients who have already had a stroke, does giving lumbrokinase prevent a secondary event? Because patients who've already had one are at risk for more strokes. It's important to point out that this was ischemic stroke, meaning lack of blood flow, not hemorrhagic or bleeding-related stroke. So the lumbrokinase was provided by the Chinese Academy of Sciences for the purposes of the trial, and they had patients diagnosed with ischemic stroke or transient ischemic attack, mini strokes or TIAs, and between 40 and 80 years of age. Strokes were confirmed by CT or MRI, and they had to have a fibrinogen level higher than two grams per liter. They also had some criteria for the mini strokes, which are usually not seen on imaging. And it was a multi-center parallel group. So they had multiple different hospitals. They were running both a treatment group and a placebo group at the same time. They actually used a two-to-one randomization, meaning twice as many patients got the treatment as got the placebo group. They talked to us about the randomization. Patients in the treatment group were given oral enteric coated lumbrokinase, 600,000 units at a time, three times a day, 30 minutes before meals, for one year. Control group was given placebo for a year. Both groups receive standard stroke treatment otherwise. This is a bit of a sticking point for me. They don't say what that is. We're gonna go down to the tables here in a little bit, and I'm gonna show you that I'm not sure that their standard treatment for stroke is what our in the Western worlds would consider standard treatment for stroke. This paper is also a little bit older, so perhaps things have changed, but um I'm concerned that the effect we're seeing here might not be seen if patients actually had after strokes. So they had two follow-up visits and they measured NIH stroke scale. They did use carotid ultrasound and measured some lab tests, including blood and plasma viscosity and some coagulation markers. Their endpoints, what they were measuring in the end, all cause mortality, recurrent stroke or mini stroke, hemorrhagic stroke. They also measured heart attack and chest pain or angina and other non-cerebral ischemia or hemorrhage. So that would be anything other than the brain, legs, arms, intestines, uh, anything like that. Safety endpoints included hemorrhage, bleeding, mortality, and other lab measurements. They had a safety committee that's excellent. They go through some details of their ultrasound examination, which I really appreciate because we talked about how a CIMT protocol really determines how reliable the test is or is not. So they go through a bunch of different places where they measured the IMT, which wall they measured, left, right, um, multiple different views. Um I think that's overall pretty good. I'm surprised that they don't they they continue in the outcomes to talk about left versus right. Um I sort of wish they had just merged that all or averaged that all into one measurement, but um we can talk about that when we go through the results. And then they also have um their definition of plaque. So anything greater than 1.2 millimeters in terms of intimal medial thickness is a plaque. That's great to have that definition. And then they also look at the types of plaques. So hypoechoic, and uh, those are the sort of black-looking plaques on ultrasound that are lipid-rich. Hyperechoic means that bounces a lot of those sound waves back. That's what calcium does. It's bright white on ultrasound, and then mixed, which is obviously a combination of the two. Plaque volume is calculated as average plaque diameter times width times the IMT. It's fine. Um, it's not the most precise way to measure plaque volume, but it's pretty common, and I think that's fine. Um, here are their statistics. Okay, so results: 310 patients, 192 in the treatment group, 118 in the control group. What I want to point out about this that I um should have mentioned in the in the methods, this is not a blinded trial. This is an open label trial, which means even though there's a placebo group, which is great, everybody knows, both the study committee or the researchers and the patients know which group they're in. They say when they looked at the ultrasound that the ultrasonographers, the imaging techs, were not aware of treatment assignment or any clinical information about the patient, but certainly the patients know and the doctors know, the researchers know. So, and I'm not sure why they did it that way. Um, if you're gonna take the trouble of running a placebo-controlled trial, why wouldn't you blind it? I don't know the answer to that, but it's a one other thing that concerns me a little bit about the study. Uh, nevertheless, all right, here we have our trial. We're gonna look at figure one here. It's very hard to read. I'm sorry about that. Um, but I'll go through this with you. 192 patients were assigned to lumbrokinase, and 169 received the full course. 23 did not, and of those, three were lost to follow-up, 10 missing doses, no mortalities, five refused therapy, and five had a medical problem. Uh 118 were in the placebo. Of those, 105 received the full course, 13 did not, two were lost to follow up, five had missing doses, no mortalities, four refused therapy, and two had a medical problem. I don't know what the medical problems were. That would be helpful. Um table one is baseline characteristics of the study group. Again, this is gonna be very small for you on screen. I'm sorry about that, but I'm gonna um just tell you that at baseline, again, a randomized trial, the groups should be equivalent, and they are the um proportion about 60 to 75% male average age is 66 to 67. Um, blood pressure here is not well controlled, but it's right, they've already had a stroke and they may have been allowing blood pressure to run higher to protect the brain. That's something called permissive hypertension. They don't state whether that was done explicitly or not, but that's one possibility. The other possibility is that these patients had strokes because they had poorly controlled hypertension and that's not being well managed. Unclear to me. But average systolic blood pressure is in the high 140s, diastolic is in the mid to high 80s. Concominant medications. They're gonna talk to us about this at baseline and then one year usage. And again, I'm not sure. I think that's the one year of follow-up, but they shouldn't have put that in the same table and they did. I don't know why. Baseline usage of antiplatelet drugs is 80 to 83 percent. Good, right? Most patients who've had an ischemic stroke should be on an antiplatelet medication as standard therapy following the stroke, as long as it uh isn't a concern for hemorrhagic transformation or bleeding events after the stroke. Um, 80 to 83 percent is not bad. It might be a little low actually, but okay, that makes sense to me. Baseline use of statin drugs, uh 30 to 33 percent. Baseline use of antihypertensive drugs, also 30 to 31 percent, which is again a little low when I see those blood pressures there, but um let's see what happens. So at a year, one year use of antiplatelet drugs is dropped to 52 to 54 percent in both groups. I don't know why that would be the case. That certainly does not comport with what I understand to be standard post-schemic stroke therapy. That should stay 80% or higher, unless there were bleeding complications, which we'll go through this, there were not. So I don't know why platelet antiplatelet use dropped so dramatically, but that does not account for standard stroke therapy. Uh, one-year use of statins also dropped 20 to 21%. Again, say what you want about statins. They are part of the guidelines for post-stroke therapy if you have had an ischemic stroke. Um, if you were gonna run a trial on standard therapies and say that people were getting standard therapies, this is a pretty low percentage of that population. And again, the one-year use of antihypertensive drugs is uh around, it's the state most stable of any of them. It's again around 30%. Um they go through past history here and they do some weird combination thing. I'm not gonna get into that. And then fibrinogen changes. So they have their treatment group and the control group, and they're gonna go through a bunch of different lab measurements in this next table. They don't actually calculate in or show us in this table which of these are significant. So we're gonna have to take their word for it in the results section, but I'll go through that with you. Uh, fibrinogen did drop in the treatment group, but not the control group. That is totally appropriate for what we would expect from this molecule whose entire job is to degrade fibrin products. That is how lumbrokinase works. Um, in contradistinction to nato kinase, it does not activate plasminogen. That is actually said somewhere here in this trial, but that's uh to the best of my knowledge and what I have read and researched, lumbrokinase breaks down fibrin, again, part of the clotting cascade. That's good, that's great. Um, but unlike natokinase, it does not activate plasminogen to plasmin and create a fibrinolysis uh that way. And so I think it's a bit safer, is my take-home message about lumbokinase based on how I believe that it works on the research that I've seen. So um, but it does reduce fibrinogen levels. Good, that's appropriate. The um high sensitivity C reactive or regular C-reactive protein came down in both groups, and uh they did say that was statistically significant from treatment to they only said it was significant within the treatment group. They don't compare the treatment group to the control group. Z dimers also reduced TPA activity was elevated, which actually goes against the statement I just made that it doesn't deal with plasminogen. The fact that TPA went up is actually suggesting. That it might have some impact on the plasminogen pathway, but it's not supposed to, based on the research I did. And fortunately, we don't see any big changes in other coagulation markers like PT or PTTINR. Those are all stable. You don't have to know what those translate to or what those acronyms are. Just recognize that in general clotting cascade markers were stable that way, the one other than the fibrinogen and the TPA that we talked about. All right, this is where it gets interesting. Plaque number and echo intensity changes. So what are we seeing in the arteries, right? The labs are nice, but does it actually move the needle for plaque? Baseline plaque numbers in both treatment and placebo group were about the same, no significant difference. After one year of therapy, there was a significant reduction of the plaque number treatment group, but an elevation in the control group. There were mainly hyperechoic plaques in both groups. That means calcified hard stable plaque. In the treatment group, baseline vulnerable plaque, which non-calcified rates of hypochoic and mixed were 28% on the left, 17.5% on the right. At one year, rates were reduced to 7.9% and 9.5%, respectively. Again, this like left-right thing, it's weird. I wish they had just combined them, but fine. And they didn't actually give us the placebo group for that. Interesting. Okay. IMT and plaque volume changes in the treatment group. Bilateral carotid IMT was significantly reduced after one year. Um 1.26 down to 1.09. Again, that's not an enormous change, but it's within the realm of what I would consider detectable and reliable by C IMT measurements through a good protocol. Right side, again, similar magnitude of change, 1.25 down to 1.06. And in the control group, IMT thickness increased after one year. So right side was 1.4 to 1.59, or basically 1.6. And on the left side, 1.38 to 1.62. So again, it's one thing to see a decrease, but actually to see a divergence, right? That the treatment group goes down, placebo group goes up is interesting, right? I'm not gonna say uh based on one study that this is you know practice changing. But again, just like the original 2022 natokinase trial, it's curiosity-provoking, it's hypothesis generating. And again, because I think that the safety profile of lumbokinase is probably a little bit better than natokinase, I am cautiously optimistic that if you were gonna switch from natokinase to something else, lumbrokinase might be a good choice for you. All right, linear regression analysis of the crowded plaque volume. I thought this was a weird component of the study. I was not sure why they included plaque parameters within the regression. I thought that was kind of strange. The other thing they tested were the NIH stroke scores. Um this is a measure of how many areas of dysfunction, right? So if your arm doesn't work and your leg doesn't work, then you get multiple points. But if only one works, then you get less points. So NIH stroke scale is a composite measure of how severe the symptoms are from the stroke. So lower is better. And they show here that everybody had an NIH stroke score that was elevated at baseline, 5.7 in treatment, 6.2 in control. And they all went down. Um, but the NIH stroke score at one year was lower in the treatment group than in the control group, 2.35 versus 3.62. Whether this is clinically meaningful or not is a little hard to say. Just not clear to me whether patients would notice the difference, right, between 2.6 and 3.2, but nevertheless, it's an interesting finding to report. And lastly, they actually do have outcomes, which is another cool thing. I have to say, the adjudication of outcomes in a trial that's not blinded is a little bit dicey, right? Because everybody knows who's in which group. However, they do report fewer total events in the treatment group versus the placebo group. And um, the only um cerebral hemorrhage was in the control group. So there was no brain bleeding in treatment. There was a GI bleed in the treatment group, but not in the control group. But overall, I would say um there was a pretty neutral safety signal over both the treatment and the placebo groups. So uh again, you can kind of look through here and see which types of events, um ischemic stroke, hemorrhagic stroke, TIAs, angina, um, they didn't really see any difference in heart attacks. The other thing that I would point out is the number of events is low, right? So if I go back to this table here, we have four total events in the treatment group and eight total events in the control group. If you made a very small adjustment, right, one or two events plus or minus in either group, that statistical significance could go away entirely. So I wouldn't put a huge amount of stock in this event result. I think it's interesting again, and it and it I should generate more studies and more hypothesis testing, but I would say this is a very um sensitive. How do I put this? This is like a small change would really change the outcome of the of the testing here. And so, you know, again, two more events would be six and eight, and maybe that's not even significant. So just be aware that non-blinded and um overall low event rate makes it hard to feel really strong about these conclusions here. So, overall, what do we know? Um, they're gonna go through this discussion. Lumbrokinase is extracted from, again, this is an earthworm thing, it's a family of enzymes, it's heat stable, optimal, broad optimal pH range. And they say here it acts as a plasminogen activator. This is disputed, right? Like when I look into it in other papers and other resources, it actually shouldn't activate plasminogen, it should dissolve fibrin by converting or by uh direct proteolysis. So it should impact the fibrin, but not necessarily through this plasminogen to plasmin factor. If you are a hematologist and you actually know more about lumbarkinase and its exact mechanisms, please hit me up in the comments and uh inform us all because I do think this is relevant to how I feel about its safety profile. But they say it has a selective affinity for affinity for fibrinogen and directly hydrolyzes. So, again, directly hydrolyzes fibrinogen to soluble degradation products. This is where I think the difference is here, and that's important. It also can reduce platelet aggregation rate and lower plasma viscosity, right? The thickness of our blood overall, and it's not like sticky clotting. It's actually truly the um the thickness of the fluid, right? So that's like molasses versus water, right? That's the thickness of the fluid and how it flows. Um, and so they're gonna go through some more of these enzymes here. Um, PAI did not change, plasminogen activator inhibitor one did not change. That's again another distinction because nato kinase absolutely affects PAI one. We talked about that in the original video, and maybe one more pathway by which it might enhance the bleeding risk. Okay. So um plasma viscosity improved, and they hope that this is partly accounting for how it is working to reduce these soft vulnerable plaques. Uh, they talked through here a little bit about D-dimer. Fibrinogen is an independent risk factor for atherosclerosis. Um, so all of this to say after one year of lumbarkinase therapy, incidence of vascular endpoints was reduced by 4.7%. Um, more interesting to me, the IMT decreased, the internal medial thickness, and we definitely showed a reduction in fibrinogen. So, do you take this or not? It's gonna really depend on where you think your plaque is coming from, what your risk tolerance is. Again, I've been looking at different products that are available. They should be enteric coated, meaning they um will make it through your stomach without getting the enzymes digested. Uh, probably should be taken on an empty stomach if you're gonna take them. And I don't have a strong body of evidence that suggests that this is gonna be a miracle cure for us. But if you want to put hang your hat on something that is not a pharmaceutical, I would say probably, in my opinion, this would be a better choice than nato kinase based on my own clinical experience, which is admittedly limited. But that's where I end up on this. Let me know what you guys think in the comments. I hope this was helpful. If you guys have more questions about lumbrokinase, please drop them down below. We will get to as many of them as we can. Until next time, take really good care.