Transcription
So good morning, good evening, depending on where you are in the world. Good L, maybe sometimes good late night. Today, we're going to talk about nyas. It's a natural blood thinner. We're also going to talk about sarapeptase, another natural blood thinner. In fact, both of them are enzymes. Both of them are made by bacteria. Both of them are pretty benign. Excuse me, I'm having a technical challenge here. Um, both of them are relatively harmless, and both of them have some challenges in terms of the evidence that supports them.
I'm also going to talk about why your doctor doesn't know this. Uh, no, I didn't learn it in medical school. No, I didn't learn it in a preventive medicine residency program. And in fact, I failed at a big opportunity to introduce nutrition training into medical training, but we'll get to that in a few minutes.
Let's go back to ninas. Ninas is an enzyme. It's, um, found in, well, like most enzymes, it's a protein. It's found in, uh, a dish made in Japan. It's an awful dish. It tastes ter- terrible. I worked for Toyota for a decade and traveled to Japan a few times. The breakfast buffets would have this dish that you saw on the, um, on the advertisement, the picture for the show. It tastes like rotten beans, and there's a good reason for it. It is rotten beans. It's fermented soybeans. Um, one of the viewers asked about, well, I'd like to take something similar, but I don't like soy or can't take soy products. That's where Sarah pepase is going to come in, and we'll talk about that in a minute. But I tried tasting that when I went back to natak in Japan, and natto. I tried tasting it, and again, the best you could say for it is it's an acquired taste. Um, it's made by a bacteria, uh, presumably one of the bacteria that's involved in rotting or fermenting those soybeans. The, your doctor has heard of that bacterium. It's called Bacillus subtilis. Uh, even if he or she never heard of ninas, it's a protease, meaning, um, it breaks apart proteins. The protein that it breaks apart is fibrin, and fibrin is a part of clots. It's also a part of, uh, cardiovascular plaque. So the mechanism, the theory is that it breaks apart plaques and even clots. When you look at side effects or bad things, it'll say, don't take it if you have bleeding diet, uh, bleeding problems. I think that's reasonable.
Um, so when would I recommend it? Uh, you know, I used to say I'm not sure I would ever recommend it because if you really needed it, you couldn't depend on it enough. But I've actually recently changed my perspective on it. You know, there are, we've changed our recommendations for baby aspirin. Naty and cepas are not really significant, uh, reliable, um, substitutions for baby aspirin, except when you, uh, have the situation that maybe you're an 80-year-old and you have cardiovascular plaque, you may have some problems with, uh, esophageal, uh, inflammation, potential esophageal bleeding, potential, uh, stroke type of bleeding, and not want to take baby aspirin. Maybe that's a good place to think about ninas or serapeptase.
Uh, back to sarap Pepes. A couple of times over the past few years, people have asked me on, on the YouTube live shows about sarap Pepes or Nyes. And yeah, I'll give myself up. I've often confused the two. And you could say, well, and, and I'll also give myself up on, yeah, I'm a doctor. Doctors tend to not know that much about nutrition. But there's a little bit more to it than that. Both serapeptase and ninas are enzymes, therefore they're both proteins. They're both made by bacteria. And you may say, well, hold up, Brewer, uh, sarapeptase actually comes from saliva of a silkworm. It's what the silkworm uses to cut itself out of its silky cocoon. Well, we're both right. Uh, it is saliva from a silkworm, but it is a bacteria in the saliva of the silkworm, and that bacteria is called Serratia marcescens. You know, so again, there's some commonalities here. Nto kyes is named after nto. The first two syllables are the same. The source, same thing with sarapeptase. It's name, the first two syllables come from the source as well, Serratia marcescens. And yes, your doctors heard of Serratia marcescens in his or her medical training, even if he or she never heard of, uh, serapeptase.
So back to serapeptase. Back to some of the similarities with ninas. Cepas is also an enzyme, also a protease. In other words, it also breaks down protein. And it also breaks the protein, it also breaks down is fibrin, again, that same component of, um, clots and cardiovascular plaques. So therefore, maybe a blood thinner, maybe a natural source. And yes, again, I didn't learn any about any of that when I was in medical school. In fact, I got a little short story to tell about, um, me and medical training.
So, um, I sort of tripped into medical school. I didn't grow up thinking I wanted to be a doctor. I had, um, I was, uh, in high school and had some, uh, thoughts that I wanted to help humanity because I'd sort of, uh, spoiled myself in terms of my own life and was getting tired of that. So I had this opportunity to get into medical school out of college. I, I tried it, got in. And when I got to, uh, I had to take two years of college, uh, got admitted out of high school. And when I got in, I naively thought that doctors were all do in training were all going to be about helping people. No, they were about learning a career, a job, and a licensed career and job. And so when you begin to look at medical training, it's really all about learning how to do the things that doctors get licensed for: medications and, uh, surgical procedures. I did love surgery. I was good with my hands, um, and so I thought maybe surgery is going to help. But it became very, very clear in med school that people don't really need prescription medications. They don't need surgical procedures to keep them from, uh, injuring their health, to, to protect the health of individuals. You learn it even in your first year of medical school, 80% of disease is chronic disease. 80% of what damages, what kills and damages us, disables us, is chronic disease. And chronic disease, it's really clear, you cannot outrun. You've heard it say it multiple times, you cannot outprescribe a lifestyle. You cannot out-stent a lifestyle. You cannot do bypasses, surgical bypasses, and bypass out bypass a lifestyle. And in terms of lifestyle, you cannot outrun a diet. You cannot outsleep it. You cannot out-supplement it. So it's all about lifestyle. It's all about diet. Again, you would think that doctors would learn about nutrition. And again, that's based on the assumption that doctors are and medical training is all about, um, protecting health. It's more about teaching careers and jobs and licensed professionals.
So I got very frustrated with that, ended up not going into a surgical specialty or, uh, or internal medicine for the reasons I just described. I got out, went to Charity Hospital, uh, for a year. And at that point in time, you could go straight into the ER. And I decided to just, uh, take some time, slow down, think about what I wanted to do. And went into the ER. I still got frustrated because these 60-year-olds were coming in with heart attacks, even 50-year-olds. I remember a 50-year-old man coming in with a heart attack. And yes, there, there were some challenges with the cholesterol metabolism that he'd inherited, but he, like so many others, could have, would have, should have prevented that heart attack.
So I had, I had a, um, a moment of truth. And the moment of truth was, well, you know what? If this is about my career, my job, uh, my licensed profession, then no, I'm going to go back and get training in surgery. But if this is about helping people, I'm going to go into prevention. And going into prevention was just such a hazard to your career. It, it made you, it made me risk three things that I'd always said that I did not want to be. The first was a teacher. And teachers, forgive me out there, but I grew up with the Charlie Brown view of a teacher, and that was my view of teachers, and I did not want to be one. I also didn't want to be, uh, a bean counter. And sure enough, when you go into prevention, you go into epidemiology and biostatistics, you want to know what actually causes disease in populations, and that's very much associated with, uh, numbers and biostatistics. So I didn't want to become a bean counter either. And finally, and worst of all, you go into prevention. At that point in time, you're very likely to go into being a government public health bureaucrat. Maybe the worst thing in the world. So I said, you know what? Despite all of that, this is about patients. It's not about my career. I'm going to do it.
I was very fortunate. I was able to get into Johns Hopkins in prevention, arguably the best place in the world for teaching doctors preventive medicine. And guess what? No, after two more years of training there, I really didn't get significant training and nutrition there either. And yeah, that's frustrating. Um, we sort of learned it. We knew it was important. We knew that, like I said before, what we'd learned in medical school, that 80% of death and disability was caused by chronic disease, which was in turn caused by lifestyle. But we just felt like everybody knew that. You just needed to tell them, and maybe things would change. Obviously not logically very smart, but that's what we thought back in those days, the days when a calorie was just a calorie.
So here's where I get into my own, may, aopa, my own, um, my own personal could have, would have, should have. Uh, I did well. I, I loved, uh, biostatistics. It really became more about probability than than bean counting. And, uh, as you see now, I am a teacher. Um, and public health policy was frustrating and dirty and ugly, but it really was a lot of what needed to happen in terms of protecting health. So I did well, and I was actually asked to run the program there. Here's where I screwed up, um, and I didn't even know it until 30 years later. I didn't add nutritional training to the preventive Medicine Residency program at Johns Hopkins either. I totally failed at that. And it wasn't until 30 years later that I realized it. To, to my own defense, it was a very, very different time. Um, like I said, at that time, a calorie was just a calorie. You put food in a bomb calorimeter, and whatever it burned, the, the amount of heat that it created, that was the calories. We didn't realize that we were feeding a 100 trillion other organisms in our gut. Uh, we didn't realize that for every 150 calories you ate of of almonds, that 50 of those calories are actually going to support that gut biome. I'm not you. We had heard of a fellow named Atkins, but that was really a fringe thing. That whole thing was fringe. We all knew at that time that it was, it was fat, low-fat diet. And again, those were not innocent days. Those were naive and arrogant days. And you know, if you want to say, well, you've got delusions of grandeur, maybe that's true. Maybe, uh, maybe I'm just an old man complaining. But here's the thing, please don't expect your doctor to understand, uh, nutrition. He or she didn't get it in training. Uh, it's not likely to happen anytime soon. Uh, to my own defense, when I was at the program at Hopkins, we had more immediate issues. We had academic, uh, credibility issues, we had financial issues, and I worked hard and did save the program from that. So I was very proud of what I accomplished, but we didn't focus on nutrition, even with the knowledge that nutrition is what drives health. So enough of an old man ranting. Jesus is going to talk today about some research that he just found about natoc kyes. Hey, seus.
So it's, it's awesome to, uh, to be here today. Uh, thank you. Thank you, Dr. Brewer. It's a really emotional and thoughtful situation because it's hard. It's hard to find a doctor who will say, you know what, I screw up. I, I, I made a mistake. I thought I was doing the right thing. And in perspective on when you see back, it's easier to find, uh, what you could have done. But it's never too late to change. I, I will say, at least on, on, on this specific aspect, then we are, we're doing something different out here. I'm going to show you something about Nato. Let me just try to show you some of the slides real quick. This is a topic that we get a lot, and you, you see those comments about, hey, what about Nato? What about Nato? You talk a lot about reversing or stabilizing, uh, cardiovascular plaque, and you don't say anything about Nato. Well, we have something about that today. And, uh, as you will see on the, on the recent topics, uh, a lot of the topics were are about plaque. So we had, uh, Dr. Mario Katz, we got Dr. Gil Carbal talking about K2, talking about insulin resistance. We, the last week, we talked about, uh, the personal fat threshold and why lean or, or apparently lean people also can develop diabetes and insulin resistance, even if they're not fat on the outside.
And let's go to to Nato. So as Dr. Bro already mentioned, uh, Nyes is an enzyme that comes from Japanese food called Nato. It is made from boiled soybeans that are fermented, uh, with some type of bacteria. So, um, it, you need to develop the special taste for that if you want to take them that way. Uh, this, this is a really interesting article from Frontiers of Medicine, uh, from, uh, last year. And the interesting thing about this is it's not such a small study that you will like the ones you will find when you're talked about supplements. A lot of the studies or research on supplements are made on maybe 12 people, 20 people, 50 if you have luck, if you're lucky. Uh, this one involved about a thousand participants. So really interesting findings on this one. We're trying to to summarize this article for you, and you can, you can just Google the title of the article. I'm going to show it for a moment right here. If you want to pause the video later, if you want to look for it yourself. And we're gonna, a small sideline comment, we're going to have a space to talk about how to find research and evaluate if research is enough. Uh, anyway, this specific article, uh, the researchers included about a thousand participants with high cholesterol, triglycerides, and evaluated the effect of, uh, almost 11,000 fibrin units of N. As Dr. Brewer mentioned, fibrin, uh, it's involved on the coagulation portion of it, and that's one of the aspects where this enzyme, uh, works, and it decreases the, the clotting that you will get on your, on, on your blood. So not such just short follow-up. They, they back actually followed this group of people for a year. So some, some of them received 180 micrograms of K2 and 100 milligrams of aspirin as well. And they compared how did Nat alone did compared to when it was combined with K2 and aspirin. That unfortunately, I did not see them having a group of K2 and aspirin alone. Um, well, however, there, there's a lot of conversation also on, well, I'm taking aspirin, should I take Nat or not? Is this, is it risky or not for me? And they just, they did not just follow up on cholesterol lipid panel. They also did a CIMT, which is one of the, the things that I caught my eye when I saw this article.
So let's, let's go real quick to the results. So nines did reduce triglyceride, total cholesterol, and LDL cholesterol. It also increased HDL for about 15%. And this is the, this is the part of, well, you might be doing some clickbait. Are you talking about shrinking or reversing plaque? Well, this is what they found when they did this, the, uh, CIMTs from 1.33, which, uh, some research, uh, consider that significant plaque or just something that when you get a CT, if you have, if you have a plaque of 1.3 millimeters, that's considered plaque that needs to be evaluated. So some of the folks went from about around an average of 1.33, uh, down to 1 millimeter, decreasing the plaque size for about 36%. The authors on the abstract that they say, oh, the effects of Nato were greatly increased or were synergistic. They had a similar component or saying another way, Nat plus K2 plus aspirin had better effects. But I saw the tables on that, and I don't think the, the difference was that big. But yes, granted, if you combine Nato with K2 with Aspirin, the effects on the, on the CIMT or on the intima media K, thickness, uh, they were a little bit, uh, more important or more, um, identifiable. So more effects with Nato when combined with K2 and aspirin. I will not say it was that big of a difference, but it was. And I think the, the, the main concept or message from this article also was Nato alone can do that.
So how does Nato do that? That's the question. And it seems that there, there are two different mechanisms of, two ways that it can do this. Uh, maybe three even. Three. So one of those is decreasing the clotting expectations and the probability of developing clots. So even, even if your plaque, if you have, especially you have soft plaque, even if it is not ruptured, you will have some platelets and some fibrin going around. It also impacts the lipid, lipid levels. So, uh, we don't, we're not, we don't know for sure if Nato was able to decrease the amount of, uh, LDL and other lipid proteins around the plaque that just did not get caught within the intima layer, and we did not have inflammation markers. But when you take a look at the mechanisms of K2 for plaque, which is basically decreasing insulin resistance, uh, I suspect that it could, it could be a good case to be made of Nato having an impact of insulin resistance as well. We don't have the data of the research to, uh, say that yet, unfortunately. But the impact is in there, at least on one article. Uh, what is one of the downsides of this? Um, is it seemed like in order to get that effect, you will have to consume about 11,000 units of Nato. And if you look at the pills, the supplements, I believe the, the highest amount that I have seen is about 2,000 per pill. So that means five capsules a day. So to me, it sounds, it looks like a little bit excessive. Um, but again, after one year, there were not significant side effects. I was a little bit curious about to see if Nato will increase the amount of bleeding when combining that with Aspirin, but it did. It did not seem like that. However, there is a disclaimer on the article about, well, if you're taking Aspirin, just be careful about that. Of course, some people will have an increased risk of bleeding if they combine Aspirin with Nat or just with Aspirin alone. So if you have risk of bleeding with Aspirin alone, and then you put that on it, theoretically, you will have an increased risk of bleeding as well. So be careful about that. But at least after one year, it, it appears like that. That, uh, I'm seeing, I'm seeing a comment right here. You should not use the term Nat when referring to N K. There are two different things. Yeah, I'll take that. Yeah. Um, we, and we just say that at the beginning, right? The natto is more like the, the, the food, and N kinase is the enzyme. I'm just trying to make it shorter, but, uh, it's basically the same substance. If you look for Nato supplements, that would be N supplements, not Naro alone. So, I, I, I'll agree with that. Um, and how do you say that, Dr. Brewer? Potato, potata. So we're talking about the same substance after all. But yes, basically the whole point here, and I know this might be frustrating for some viewers, it's, it's like whenever we talked about supplements, it's like, give me a clear stance. Should I take it or should I not? Or should I not take it? And we are, we're almost always saying, it depends. It depends of what you want to achieve. It depends of your own conditions. It depends of your own risk in this, in this case of bleeding. And if you want to have a, I, I think one way to look for the advantages of a supplement is when you have a way to measure it. And in this case, especially for nines, uh, if you have, if you have a CIMT and then you try nines, and then you repeat the CIMT after one year, that would be a good idea to take a look at it. Just remember that any, any nutritional research, we have limitations in regards to what else are you eating, what other lifestyle components you're making, and how do you take in count what is doing the most, taking the most credit for the benefits that you're seeing, if it is the supplement alone or all the other lifestyle components that you're making. So those are, those are the things that I'll, I'll, I'll consider whenever you're talking about any supplement, and I'll include nines on, on that.
Dr. bre, do you want to translate my whole run? I, I kind of tried to squeeze it in about 8 minutes, but maybe less. Um, any other comments of nines? No, I'm glad you, uh, acknowledged Long Tong Tall Sally's comment that natto is not the same thing as NATO kyes. And you also did bring up one of the major concerns that I have, that, and that is that natto also has vitamin K2 in it. And when you start looking and seeing that, you've got two things in there. Another vitamin K2, uh, has also shown some positive impact in terms of, uh, cardiovascular disease, which is it. And so I think you're being very, very, um, appropriate in terms of that those responses. That's why, you know, I hate it. A lot of people say, well, you just tell, you know, just like you said, just tell us what to do. I mean, I can tell you what to do. Uh, take natto. I took, I took natto powder for years. Uh, you can get it in, uh, Amazon. You can get it other places. Uh, my focus was more on, uh, K2 though, than on, uh, nto kinas. Is that going? Am I gonna try to guarantee that you're gonna get, you're gonna save yourself from heart attack if you take natto? Not at all. And here's the thing, the evidence behind natto, ninas, serapeptase, uh, all of these things is very, very minimal compared to the evidence behind metabolic health. There's just little, there's no question about looking at something like your triglyceride over HDL and the impact of that on your health. Nothing like the questions that you see associated with something like the evidence behind nyas. So not sure I can add a lot more. Jesus, I, I have two things to add. And I do this all the time. I like kind of, uh, give you a chance to intervene, and then it gives me a chance to regroup and think, what else am I missing that I wanted to say? I don't work really good with scripts, so I don't have anything written down, written down. So one thing they also did on the research that I wanted to mention, they did compare that to 3600, um, fibrin units. And 3600 fibrin units seem not, seem not to be working. So if you're taking only one or two pills a day, uh, um, it might not be enough. That's one thing. And the other thing is whenever we talked about plaque reversal, we, and I'm, I'm going to make sure I recover one of those articles that we covered last, last year about what is more important. Is it more important how much plaque do you have, like the amount of plaque that is in there, how many millimeters do you have on it, how many plaques you have on it, how big the plaque is, or is it more important what type of plaque do you have? So when you do a CT angiogram, when you do a CIMT, when you do a calcium score, when you are evaluating how much plaque you have, you will have different scores, like total plaque burden, that they call it, or will you have a risk assessment of total plaque on the CIMT as well? And when there's just so much plaque on it, the risk automatically goes high, like, oh, there's too much plaque, it's the plaque is too big, that's really concerning. And especially if you're getting a CT angiogram in order to get a stent, they tell you, well, it has to be 50% occluding or obstructing the flow for 50% or more, which they call, which is called a stenosis. So until that point, uh, you might get a stent, or, or you may even get it on, on the stress test, you will get that identified. But what I, what I will, where I will advise some caution is even if this article said, yes, you can decrease the size of the plaque, uh, they, they missed the point on telling us what type of plaque it was. Because if this is soft plaque that not only reduced but calcified as well, that's the big deal. If it calcifies plaque, because that plaque is not going to rupture. But if you're having plaque that is less, is not, it's not that big, but still is soft, we're not going through that healing process, we're just maybe taking some goo out, but not, not stabilizing the plaque. The benefits might not be as, as good as we think. So that's, that's the, the thing that you see on research. It's hard to find, uh, research that really goes to that point of telling you, yes, we can decrease the amount of plaque, but also we're changing how that plaque is, and we're turning that plaque from soft to calcified, stable plaque. Thank you for your patience, everybody. Also, Dr. Brewer, I think you're absolutely right. I mean, you bring up a point, and I'll bring out that old joke of what the Jesus meant to say, or was, you know, risk is not risk. You got to define risk. Risk is not just risk. Plaque is not just plaque. And again, I think that's the major part of your most recent statements. It's soft plaque versus stabilized plaque. And I'm, I keep getting reminded of that. Uh, a couple of other statements like Lustig says, a calorie is not just a calorie. Back to your point about a, a plaque is not just plaque. It's soft plaque versus, uh, stable plaque. Will you go, go back and quote that article that you pulled up that talked about risk for people with calcium scores over a thousand versus risk less than a thousand? It helps really make that point. And I wish we had that, that actual image that we could show. Hope, hopefully, we'll have to just show it in one a later show if you don't have it available. Describe it. That's a good marketing tool if you want to see that graph about how people with a calcium score of over a thousand, uh, have less heart attack risk. As you heard, just like you heard it, the higher the calcium score, the lesser risk was on this one study. I'm going to bring that, uh, graph next week. That's a pause for you. And again, it's, it's a point. People just, they, when they talk about LDL, it's not just LDL. It's small dense LDL versus large fluffy LDL. HDL is not just HDL. It's large fluffy HDL versus the other, the rest of the HDL population. Risk is not just risk. And again, a calorie is not just a calorie. And like you said, plaque is not just plaque. People look at a calcium score and assume that the higher it is, when it's increasing your risk is increasing. Not, not so much. There are times when a higher, a higher calcium score correlates with more risk. But it's sort of like saying all LDL, all LDL is the same. Wonderful. Now, no, no, no, no. More question remarks on natto. I know you want to wanted to talk a little bit about about a senic. Go ahead. Well, I, I don't think I'm, I'm really prepared about talk specifically about a senic. I will only, I will only say, I will give you an introduction. So Dr. BR shared with me a few days ago an article from The New Yorker, uh, from December. And it's a really good article. You can just Google for it. The author is, I hope I don't mess this up, is Dru Col. And he gives a summary, really important summary about the development, the history behind OIC. I know it's going to be a comment about big pharma. And if you're a conspiracy theorist, I'm, I'm with you. But there's some stuff to be recognized regarding the development of some medications. So in this one, it says a lot of things have changed since the discovery of GLP-1s. What we have found on the experience with a senic, especially last year when it boomed, it has some benefits like improving insulin sensitivity, weight loss, decreased cardiovascular risk, and fatty liver. It was a surprise to find that it, it also can reduce cravings for alcohol and tobacco, and even some compulsive behaviors. But it doesn't work for everybody. So it's not a one-size-fits-all solution. There are side effects like nausea, constipation, diarrhea, GI symptoms. And the article did not mention this, but also thyroid cancer, which is, which is not that common, but still, it's on the label. However, it, the benefits outweigh the risks. So, diabetes is killing more people than thyroid cancer, of course. Other population might lose body fat, bone density, and muscle mass. That's kind of a risk. I, Dr. Brew has a perspective on that specific point. The downside is senic is really expensive, at least in the US. And just to remember, obesity itself, it's a major epidemic, and GLP-1 hitters are just another tool for physicians to address it and try to go in it. I saw a, a, kind of a documentary on on YouTube a few days back on, oh, how bad a senic is, and people just staying off a senic and gaining that weight back. And, and that is just such a bad drug for you. And the only thing I will argue is if you are depending on a senic for your weight loss journey, for your prevention journey, then we have a problem. Because when you talk specifically about prevention, there's no supplement, there's no medication that is going to replace all the other lifestyle components that you need to put in place. So it is possible to stay off a symic for, after taking it for some time, if you are doing the work and you're training your body to be in that place. And of course, the journey will be harder for some people than it is for other people. I'm, I'm, I'm a little bit inspired today. Don't let me take your tea. You are. I'm impressed. I'm impressed.
So actually, thank you for bringing that up. OIC has gotten so popular that it's the thing that everybody loves to hate now. Um, and I, I get it. Asmic is a prescribed drug. Like any prescribed drug, the reason for the prescription is there are dangers associated with it. Clear dangers, as Jesus mentioned, like cancers, um, pancreatic cancer, thyroid cancer, especially. But we've begin, we forget, what, what, uh, it's dealing with. It's sort of like, it reminds me, I did a lot of my early work in medicine and public health with the HIV epidemic. And, and, uh, there's so many parallels. Um, we're binge-watching Robert Lustig right now, and he makes a good point about personal responsibility. And it really holds true for the diabetes and, and obesity epidemic. What, what does this have to do with HIV? So here's what happened. So the HIV epidemic, when I was working with it, was just transitioning from the, the gay population to the IV drug user population. And people said, you know, that's the pro, that's a personal responsibility. People have made bad choices that increase their risk, and that's what happened to them. And then Magic Johnson, a respected super athlete in basketball, and a heterosexual, announced that he had HIV infection. Pretty soon, things changed. And instead of becoming so much a, an individual responsibility, yes, it was still an individual personal responsibility, but it also became a public health crisis at that point in time. When you look at obesity and, and, uh, diabetes, we seem to be struggling with the point that yes, obesity and diabetes are both, uh, involved with food misuse of food, and therefore personal responsibility. But we talked about this before, it's becoming clearer and clearer, and the use of GLP-1s like a zic have also made it much clearer what the obesity specialists, what the addiction specialists have been telling us for a long time. The obesity epidemic is an addiction. It's not just personal responsibility. It's not just personal bad choices around food. All you have to do is look at what's going on around you in terms of obesity, diabetes, and this hot new drug, asmic, to realize that there's something bigger going on. You know, I talked earlier about those innocent, maybe naive, arrogant old days when a calorie was just a calorie. You got some of that now. These, uh, lack of understanding that, I mean, it's more than obvious to us that sexual behavior among young adults is driven by hormones. But for some reason, we seem to miss the point that food behavior among all of us, and especially among Boomers, middle-aged and older adults, it's driven by hormones as well. Leptin, insulin, of course, but leptin, adiponectin resistance. Um, again, GLP-1s, OIC is nothing but a hormone, a hormone associated with food behavior. And, and there's a reason why it's had such an impact on the obesity epidemic, and also therefore the diabetes epidemic. So again, I'm going off on a rant too. Maybe we ought to, uh, cut it for our rants and, and go ask, ask and answer some questions. Go into the Q&A. What do you think? Maybe it's the coffee. I don't know. Do we have the same brand of coffee? Maybe. All right. So let's go to a Q&A. Uh, Gilver, if you will give us the water.
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So let me see if I can share the stage with the host of the show right here. We go. Uh, Gilbert, can, can you give us that image that I love? Oh, there he goes. I mean, I had to take answer. Yeah. And, uh, you know, we're getting better and better on being more direct with our main topics. Um, do you, do you hear some background noise on my side? Not on your side? No, okay. Perfect. I don't. So if you're not a YouTube member, there's a button next to the subscribe button for you. Just click on it. It says join. It's a couple of bucks a month. Uh, the idea is not so much about the money. It's about us being able to answer as much questions as we can. So what I, what I will try to do is, um, address questions from YouTube members first. If you're not a member, no answer for you. No, I'm, we're gonna try. But we're there afterwards. You're such a big corporate conspiracy guy. I can't believe it. Well, I think people are starting to to see that, uh, Dr. Bru, uh, uh, it's, it's, uh, a gentleman. He will answer stuff when I'm not looking around, and I'm okay with that. Uh, but take a look at this. Brad, for example, Brad has an icon next to his name. So, we, we sometimes have that a show when we're answering the same person's questions over and over again. And I mean, that's, that's the perk of becoming a YouTube a member from your YouTube channel, not YouTube Premium, a member of your or channel. So premium is very different. That's very different. And you might end up paying more. So Brett, good morning. Regarding the abdominal MRI, is it worthwhile to obtain, or does CT angiogram give the same degree of knowledge plus additional information? Cost the benefit, radio of one over the other? Really good question. I don't think we have ever had that specific question. We, we talked about MRIs and CT angiograms separately. Uh, do you want to take this one? I'll start, and that give you a chance to think and really give the right answer after I blather around a little bit. They're, they're two totally different things. So a CT angiogram is telling you, do you have plaque in the arteries around your heart that supply your heart? That's what people are wanting to to look at. Unfortunately, you know, I don't like them because once you start look, the anatomy is so good, you start to make an assumption that, hey, if I just put a stent right here, that would fix my problem. And what we know and see all the time is that cardiovascular disease is not a plumbing issue, it's a metabolic issue. So we know that even looking at the arteries in your neck, I mean, if you have plaque in arteries in one arterial bed, you're going to have them elsewhere. So we recommend that you, uh, don't get too focused on the artery specifically around your heart and thinking that you just put a little stent in that one place and that's going to fix your metabolic problem, because it's not. But Jesus is, you know, just like everybody else, he doesn't agree 100% with me, and he's got a little bit of different perspective on CT angiogram. I'll let him talk about that in just a minute. But abdominal, uh, abdominal, uh, MRI is a very different thing. It's looking at abdominal fat. And we talked a bit, a good bit about that. That's one of my most favorite recent topics, and that is fat threshold. We all know that fat is a big deal, or most of us do. We used to think it was an inert energy storage tissue. It's not. It dies. Fat that's growing. And fat cells that are expanding to the point to where they're saying, look, I'm full. Your fat tank is full. Don't put any more fat in here. What it does is it starts decreasing leptin, which is a different issue. Leptin is the satiety hormone, and it starts getting, it looks like maybe it's getting injured or it creates resistance to leptin. So that's a confusing issue. But again, a hormonal driver for more eating. Resistance, which is another hormone that's made by, uh, fat cells as they expand, creates insulin resistance. Adiponectin, which is the insulin sensitivity hormone, when those fat cells start expanding, they quit making adiponectin. Ghrelin, all, all of these different hormones that are associated with food behavior end up getting impacted by fat as it grows. Now, why did I go down that bunny hole? Because it's far worse. The fat that's associated with your abdomen, per organ fat, visceral fat, that's the fat that really drives this problem much more than fat that's under your skin. Fat that your doctor will call subq, meaning subcutaneous fat. So as we talked about with Mario Katz a couple of weeks ago, most of us, if we're going to put in, put on fat, we put it mostly subq first. But then we get to a point where we can't, we don't have any more room subq, and then we start putting it in the organs. That's what abdominal CT is all about. And I can't remember the guy's name. I think it's Shan Amira or somebody something like that. He's basically got a whole YouTube channel about looking at abdominal CT or abdominal MRI for this point. One of the things he does, I've seen a few of his, uh, videos. It's a good concept. It's a good point. And I will say one of the things that he is a big fan of, and that is HIIT intervals. I'm a big fan of that too. In fact, I'm beginning, I'm going to go just for half a second, a teaser, down another bunny hill, uh, hit training, hill interval training. Have you heard of REHIT, reduced exertion high-intensity interval training? Maybe that's got a big opportunity for the future. I'm going to just leave that as a teaser though. And let Jesus you talk about how you like, uh, CT angiograms, even though I don't.
Well, and, and I will say to, to the point of those of this specific questions, the, the goals for each study are absolutely different. So advantage of an MRI doesn't have radiation. And if you have obesity, if you're overweight, you might want to have one of those just to see how much visceral fat. And if you're thin on the outside, you don't seem to have that much fat on your belly, you will pass the jiggle test, which is, you take your shirt off. Uh, this is a test that Dr. Brew taught me. This is not mine. This is not my credit. I don't know where Dr. Brew learned about it. You take your shirt off. Oh, yeah, see there. So you, you take your shirt off and stay in front of the mirror and you jump. Anything that jiggles, that's fat under your skin. That's dangerous. But it's more dangerous to have visceral fat. So, so if you're thin and you don't have that much body fat outside, uh, you might want to get one of those abdominal MRIs just to know if you have a lot of visceral fat on it. Another option is to have a DEXA scan with a body composition report that can give you a similar response as well. But going back to the CT angiogram, as Dr. Brewer said, the CT angiogram will give you a perspective on your coronary arteries. I'm a fan of the CT angiogram a little bit more than Dr. Brewer is, especially the latest version of it, which is the artificial intelligence driven, the AI driven CT angiogram, because the machine itself, it's measuring how much plaque you have, but it can tell you how much soft plaque you have in the specific vessel around the heart. Um, if you go to get the standard CT angiogram, uh, if the interpretation is made by a physician or another provider, we have seen plenty of CT angiograms where they are only focusing on if the plaque is obstructing the blood flow or not, and not giving a report of if it is soft or calcified, the stable plaque. So if, if, if I would get a CT angiogram, I'll probably get a Cleary one. The risks, risks regarding the procedure are not that high, but still involves getting a, a dye on your arm, which is some people will can develop allergies to that. It involves some radiation, which is not that much, but still some radiation on it. And the major risk is if they find plaque, then they, they making you sign even before the test starts, oh, if we find plaque, we're going to put a stent on it. And that's one of the major risks of getting one of those. Be very afraid if they ask you to do that. Yeah. If, if the idea is, I just want to know if I have plaque and what type of plaque is it, and I have access to a CIMT, I'll probably get that. Some people already had already have stents or bypasses are and are not candidates for a CT angiogram, then you'll have to look for a CIMT. For those who are new to the channel, CIMT is a carotid intima media thickness test, which is an ultrasound to your neck that can tell you if you have soft plaque or no. So thank you for your question, Brad. Give us the opportunity to go a lot on that, which is a really good topic to, to talk about. A good guest recommendation, maybe good. You have any other comment on that?
Yes, thanks. Let, let me just make a qualifier on my last comment about be very afraid about getting a stent. The reality is, I just wrote a book on it a couple of years ago. Stents are not that dangerous. In fact, I know of a fellow that used to manage a couple of, um, of, um, cath labs, and he talked about a couple of the cardiologists hopping up on the table and doing stents on each other just to see what it was like. They knew that these things, not that dangerous. Wow. But the bottom line is, here's where the danger is, assuming that a plumbing fix is going to solve a metabolic problem. And that is the problem. Yeah. And, and a remark to the remark, if you're having an active heart attack, if you're having the chest pain, if you're sweating all over, you have a numbness on your jaw, your arm, you cannot breathe, all the symptoms of save your life, a stent will save your life.
Definitely, we're not talking about just a plaque. We're talking about a plaque that ruptured, released goo, and created a clot that is obstructing the flow completely. Uh, so yes, a stent will save your life in that moment. So we're not against a stance. We're concerned about the stances that are placed, quote, to prevent heart attacks, which is, uh, when you ignore metabolic health. It's just people thinking that because they have a stent, they're safe, and that's not reality. Thank you, Brad. Again, you, you, you place us in a really good conversation about that, which is core to to our channel. A good guest recommendation might be Dr. Robert Lustig. He does a great job explaining IR progression, has a metabolic. Dr. Brewer already, as I say, spilled the beans. Spilled the beans, sorry about that, from Dr. Brewer. We're in the middle of it. Um, uh, yeah, we're big fans of Lustig, and we invited him to the show. He agreed, he accepted, we have a date, we're going to record something. We're going to bring that out to you guys as soon as we have it. Oh, and you know, I'm a big, we've got a couple of people, we got some a little bit of argument going back and forth about, oh, it's all plant-based. No, no, no, no, it's all, um, carnivore. You know, we have that argument going on all the time with folks that watch our channel. And the bottom line is, we're from Switzerland, meaning we've got a position similar to Lustig. Uh, we've seen people have healthy diets and do very well on both plant-based and animal-based. It's not quite so much where you get your macronutrients. I hate to tell you that. And you know, we're going to get a lot of haters for that comment. But the bottom line is, it's knowing your metabolism and knowing what poisons it. So, when you look at the fact that over half of us have a problem, uh, metabolizing carbs, starting at age, not 30, not 25, starting at age 18, you got to ask yourself the question, are you feeling lucky? Meaning, are you ready to eat, continue to chow down on those, uh, ultra-processed carbs? How, how did Dirty Harry just to say that? You do a really good impression of it. Are you feeling lucky, punk? Yeah. So, any people give us a hard time about being too light. Uh, they say that, uh, this is a serious health, is serious death and disability, serious. We deal with it all day, every day. So, and we don't want a sleepy audience either. That's the truth. Hey, Jesus, can I, can I pull a Ford on you and go back and do and feature a, um, a comment from you? Do a non-channel member? Or are you done? The channel members, or you there? There are a couple of questions from channel members, but go ahead. Uh, I'll, I'll, I'll give you the chance. Oh, it's, it's JMK. I mean, I've been trying, I've been trying to convince JMK to become a member. I don't think I'm gonna be successful any anytime soon. He knows I keep, I keep showing his questions anyway. So, yeah, is asking, brings really good questions though. I mean, that's, that's the, it really does. Maybe it doesn't need to be a member because brings really good comments. And this is a, a question that has a, has a, it has to do with the channel. It has to do with a very important issue. There's a major debate out there about saying that LDL and more maybe more accurately ApoB causes cardiovascular disease. And then the folks saying it, it's Peter Attia, who's basically just listening to Dubring and Sniderman and some of the other folks that, uh, there's, um, Mendelian, uh, randomization studies, etc., etc. I've looked at those studies. I agree that there is some causation there. Um, but I also say when we say there is no question, that's not true. Or, or when the lipidologists say there's no question that it's all causal, that's just not true. The study that JMK is talking about is a study that we covered. And yes, we tweaked Peter and the and the lipidology crowd on this issue. And it was interesting. The point we featured Dave Feldman, Nick Norwitz, and the point is exactly this, that maybe for a lot of people, LDL is really more of a, of a bioindicator of metabolic status. If you listen, you know, we're talking about Lustig, a lot of these, uh, on in this, this video and on this show, and yet he says the same thing. He's got a position similar to ours, and that is that LDL may be more of a metabolic indicator. Um, I pinned a comment. I, I'm maybe I shouldn't do it, but I was being factious and a little bit, uh, snarky. A comment came today on that video. It's been a very popular video coming out of the blocks. It was a, it was a presentation. Nick Norwitz and Dave Feldman came, set up a, a Zoom meeting with us and actually presented the data that you're that, uh, JMK's talking about, that's basically showing that there's some people, excuse the cough, some people who go on a low-carb diet and their LDL shoots out the roof, 200 or more. And in fact, in these people, the average LDL that they had, about 100 people, the average LDL for those folks was 272. And they didn't have any more plaque than anybody else. And the point was, gosh, if you've 272, in case you don't know it, is one in a, a level of LDL and related ApoB. And so if LDL and or ApoB causes cardiovascular disease and plaque, then how can these people have such high numbers and not have any more plaque than anyone else? One of the, one of the folks, one of the comments, a couple hours ago, was, well, basically to be paraphrased, it said, well, you idiots, it's because the BMI was so much smaller. I responded and said, well, you missed the point. That is the point. It is metabolism. It is the BMI. And that was exactly why the study is so interesting. And I couldn't help it. I pinned the comment. Jesus. Any other explanation or, uh, what Dr. Brewer meant to say was something nicer than what he said? Or leave it alone. I'll learn. I'll learn from from being on YouTube for a few months now. Uh, I just, I just jump the comments that are not that are not polite. I'll, I'll take, I'll take criticism. I'll take other points of view when they're respectful. So I will, I probably will not have pinned that comment myself. But, uh, that's okay. I mean, it's, it's perspectives. Uh, one thing, oh, go ahead. On your to your point about being respectful, uh, there is a little bit of snarkism going on. But the bottom line is, uh, I do think that this is a debate that needs to happen. I do think that at the end of the day, we're probably mostly going to end up all being friends again, but there's going to be some dust flying a little bit as we get to the bottom of this that, you know, what exactly is the relationship of LDL and therefore ApoB to cardiovascular disease? There's no question that there's a relationship. How much of it's correlation and how much of it is causation? Yeah. So, so I'm gonna play the devil's advocate for one minute regarding LDL and ApoB because I'm gonna say, uh, that they are right. However, I think this is a situation of, uh, what do you say, the six blind men and the elephant? Yes. I would agree. This is a chicken. They're looking at the trunk. We're looking at the tail. Exactly. So if you say to me, because I read that, I read that, read that research, and they, there's compelling arguments on it. They say the higher the LDL, the higher the ApoB, it starts an inflammation cascade. When the LDL gets oxidized, the ApoB gets oxidized, it gets accumulated, uh, below the intimal layer, and that starts plaque. So I agree with almost all of that except the part of starts. Because yes, if you have LDL that or ApoB that gets oxidized, myeloperoxidases and other inflammatory things, cells and substances will increase inflammation as a response to that. That is through. However, you're missing other components that also cause inflammation. And that's our whole argument. And that's the bail, the position as well. Oxidative stress doesn't come only from LDL and ApoB. So if you say ApoB and LDL can cause inflammation and plaque, yes, that's true. But there are other factors that are, I would say, more important than ApoB and LDL causing inflammation. And when you have inflammation from other sources like insulin resistance, high triglycerides, autoimmune diseases, if you have a lot of ApoB and LDL, you might be at a higher risk of oxidizing all that stuff and incrementing the amount of plaque and incrementing inflammation that you have in the inside. But if you close to the idea that it's LDL and ApoB alone, you are missing the whole elephant in front of you. Now, if you don't know that much about this topic and you're sitting there listening and saying, you guys are a bunch of nerds and you're being impolite and you're arguing with each other, it's this is just some really arcane biochemistry. Here's where the issue is. And here's what Jesus's point is about. And here's that point about CT angiogram and the problem associated with stents. All of us would like to take the easy way out if it turns out that you can lower your risk, take the majority of your risk for cardiovascular disease off the table by lowering ApoB or LDL. You can do that with a pill or an injection. And therefore, you don't need to manage your metabolism. That's what this fight is about at the end of the day. It's not about ApoB or LDL or metabolic disease or any of or biomarkers. At the end of the day, it's what's the best way to protect yourself from cardiovascular disease? Is it managing your metabolism or is it a medication? I saw, and I share this with you, very interesting discussion between three personalities that if you are on YouTube a lot searching for these topics, you will be familiar with, uh, Dr. Mike, which is more mainstream media doc, a family medicine doctor, Dr. Daniel Bardo, which is a doctor who works a lot on guidelines of nutrition and cardiovascular prevention, and Dr. Gundry, which has multiple books about gut health and inflammation and how liver, liver function and disease and all related to inflammation and cardiovascular disease. Two different perspectives colliding. And I told Dr. Brewer, Dr. Gundry just got bashed. And there's one thing Dr. Bardo says that we know for a fact that the main intervention to decrease cardiovascular disease and death is lowering ApoB. And when I heard that, I was like, well, I mean, there are just so much we agree on. We agree that ultra-processed food issues should be avoided. We agree that diabetes is an issue. The thing is that it, it appeared to me that their perspective is diabetes is a secondary thing to consider, just a factor. And we're more involved on insulin resistance is a major factor, not just a secondary player on this. And I, I mean, there's so much things on which we agree. But when we focus on the things we don't agree, we're not getting anywhere. And the point, the bad thing is that guidelines are focusing on one thing and mentioning other stuff that we agree on regards to lifestyle. But the, the, the approach when you go to see a doctor, the approach is on statins. It's more about the statin that lifts. And I know they recommend lifestyle, they say things about lifestyle, but it's not being enough. But I'm, I'm, I'm sorry, I did not mean to drag this conversation that long. So just wanted to take put that out there. Well, you did take us back to my very, my original point in my introduction, and that is, uh, assuming dangerously so, that your doctor is going to know nutrition. Your doctor's going to go back to his or her profession. It's a licensed profession where they are the ones that can give a prescription medications or do surgical procedures. Um, and, uh, assumptions that they're going to understand exactly the best way to protect your health are not very realistic. Make that assumption at your own risk. Definitely. All right, I'm gonna jump to another YouTube member's comment. Brett Jones, if one has trouble with aspirin, maybe it's a good alternative. He's talking about Nattokinase. I, I think it's if, if you're, your goal is to decrease the risk of clots, I'll make an argument that omega-3 or fish oils might have an effect more similar to aspirin than Nattokinase. I think you're right. I mean, it's not the same. And if you go to a medical degree, one, you're going to get other medications like Plavix. What's, what's the, the standard name from Plavix? I blanked on it. Clopidogrel. Yeah. Clopidogrel. So those are different mechanisms. But, in order to make prevention, and I'm not going to go into the deep argument of aspirin when to use it, when to not use it, but if you're looking for a, um, substitute for aspirin, I think there are other options before Nattokinase. Uh, they, there are other types of blood thinners as well. There's a couple of different prescription types. Jesus mentioned Plavix or clopidogrel. There's also the what we call the NOACs, novel oral anticoagulants. That's like Rivaroxaban or Xarelto. And, uh, Eliquis. And some of those. Those are are best for things like, uh, atrial fibrillation. People will often ask me, do I recommend something like, uh, baby aspirin for atrial fibrillation? No. Baby aspirin has been demonstrated that it doesn't manage atrial fibrillation very well. How about the other ones that we're talking about? The natural ones, the, uh, fish oils, krill oils, uh, nope, they don't do it either. How about, uh, Lumina, serrapeptase, nattokinase? No, those are, I would not recommend depending on those to, uh, decrease your increased risk of stroke from atrial fibrillation. So there's a whole lot in terms of blood thinners. Definitely. Col Red Racing, yes, we would love to have Dr. Brewer on the channel. I'm gonna try to invite him. Let's see if if we have, if we're lucky, we have success of having on the show. Um, shout out to Laser Harvest and David Mines. My aggressive efforts of having people becoming a YouTube member are being successful. We appreciate the support and give a, um, warm, uh, salute. Hi, today, friend of ours. Yes. Yeah. Uh, I saw a comment over here that I wanted to bring out from another YouTube member, which is, and I'm going to go back to some of the Laser Harvest. Laser Harvest commented a lot today. I'm going to try to recover one of your questions to honor my word, of course. I just want to make sure that I, I saw one question around here, one question around here. Um, I'm gonna, I'm gonna briefly say the question. I hope I find it. Somebody said that calcified plaque or calcium score, it's only about 20% of the plaque that is in there. While I look for that question, Dr. Brewer, do you have any comment on that? Yes, it really depends on what you're looking at. I think one of the studies that you uncovered said that for most calcium score folks, for the typical person walking in and getting a calcium score, wasn't it like one-third, two-thirds, maybe, yeah, around that, with one-third being the soft plaque? Yep. No, I would say two-thirds or the other way around, the two-thirds being the soft plaque. So therefore, when somebody comes in, they get a, they come in to us with a calcium score of 400, they lose 30 pounds, they get their metabolic health improved, and their calcium score doubles or quadruples. They're really in a much better shape. And this helps people understand why they have calcified all that soft plaque that was there when they started and they didn't see it. And I will say one more thing about that, and this is kind of the point that I've been, if you look at the videos, I know they're like one hour long, and we are about to finish this one as well. Yeah, to me, from what I have learned, and Dr. Bird taught me most much of that, is the calcium score number alone doesn't tell you the full picture. It depends on your specific situation. So to me, a calcium score of 300 is not the same in a person who has been on the standard American diet, the standard American diet for years, who's dealing with diabetes, high blood pressure, and other stuff. And a calcium score of 300 to me will be like the tip of the iceberg. And I will agree with Lori. I'm not concerned about that calcified plaque. That's plaque that has been, that is healing. I'll be concerned from all that soft plaque that we don't know about just yet that is in there, but we don't know how much is it and which one of those are ready to be ruptured and waiting for the event to happen. But if you have a 300 calcium score, even higher than that, you're lean, you're building muscle, you don't have significant insulin resistance, you're changing your lifestyle, you're doing other stuff. I don't think I will be that much concerned about a 300 calcium score, even higher, if you're doing the work that you need to do. Then then comes the CT and the CT angiogram just to verify that you have indeed not so much of of that soft plaque that is actually the dangerous one. Very good. No, I was going to say thank you for, as you said earlier, you've, uh, taken the responsibility of keeping this, uh, close as close to an hour or less as possible. We've gone beyond it. Um, I think maybe the last two or three questions and we'll need to go. I think I'm going to, I'm going to refer to Laser Harvest, who just became a member, and I'm going to honor that. Uh, he commented a lot. We appreciate the participation. That's really important. We just have, we have just so much time. So Laser, I have been taking, pardon the rasp, boys, been taking very large amounts of nattokinase for a year. Don't know yet if I'm receiving the benefit, and 50,000 firing units a day. So if we refer to the research that we presented today, I'll make a case that 50,000 is maybe just too much. Not maybe not for side effects, but maybe for benefits. Maybe it's not necessary to take that much. And if you refer back to that article, if I was looking for the benefits of nattokinase, I'll probably look for my lipid panel if I have something as a reference as a baseline. And I'll probably get a CIMT as well, a carotid intima media thickness test, and see how much plaque I am building and if there's any difference. But again, it's going to be hard to isolate the benefits of nattokinase because, or nattokinase, because you will have to make sure that your other lifestyle components have been the same and they're in the good place. Uh, I'll, I'll say that nattokinase will be one of those. Again, it's on the name, it's a supplement intervention for the things that you are already doing. Do not rely on supplements or medications for your preventive efforts. Dr. Brewer, closing remarks. Thank you. No, we got a couple of remarks about, well, you talk about nattokinase. We did go back to the original. We started with it. We ended with it. And we had a lot in between. But this is a YouTube live. So the whole point behind YouTube live is responding to questions and topics that are brought up by the audience. Speaking of the audience, you guys are the ones that make the channel. So thank you very much for your interest. And we'll see you next week.