Heart Surgeon: REVERSING PLAQUE is 100% Possible! Here's How...

0:00 90 to 95% of the patients that end up on my operating table would not have ended up there if they knew how to prevent this. >> Philip Ovadia is a board certified cardiothoracic surgeon focused on preventing heart disease through metabolic health and lifestyle based approaches. 80% of the plaques contain microplastics. And more importantly, the amount of microplastic that was in that plaque was then predictive of how that patient did over the subsequent 10 years. Now, I would like to ask you a big question. Can we reverse plaque?

0:35 Yes, it is possible. And And this has been shown over and over again, right? Whether you're looking at CAC scans or you're looking at CT angiograms, I have [music] patients who have taken and their CAC scores, right? So, only [music] looking at their calcified plaque, have decreased. We've been seeing a lot of people having estrogen dominance from women and also men from them. Elevated levels of lipoprotein A, what can you do about it? It's even more important for them to be looking for plaque. Get the CAC scan. Get the CT angiogram. Follow it over time. ApoB uh has been [music] shown to be a better predictor, but I would still say it's not a great predictor of heart disease.

1:17 And the reason is Dr. Ovadia, it's great to see you again. Congratulations on your upcoming book, Stay Off My Kitchen Table, launching in July. And so, to start us off, what inspired you to write this book? And what problem were you hoping to solve from it? Yeah, so it's been uh almost 5 years now since I did released and wrote uh Stay Off My Operating Table. Uh hard to believe, time flies.

1:47 Uh and a lot has changed since then. Uh a lot of my thinking has evolved. And while the core kind of uh tenets of Stay Off My Operating Table uh remain true, what I really want to do with this book is go a little deeper. I wanted to explain why, you know, the foods that we recommend are the right foods to be eating. Um, why some people, um, you know, can do what is a good diet, right? Mostly carnivore, low carb, and still struggle to get the results that they're looking for. And this is something I see in practice a lot, and understanding, you know, uh, that if, for instance, you're not absorbing the food that you're eating well, uh, that can lead to problems. So, we talk a lot about gut health, we talk about bioavailability, nutrient density, and really, you know, go deeper into, uh, why what I recommend in stay off my operating table, uh, is the right thing to do. And ultimately, it comes down to what should stay on your kitchen table, and what needs to come off your kitchen table. Yes, and I really appreciate that because people are starting to realize that health is not just about the foods that you're eating, but the environment that you're being exposed, how they're cooking their food, and many other things that we cannot even measure that is part of that variability that you need to consider for being health overall, healthy overall. And how important would you say is cookware quality for your health?

3:22 Yeah, I think it's certainly a factor that people should be thinking about, right? You know, as we move beyond just, you know, what is the right food to be eating, we have to think about what might be coming with that food, right? And this relates to perhaps how the food is, uh, packaged and transported, and then how we cook it. Um, cookware, you know, can, uh, become problematic. Uh, if there are things that are on that cookware, right? That are then being transferred into the food and you're now consuming them, uh we, you know, that can lead to some problems.

4:01 Um I would say one of the most prominent things that is, you know, come to light are things like microplastics, things like uh coatings that are on like the nonstick cookware, right? And realizing that, you know, you're putting your food in it, you're heating these things up, uh and there can be transfer of those materials. And um we're starting to see some concerning signals around that. So, um once you've kind of established this is the good food to be eating and you're committed to that, uh this is one of the next levels that I often times see people starting to think about. And I do think it has some relevance. What are some tools that you normally keep off your opera- uh I mean, your kitchen table?

4:48 >> [laughter] >> Hopefully, I'm not moving too many tools between my operating table and my kitchen table. >> Exactly. Yeah, so um I generally am trying to avoid uh plastic um you know, cookware, right? So, the spatulas and the, you know, other um uh things that you're going to be using that especially you're going to get heated up. Um you know, if you want to use uh and again, as a mostly carnivore, um I don't end up doing a lot of recipes, so things like, you know, mixing and whatever don't come up uh too much for me, but one of my main focuses, right?

5:23 Most of my cooking is done either on the grill or in a cast iron pan, for instance. And you know, I don't want to be grabbing the hot steak with a plastic set of tongs, right? You know, I go for stainless steel generally. Um uh so, plastics are probably the biggest thing that I think of. And then the cookware itself, like I said, avoiding the nonstick, you know, coating. Uh I am a big cast iron user.

5:51 If I'm not, you know, just cooking on my grill, it's usually going to be in a cast iron pan. Yeah, the one of the things that I started to research recently is about the coatings. I had no idea. So, for example, there's no legal definition for you to say if your pan or whatever is non-toxic. So, they do not need to tell you. They just can just say it without any legal reasons from justifying that. And that that is a big problem because many of them contain coatings in which has a lot of titanium dioxides and many other harmful compounds that are leaching to your food and you don't want that. So, it's really harmful and I really want everyone that is watching this to really understand that sometimes they can be spending a lot of money on a brand that is not trustable, for example, because they contain those coatings. They say they're non-toxic, therefore they're not.

6:42 And and that's a big problem. So, talking about microplastics, why is that so important to be acknowledged for your heart health and overall health? Yeah, so we now have studies where they have looked at plaques from arteries in the heart, from arteries in the neck, you know, in people that are undergoing operations because they've built up, you know, enough plaque blockage and you can actually find the microplastics in those plaques.

7:18 More perhaps even more importantly, right? So, there was a study a few years ago where they were looking at patients undergoing what we call carotid endarterectomy. So, this is basically a cleanout of plaque from the artery in the neck. And they looked at the plaques under the microscope and they saw did they contain microplastics and how much. And I forget the exact numbers, but it was something like 80% of the plaques contained microplastics. And more importantly, the amount of microplastic that was in that plaque was then predictive of how that patient did over the subsequent 10 years. So, it wasn't just that the microplastics that were in, you know, were maybe contributing to the plaque formation, it's that microplastic burden having a higher burden of it uh predicted that you were going to have worse outcomes even after the operation, right? So, that tells us that there's something systemic going on here, more so than just within that plaque. And um you know, I think in in some level, right? It's a maybe a marker related to your diet quality overall, uh but it's certainly very concerning.

8:32 And um you know, as we're becoming more aware of where these microplastics are getting into our food supply, um it's one of the things that I have people paying more attention to, right? And there are some simple things that you can do. You know, try whenever possible your bottled water, you know, not in plastic bottles. Uh the the um bottle you're using, right? You know, throughout the day with your water, right? Try and make sure that that's not plastic.

9:03 >> Yeah. Um um you know, just simple things like that that are going to reduce your exposure. Uh generally, I have become a lot more aware of what I call now the non-food environmental toxins, right? So, it's not necessarily the food itself. It might be, you know, what the food is transported in, um again, how it's cooked, and all of that. Uh that's now introducing these other toxins into our system. And ultimately, they contribute to inflammation, which then contributes to cardiovascular disease. And that's why I'm so interested in them.

9:39 Is there any mechanism that we know right now in the literature about microplastics being um contained in our plaques and also harming our endocrine system? Yeah, so I think we're still figuring a lot of the mechanistic stuff out, right? At a high level, it you know, these are foreign bodies, right? That our body cannot process and get rid of, right? Yeah, we're not used to it. Yeah, sorry to interrupt you. Exactly. We didn't evolve with these things in our environment and we haven't evolved the defense mechanisms against them, right?

10:10 So, many of the toxins, you know, that have been around forever, right? Our body can process them safely, detoxify them, and then get rid of them, you know, usually we either pee them out, right? Or they they exit within our bowels or the liver, you know, can kind of break them down and get rid of them. Uh microplastics we can't do that with. Um it seems that these things really get trapped in our tissues and the body's reaction to things like that is, "Okay, we're just going to try and sort of wall them off, right? Sequester them and in something like a plaque, right? That that the plaque becomes a defense mechanism that we're just sort of wrapping this thing in, you know, cholesterol and the other components of the plaque and it's a way to sort of you know, get it out of the bloodstream, but obviously the plaque continues to build up, that becomes problematic. Now, the endocrine system is a whole 'nother interesting topic and again, the main harm here seems to be that these plastics, uh many of them are close enough in structure to our natural hormones that the body starts to mistake these things and you know, the receptors that are on the cells for the hormones get these plastics can attach to that and then block what the normal hormone is supposed to be doing. We've been seeing a lot of people having estrogen dominance from women and also men from that. And mostly from what we've seen by microplastics is that they're mostly xenoestrogenic. They're very similar within the compounds from estrogen. So that's really harmful for them. And I was also wondering one thing that so for example I was I was looking at the diet of pigs like not normal pigs that's sold in the grocery store and they're normally fed garbage like literal microplastics. I wonder if because they cannot sweat or anything like that they have a really bad um system to push toxins out so they just store in their fats and I just wonder like if we're eating this or or anything like that we're getting contaminated from it.

12:22 >> Yeah, you know, and again non-ruminant animals, right? Like pigs, like chickens, like humans, right? They generally have a harder time detoxifying these things. Ruminant animals, right? One of the things that's sort of magic about the ruminant animal with the multiple kind of stomach compartments and they're able to process a lot of these toxins better and detoxify them so that they don't, you know, as much end up in the in the meat and in the fat when you're eating the animals. So that's one of the things that guides us more towards, you know, ruminant animal-based diets. And I always tell people, right? People get often times fixated on, you know, grass-finished versus grain-finished beef and understand that that difference ends up being a lot smaller than when you're talking about your non-ruminant animals. So I help direct people's energy towards if you're going to be really starting to think about, you know, what your food is eating, Um, becomes more important when we're dealing with non-ruminant animal proteins and fats.

13:36 One of the main problems I see is that there's no legal definition for you to consider your product non-toxic. [music] And that is one of the reasons I partnered with Magnifiq because with all transparency, they actually prove with third-party testing that their product do not leach harmful compounds into your food. The Magnifiq pot is made entirely of kaolin clay. It's all natural, zero coatings, and zero toxins. The problem with coatings, for example, is that they contain titanium dioxide, which is widely present in other brands and that leaches into your food, which is not good and we don't want that. And that's why I trust 100% on Magnifiq. The clay pot cooker is the only multi-cooker in the market. It can sauté, slow cook, sear, and even put it in the oven just by taking this off. So, it's really simple. And the micropores from the clay keeps the moisture inside and alongside that keeps the heat well-structured inside. Clay is actually one of the oldest materials found in cookware used by many civilizations back in the day.

14:35 If you're interested in the Magnifiq cookware, you can find on their website. I'm going to be putting a link in the description and you can use Hugo for 10% off on your purchase. Thank you very much, Magnifiq, for sponsoring this video. Let's get back to the podcast. [music] I would like to know so your thoughts on microplastics, for example. Is there any other any other main sources that we're getting contaminated besides our plastic water bottles and uh, the tools that we're using on our uh, kitchen?

15:06 Yeah, so one of the other things that might be important is, uh, these things have now, uh, contaminated our water, right? Our oceans, our lakes, our, you know, ponds. And the seafood, therefore, uh, becomes a concern because as the fish and you know other aquatic animals are living their life in the you know their water they're absorbing these things. So that's one of the other areas of concern that I've seen around the microplastics and that might be another potential way that it's getting into our diets and into our systems. I've seen how our world is being very intoxicated today and people get really overwhelmed.

15:49 And this is just for them to know that knowledge is power and not to be overwhelmed about how our how our world is intoxicated right now. It's mostly about that. One of the things for example that I that I was that I had was that one of my podcasts I don't remember the guest right now but we were talking about those things and what we can avoid and things like that for to optimize our health. It's not just to improve it's optimize and we were talking about the same theme and people think that it is just to scare them but it's not it's just providing information that is useful for you and if you can apply that does do it. And if you cannot that's okay but at least now you know that when you have the resources you can do that for your for your overall health. Yeah you know one caution though that I do you know give people is you know you don't want to get overly right you're not there is no perfect when it comes to this right and you know you do have to eat something ultimately and you know sometimes because of all these discussions right people can really get like almost every food has something that could potentially be a problem with it and it's really about making the least harmful choices you can. It's also about strengthening your body overall to be able to deal with these things because clearly um, have different levels of reaction, right? And what I find is generally the more unhealthy you are, right? If you are insulin resistant, if you are metabolically unwell, um, it becomes more difficult for your body to then deal with some of these other toxic issues. So, um, you know, I want people to understand, right? You have to You have to live your life. Uh, you don't want to get overly obsessed with these things and always be like trying to find the perfect food.

17:50 Um, you make the best choices you can and you have your overall strategy so that your body is going to be, uh, best able to deal with There is going to be some invariable exposure to these various toxins throughout our life. One thing that I want to shift a little bit our conversation right now on salt and high blood pressure because that's also really important topic on cardiovascular health and overall metabolic health. It does not involve only your heart, but also your overall, uh, system, especially involving the, uh, renin-aldosterone system and your insulin signaling for your kidneys. So, what is the actual relationship of salt intake and blood pressure?

18:37 Yeah, you know, before we get to salt specifically, uh, what's important to understand about blood pressure, right? Hypertension, high blood pressure, it is one of the five basic metrics of metabolic health, right? It is an indicator of insulin resistance. Um, and one of the biggest mistakes, I guess, I see out there, right? And this is a lot on my medical colleagues, is doctors don't recognize that, right? So, when the patient shows up to them with high blood pressure, um, most often, right? When we're diagnosing the high blood pressure, right? We end up calling it idiopathic hypertension, which means we don't know what caused it, right? Um, there's no specific thing that we can identify. And so we put it in this bucket, right? And we fail to recognize that it's usually going to be an indicator of underlying insulin resistance and metabolic disease. And since doctors again just aren't really attuned to checking for that, it's a huge missed opportunity, right? Cuz the patients that ultimately then show up uh, on my table, right? With the advanced heart disease, um, you know, hypertension is almost universal in that population. And you ask the patient, well, when were you first diagnosed with high blood pressure? And the answer is usually decades ago, you know, 20, 30, 40 years ago. And that was a missed opportunity because if someone at that point said, you have high blood pressure, you're probably insulin resistant, check for it, and then we can intervene.

20:21 Now, the salt um, ends up being, I think, a much less important issue when it comes to high blood pressure than people perceive. Um, there is a specific form of high blood pressure, right? It's called salt-sensitive hypertension. And these people are uniquely sensitive to the effects of salt uh, in raising their blood pressure. But it turns out that's a small percentage of people with high blood pressure. I think the numbers I see are usually in the 5 to 10% range of people have truly salt-sensitive hypertension. Ironically, when someone comes into the emergency room with very high blood pressure, right? And we're worried that, you know, their blood pressure is so high that it might lead to them having a stroke or having a bleed uh, within their brains, right?

21:11 One of the acute treatments that can be given in the emergency room is a high dose of salt, what we call hypertonic saline solution, which means it's a IV solution, right? That has a salt concentration that is higher than our normal salt concentration in our blood. And that actually brings the blood pressure down, right? Working through, you know, Yeah. renin-aldosterone system, angiotensin-aldosterone system, like you mentioned. So, you know, that tells you that salt doesn't always raise the blood pressure, but in a small percentage it does. And I think, maybe similar to the saturated fat story, right? The reason that salt got associated with high blood pressure is in the Western diet, in the American diet, most of the salt is coming from processed foods. So, the salt intake really became a marker of processed food intake, and we know that, again, the processed food is leading to things like insulin resistance, which ultimately is causing the high blood pressure. The salt took the blame because that's a sort of easy to measure component, right? So, we looked at salt levels and we said, "Okay, this is what's contributing to high blood pressure."

22:27 But, the salt that's in the processed food is a lot different than just your good high quality table salt that you might be putting on your steak. What if I told you there was a better way to take low carb on the go? To go where your mission takes you, you need a food that's as mobile as you. Solved this problem. We've engineered a zero carb meat bar that's shelf stable, allowing you to take it wherever you need to go.

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23:42 >> [music] >> The Carnivore Bar. Eat meat. You said for them then actually, if you have a higher blood pressure, you should focus on the insulin sensitivity. Improve your insulin resistance. How do you do that with your patients? Yeah, so again, we can start with the basics. Uh and I think we talked about this last time, but five basic metrics. Uh blood pressure, we already mentioned.

24:12 Uh your waist circumference, your fasting blood glucose level, your triglyceride level, and your HDL cholesterol level. Um and again, you know, those are the five basic measures. Now, typically, when I'm seeing a patient and uh if the patients out there are listening and saying, "Well, you know, how do I go beyond that?" Uh you need to measure your insulin level, right? If you want to know about insulin resistance, it makes sense to measure your insulin level. And um if uh your fasting insulin level is raised, um what we call hyperinsulinemia, um you are almost by definition, you know, insulin resistant. Now, it's important to understand that you can have a normal fasting insulin level and still be insulin resistant.

25:03 >> Yeah. So, I love the insulin test. I really advocate for people to be asking their doctors or, you know, go order it yourself. You can do that here in the US freely. Um but again, it may not be enough. Uh we probably want to look at a measure that's more specific to insulin resistance. And there are a couple that we can look at. So, one is called the HOMA-IR score. Mhm. And what this is is you take your insulin level that you've checked, your fasting insulin level, you take your fasting glucose level, the sugar level, and you put them into an equation, and there are lots of, you know, online calculators for this, and it will give you an indicator of how insulin resistant you might be.

25:49 And then finally, the one that I really like most is what's called the LPIR, the lipoprotein insulin resistance score. So, lipoproteins, right? Yeah. The cholesterol in our blood, Uh-huh. or the particles, more specifically, that are transporting the cholesterol around. Uh looking at the size distribution of those particles. How big and small are your LDL particles? How big and small are your HDL particles? How big and small are your VLDL particles? Um that can be put into an algorithm that uh then tells us how insulin resistant a patient is or isn't. And that's really, I think, the I would put it as the gold standard practical way to measure Yeah. insulin resistance, right? There are the laboratory tests that can be done, things like a craft test, but those are kind of impractical. The LPIR score, in my mind, is probably the best way to easily, and again, it's just a simple blood test done when you're fasted, and you can then determine how insulin resistant a patient is. LPIR, is it the same thing as measuring if you have a high amount of small dense lipoprotein particles? Is that what it is?

27:08 >> Um it goes beyond that, right? So, it's not just looking at your LDL particles. Like I said, it's looking at your HDL and your VLDL particles as well, and putting that all together. But, yeah, it's based on the premise that insulin resistance is one of the biggest factors affecting the size, the quality of our lipid particles. Yeah, okay. I never I never heard about it, and interesting. And is it is it easy for you to to have a test like this? Um yeah, so you just need a doctor who knows how to order it, right? The LPIR score is widely available.

27:45 Fasting insulin, right? Very easy to do. So, the HOMA-IR score becomes the most accessible of the ones that I just mentioned, because, you know, you can go to any lab and get a HOMA-IR and a get a fasting insulin and a fasting glucose, and then calculate your HOMA-IR. LPIR is specific to certain lab testing companies, and so again, if your doctor is knowledgeable about this, right? You can get it tested anywhere. You just need to know which labs do that and which ones don't.

28:19 >> Exactly. I wanted you to talk about other biomarkers too that we didn't have the opportunity to talk in our first podcast, and one of them is apolipoprotein B. There has been a lot of disagreement between apoB if it is really determinant of your overall heart health or not. What is your take on that? Yeah, so first to understand what apoB is, right? So, we've mentioned you have these lipoproteins, right? These particles in the blood that are transporting the cholesterol around, right? Cholesterol is a fat and our blood is essentially water and so you can't mix fat and water. So we wrap these things in these proteins that then transport it around.

29:06 And you know, these proteins become markers of sort of what they're carrying. And apoB is a marker that appears on LDL particles and VLDL particles primarily. We talked a lot I think the first time about, you know, why LDL is not really an ideal predictor of heart disease. >> Exactly. >> It's almost a coin toss it turns out when you're looking at LDL whether or not it's actually predicting heart disease. It needs context.

29:37 >> Yeah, it needs context, right? apoB has been shown to be a better predictor, but I would still say it's not a great predictor of heart disease. And the reason is apoB is on all LDL particles, right? So it's on the small particles and it's also on the large particles. apoB is on VLDL particles. Now VLDL and small LDL particles are atherogenic.

30:09 Large LDL particles are non-atherogenic. So the problem is when you're looking at an apoB level by itself, you still don't know, okay, what particles are you looking at? Are you looking at mostly atherogenic or you looking at mostly non-atherogenic? And that can vary a lot between people. Metabolic health, insulin resistance becomes one of the main factors there. So two patients both with what might be considered to be high apoB may have very different risk profiles.

30:44 Same with LDL. Same with LDL, right? Because it's it's it's uh suffering from that same problem, right? Because it's measuring all of the LDL, you don't have that fidelity to know, well, what type of LDL does this patient have? And therefore, what is their true risk? Yeah, it's a little bit different than the LPIR because it measures the small atherogenic particles, correct? If I if I got that right? Right. So, when your LPIR is higher, meaning that you are more insulin resistant, that's going to be reflected by you having more of these small dense LDL particles and more of those VLDL particles, right? That are truly atherogenic. Yeah, similarly to apo B because essentially it's like a tag on your LDL particles, for example.

31:36 So, if you have a higher amount, it's a higher tendency for you to have smaller particles. There's something called we talk about this concept of discordance in in you know, lipids. And um if you have if you have two patients with the same level of LDL, right? So, LDL is measuring mass of cholesterol essentially, right? You take all the cholesterol out of your bloodstream, you put it into one big ball, how big is the ball?

32:08 Apo B is really looking at more the number of particles, right? And like I said, it's not differentiating what type of particles, but number of particles. Now, it makes sense, right? If you have the same mass, the same amount of LDL and you have a higher level of apo B, more particles, on average, those particles are going to be smaller, right? So, this is why apo B can help us refine the predictive value of LDL essentially.

32:38 But, you still uh right so the problem we got into, right, is if you have what's considered a high LDL level, >> Exactly. your apoB is probably going to be again in that high range cuz more mass, more particles, right? But, those particles are probably going to be larger. So, two patients with the same apoB level, right, but different LDL levels, Exactly. you're going to be getting a different risk profile ultimately. Yeah, very similar to the lean mass hyper-responder phenotype, for example, right?

33:14 Yeah, with the keto CTA trials, they tested with CAC scores. I'm not sure if they did CT angiography or CAC scores. >> CT angiography in that trial, yep. Yeah, and most of them had very high LDL cholesterol. If you don't know, usually lean mass hyper-responders is a metabolic response by being lean, is that correct? And they have a really high LDL and apoB. Correct. Yeah, these are patients who go on low-carbohydrate diets and see a dramatic response in their LDL and apoB levels. They go up dramatically.

33:50 They tend to be leaner is one of the things that has been kind of discovered about them, and they have what has now become known as the lipid triad of high HDL, low triglycerides with the high LDL apoB level. Now, so the study that you know has been done over the past few years um did CT angiography on 100 of these patients 1 year apart looking at progression of disease.

34:25 And I think the most important finding out of the study so far is Um, the LDL or the apoB level, they looked at both, in no way predicted what happened to plaque over that year, right? So, if we accept the lipid hypothesis as it is, right, that LDL levels are what drive plaque formation and plaque progression, we would have expected these patients with very high LDL levels to progress their plaque kind of in um, in concert with their LDL level. The higher the LDL, the more the plaque should have been been progressing. And that was not found to be a predictive factor at all as to whether or not plaque progressed. Now, understand, yes, there were some patients that their plaque progressed. There were also some patients, despite these incredibly high LDL levels, that their plaque regressed over the year. And for the majority of the group, the plaque didn't change over the year. Uh, but again, they looked at what predicted whether or not people progressed or not, and LDL and apoB both had no predictive value when it came to figuring out who progressed and who didn't progress. And how can we change that dogma, for example, because even though we have a lot of data showing that insulin resistance is a much bigger factor, risk factor for heart disease compared to LDL cholesterol, specifically, and maybe apoB, depending on the context, how can we make this not a dogma, but rather a search for nuance in every single patient, not treat a patient like an average, but treat them as they are based on their genetics, the genetic predisposition, predisposition, etc.

36:18 Yeah, so this is certainly one of the challenges, because medicine in general these days uh, is very focused on guidelines on treating populations, right? And that translating that to individuals, right, is where the challenge now comes. Cuz if you say something like LDL when it's high is always problematic, right? And now we have this population, right, that we've brought to light these lean mass hyper responders where it seems that LDL is not problematic in these people. And I think, you know, a good physician individually, right, and a responsible medical system as a collective should be wanting to understand why that is. And that's what was so important about the Keto CTA trial, about the work that Dave Feldman has kind of pioneered. And definite shout-out to Dave.

37:17 One of I'll put a little plug in here. One of the things we want to do, right, is educate individual patients about this. So they can be bringing this issue up with their physicians. Go see the movie. It's called The Cholesterol Code. It's all about the trial. It's out now on Amazon. And I highly encourage people to go watch that, get yourselves educated, and then take those questions back to your doctor. And if your doctor isn't equipped to answer those questions, right, you know, it's not that you get mad or anything at the doctor, but you know, understand, right, this is not something that most doctors have been educated about.

37:55 But you empower yourself, right, and then maybe you can start to influence your doctor a little bit. Or maybe you say, "Okay, maybe this isn't the doctor for me. I'm going to go find a different doctor who does understand these things, who does think about these things." Your shift from the idea of a low-fat diet to eating a low-carbohydrate diet, what what did that come about? Did Did learn from a patient or did you learn by yourself watching something?

38:23 >> Yeah, so for me it started with me, right? I was morbidly obese, I was pre-diabetic, and I was trying to figure out how to address that. And that's what brought me to a low-carbohydrate diet. Now, similar to Dave Feldman, right? I went on the low-carbohydrate diet, and my cholesterol went up some. Wasn't as dramatic as a lean mass hyper responder, but you know, it went up some. And I started getting curious about that, and this happened to be right around the time that Dave was really, you know, talking about this. And he was actually one of the earliest people I found talking about this.

39:04 And you know, I then started asking, well, you know, Dave's an engineer, right? Why aren't there doctors talking about this? And in in no way is that a knock on Dave, right? I've told Dave I've told Dave, and I've said this many times publicly, right? I learned more about lipids from him than I learned from any of my medical colleagues or any of my medical textbooks. But, you know, it did get me curious, like why aren't we talking about this in the medical system? And that, you know, has been a big part of my journey as well. Hello everyone, I just came back from my running, and as you can see I did sweat a lot. And the main problem with sweating is that you lose sodium, potassium, and magnesium.

39:45 And you need to replenish that. And the best way that I do is with good quality electrolytes. That's why Salter is sponsoring this video, because I truly trust on their brand, in which they have good quality electrolytes, sodium, potassium, magnesium, in which is going to replenish what I've lost on my running right now. And they have many different flavors. They have lemon-lime, they have grapefruit, and even unflavored if you would not like to have any flavor on your electrolyte. I really trust them. I'm going to take them right now, and get back to the podcast.

40:16 I would like to shift a little bit our conversation right now on lipo lipoprotein A. This is a genetic marker and I would like for you to let us understand what is the relevance of it? Lipoprotein A, right? So, this is another one of these special markers, special proteins that are on some uh of these lipoproteins. Specifically, these are all on LDL particles. Um but a subset of them have this lipoprotein A attached to them. And what that lipoprotein A does is it basically makes that particle uh interact with the blood clotting system. Um you know, I kind of describe it that it becomes a more sticky particle. So, when we have a disruption of the endothelium, when we have damage to that lining of the blood vessel, um these lipoprotein A uh are going to basically cause these particles to start to stick to each other. And it's not again in the sense of forming plaque, it's actually in the sense of forming blood clots. Uh and these microscopic blood clots can then contribute further to plaque formation.

41:32 Um whether or not you have high levels of this lipoprotein A is largely genetically determined. However, there is some influence of diet, metabolic health, inflammation can increase lipoprotein A levels in patients that have this sort of genetic predisposition. Um but ultimately, lipoprotein A becomes a marker for increased risk of micro blood clots, which then can contribute to plaque.

42:03 Um very important, very under recognized. Again, it's not a test that most people get done when they're getting blood work done. But again, I encourage people ask your doctor for it. And then if you have elevated levels of lipoprotein A, what can you do about it? >> case. I want to hear it. Yeah, so >> My case, my mom's case, my dad's case, everyone. Yeah. Exactly. If you come, you know, if you're genetically predisposed to it, what can you do about it? So, mechanistically, like I said, blood clotting is the issue. It's not because of the cholesterol that these lipoprotein A particles are are transporting around, it's because of the blood clotting issue. So, you can do things that might mitigate against blood clotting. Taking an aspirin, taking a supplement called nattokinase, which can help counteract the potential negative effects about LP little A. Now, the first thing it should make you do is make you hyper aware, right?

43:05 of am I accumulating plaque? So, patients that have elevated levels of lipoprotein A, it's even more important for them to be looking for plaque. Get the CAC scan. Get the CT angiogram. Follow it over time. Um the other important interaction becomes inflammation. We know in patients that have elevated lipoprotein A levels that if they also have inflammation, most commonly measured by your HS-CRP level, that that is going to magnify the risk.

43:39 So, we don't have any reliable way of lowering LP little A levels today. Maybe coming. There are some medications that are under trial looking at that. But we can definitely lower inflammation levels. So, if I have a patient that has elevated LP little A, one of the things I'm going to be talking to them about is it is even more important that you keep your inflammation low, and what can we be doing for that? What can we be changing in your diet? What other lifestyle things can we be doing to lower your inflammation and therefore make the LP little A less impactful? Now, what's interesting to me, what I have been seeing is there is some effect of diet on this. I oftentimes see patients that go on low-carb diets.

44:27 Uh they improve their insulin resistance. They lower their inflammation. And their LP little little A levels do come down some. Um it may not take it from elevated to a normal level, but it at least becomes less elevated. And you know, that is probably lowering risk over time. Um and then finally, yes, there are some medications that target lipoprotein A. Uh they are in trials. Mhm. So far, they have demonstrated that they can lower LP little A levels um a fair amount, probably 50, 60, maybe 70% uh in some people. They It's not a universal response.

45:12 Uh what we don't know yet is will that translate to lower rates of cardiovascular disease ultimately. That's what's still being uh tested in the trials. Is there any story from someone you know or a patient that you're allowed to say that lowered their LP little A by doing diet, improving their inflammation, etc.? Yeah, I have a number of patients in my practice that have been able to uh pretty significantly, you know, 30, 40, even 50% lower their LP little A levels.

45:45 Uh combination of diet. And then uh there are some supplements that also have been purported to help. You know, I'll tell people in my experience with patients, the response to these is variable. But the two that come up most commonly are niacin and uh vitamin C. Okay, yeah. Both have been at least suggested to help lower lipoprotein A levels. The problem with both is you need to have fairly hefty doses of these and they both have limitations mostly around GI effects of high doses of these supplements. So neither one is ideal and like I said in the patients that I've had that have tried this and tested it I've seen variable. Some patients do respond significantly to it, others do not.

46:39 Yeah, my case for example when I took niacin, I think that was that was 2 years ago. I had a big skin reaction to it. I don't know if many people has had suffered this but I took it for the first time and I was really scared so it was crazy. >> is a big limitation. We get what's called a niacin flush syndrome and you know, and again the dosages that have been shown to be effective for lowering LP little A you got to get pretty high and in most people you know, you either have to increase it very slowly over time to try and give the body a chance to adapt or they just can't get to those high levels that are needed. So it's not something I generally recommend. You know, my focus because we can't really you know, effectively lower LP little A levels is okay, what can we do to mitigate the effects and it's an increased awareness of you know, you need to track your plaque over time. I would like to shift a little bit of our conversation now to CAC scores and CT angiography scores.

47:47 Yeah. That is something really important because we talked about apoB, we talk about LP little A, we talked about LDL, HDL etc. But these are just hypothetical markers of you having plaque or not. And I would like for you to explain what is a CAC scan and why that is even more powerful than having or apoB checked, or LDL, and other biomarkers. Yeah, so again, like you said, conceptually, right, the blood work is trying to predict our risk of plaque.

48:20 But it would be much better to measure the plaque, right? You know, measuring the disease is always going to be more important than, you know, predictive value. So, we have two ways, practically and non-invasively, of measuring plaque within the heart. We have the CAC scan, coronary artery calcium scan, and we have the CCTA scan, the coronary CT angiogram. So, these are both imaging studies. They are both CT scans, non-invasive.

49:02 The CAC scan easier to do, less complex. Um Both of these are non-invasive, I should say. But the limitation of the CAC scan is it only looks at calcified plaque within the blood vessels. Now, this is a good screening test. Generally, if patients don't have any calcified plaque, they get a CAC score of zero, we know that their risk of cardiovascular disease over at least the short to medium term is very low.

49:40 Um but again, we're only seeing the calcified plaque with the CAC scan. We're not seeing the non-calcified plaque, and we can't directly say how blocked up your blood vessels may or may not be. So, the ideal CAC score is zero. Um the highest CAC score I have ever seen is about 8,000. Oh, wow. Yeah, it can be a pretty long a pretty widespread. And within that, you know, patients always want to know, well, what the you know, what's the bad number?

50:12 What's the number that predicts my risk of having a heart attack? Um there really isn't an absolute cutoff for this. The higher it is, the more likely it becomes that you're going to have one or more blockages within your arteries that may be significant and we need to consider an intervention for. But, there can be a lot of variability in this. I have seen patients on the low end, CAC scores of two or 300, uh that end up having a blockage that might need a stent or something like that. I have a couple of patients within my practice with CAC scores in the multiple thousands, uh who have not needed a stent, have not needed bypass surgery, and they don't have a significant blockage. Uh the variability comes from, first of all, distribution of calcium. You can have a relatively smaller amount of calcium all in sort of one place in one blood vessel, and that might be associated with a significant blockage. You can have calcium that's sort of spread throughout the blood vessels, and no one area is significantly blocked. Um so, I used the CAC scan as the initial screen.

51:23 Um do we need to be worried about this patient or not? And then the progression of the score over time, how it changes over time, becomes an important predictor. So, um the nice thing about the CAC scan is it's easy to do, uh relatively low radiation exposure, uh and pretty inexpensive. Here in the US, usually you can get it done for 100 or 200 dollars. Um the CT angiogram is the more detailed study. Uh more radiation exposure, not a massive amount, but more. Uh you need to put an IV in the patient.

52:04 You need to administer intravenous dye, intravenous contrast. Um so now we can see the finer detail of those blood vessels. And now we can see how much soft plaque, non-calcified plaque is there in association with the calcified plaque. And we can actually now measure directly how narrowed is that blood vessel. So the CT angiogram becomes uh the next level of plaque assessment. Uh but you have to balance that sort of, you know, extra radiation, extra expense, uh more complex, uh versus, you know, the information that you're getting from it.

52:42 >> What would you consider uh to get this uh CT angiogram compared to see a CAC score, for example? >> Yeah, so generally I use the CAC score as the initial screen. If the CAC score is high enough, we are going to consider getting a CT angiogram. If a patient is uh having symptoms that might be suggestive of a significant blockage, I think a CT angiogram is a great step before you go to the invasive, definitive test, right?

53:14 What we call uh coronary angiogram or a cardiac catheterization, right? Where now we're actually feeding a catheter up the patient's arteries into the, you know, into the heart, and we're directly, you know, getting into those coronary arteries, putting dye in there, and seeing exactly what's going on. But that's an invasive test, uh has some risk associated with it. So the CT angiogram becomes a first um test where someone that's coming with symptoms that aren't maybe quite as definitive, right? They're not having a heart attack, but they're, you know, having some symptoms and we're not sure could this be blockage, may it not be blockage, a CT angiogram becomes a great test in that situation for us to start to figure that out. Now, I would like to ask you a big question.

54:05 That was talked a lot on our first podcast. And can we reverse plaque? Yes, it is possible. I am now seeing it routinely in my practice. People always want to know how, right? Obviously. But yes, can it be reversed? Yes. And and this has been shown over and over again, right? Whether you're looking at CAC scans or you're looking at CT angiograms, we know that some people experience plaque reversal, plaque regression, we call it. Um and what might lead to that? So, I always again, you know, high-level thinking, right? Yes.

54:41 >> Before you can get your plaque to get better, you have to stop it from getting worse. So, again, we go back to those root cause factors, insulin resistance, inflammation, poor quality cholesterol, right? Which is not quite the same thing as high cholesterol, but um if you have a lot of those small dense particles, a lot of those VLDL particles we talked about earlier, um and you're having ongoing damage being done to your blood vessels, there's really no chance that you're going to get it better if you don't stop making it worse. So, my first step is always let's stop making it worse and let's talk about the diet, the lifestyle, you know, the things that might go into, okay, we've we've created an environment now that there isn't ongoing damage and we're essentially giving the body a chance to do what it does, right? The body can heal itself Uh, as long as you stop doing the damage, and so, um, first step is address the insulin resistance, address the inflammation, address the quality of your cholesterol, and now you've created the environment where we can potentially start to see plaque reversal. What are some foods that you normally tell your patients to avoid at all costs to prevent that plaque, uh, progression and also to improve their insulin sensitivity? Yeah, so, um, highly processed foods of all sorts, and especially highly processed carbohydrates. Uh, that's first on my list.

56:13 >> [clears throat] >> Um, adjacent to those are going to be the highly processed fats, vegetable and seed oils. Uh, these are probably, you know, those two combined, and the honest truth is I don't know which one's worse, but they usually come together. Uh, so it's kind of a moot issue, but if you eliminate those things from your diet, right? And what does that leave you with? That leaves you with eating whole, real food, right? Meats and vegetables, animal proteins, animal fats, um, you know, vegetables, uh, and fruits, right? And you have to be a little careful with the fruits. The more insulin resistant to you are, those are carbohydrates, and you know, you may not be able to tolerate them well. But that those are the basics, right? That I talk about in Stay Off My Operating Table, I talk about in Stay Off My Kitchen Table, and that remains our, you know, kind of my first high-level advice to everyone is eat whole, real food. Uh, and that's going to get you a long way towards this. And, you know, the carbohydrate content of the food, uh, becomes important as well. The more insulin resistant you are, the less you can tolerate, uh, carbohydrates, even if they're coming from whole, real food, right? Even if they're coming from fruit or higher carb vegetables, you're going to have to be careful if you are more insulin resistant. Exactly. And one thing that you mentioned right now that is really good to address is that you're not against carbohydrates, real carbohydrates from food, etc.

57:44 Obviously, it depends on the context, how the insulin resistance is for each patient. Because on our previous podcast, when you when you mentioned about the carnivore low-carb diet, they really thought that you were against carbohydrates in general and they were taken out of context at all. So, is there anything that you would like to say about that? So, you know, what I tell people is um you um carbs are not essential, right? No one needs to eat them.

58:11 Um and so, something like a carnivore approach, a very low-carb uh you know, carnivore approach is a perfectly valid dietary approach. Uh I am very confident in saying these days it does not contribute to worsening heart health, it does not contribute to cancer, uh or really any of our other significant uh metabolic diseases. Um that does not mean that everyone needs to do a carnivore diet. Um your tolerance for carbohydrates, when we're talking about real whole food, you know, carbohydrates, is going to depend on how insulin resistant you are, how active you are, and how much muscle you have. Those are the three biggest factors that determine how much carbohydrate you might be able to tolerate in your diet, right? Um again, is it essential to have any carbohydrates in your diet? No, it is not. Flat out, you can do a you know, carnivore diet that essentially has zero carbohydrate, you can do that long-term, and you can be very healthy.

59:17 Um but if you want some carbohydrates, it's important to understand how insulin resistant am I, uh how much muscle do I have, because muscle becomes one of the places that we can kind of store away some extra carbohydrate, and how active am I? Am I going to be able to burn off those carbohydrates? Um and that will then lead you to understand how much carbohydrate you might be able to uh tolerate safely. A great tool for this is the continuous glucose monitor.

59:50 Um the continuous glucose monitor will show you how you react to whatever carbohydrate it might be, right? How many blueberries can I tolerate without my blood sugar spiking? How much rice, how many baked potato, you know, uh that is really the best tool that we have as individuals to figure out, you know, what my carb tolerance might be. Yeah, and one thing that it is really good that you mentioned is about the amount of muscle that you have because many people try to focus on improving their health just focusing completely on cardio and losing weight all along and they completely forget about muscle and that is very crucial for us. Yeah, there are two unique advantages that muscle give us, more muscle mass gives us.

60:35 Number one I mentioned, um we store something called glycogen within our muscle. And so if you're uh you know, have excess sugar in the bloodstream, you're you know, have carbohydrates coming in, right? Glycogen becomes one way that we can get that sugar out of our bloodstream. We put it into our muscle and our muscle then can use that for energy, you know, later on. Uh and the more muscle mass you have, the more room you have to store glycogen. The other advantage of muscle is muscle is very metabolically active tissue. Uh even when you are not moving around, even when you're asleep, right? Your muscle is still burning through some energy. And so um the more muscle you have, the more energy you're you're to be burning through uh burning throughout your day and that's going to give you again some more leeway as to you know can you tolerate more energy coming in and what forms that energy might be in.

61:34 One other thing that is widely used to reverse plaque as a as a tool would be nattokinase. I would like to know from your perspective why nattokinase mechanistically is really important for reversing plaque and has been widely used for therapies like that. Yeah, so we mentioned nattokinase earlier in the context of LP little a, right? So nattokinase is essentially a natural blood thinner. It actually assists with breaking down blood clots if they start to form. And because blood clotting is part of this plaque formation process, therefore nattokinase may be able to protect against plaque formation and lower plaque levels.

62:24 There is one good trial that has demonstrated this. I always caution people when you only have one trial, you might you know we really ideally will get further confirmation of this but this trial done in Japan it was about a thousand patients. They were looking at plaque within the carotid arteries in the neck that we mentioned before and they looked at patients on two different doses of nattokinase compared to patients not taking nattokinase.

62:55 And what they found at the highest dose of nattokinase, 10,800 units a day, was that there was a statistically significant reduction in plaque within the carotid arteries in these patients taking that level of nattokinase. At the lower dosage of nattokinase, 3,600 units a day, they did see reduction of plaque, but it did not reach that statistical significance. And of course, patients not taking nattokinase tend to progress their plaque over time.

63:27 So, you know, that gives us very good reason to suspect that nattokinase may help stop plaque progression and actually lead to some plaque regression. Nattokinase is fairly low risk, right, to take it? >> Yeah. So, very low very low collaterals, you would say. Yeah, side effects, exactly. So, low risk associated with taking it.

63:57 Certainly maybe some benefit, and therefore I typically recommend it to any patient who's dealing with plaque. I don't say everyone should be taking nattokinase. We have absolutely zero evidence, right, that if someone who does not have plaque today takes nattokinase that it's going to prevent plaque from forming over the next 10 to 15 years. So, I don't universally recommend it, but anyone that has plaque, I think it's a good idea for. If you have an extra risk factor like LP(a), probably a good tool to consider bringing in. Now, I always say supplements are supplementary, right? They shouldn't be the main you know, the main approach, right? So, if someone's insulin resistant and they have inflammation, and they think taking nattokinase is going to like counteract all of that and they can continue eating a poor diet and you know, having other poor lifestyle factors, probably not going to end up well for you. But if you're already doing the diet and the lifestyle, and you want a little bit extra that might help, you know, stop the progression and and reduce the amount of plaque you have, I think nattokinase is a great option there. I would like to know also if nattokinase can only help with soft plaque or also calcified plaque? Uh unclear, I'll say.

65:18 Uh the studies really didn't uh look at that, right? You know, I would love to see a study looking at CAC scans or looking at uh coronary CT angiograms, right? They were only looking at amount of total plaque uh with ultrasound of the carotid artery. So, it uh although you can sort of differentiate on ultrasound between calcified and non-calcified plaque, uh it's really they didn't look at that. Yeah. So, um what I can say from my clinical experience, I have patients who have taken nattokinase as part of our overall plan, paying attention to metabolic health and all that, and their CAC scores, right?

65:58 So, only looking at their calcified plaque, have decreased. Um so, uh one piece of data, you know, and uh So, I do believe it can contribute to the overall plan of lowering both calcified and non-calcified plaque, but we really don't know like mechanistically, you know, what nattokinase can uh you know, attack and not attack essentially. I have seen that there's a lot of heterogeneity on that. A lot of people can reverse plaque, a lot of people have a hard time doing that. What has been your experience with it?

66:35 Yeah, I do think there, you know, some people do, right? >> Yeah. The overall plan that we've talked about, and uh see plaque regression. Others, we just stop plaque progression. Now again, going back to the CAC scan, we have very good data from CAC scanning that if you stop your progression, right? So, on average, a CAC scan uh when you look across the population, uh you scan someone today, you scan them a year later, uh we expect to see it's going to depend on your age and other factors, but we expect to see on average about a 10, 15, maybe 20% progression per year in CAC scores. We know that patients that progress slower than that.

67:21 So generally under 10% per year is the number you'll see. Their risk actually goes down. Despite what their absolute score might be. So to really explain this well, you know, put some numbers to it. If I have a patient with a score of a thousand and a year later their score is still a thousand, I'm actually going to be less worried about that patient and they have lower risk over let's say the next 5 to 10 years of a heart attack than a patient with a score of 800 or I should say a patient with a score of 400 that then goes to 800 the following year.

67:59 Right? So at year two, right? We have someone with a thousand, we have someone with an 800. The 800 person may actually be at higher risk if they've had that significant progression versus the thousand that has stayed a thousand. Because you got to let's say decrease the delta that is making that plaque to progress. So there's more stuff for you to do for that person that is increasing on a higher rate than the person is that is staying stable. Yeah. And at a high level it's telling you, right? You have not addressed the underlying driving risk factors in the patient that's progressing where someone who had past damage, but now we've addressed those risk factors, they're not having active plaque formation and therefore they are at lower risk of ultimately having the cardiac event.

68:49 Is there any other supplements? You mentioned niacin, I don't know if it was specifically for prac plaque regression. What does niacin do? Is that Is that correct? You said for plaque progression? >> Well, niacin was specifically targeting lowering LP little A. >> Okay. Niacin has also been reported to help lower LDL cholesterol levels, which is why some people think it can help with plaque progression. Yeah. I don't put it in my generally recommended bucket.

69:21 The other I guess the other big one besides nattokinase that I would point to is vitamin K2. Mhm. Vitamin K2 is specifically directed at the calcified plaque. Yeah. Vitamin K2 helps regulate where calcium ends up in our body. So, again, the way I explain it to people maybe a little simplistic, but vitamin K2, when we have higher levels of it, it's signaling the calcium to go into our bones, to go into our teeth, where we want it, Mhm. and not hang around in our blood vessels where it may end up contributing to calcified plaque. So, the evidence honestly is not quite as robust as nattokinase, but there is some evidence that vitamin K2 may specifically help protect against progression of calcified plaque. So, that's another one that I put in as a useful. And then the other supplements that I think about are directed towards Right? The reason that plaque forms to start with is because the endothelium, the lining of the blood vessel, has become damaged. So, what can we do to protect the endothelium? And there are two substances, supplements that come into play here. One is nitric oxide. Nitric oxide is something our body makes and helps promote healing of the endothelium, helps protect the endothelium from damage. Also helps relax our blood vessels. So, it tends to lower blood pressure, and if you do have a blockage, right, And you can get that blood vessel to kind of relax and enlarge and open up a little bit, you're going to get more blood flow through there. Uh so, nitric oxide becomes a good target for supplementation. And then vitamin E is another one that comes into play here that also helps that endothelial health overall and can protect against the damage to the endothelium. Yeah, fighting against any reactive oxygen species or anything like that that can harm your endothelium in general. Would you say that because our knowledge of vitamin K2 supplementation with vitamin D is fairly new, I would say, for the last 10 years, 5 years.

71:36 And from what I know, a lot of people have taken vitamin D by itself, which could have harmed their arteries in a way for progression. Would you say that could be something that could have harmed? Well, yeah. So, the concern is so vitamin D, vitamin K2, and calcium, right? Interact with each other. And if you get out of balance, right? Uh if you have too much vitamin D with not enough vitamin K2, you could end up uh um you know, increasing the amount of calcium pulling the calcium out of your bones, right? Increasing the amount of calcium therefore in your bloodstream that could ultimately contribute to more calcified plaque. Uh so, that is a concern and we do routinely uh advocate for people to take vitamin K2 with their vitamin D. Now, vitamin K2 is not actually new. Um >> Really? Okay. Uh probably the first discovery or the first recognition that vitamin K2 had something to do with health uh goes way back to uh Weston A. Price.

72:39 Uh Weston A. Price was a dentist early 1900s. He was going around studying uh native populations and he was interested in uh you know, the health of the teeth. But, you know, and what he ultimately recognized was there was something that he called substance X. The X factor. >> The X factor, right? That helped people be healthier as evidenced by better jaw formation, better tooth better tooth formation, better oral health. And we then discovered subsequently that his substance X is actually vitamin K2 that was more present in the diets of these native people whereas people eating Western processed diets were getting lower levels of vitamin K2.

73:29 So, interestingly the history goes way back. We just didn't recognize it as such. Yeah, I had a crazy story because I've read the entire book from Weston Price. It's it's a fairly big book because he goes all the way from the entire story that they found the indigenous species and and all of that. And also all all all the scientific data that they had at that time. I think it was in the 50s, something along those lines, 30s.

73:56 That he visited the whole world and comparing people who were in the cities and people who were eating eating healthier foods. And one of the interesting stories is that I had this book and I was going to gift it to a friend that had that he was a nutritionist and he read it himself some of the work from Weston Price, but he didn't have it available for him to buy. And then I told him, "Okay, I can buy one for you and gift you." And I was going to give that to him. But then I saw a I was talking with a Uber driver.

74:27 Usually they don't have as much, you know, money and anything like that. And he was he he was mentioning that his son was doing dentistry. And that he's really he's really focused on overall health, diet, and how that is really important for it. And then I was like, "Okay, let me just give that to you. I have a gift for you. And then I just give that to him. And I told my other friend, man, I can bring you next time.

74:52 This guy really needs it more than you. I know you like it. I know I was going to gift you that, but I can I can bring it back and give you an online version after that. So, that's pretty much the story I had it from it. And I love the story from Banting Prize. Yeah, he really did amazing and groundbreaking work. And it remains very relevant today. And like I said, he was one of these people that was sort of ahead of the science that was available at the time, right? He couldn't identify what substance X was.

75:23 But his work has remained true, you know, a century later, a cent you know. And Dr. Ovadia, to close off our podcast, after seeing thousands of hearts from your experience as a cardiothoracic surgeon, what do you wish everybody to understand before it's too late to be in on your operating table? Yeah, so the big thing I want people to understand is heart disease is preventable. I would estimate, you know, based on kind of everything we know today, that 90 to 95% of the patients that end up on my operating table for plaque in their arteries, blockages in their arteries, would not have ended up there if they knew how to prevent this. And so, that really should be our focus when it comes to heart disease. Yes, we have had success, right? We are much better at treating people with heart disease today than we were, you know, 20, 30, 40, 50 years ago. We can keep people alive longer with heart disease. But we have done an absolutely miserable job of preventing heart disease. And if we're really going to have impact, right? And I want to have impact. My mission is that heart disease will no longer be the number one killer.

76:50 Um it has been the number one killer here in the US now for nearly 100 years, and it is not slowing down. We are not making progress against it. And the only way we're going to do this is prevention. So, uh that's what I want people to understand. You don't need to end up on my operating table. Uh take control of your health now. Uh figure out what needs to stay off your kitchen table so you can stay off my operating table. You have many problems, but when you have a health problem, you just have a single problem.

77:23 And lastly, where can our viewers find the book? Yeah, so uh the book Stay Off My Kitchen Table widely available uh for pre-order. It's going to be coming out end of July. You can go to stayoffmykitchentable.com. Uh you can get all the links of where to order it. We have a lot of uh bonuses going on around people that are ordering it. So, uh stayoffmykitchentable.com. That's good. Thank you very much for having you on my podcast, Dr. Ovadia. It was great talking to you. Pleasure being back with you.