55. Biophysics of Aetherosclerosis, Beyond Cholesterol with Stephen Hussey

Stephen and I explore the causes and prevention of aetherosclerotic cardiovascular disease (ASCVD) from a biophysics perspective, leaving behind the biochemical, lipid-based model of heart disease. We discuss the role of clotting in acute myocardial infarction, endothelial health, fourth phase of water, sunlight and the impact of deuterium on mitochondria plus much more.

Stephen Hussey, MS, DC a chiropractor and functional medicine practitioner, Type I diabetic and myocardial infarction survivor.  He is the author of the recently published book, Understanding the Heart.

I personally believe Stephen is closest to the mark of understanding the true causes of ASCVD and I think his message is frankly paradigm shattering. Be sure to share this one with anyone who is interested in preventing heart attacks.

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TIMESTAMPS
00:03:00 Type 1 Diabetes and Glycemic Problems
00:13:00 Acute Myocardial Infarction and Clotting
00:24:00 Traditional Risk Factors and the Role of LDL
00:32:00 The Role of Cholesterol and the Flaws in the Lipid Hypothesis
00:41:00 The Importance of Structured Water and Endothelial Health
00:49:27 Structured Water and its Role in Cardiovascular Health
00:52:50 The Paradigm Shift in Cardiology
00:56:43 The Importance of Sunlight for Cardiovascular Health
01:04:54 The Benefits of Grounding
01:18:44 The Role of Deuterium in Mitochondrial Health

LINKS

Understanding the Heart by Dr Stephen Hussey - https://www.amazon.com/Understanding-Heart-Surprising-Evolutionary-Disease_and/dp/1645021300

Follow Dr HUSSEY

Twitter: https://twitter.com/DrStephenHussey
Instagram: https://www.instagram.com/drstephenhussey/

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DISCLAIMER: The content in this podcast is purely for informational purposes and is not a substitute for professional medical advice, diagnosis, or treatment. Never disregard professional medical advice or delay in seeking it because of something you have heard on this podcast or YouTube channel.

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Transcript

Speaker 1: 3:34

In this episode I'm speaking with Steven Hussie. Now he is bringing a quantum biology and circadian biology lens to the problem of atherosclerotic cardiovascular disease or heart attacks, and his analysis of this problem with regard to the fundamentals of biophysics and what is occurring at a mitochondrial level are incredibly insightful and incredibly refreshing for those who are trying to understand how to prevent the development of heart disease or stop them from getting another heart attack. So if that's you, then I would highly recommend listening to this podcast. And why I believe this is so important is because, despite improvements in acute management of heart disease and acute myocardial infarction, we don't seem to be getting any further in really preventing the onset of atherosclerosis and we really can't solve problems within the same paradigm and intellectual thought pattern that these problems arose in. So, moving past this biochemical biochemistry, lipid model of heart disease, I think, is what is needed, and what Steven is bringing to this problem and his perspective and analysis is just amazing. So I really encourage you to listen to the end of the podcast. And, as always, this is not medical advice, so please always consult your treating clinician before making any medication changes.

Speaker 1: 5:19

Now onto the show. Steven, I see you. Welcome to the show Thanks for having me Happy to be here. Maybe start with a bit about yourself, what you do and your perspectives on heart disease.

Speaker 2: 5:38

Yeah, so for a living I'm a chiropractor and a functional medicine practitioner. I have, obviously, dr Chiropractic and Master's degree in human nutrition, functional medicine, and so my day in, day out, I'm neuromuscularly scalodally treating people, adjusting their spines, helping them with various problems with the musculoskeletal system. But I also have a passion for heart disease because of my own health journey, and so I spent a lot of time diving into that topic and the things that I found were shocking to me along the way, and it's been probably a close to 15 year journey now of doing this. But yeah, I've always been very passionate about health in general, ever since I learned whoever, since I had health conditions as a child that my parents and I kind of relied on Western medicine to help us get through, and it wasn't until college when I started figuring out that the way I lived my life impacted my ability to manage and even reverse lots of these conditions I had.

Speaker 2: 6:45

As a child. I thought it interesting that I never heard that from doctors, and so that kind of pushed me into this direction of how can I live my life, the best way possible to get rid of these conditions and to keep them away and achieve health, and so I've always been passionate about that, and specifically heart disease, because of my own journey. So eventually I found myself with a bunch of information about heart disease and I started sharing it on social media. Eventually I wrote a book about it, and here we are today. People seem to enjoy the information that I share and it's benefiting people, so that's what I'm doing today.

Speaker 1: 7:28

Yeah, and your history includes a diagnosis of type one diabetes that you had in adolescence and then you had an acute myocardial infarction several years ago. So I think those two events make you uniquely qualified on an experiential level to delve into this topic, and obviously all your own private reading and self education around that and has led you to this point. And the thing that I really admire about your work is the fact that you're not anchored within an existing paradigm of thought with regard to atherosclerosclerosis cardiovascular disease and I'm always excited to talk to people like you who approach these traditional problems in medicine from this orthogonal, out of the box way, because we get very refreshingly unique perspectives. So maybe start with the type one diabetes and maybe explain to people why glycemic problems are an issue for atherosclerosclerosclerosclerosis and maybe build us up to where you are now in terms of your journey.

Speaker 2: 8:36

Yeah, definitely. So you know, at age nine I was diagnosed with type one and my only inclination that something was wrong was that I was peeing more often and I felt weird. I just felt like you know, as a nine year old kid, I just felt like claiming weird. And I went into the doctor and they my blood sugar was like over 700 at the time. And so, you know, learn to manage type one diabetes by insulin injections and things like that.

Speaker 2: 9:06

And the reason that diabetes of any nature, where there's type one or type two, contributes to vascular issues, cardiovascular issues, is because blood sugars are fluctuating. Blood sugars are higher than normal. I might have. Well, I manage my blood sugars, which I have very tight control. They're still going to be higher than the average person without type one diabetes. And type two is different because it's not that my, not that your body just stopped making insulin like mine does, it doesn't make insulin anymore. It's that you're still making insulin but your body has gotten so sick that it's not even responding to that insulin. So type two is oftentimes worse and the damage becomes or the damage happens faster because that person's already gotten to this poor state where they're not even responding to insulin, whereas in my case it doesn't happen as fast but it still happens.

Speaker 2: 9:58

And the reason that it happens is because two things One especially like in the arteries. One is that when your blood sugar is higher, you know a certain percentage of your, you know tissues but especially red blood cells, and are elements of the blood are supposed to get quote unquote glycosylated or filled with sugar over a certain period of time. But obviously if my blood sugars are higher than the average person, then that's going to happen to more of them. And when they're damaged by glucose like that, they become problems. They can become damaging to other tissues in the body. So that's one thing. So the elements of blood become more damaged by glucose, or more of them do. And the other thing is that fluctuations in blood sugar because I'm not a pancreas, I can't work like one. I'm trying to predict how my blood sugars going to react and get myself insulin. I'm only assuming that insulin gets absorbed well wherever I injected. It's just there's all these variables. Because of that there's more fluctuations in my blood sugar than normal Same with the type two diabetic and those fluctuations are very damaging to the lining of the artery when we get these abrupt increases and decreases in blood sugar. The fluctuation seems to be even more damaging than just having higher blood sugar in general.

Speaker 2: 11:21

So my number one goal is to try and keep things as stable as possible. But that's why type ones are predisposed. And so, you know, I spent a long time figuring out that I could help manage that. Because the advice I got from Western Medicine was oh, here's this book with every fast food listed that you could get anywhere, listed, and the amount of carbohydrates in it, so that when you eat these carbohydrates you give yourself insulin for it. That's all you got to worry about. And so that's what I did for years, you know. And so eventually I figured out that was not the best way and it was way easier if I didn't eat these processed foods. And I exercise regularly and just on and on and on and on and on. I've gone way down the line. It's not just to have an exercise.

Speaker 2: 12:05

And so over the years, you know, I would go to endocrinologists and I'd see the. You know the postures in their office. Like diabetics are predisposed to eye damage and you know diabetic neuropathy and kidney damage and amputations and other things. And it was all because of these vascular issues. That can happen Because the smaller arteries get damaged quicker, faster, and those areas of the body you know have smaller arteries and they can get damaged because of that.

Speaker 2: 12:35

And so, you know, I eventually started changing diet. It was like, you know, it was just eating a little bit better and then a little bit better, and then I went vegan for a while, which was a mistake. It is about a year and a half. I did that maybe like 12 years ago now, and then we'll pay Leo and then eventually went low carb. And I went low carb and I'm what some in the space in the biochemistry, lipidology space would call lean mass hyper responder, and that when I went low carb, you know, and people who are lean and relatively fit then they send, they can see these elevations in LDL or cholesterol. Ldl cholesterol but and I was one of them, I mean my skyrocketed. But it varies. Sometimes it's only like total cholesterol is only around two, 300, other times it's 500. You know, it's just, it's very. We can talk about why that is and why I think that is. But so, yeah, I was concerned about that at first but then found that, you know, there's not so much of an issue if I have metabolic health and so then you know if my, if my treat ratio ratio is good and other things that signify metabolic health were good, that's not so much to worry about. And so that's kind of what I went into or went in, lived my life by those things that I should be good right, and so I'm doing that.

Speaker 2: 13:54

And I went through a period of a very high stress, and probably One of the most stressful news that I got in my life happened a day and a half before I woke up one morning, did a very intense workout and had a heart attack and it was not you hear people talking about. Oh, I was walking around with the heart attack for a few days and I felt this weirdness but I couldn't tell what it was and eventually went in as heart attacks. It wasn't that at all. It was very, very straightforward. It was yes, I have intense chest pain right here. I can't really function or do anything. I should probably go to the hospital.

Speaker 2: 14:35

It was very it grabbed my attention for sure, and it was 100% blockage of the left anterior descending artery, which is the biggest artery in the heart. It's the most common place for a heart attack to happen and it was just a giant clot. You know I, previous to this, about six months earlier, I got a CAC score, which is a measure of how much calcified plaque there is in your arteries, and I had zero, completely normal arteries as far as heart and plaque, and they say that's a good predictor whether or not you have a heart attack. Yet here I am six months later having a heart attack. And when they went in to check things out and open up the put enzymes in there to bust the clot and go in there and see if they needed to place a stint, they found no atherosclerosis anywhere. So you know, they said very, very mild, if anything soft plaque in an area that wasn't even where the clot happened. And then then there was just giant clot. You know there was no narrowing of an artery before there, it was just clotting material right there. And so they busted the clot, they placed the stint, which I could argue they didn't need to place the stint. But that was their clinical call and I'm grateful that I'm here today because of what they did. So I'm not really going to harp too much on that.

Speaker 2: 15:56

But you know, after the fact, you know they saved my life and here I am laying in the hospital completely doubting everything that for about you know, six hours I'm just laying here like doubting everything that I think I know and then, after the fact, I received this care in the hospital and for the three days that I was there, it completely reinforced everything that I've learned about health and how the body actually works. Because what they were telling me to do was three things. One, it didn't make sense logically. Two, it was clearly being pushed by pharmaceutical and big food and things like that. And three, it was not reflective of the research. You know, if the research is how you dictate what you do, which for some people it is, some people it isn't, and I can make both arguments.

Speaker 2: 16:51

What they were saying, what didn't even reflect what the research says and I was very familiar with it at that time, especially about cholesterol and that's what they kept harping on it's like oh, your cholesterol is high, that's why you're heart attack. And I was like well, are you aware of the study that shows that? You know, they did, like 60% of the heart attack admissions and they measured their cholesterol within 24 hours and their cholesterol most of them were normal or ideal and they still had a heart attack. Like what about that? You know? And they weren't aware of that when I brought that up. So it was clear there was a lack of knowledge about the subject and it was I was a cookie kind of thing, you know like someone has a heart attack, this is what you do to them, because this is what we were taught in school.

Speaker 2: 17:29

Here it is, and it's based on this cholesterol theory of heart disease, this lipid theory of heart disease, and so I was open to listening to them because, hey, I just had a heart attack, like give me your opinion, I want it. I don't know if I'm going to do it, but I want to hear it and I was taking any information I could at that time. And so the other thing was that clearly there was something that I missed too, because this still happened to me. And, yes, I'm predisposed to type one and there's even evidence that type ones are less able to handle, especially when under stress. Let's say, we'll handle stressful things like the workout that I did, which I think I should not have done. Based on my stress levels and how I was feeling at that moment in time, I shouldn't have tried to do that workout.

Speaker 2: 18:19

But yeah, there's lots of different factors and clearly I missed something, and that's I was aware of a lot of different things when we talk about more of a quantum or biophysics perspective.

Speaker 2: 18:32

I was very aware of them, wasn't doing them and I have gone much deeper into them in the last three and a half years since this happened and learned a ton, and it all makes sense based on everything I knew before, everything I know now, and to me it's the path forward and it's what I've used to completely heal my heart. It's 100% recovered, which they told me would not happen if I didn't follow the recommendations, and I also reversed atherosclerosis in my leg that started to develop because the procedure they did place the stent. I reversed that when they told me that that would never happen either and I didn't take any medications or follow their advice. So I'm kind of this living example of the fact that there's more to it than just this cholesterol theory and placing stents and taking drugs, and you can do it in other ways and I hope that they figured that out soon.

Speaker 1: 19:25

Yeah, and this is a fascinating example of this concept of you being an N of one, which means you're an experiment in and of yourself, and that has amazing power in terms of mechanistically understanding what is actually going on here. Couple of points and some context for my listeners. So what you mentioned earlier in terms of the fluctuating blood sugars and glycemic problems, either, as you mentioned, in type one or type two diabetes, are a risk factor. As you mentioned, the fluctuations in blood sugar, is damaging the endothelium and I think that is just for again, background before we delve into the minutiae. But for everyone that is imagining a blood vessel, if they imagine a pipe, there's basically three layers of the pipe and there's a really thin layer of cells called the endothelial layer which is lining that inside blood vessel, and in that endothelium is what's called a glycocalyx, which is a bunch of glycoproteins that stick out of the blood vessel wall, into the lumen, into the flowing blood of the vessel, and they have a mucin-like, mucous-like effect which is, if you ever touch a fish, it's very mucous-y. That's similar to what's happening on the inside of the blood vessel. So what Stephen was mentioning in terms of the glycemic dysregulation is you're going to damage that endothelium, you're going to damage the glycocalyx, and what I believe is going on, and what you believe too, and we're going to explore this, is that it's endothelial dysfunction and endothelial injury that is at the root of this whole atherosclerotic cardiovascular disease problem, and insulin resistance and hyperinsulinema is also going to be generating endothelial damage.

Speaker 1: 21:05

The interesting point you made was, and then coming up to your heart attack event, your acute myocardial infarction. You had this CAC score the year before. It showed symptoms 0. And the CAC score is a risk stratification tool and, as you mentioned, it shows hard plaque, it doesn't show soft plaque. So we use it to simply really further refine someone's risk score, but it is not a functional test and it shows nothing about flow or stability or instability of the endothelium, which is a really, really key point.

Speaker 1: 21:37

So what I think your story illustrates is that you had a couple of issues at the same time that precipitated what sounds like an acute thrombotic event in your LAD artery and you were stressed, you were working out intensely. Those two are really important and it flies in the face of this concept of heart disease, this kind of slow buildup and stenosis of the vessel and then suddenly I've had too much fat in my diet and now the artery is blocked. What happened to you was an acute thrombotic event, sudden onset of symptomatic chest pain, like it's on and off. So obviously you just threw off a massive clot. So I think what we're going to talk about in this interview, what I think is the crux of the problem is that we have to understand what causes someone to clot and in order to help prevent this problem. So maybe talk about why you think you had that acute myocardial infarction.

Speaker 2: 22:37

Yeah, and so my I'll call it best guess because it's all I can do. No one's ever really going to tell exactly what happened in that instance. All I know is that there was no atherosclerosis. Atherosclerosis present first, and then all a sudden boom of a giant clot and that's all they found. That's what they told me was clotting material. But if you look at atherosclerosis, it's clotting material, like a large percentage of it, almost 90% of it, is fibrotic material. So the people like clotting material, like if you cut your skin, clot forms a scab. So think of kind of similar to scab formation on the lining and inside lining of your artery. And so what causes clotting to happen?

Speaker 2: 23:22

And then when we talk about those things, I'll talk about the specific things that I think happened, that caused my clotting to happen, and so anything that can damage the lining of the artery. So, and there's lots of layers, there's even another layer than the ones that you talked about. You know, there's the endothelial, like calyx, but then there's a layer of structured water which I'm sure we'll get into. But all those things can get damaged, and they can get damaged by things that want to steal basically energy from them, everything's we're all just trying to harvest energy from our environment and maintain our body. And the endothelial cells in the lining of the artery are the same way, and so when that energy gets stolen it creates damage. So what can steal that energy? Well, you know, in the health space everybody throws around the term like free radical or oxidative stress or inflammation, and all these things are kind of you know they're different processes, a little bit that oxidative stress and inflammation, but they're mostly the same thing. In my opinion. They lead to the same kinds of imbalances in the body. And so just a kind of hit list of things that can create oxidative stress and damage the lining of the artery. One psychological stress can definitely do it.

Speaker 2: 24:33

Toxin exposure everything from plastics to heavy metals to air pollution, lots of different things like that have definitely been shown to cause damage to the lining of the artery. Toxins that happen when we get bacteria that's in the body that goes into the wrong place, so it's in the gut or it's in the mouth or something and it leaks into the bloodstream and it shouldn't be there and the body tries to kill them and then releases endotoxins. So that can happen for dental health or gut health. Those things lack of, like I said, lack of energy, so like lack of sunlight or grounding or things like that, like decreasing the amount of protection of the lining of the artery and of the elements of blood, all these things can contribute to this eventual damage. And then insulin resistance for poor metabolic health, which is type 2 diabetes, like that's what leads to type 2 diabetes, but it can be present well before type 2 diabetes happens.

Speaker 2: 25:32

What that plays a role? Because when this damage happens, the body can repair itself. However, it's really dependent on insulin signaling for that repair to happen in the endothelial cells. They really dependent on that, and so if you become insulin resistant, which is that precursor to type 2 diabetes, and if you become full blown type 2 diabetic, then your cells are not getting that signal to repair. So the damage happens and the repair is malfunctioning, and so that leads to the body having to do something else. To quote unquote repair the tissue and just like it would repair a scratch on your arm with the clock, it does the same thing on the lining of the artery.

Speaker 2: 26:16

And so those that can happen gradually over time, and it can happen on the lining of the artery, that clotting material can form right there and that's what we call atherosclerosis, and at first it's soft and it gets there. If it's been there long enough it can form hard plaque, and so that can happen gradually from kind of low grade inflammation that can be there chronically for a long period of time and we can develop this atherosclerosis. And it happens only in arteries. We usually don't see it in veins because the arteries are under more pressure, so things are getting pushed up against the lining of the artery more. We usually see in lining areas of the artery where there's a curve or where there's a bifurcation of an artery, where they split, because those are areas that are usually under more pressure and the heart arteries happens the most or it's at the most risk for intense clotting because those arteries are under the most pressure of any arteries in the body, especially the left anterior descending artery, and so, like I said, that can happen gradually over time. Or if you get yourself into a situation where there's enough inflammation and enough pressure, then a clot can form. When this happens, sometimes in people's legs, they call it a deep vein thrombosis. It can happen in lots of different areas, happens in the brain, called strokes, and so the theory is that you get soft plaque and the soft plaque rupture is causing a clot. But there's many issues with that theory. We can talk about For me, the fact that I was under a lot of stress for about eight months to a year before this happened.

Speaker 2: 27:57

And then I received some very stressful news about a family member a day and a half before it happened. And I tried to do if anybody knows anything about trying to manage blood sugars when you're that stressed it's very difficult. So my blood sugars were up and down a little bit more than usual at that point and then I did that workout and I think that that, because it was like 15 minutes after, my blood flow kind of calmed after the workout and then I was just sitting there making some food on the stove and then boom, clot happened as soon as my blood flow got low enough. And it all happened because I think I created a situation, unfortunately, that there was this kind of maybe lower grade inflammation from blood sugars that are always going to be higher than the average person going through that stress, having the acute stress, and it was the stress.

Speaker 2: 28:46

The stress affected me most because it was the inability to do anything about the thing that caused the stress. Me or my family could not get to this person and help them. So it was just kind of like this waiting game we hope everything's okay and so that was an issue. And then I did the workout and inflamed everything and as soon as the blood started slowing down from the workout, the clot formed in that most vulnerable area, which is the left hand here descending artery of the heart. And there we are, and it was a big enough clot that it blocked the whole artery. Pretty much that's what happened.

Speaker 1: 29:24

Yeah, very interesting, steven, and there's a couple of points I want to make. And one is really relevant to this issue, which is Workhouse Triad. And this is an old physiological kind of framework of thinking about blood clotting and it involves three factors and they are endothelial injury, hypercoagulability and blood stasis. So those three factors influence the likelihood of forming a clot or not. And if we think about what you've talked about, then it makes sense when we're considering what's going on here. Endothelial injury is the blood glucose dysregulation. It's those factors that you mentioned briefly before. Hypercoagulability is the state that you get into when we're insulin resistant or when we are on that scale of metabolic dysfunction, and there's blood markers like fibrinogen which kind of can give insight into that hypercoagulability. And venous stasis, and I think that that means or venous arterial stasis is occurring when, as you mentioned, there could be some interruptions in flow, especially around breakpoints or branching in the artery. So that is a fundamental thing to think about in terms of blood clotting, and the person who I have read a lot about, who has talked about this, was Dr Malcolm Kendrick, and he has also given a really good framework to think about the effect of stress on vascular health and the fact that you had that year of leading up potential of stress in the background. One of the mechanisms that he mentions is that prolonged hyper, having raised cortisol level related to stress for a prolonged period of time, actually inhibits the action of vascular endothelial progenitor cells. So your ability to heal the background endothelial damage that's occurring through maybe those blood glucose swings or any of those other factors, is impaired when you're stressed. So perhaps you had a bit of a vulnerable vessel wall in this background because you've got this stressful milieu and then bam, the acute stress of exercise which is both increased barotrauma because of the demands of the exertion and potentially even temporarily higher blood glucose if it's a really intense workout. That was enough to bang pop off a clot. The other interesting point which is born out in long term studies to do with the social determinants of health and these observational studies showing that lower socioeconomic people in Glasgow, scotland, I believe, particularly, were at high risk of getting heart disease. And it goes to show what you're talking about, or the impact of hopelessness and that unresolving, unrelenting, prolonged hyper cortisol state that we get from hopeless type of stress. So that's very interesting and I think that gives us an explanation of why you had your event.

Speaker 1: 32:32

I just want to make a point about the traditional risk factors, because what we're going to discuss next is very much beyond the scope of the points that. I was taught in medical school that my colleagues in both general practice and cardiology approach this idea of vascular health and atherosclerotic cardiovascular risk, these so-called traditional risk factors, the main ones being family history. So if you had found the history of having heart attacks, high blood cholesterol, but that concept should be atherosclerotic, sorry, should be dyslipidemia, but it gets confused with or lumped in with isolated hypercholesterolemia, smoking, diabetes and hypertension. So those are the traditional risk factors, but what you gave us a prelude to is these kind of non-traditional factors that are also going to be harming endothelial health. So I just wanted to kind of put that flag in the sand for people who are listening, especially the doctors in the audience. So we're not saying that the traditional factors don't play a role, because they obviously do, but they are all impacting the vascular health in the context of clotting, which is a point that I really want to make.

Speaker 2: 33:46

Exactly, and I'm glad you make that point, because there are people out there that well, first there's people out there that claim that it was just high LDL and that is what causes heart disease and that's been the theory for a long time, based on some more science and a whole history of that. But then there are also people that accept that that's not the reality and that they're still trying to analyze lipids and get the answer through this analysis of lipids. And I think that, unfortunately, blood lipids, while they may play a role in certain situations, have become a huge distraction to the actual causes of vascular damage and ultimately, you know, clotting, instances of clotting that can cause events and so yeah, so that's kind of what I had to discover on my own was what are those risk factors and how? Usually the traditional risk factors that they're looking at, which there's actually a study that came out that called the SMERFs, the standard modifiable risk factors that actually more of them, more cardiac events are not being predicted by those traditional, which are hypertension, smoking, diabetes and cholesterol, and so, in addition, like those things and how they're affecting, like you said, the clotting, the likelihood that we will see clotting, whether it's a minor scale, on the line of an artery, or it's a major scale and actually causes an event like in my case.

Speaker 2: 35:19

So very, very important to make that distinction and, I think, steer us away from this very myopic view of let's look at the lipids. They're going to give us the answer, but just analyze them in the right way. They're going to give us the answer, which I think they never will. They may give us an indication of if your lipids look like this, you're at more increased risk. But why do the lipids look like that? That's the more important question.

Speaker 1: 35:43

Yeah, and my interpretation of lipid panels just the standard lipid panel is that it's simply a insight into insulin resistance, particularly the triglyceride to HDL ratio, and, yes, it's predictive of different kind of patterns of LDL, but essentially it's giving us an idea, another kind of window into the same room, of insulin resistance. But it is as you mentioned. It is fundamentally limited in its predictive ability. And the study that you quoted I believe it was 2012,. It was a US study and they basically retrospectively looked at the lipid panels post-admission of over 100,000 people that were admitted for various cardiovascular pathologies and yet more than 60% had LDLs within the limit, the reference range. And the conclusion of the paper wasn't and hang on, we're obviously using a kind of a standard, we're not using the best tool here. The conclusion was we need to lower the lipid parameter even further. So I mean, you can't? You know it's trying to solve the problem with the same thinking that created it.

Speaker 1: 36:57

But let's talk about this cholesterol, and I really want to make a couple of distinctions here, because I hear this getting discussed and the lack of precision kind of annoys me. I want to make the point that cholesterol is a molecule, it's a sterile and it's not a fatty acid. It's actually sterile and it is a component of the cell membrane. It's component of red blood cell membrane and that gets to the point you were making, stephen, about the presence of cholesterol in the plaque is because it's gotten there through the presence in red blood cell membrane and then it is poured it around the body in low density lipoprotein, which is essentially a big ball that has an apoby protein or a different type of apolipoprotein, and that allows these cholesterol molecules to be soluble and to be transported around the body. So I just want to make that point, because people say high cholesterol, but it can be a little bit ambiguous. So why is this? With that background, why is this problematic in terms of the explainability of afterscolar plaque formation?

Speaker 2: 38:08

Why is the theory of high LDL problematic?

Speaker 2: 38:12

Yeah yeah, yeah. Well, I mean, first of all, if you just back up in like big picture, like wisdom of the body, like if the body is creating higher LDL for a reason and the person is not having this overt symptom because of it, like obviously there's pathological reasons why we could see imbalances in something, but if it's happening and the person is experiencing good health, then it must be doing it for a reason. And there are people that theorize that it's because I mean, like in the case of a low carb diet, that it's because more energy needs to be delivered to the system, which is lipids. We can use lipids for energy, or it's one way we can get energy, and so your body puts more of it into the bloodstream. There's theories that when the liver is on a low carb diet, the liver is making more ketones, which you can also burn for fuel. The process of making ketones is very similar to the process of making cholesterol, so more cholesterol gets made and it ends up in the blood. Or the liver shuts down the absorption of cholesterol because it's wanting to leave more in the blood for energy delivery, and so, instead of reabsorbing cholesterol, it leaves more in the blood and that's why it goes up, but there's always a reason for it. There's some metabolic reason for it. There's also circadian reasons why it could happen too, because we're all on this biological clock, and so the point of being that there's reasons why LDL could fluctuate in the blood, just like lots of things fluctuate, just like your blood pressure is supposed to fluctuate. If it goes elevated and stays elevated for a long time and never comes down, that could be an issue that could be an indication of pathology. But fluctuation depending on when you measure, that one snapshot in time is normal. Even blood sugar is supposed to fluctuate not as much as mine, because I'm trying to control it as a type one but it's supposed to go up when you eat something and the ability of it to come back down, that's normal, and so it's that kind of mentality.

Speaker 2: 40:23

Now the other issue with the theory is that when we look at atherosclerosis and we measure that clotting material, that's what it is. It's clotting material, and very little of it is cholesterol or lipoproteins or whatever you want to say, which suggests that the little amounts of cholesterol that we do see in them is just a byproduct of A. They're already there in the endothelial cells or there just happens to be some around whenever the clot forms and it ends up being in there because it kind of sucks in everything that's there. And so there's these flaws in this theory. And then scientifically, if you want to go the scientific route, there's lots of evidence that people with higher cholesterol levels, ldl levels, have just as little or they don't form atherosclerosis any more than people with normal quote, unquote normal levels. And there's, you know, there's associational studies that show kind of both, and some of those associational studies are funded by pharma and they push you in one direction, others are not. But what we do know is that, logically, you know, we have people with higher cholesterol who have lower all-cosmortality, they have higher cognitive abilities, they have lower rates of infection, lower rates of cancer, lower rates of heart disease, associationally. And so if something was that bad for us or that causative on its own of disease, why would these people be having these other better health outcomes, right, and not dying more frequently? And they've shown that with people with familiar hyper-cholesterolemia, which is genetically high LDL, they don't live any shorter of a lifespan than people with quote, unquote normal LDL. And if they do, it's because of their lifestyle habits, not because of the high LDL. That's literally what the researchers say when they look at those studies.

Speaker 2: 42:29

So anyway, you kind of slice it up. There's really no evidence for this theory that this one molecule on its own can be a driver of a whole disease process which is fundamentally flawed in general. Like the body is a very complex biological ecosystem, it's never like one thing is never gonna cause a whole disease process. It's always gonna be a combination of things, just like we're always a combination of what happens to us in our environment. Yeah, many, many flaws and holes in that theory. But it's a very convenient theory for pharmaceutical companies Because if you can say that a disease is caused by one molecule and you have a drug to lower that molecule, then you can sell more of that. If your theory is that stenosis of an artery is what causes heart attacks, then you can make a lot of money doing stent and bypass procedures which studies still don't work to fix that stenosis. And it's very profitable, very convenient for that system to thrive. But people are left with poor results and in higher rates of heart disease.

Speaker 1: 43:33

So yeah, and you're specifically referring to the practice of stenting. Asymptomatic people who might have undergone a angiogram, discovered to have a degree of stenosis don't get exertional chest pain or any other exertional symptoms and then get stented. And there's not good evidence that that is benefit and there's lots of reasons for that, one of which is the fact that the body develops collateral flow if there's stenosis that's occurring over a long period of time. I wanna make a comment about what you talked about in terms of the LDL and the lipid hypothesis, because I've called this the original sin of having apoby, and what I mean by that is the way that it's framed by mainstream thinkers in the space, so particularly Dr Thomas Dayspring, dr Peter Atia, who are some of the most fierce proponents of the lipid hypothesis and the causal role of apoby and LDL cholesterol in atherosclerotic cardiovascular disease is that they would have you reduce your apoby to basically almost undetectable. They and I believe it's 70, I think they want it under 70 as a kind of in the US unit as a treatment goal. And the why I call this the original sin is because it's presuming that the body made a mistake and it's presuming that mother nature made a mistake in giving us this LDL particle and it's huburistic because it excludes this or presumes that there is no other reason for this molecule. Effectively and it's not specifically what they've said, but that's how it's interpreted is that there's no other value for this molecule other than kind of giving us atherosclerosis starting at a very young age. But what I think both of us are agreeing in what we're saying is it's the context of which the this particle exists in the body. It's the context of the endothelial damage, it's the context of the coagulating, the pro-coagulant environment of the blood vessel that, ashley, is gonna determine the degree of pathology or disease causing capability of LDL.

Speaker 1: 45:50

And I think you make a really good point about when there's a monomaniac or a myopic focus on one metric. It's because that there is a medecatable endpoint. And it's not a surprise that we're not emphasizing triglycerides, because the satin therapy doesn't do a lot for hyperdrugless rightemia. What does getting in the sun and cutting out carbohydrates? That's what gets you at fixing metabolic health. So you know, it's definitely a focus of this paradigm because that is kind of where we're at. And in terms of the effect modification, that's a concept that no one's talking about. Is that the effect modification of LDL and having this apoB is metabolic health, ill health and all these things that are damaging in the lining of the blood vessel. So maybe let's quickly talk about the exclusion zone, because even within metabolic medicine and metabolic doctors who acknowledge the presence of the glycocalyx, then I don't believe they've got the full story, because we do actually have a protective layer above those glycoproteins that are sticking out of the endothelial cells. And if you wanna comment on anything else I've said, please go ahead.

Speaker 2: 47:03

Yeah, yeah, so you know. I think that, like you said, we're over analyzing these lipids because we're stuck on this idea that the lipids have to be the answer. But when you broaden your like, instead of asking do lipids or what ratio of lipids is more atherogenic, you're gonna. We'll probably find a ratio or a certain way that the lipids are presenting themselves that is indicative of more atherosclerosis. But it's not the lipids driving it, it's always the context of the environment the lipids are in, and so now we have to learn about this environment that the lipids are in right.

Speaker 2: 47:43

And one thing that has been completely missed is the more quantum biophysics side of the cardiovascular system, and that has to do with water and basically it has to do with your body's ability to hold energy and use energy to create structured water. So what is structured water? So we're all made of water. We're all told we're 80, 90% water, whatever you wanna say, but we're a large percentage water, and the water in our bodies, most of it, is in a structured state, meaning it's more like a gel. It's not fluid, liquid, like water, and it's not ice solid, it's in the middle, it's more like a gel, like jello or like the consistency of a raw egg yolk, like it's kind of that gel, and so most of the. That's why, if you can touch your forearm, it feels like a gel. It kind of responds and bounces back, and so structured water forms. When there's a water-loving surface which all biological surfaces are water-loving and you have water, obviously, and then you have an energy source. There's lots of different energy sources, but the main one is infrared light. It's the most structuring to water. When that happens, water will become this. It'll form a layer of this structured water on the biological surface and the lining of the artery. The endothelia, with glycochialis on top, is one of these biological surfaces, and in the lab of Dr Geopolic they found that it does indeed form on the lining of the arteries.

Speaker 2: 49:11

Now the thing about this structured water is that it's got different names. It's called fourth-phase water, but it's also called exclusion zone water, and the reason that it's called exclusion zone water is because the way that it forms it becomes this nearly impenetrable barrier. There are certain very small hydrated ions of minerals and certain metabolites that can get through it for good reason. But anything larger than those things, which they're very small they're like fractions of a nanometer cannot get through there, and so red blood cells are too big, bacteria is too big, all the lipoproteins are way too big, platelets are too big, the protein albumin, which is the smallest protein in the blood, is too big. Nothing really gets in there if you have this intact structured water there. And so the thing is that structured water is very electronegatively charged, and so earlier, when I was talking about all those that inflammation and oxidative stress, those things can interfere with and break down this barrier of water that's protecting the lining of the artery, and so eventually, if they break that down, then they damage glycocalyx and they can damage the endothelia, and then that leads us into this situation that promotes clotting right, this inflamed endothelia and poor blood flow and aggregation.

Speaker 2: 50:32

Now, so we have this water protecting the lining of the artery, but the other thing is that structured water forms on all biological surfaces. That includes elements of blood, and so red blood cells and lipoproteins. They also have structured water on them, and that gives them what's called a zeta potential. It gives them this charge around it that protects them. So you think of it like you know, there's two lipoproteins next to each other and they have the same charge, so they kind of repel each other, but the water around them is positively charged, so they kind of attracted to that. So then they repel each other to get too close. So it's just like this everything's evenly spaced in the artery in the blood floating in this water, evenly spaced but they're kind of hooked together a little bit called electrostatically like train cars hook together, and that keeps everything evenly spaced, protects the lining of the artery. And then the last piece of it is that in Pollux Lab they've shown that the formation of this water is actually what creates blood flow.

Speaker 2: 51:27

And so here we are. We've already predisposed everybody to these three factors that generate clotting. And that is damage to the lining of the artery. It is aggregation of elements of blood clumping together and it is poor blood flow. And I just told you that structured water is responsible for protecting the lining of the artery so that it doesn't get damaged, keeping things evenly spaced in the blood, not clumped together, and promoting blood flow.

Speaker 2: 51:56

And so if we look at what atherosclerosis is, what damage to the lining of the artery is, and what clotting is, whether it's acute or chronic clotting over long periods of time it's basically an inability of your body to maintain structured water in the few places where water is still liquid, and then structured water onto elements of the blood and lining of the artery within that liquid, and that is lymphatic tissue, cerebrospinal fluid and blood. And so it's all about giving your body enough charge and water the raw material so that it can do this and prevent atherosclerosis. And so this is the things that solidify this for me are if you look at what actual risk factors for heart attack, heart failure, atherosclerosis, stroke are, one of them is rithicite sedimentation rate, which is measuring how fast items of blood clump together. Red blood cells clump together. We don't want it to be that fast, we want them to do that slowly, and so you can measure this in how, if they clump together too fast, that's definitely one of the best predictors for if you're gonna have a clotting issue.

Speaker 2: 53:14

Also, poor blood flow has definitely been associated with higher risk of clotting, which makes sense. The more stagnant something is, the more like it's gonna clot. Just like if a river is always flowing and beautiful, but you get an area of the river that goes off to one side and kind of eddies and it starts to treat this pool and we always see things in it. We see the sticks and leaves and stuff that can not get accumulated in it and that's gonna increase clotting of that area. If that was blood, which is why we always see like vasodioid and I've talked to cardiac surgeons about this and the vasodioid at the time we see clotting happen in areas of a bend in the artery where turbulence is supposed to happen, or if it's poor blood flow, things can get stuck or areas of bifurcation, things split and so maintaining this water is what keeps artery healthy.

Speaker 2: 54:03

And if you think about it like that, if we are assessing lipids and we see a lipids present themselves in a way that suggests that there's poor metabolic health or inflammation or whatever, it's all a reflection of how healthy that structure of water is in your body. If that structure of water is not there, it's because you have poor metabolic health and it's because you have high inflammation and oxidative stress because you're not doing things to get energy into your body to maintain that structure of water. So I hope that makes sense. But it's kind of this overarching thing that just looks at all, takes all of it and says, oh, that's what's going on, I don't need to overanalyze lipids, this is the solution.

Speaker 1: 54:45

Yeah, thank you for such an excellent summary, stephen, and I think what you've just talked about and what you've described is so fundamental and so pivotal and so paradigm-shattering that it's almost very it's difficult for me to overstate the importance of what you've just said and I'm gonna go over it again, and really slowly, for the doctors in the audience, because they really need to understand this concept and what you talked about in terms of structured water. This isn't not some woo-woo topic. This isn't some kind of obscure, esoteric concept not based in scientific reality. This, what Gerald Pollock described in his lab, who is an electrical engineer turned water researcher, is a fundamental truth about the biophysical properties of water that respond to electromagnetic radiation in the form of infrared light. So the structure, the actual molecular structure of water is taking on a completely different configuration and confirmation under the influence of infrared light in biological systems, and the power of structured water to exclude solutes is so great that this has been looked into as technology to filter water, meaning that if they can harness the structured properties of water by passing current through it, by putting light on it, then they can actually use it to filter sea water, to filter all kinds of solutes out of water. That is how powerful this is.

Speaker 1: 56:26

So what you've described and what makes sense is that we have got this exclusion zone structure water on the inside lining of the blood vessel beyond the glycocalyx, and this is our force field barrier effectively.

Speaker 1: 56:39

That is, preventing contact of lipoproteins and anything larger than potassium ion which is what we talked about in your recent talk from contacting the endothelial layer.

Speaker 1: 56:49

So what Peter Atia and Thomas Dayspring and these people don't understand is that if the body is healthy and there is, the charge of the body is within its physiological optimal level, then there should not be contact with the glycocalyx, with the endothelial layer of any of these contents of the blood from the lumen, because that protective layer should be preventing anything from effectively contacting it. And whatever causes the breakdown or the impediment of the formation of structure water, as you've just talked about, is therefore gonna cause damage to the glycocalyx, is gonna cause those microclots which over time or suddenly, as we talked about in your situation, form into a full blown occlusion of the vessel and you get acute myocardial infarction. But I just really wanted to emphasize that point because I think what you've just described is simply paradigm shattering for the entire field of cardiology, preventative cardiology, lipidology, and it's groundbreaking and I'm really struggling to not overstate this, but I think it is that important.

Speaker 2: 58:04

Well, first of all, just to your point too, like it's not just Gerald Pollock he is the one who has popularized fourth phase water because of his book but Gilbert Lane, albert St Georgie, who won the Nobel Prize, jim Oshman, may Wan Ho, james Clegg, like there's so many scientists that are talking about water. And it's like, if we talk about charge, like we all know, we all learn in cellular physiology that there's a net negative charge in the cell. Well, guess where it comes from? Structured water. And if the charge of the cell is altered, we know that that's a disease, cell right, and that's because structured water, whereas lost the capacity to hold structured water into it. Structured water is this net negative. And, like you kind of mentioned there, like cellular physiology, we know there's a separation of sodium potassium inside and outside the cell and I just told you that the, or you just told us, based on my talk, that sodium potassium is the cutoff. Sodium is not allowed, potassium is allowed. So structured water is playing a role in this separation of charge. So this is very well-established physiology and there's tons of literature on this. But also it's kind of, like I said, overshadows this whole lipid theory, cause we're so focused on this biochemistry and we step back and we see that there's this biophysics side to our body that makes all that biochemistry. It changes the way we see it, it changes the way we look at it and it's very, very simple.

Speaker 2: 59:37

Like heart disease and most disease in general, is a result of two things. One is that in our modern way of life we are exposed to things that interfere with our body's charge, and that is electromagnetic fields, it's the wrong types of light, it's all the toxin exposure, the poor diet leading to poor metabolic health, which is mitochondrial dysfunction, Like all these things are decreasing our body's ability to maintain that net negative charge that we know as physicians we would learn right. And then it's also the second thing is a lack of stimulus of the things that increase that charge, which is the sun and contact with the earth and movement. You just moving your body, you create a piezoelectric effect that generates electricity. So it's pretty much that simple. Now all the details of different disease processes and everything can get really complicated, but it's really is that simple. We've too much in contact with things that interfere with our ability to get charged and we're not in contact with things that maintain our ability to get charged Like. That's what life is. It's literally your body.

Speaker 2: 1:00:50

Define the second law of thermodynamics, because the second law of thermodynamics is things tend toward disorder. But life has figured out a way to take energy and create temporary order for something to be alive, you know, through its lifetime. And if we lose the ability to take that energy in and create order, we get disorder. And that's what all disease processes are. There's just a fundamental lack of energy for your body to create that order, because it knows how to create order. It's well designed or evolved, however you want to say it, to create order.

Speaker 2: 1:01:21

And the lining of the arteries is one of the first places we see disorder, because it is kind of like the front lines right, it's where what your body is trying to send everything to process or detox or metabolize all the things. So it's, it's frontline in defense and that's why we see it more common. That's why heart disease is the number one killer, because in this state where we're removed ourselves from energy and doing things to damage energy, the blood vessels see it first. So it's when you look at it from that perspective, it's very simplified. Even though the science can be very complex, it's very simple from that perspective.

Speaker 1: 1:01:55

Yeah, and it reminds me of that little story of the two fish swimming in the ocean. And you know they, I think an older fish comes by and is like you know, are you guys enjoying the water? Or something like this. And one fish looks at the other fish and asks him you know, what is water? And that that I feel like is is the lipid centric model of looking at cardiovascular disease, and it's, it's it's physicians who aren't understanding or realizing the context in which these lipoproteins and these blood constituents are really operating in. But it makes all the difference and it, as we've just talked about and I think you know, in analyzing this, this problem you really have, you've got a couple of layers of it, because you've got biochemistry, lipid analysis based on pharmaceutical treatment and apoB lowering, which is, you know, mainstream Western medicine. Then you've got, and still, a biochemical lens, but the work of Dave Feldman, you know Dr Paul Saldino and all those looking at reducing vascular risk through modifying insulin resistance, which is effective, and but I just think it's still limited in a scope. And the reason why I'm going to emphasize this point is because if you send a patient out or you send someone out and they're eating a carnival type diet. They're highly insulin sensitive again, but they're working out into a blue lit gym, they're sitting next to the Wi-Fi router every day. They get stressed and they pop off a heart attack. They pop a clot off like you. Like you and that biochemistry insulin resistance model of atherosclerosis can't explain to that person why they had that event. And that is comes to this, jack Ruz's idea of you know half truth always lose these to a full lie. So to me it's not satisfying enough.

Speaker 1: 1:03:49

We need to go to this physics level and what you talked about with charge structured water makes elegant sense in my mind and has a much higher degree of explainability of what is actually going on. And you know Malcolm Kendrick made the point that you know your theory. Someone's theory needs to be able to fit, it needs to be modular, it needs to be able to fit, you need to be able to test it with different clinical scenarios or different pathophysiological factors and you need to be able to explain that in your theory. And what you talked about, stephen, is gives us amazing explainability of all the factors that damage the endothelium. But they're doing it through these effect on charge.

Speaker 1: 1:04:30

And you know I listened to a podcast of Peter Ateer and Alan Sniderman. And Sniderman couldn't explain how smoking has any effect on atheroscopic or plaque formation, and to me that shows that he's so mired in this lipid hypothesis that his explainable theory of reality isn't able to account for one of the most damaging effects on cardiovascular health, which is smoking. And we can, you know, I think the listener can infer from what we've just talked about for the past hour how that might be the case. But it involves structural water, involves the endothelium. So I want to congratulate you for pulling these pieces together and presenting them so in such an explainable way, because what you've just talked about and what you continue to talk about, I think, is getting closest to the truth. As I see it, as I can interpret it.

Speaker 2: 1:05:21

Yeah, and like you know, like you were saying, like you got the lipid hypothesis people and then you got the people that are disagreeing with that lipid hypothesis or saying that there's holes in it, and they're showing that it's more in the context of metabolic health and that LDL is not the whole deal. But, like you said, that's limited. That's only going to get us so far. However, it is very important because we need that data that they're creating to prove that it's not LDL. But once we prove that, we have to take them somewhere Right. And then we have to say, oh, it's not that and leave it at that. We have to say we have to give them. Well, this is what it is. This is what explains it all. Here's the theory and that's what I am more interested in. You know I'm not interested in overanalyzing lipids to just prove that theory. I think that's going to be done, regardless of what I care about it or not. But I want the next theory, like, where is it going to take us? Here's some more information. Some of it makes the most sense. But let's prove it, let's mess with it, let's see if there's where's the reality, let's figure it out Right. So that's what we have to take people and it's not, I think the medical establishment is going to be stuck in the lipid theory as long as the power is held over them by pharma. And so it's really going to start with people. You know like it's great if we take here's the thing, so, like Dave Feldman's group is doing great work and we're going to take that to people, people are going to be like, oh, that makes a lot of sense, you know, and that's that's that makes way more sense than what my cardiologist is telling me. And so they're, ldl may skyrocket and without another theory, without another path from that, they're going to get scared and that fear is going to shut down the decision and they're going to go right to taking statins or that approach.

Speaker 2: 1:07:03

And I work with people day in and day out guiding them through this information and they're like I think I need to, I think I need to do the bypass, I think I need to do this, I think I need to do that, and I say, okay, well, here's what the data shows.

Speaker 2: 1:07:15

I can't tell you what to do, but here's what it shows. If they don't have another path forward, they're going to fall right back into that because of fear, and we've seen what fear does people over the last three and a half years, and so we have to give them this other information, this path forward that takes that fear away, gives them the confidence I know I'm protecting my arteries, because I'm doing this right, and that's it's a critical piece. You know they're all different pieces. What Dave Feldman's group is doing is one piece, but we have to give the other piece that really pushes everybody, because that's how we're going to affect Western medicine is we're going to take people away from it. And if people end up in fear and go right back to it, we have to give them another path, because a large percentage of them will take that path rather than buying into the fear.

Speaker 1: 1:07:56

Yeah, and I want to. I want to congratulate Dave Feldman and his citizen science project because, as you mentioned, Steven, he's doing incredible work and especially with this concept of the lean mass hyperexpondent, which is describing what happens to to someone's lipid, to apoB and LDL, and particularly on a low carb diet and particularly in those with low body weight or normal BMI, and that that data came out recently, a meta analysis showing that it wasn't the saturated fat intake but rather BMI that was the greatest predictor of developing quite high LDL on a low carb diet. So what Dave Feldman's doing is amazing work and again, his study that on the lean mass hyperexpondent, they're doing CT angiograms of people and you know yearly CT angiograms to look inside the vessel, get an idea of plaque formation on low carb and they're not forming any, which is again kind of as if, as if the lipid hypothesis needed another nail. I mean this is like the Rasputin of theories, it like it's never dying, but even even all this contrary evidence, but it keeps piling up and it's, it's exciting what he's doing. And I think Nick Norowitz did a recent N of one experiment where he ate Oreos and that was sufficient to drop his, his LDL very acutely again showing the ridiculousness of and the holes in in in this whole theory.

Speaker 1: 1:09:22

But, like you said we, it's not explainable enough and I really invite Nick and Dave and anyone else to start delving into the biophysics of what's going on here. Try to understand structured water, try to understand charge, because I think it's closer to the truth. Maybe a good point now we can talk about sunlight, because I had a recent conversation with dermatologist Richard Weller and he's done amazing work epidemiological work showing reductions in cardiovascular mortality and with greater UV light exposure and and non vitamin D mediated effects. So talk to us about how the importance of sun for cardiovascular health, how you think about it and maybe also how it relates to structured water and exclusion zone water.

Speaker 2: 1:10:07

Yeah, definitely, um. Before I get to that, I want to comment on something that you said, um, and that is that you know, just to kind of a big picture, look at this. You know, when we determined what normal LDL or lipids in the blood was, it was on a population that was eating a process food diet, right? So what Nick Norwood showed when he eats those Oreos, it lowers cholesterol. Does that mean that it's good or does that just mean how we determine normal? Right, but what if? How we determine normal was completely abnormal for humans? Right? So what if it's like? It's like if we took a, you know, a wild animal and we put it in the zoo and we put it in a semi natural environment, but then we fed it on that unnatural diet, um, and we disrupted it social network and whatever, and then we sit, took it slow, but it said, okay, this is what's normal for this wild animal. Like, it's the same kind of idea.

Speaker 2: 1:10:58

So if you think about it like that, then what's normal, what's been determined as normal, is completely wrong. Based on what humans, how humans lived, you know, millions of years before, hundreds of thousands of years, I guess, modern humans, um, before we had these process foods. So think about it in that context. And then you start to realize that when someone eats a lower carb diet which would have been, you know, traditionally what happened in humans at least part of the year um, then an LDO goes up. That could probably be normal, right? That's probably what's supposed to happen. Um, you know, and they're trying to prove that in the context of metabolic health, that's fine, but I'm trying to tell you that that's probably just the way it's been forever.

Speaker 1: 1:11:37

Yeah.

Speaker 2: 1:11:39

And one of those other natural parts of of of life for humans was being outside and being in the sunlight. Um, and so, to context this, all life on earth is in all energy. Energy on earth comes from the sun, right, it's what's driving everything. It's the only reason that life is here, and it was only when life figured out how to harvest that energy in various ways. Um and uh. Cells, you know, initially harvest that energy in in various ways, um, that cells could come together and make multi-cellular things, and then evolution kept happening. We had more complex, um, multi-cellular organisms and eventually, you know, plants, and then um uh, fish, and then amphibians, and then reptiles, and then humans Well, mammals, and then humans, and so they just kept going like that. And it was all of this ability of life to use energy. And so the idea that the Sun is bad for us is it makes no sense whatsoever. It's where all of our energy is coming from. Even the food you eat. Yes, you get energy from that. The energy that food came from the Sun, and so when we look at our ability to take sunlight and make energy from it, there's a few different ways we can do this, because people talk to a long time about vitamin D. That's what the Sun gives us, that's why it's important, and that's UVB light, which is midday light. But we have other ways that we can take energy from the Sun and use it to make electricity in the form of electrons to power the body. One of them is the molecule DHA, which animals are made of. Dha is a fatty acid, high amounts in seafood, but you can also get it, especially grass-fed forms of animals, and DHA literally takes the sunlight and has the ability to take that sunlight and convert it into DC current, electrical current, electricity electrons that are transported throughout the body, and most physicians listening to this should know that we use electrons to make energy, to make ATP, or at least an ATP molecule, which could be seen as energy, could be seen as other things, but so for the average traditionally trained physician or anybody familiar with solar physiology should know electrons are important and DHA can make that.

Speaker 2: 1:14:02

Another one is melanin. We're told that melanin is this pigment in the skin that determines our skin color, and that's pretty much what it does. But actually melanin is concentrated in many different places in the body in the nervous system, in the eye Lots it's pretty much everywhere when light or any energy form, like sound or anything, hits melanin, melanin can take that energy and what they say dissociate the water molecule breaks it open into hydrogens, oxygens and electrons. So it makes electrons and those electrons can be used by the body, especially mitochondria at the beginning. So we can take the sun and do that through melanin and DHA. Now also, we've talked about this, we've alluded to this infrared light is the light that's most absorbed by water, especially the 3000 nanomerewoven, which is the far end of infrared light, and so 42% of the sun's rays are infrared at all times.

Speaker 2: 1:15:04

And so we take that infrared light and it energizes the water in our body so that when it gets next to those biological surfaces which is already next to it, builds more structured water, and the structured water is electronegatively charged, contributing to our charge. It also creates a battery situation, because the electronegative area is lined up right next to the positive area, because the hydrogens are cleaved off and that leaves a line of hydrogens, and so this is a positive and a negative area which is a battery, which is why you don't put batteries in your remote control car or whatever, and that you have to align the charges right, because that's what creates the energy to move the car, and so that's what happens in our body. It happens literally everywhere, including the lining of the artery. So sunlight does this. And so when we talk about all those benefits of structured water in the vascular system to the vascular system and preventing clotting and preventing damage, and then we see that infrared light from the sun is what's providing that, then we start to see oh well, that's why the research shows that when you do infrared sauna or get infrared light from the sun, that you get increased blood flow and you get decreased risk of clotting and you get lower incidence of all kinds of heart disease, whether it's stroke or atherosclerosis or heart attack.

Speaker 2: 1:16:25

And it's not just the infrared, like the UVA and the UVB also have benefits too. They've been associated with health benefits, cardiovascular health benefits, and the research is very robust on that that this sunlight is what is charging our bodies. And so when you use this quantum lens and you see how your body takes sunlight and makes energy and you understand that the body's job is really just to make energy to maintain older in the tissues, you see why the effect that is. It's not some strange thing like oh, that's interesting, the sun helps your vascular system. It's like no, when you see it in this quantum lens, you're like that makes complete sense. So that's why we see that with sunlight.

Speaker 1: 1:17:09

Yeah, and I really want to make the point that you mentioned, which is Pollux work, which they found that the blood flow was occurring on, basically irrespective of or after the heart was essentially removed. The blood flow was potentiated around the body with infrared light. So when we're in, naturally outdoors, that to me is like we're reducing the, you know, we're reducing the strain on the heart. Effectively, we're relieving the ventricles of their need to pump blood because the blood is simply being potentiated through both the arterial and venous circulation by infrared light. And if we're inside all day then we are not getting that free boost of blood pumping ability in addition to all those other benefits that you mentioned from simply being outside.

Speaker 1: 1:18:05

And there's to quickly make a point about on the biochemical lens once more, is that you're making nitric oxide through UVA exposure. So that is a very potent vasodilator and it is helping assist in that endothelial health. There's also melanocortin receptors inside the endothelium and they're having an effect on the on vascular health. And again, I believe that that's mediated through nitric oxide and there was some mouse models of knocking out the melanocortin one receptor in the vasodilator endothelium and those mice developed stiff arteries and essentially endothelial dysfunction. There's also photo there's blue light mediated photo relaxation effect of melanobsin receptors in the endothelium. So being outside in natural blue sunlight, I bet, is having a beneficial effect as well. And possibly being under blue light all day artificially and kind of wrecking those melanobsin receptors or destroying them is probably contributing to disease. But just to emphasize the point that the benefits of natural sunlight are so immense in terms of cardiovascular health that yeah, again, it's hard to overstate.

Speaker 2: 1:19:28

Yeah, and here's the kicker is that we talk about how this is what's responsible for the blood flowing, and you know, there's experiments and studies back in the 40s and then repeated in the 60s, that show that when they stopped the heart beating of dogs these studies were done in dogs that the blood continued to move for up to two hours. And then in Pollux Lab they showed in a chick embryo that if they euthanized the embryo and the heart stopped, the blood continued to flow. If they put infrared energy to it, then it would continue to flow indefinitely. So these mechanisms definitely happened, and so the real kicker is, if you look at the research on infrared sauna and heart failure, it is absolutely phenomenal and, like people with heart failure, it's not the heart that's failing. The heart is a vortexing hydraulic ram. It's not necessarily a pressure propulsion pump that's supposed to be forcefully pumping blood throughout the body, but it's not Cardioid, just head explode.

Speaker 2: 1:20:29

Yeah, it's not failing. It's being forced to do more pumping than it's supposed to because the mechanisms of blood moving are not up to par, and that is poor energy. It's poor mitochondrial function in the heart itself and in the rest of the body and in its lack of structured water of the vascular system. And so if you apply this infrared light to the system and they have enough raw material, which is water, it's been shown to A heal the lining of the artery and increase nitric oxide production, endothelial nitric oxide production. But also in people with heart failure, it increases blood flow, decreases edema. It increases ejection fraction. There's people with cardiomyopic hearts that come back to normal size. Like it's just phenomenal, Right this.

Speaker 2: 1:21:14

So I don't understand why there's not infrared sauna in every cardiac rehab center everywhere in the world. But it's not very profitable to do that. That's probably why. But it's really just, it's really great and it's not just. I mean just heating your body in general is good, but infrared sauna has specific benefits to the heart and the reason that makes sense is because 42% of the sun's rays are infrared. That's why it works. But infrared sauna is kind of this modern hack we can use to help these people who have gotten themselves in this situation.

Speaker 1: 1:21:41

Yeah, and what is happening when someone has heart failure, either heart failure with reduced ejection fraction or heart failure with preserved ejection fraction this is a problem that's occurring over a matter of years, decades, and you're getting hypertrophy of the cardiac, of the cardiac, the ventricles, the heart isn't lodging. And just as you hypertrophy your skeletal muscle if you do lots of push-ups sorry or bench press, if you're asking your heart to take up the role that maybe infrared light was helping in terms of vascular flow, then it's not surprising to me that hypertrophy of that cardiac muscle is something that could happen. Yeah, the point about infrared in the cardiac ward that makes so much sense, so cheap, so efficient. Obviously, if someone's acutely unwell they might not be able to get in the sauna. But even having a red light panel that has infrared I mean, I've been in cardiac care wards and there's been it's pretty distressing a patient going into acute pulmonary edema right in front of you and everyone's. We're scrambling, we're scrambling getting the oxygen on. But imagine if we had a full body panel and simply just shining infrared light on that patient.

Speaker 1: 1:23:07

I don't know, maybe some clinicians in the audience can go to their CCU and buy a panel from Kyle at Midwest Red Light Therapy and give it a rumble, but what's the downside? There isn't any. So it's an amazing thought about how we could revolutionize cardiac care with the framework that you've described and given us, stephen. And then grounding I mean let's feed that into the mix, because you talked about electrons and energy, currency and charge. The earth is a massive negatively charged ball. Feynman wrote about that early on, so maybe just talk a little bit about grounding and, as it relates to what we've talked about, yeah.

Speaker 2: 1:23:57

So the evolutionary consistent thing is that we would have been in contact with everybody outside. We didn't have rubber sole shoes. If anything, we were wearing something natural like a mandrel skin shoe that was still conductive. So the earth is this big ball of energy. Electrons, and it's because the sun is. The solar rays from the sun are being deposited and turned into electrons in the ionosphere, in the atmosphere, and every once in a while well, actually more often than not, around the world, very frequently that discharges in the form of lightning to the earth. That's why metal things that are conductive are attracting lightning, right and so because it's trying to find its way to the earth. And so this earth is this huge reservoir of electrons, and the law of electrostatics tells us that when two conductive surfaces are next to each other, that the area that's more concentrated in electrons will flow into the area less concentrated. And, try as we may, we're never going to be as concentrated as electrons as the earth is. So if we touch bearskin to the earth, we conduct electrons through the conductive, hydrated fashion network of our body, and they've shown this over and over again. This happens if you put your feet on the earth and you test the voltage of your body. You are like your toes are like about 200 times more electro negative than your head right, because you're in contact with that and you're soaking those electrons into your body and so they've shown some benefits in this.

Speaker 2: 1:25:28

As far as the vascular system, in that you remember that Zeta potential I talked about. As far as the structured water that gives this kind of net negative charge surrounding elements of blood like red blood cells, lipoproteins and everything. When you ground you increase your Zeta potential, which keeps everything nicely spaced in the blood, which decreases blood viscosity, which we know is a risk factor for clotting, and keeps things moving through the blood nice and evenly. And so that's, you know, one way that grounding can help with that. But also we know that if it forms structured water on those elements of blood, it's forming structured water elsewhere in the body because it's giving the body that negative charge, that ability, that energy for water to structure itself onto that biological surface.

Speaker 2: 1:26:16

So it's like people say, oh, putting your feet on the earth for hippies. You know that's a woo-woo stuff, right, but there's actually a lot of research on it. And when you think about it from the perspective I just told you about how the physics works from the energy from the sun to the earth and into us, like it makes sense, like it's really happening, and it makes sense evolutionarily, because humans would have been outside in the sun with their feet on the earth or in a natural body of water. That's an incredible way to conduct that energy from the earth, those types of things, so definitely beneficial.

Speaker 1: 1:26:49

Yeah, great, great answer. Maybe some final thoughts. Have you looked into the role of deuterium in terms of mitochondrial health and specifically with regard to cardiovascular health?

Speaker 2: 1:27:02

Yeah, so I mean again, cardiovascular health is all about maintaining this charge and one of the ways that we do that. So if we think about, you know at least the way we're traditionally trained what mitochondria does. It's job is to make ATP, right? Well, actually there's a lot of other things we've learned that happened in the process of making ATP through that electron transport chain. You know, the glycolysis and Krebs cycle is all just. You know how can we take food and get electrons from it, right, so we learn about all those annoying, you know names in medical school. But then it's all about the electrons, and as the electrons are passed, we get hydrogens pumped into the inner brim, brain space, and those are used to make ATP in complex five in the mitochondria. However, the mitochondria also generate heat in the form of infrared light, and they also produce carbon dioxide and they produce water, and this is this perfect energize to a. Construct yourself water, right? And? But the other thing is is that so you know, if you think about it in that way, mitochondria are making all that we need. They just need electrons to do it Right. They're making the water, they're making the heat that we need, which is why, if we put on infrared goggles, someone will light up. You know we're making infrared heat and then they're making ATP. And ATP can provide energy for some things. But it has another important role.

Speaker 2: 1:28:28

But the making of that ATP is dependent on those hydrogens that are pumped into the inner membrane space and those hydrogens are specific. That form of hydrogen, the isotope of hydrogen, is specific for that and it's what can go through complex five and make ATP. There are different isotopes of hydrogen. One of them is deuterium, and deuterium, you know, largely comes from like eating foods out of season. That's the main way, Because if we're eating, you know, foods that are higher in deuterium, like plant foods and stuff in the summer, you know, then the sunlight gives us the ability to kind of process that deuterium and get rid of them. However, if we're eating this in the winter, out of season, because we ship foods around the world, we concentrate the deuterium and deuterium without the sunlight that we would get in the summer, in the winter they can get, we can get higher amounts of it, and when we get higher amounts of it, that deuterium is a different isotope of hydrogen than when it goes through complex five.

Speaker 2: 1:29:25

So we make ATP kind of jams up the system. It's too big, it doesn't fit, but the body still tries to use it and that kind of messes with complex five and then we have mitochondria. They're doing all these things and they can't get ATP at the end of it. That can create lots of issues. The main issue is that ATP is responsible for unfolding proteins, like cytoskeletal proteins in the cell, and those proteins are the hydrophilic surface that water structures itself on. So if those are not able to be unfolded and creating surface area for water to structure, the cells dysfunction because we've got these tightly bound proteins, not as much structure water can form. That interferes with this negative charge of the cell and interferes with cellular function. We start to get dysfunctional cells, dysfunctional mitochondria, and so that's this problem with deuterium.

Speaker 2: 1:30:15

And so, like I said, deuterium can come from a lot of places tap waters, unfortunately lots of deuterium in it, and so the better forms of water are like spring waters and glacial milk waters and things like that. They're lower in deuterium and, like I said, they're lower in deuterium. Some might as well gives us the ability. Same with heavy metals, like some might as well gives us the ability to get rid of these things. And if we're doing all these eating or drinking you know this poor quality water and eating these high-deterior foods like plant foods in the wrong season, then we really increase the amount of this concentrated deuterium. So, like lots of the reason that people on carnivore diets see benefits, probably one is that they're not eating plant foods out of season anymore, which is not giving them different live information, and the second is that they're not concentrating this deuterium in their body at the wrong times of year. So they're starting to see these benefits because their mitochondrists are functioning better and that's going to help literally everything. So that's kind of the story on deuterium.

Speaker 1: 1:31:17

Yeah, I really think the benefits of carnivore are a low deuterium diet and basically essentially helping to deuterium to please yourself, and that's having consequent effects on beneficial effects on mitochondrial efficiency and therefore energy and insulin resistance and metabolic health. But it all effectively comes from that mitochondria function functioning more properly. Yeah, thanks for that summary. I mean this is such an interesting and in-depth conversation and I think we've touched on a range of topics that mainstream cardiology and preventative cardiology have no concept of. I'm really not optimistic that a lot of lipidologists, conventionally trained, have any interest in kind of learning about. But I'm hoping that by having these conversations and helping to educate people who are interested individuals, medical students, doctors then we can slowly point people's curiosity in the right direction and they can make their own mind up about what they want to do and what they think makes the most sense for their health. So in closing I just want to emphasize one point myself and then I'll ask you, stephen, to emphasize a point that you want to make For me.

Speaker 1: 1:32:36

One of the most kind of mind-blowing parts of this interview was understanding that Vercow's Triad, that there's three components of blood clotting, which are hypercoagulability, endothelial damage and stasis. That's simply a story of structured water and exclusion zone water and the way you describe that is so elegant and it feels like a lock has kind of been put into lock in my mind when you put it that way. So thank you for explaining that and I really want people to take it at home and mull over it because it's a critical part of not only the atherosclerosis cardiovascular disease story, but it's also part of metastromboembolism, part of a lot of autoimmune disease, anytime where you've got these blood clots happening. So, yeah, any point you want to emphasize, particularly before we sign off.

Speaker 2: 1:33:30

I guess just more of like a practical kind of guideline for people. We just do a lot of information at them and some of it can be paradigm shifting or the first time they heard it or something like that. But just advice for navigating this world of health information that we have, which can be very confusing. A lot of the times when I work with clients online, like in health consulting, it's what I end up doing. Most of the time it's just helping them navigate the situation. Well, this person said this and that person said this Like who do I believe, and I think that it's really important to understand that we live in this world of hyper realities and hyper reality is just something that we take as more real than what's actually real.

Speaker 2: 1:34:18

So an example is like the weather channel and how you can look at that green blob going across the screen and you can say, oh, it's raining right there. And I'll never forget the time I was driving in my car and I had about two, three hours to go and it was pouring rain. I was like man, I wonder how long it's going to rain. So I pull up the weather on my phone and it says it's not raining and I was like it's pouring rain outside.

Speaker 2: 1:34:39

So, like this weather channel app, has become this hyper reality that we tend to take as more real than what's actually real. And, you know, while things like medical testing and medical research and lots of different forms of research can be helpful and they can help us clue us into certain things, they are, to a certain level, hyper realities that we take as more real than what's actually real. Which is what is real. Is us Right? What is what we feel day in and day out? And so, taking that to the next level is, when you're trying to figure out what to do to achieve health, ask yourself what's real, what is real? Is the statin drug real? No, that's a man made thing. That's, you know, totally defies this complex biological exercise that affects one pathway in the body. That's a hyper reality that this will give you health, right? Instead, focus on those real things. What is real? Real light that's been present on the earth since the earth's been here, real earth, you know. Cut yourself to that real food and the real way of eating food, which is, which would only be available in your local environment in season. Real relationships, not artificial ones or things that we think we know online, like. Have those relationships that are actually real and rely on those more than artificial ones or ones that aren't serving you. Maybe negative relationships, real positive emotion, real gratitude. These real things even feel real negative emotions, but learn how to process them in a healthy way, like these real things are.

Speaker 2: 1:36:10

Focusing on what's real is way more important than hyper realities Like what does this medical research studies say, which is fundamentally flawed from the beginning? Because the idea of trying to eliminate every variable and test if that's going to have an effect is a hyper reality, because I've never exposed one variable at one time. So what does that? Does that really tell me anything about how my body is going to react to something? Probably not, but it's informational. We can get information from it. So, just, I always give people that because it really helps them navigate this world and think about the information they're consuming. Is this real? It's a hyper reality. Should I get information from this and use that to to guide me a little bit, but never take it as as in all be all? It's really important to have that context and I think when I tell my clients that it's really helpful for them for as far as navigating this information they're just embarked with all the time these days.

Speaker 1: 1:37:05

Great advice. Maybe wake yourself up from the matrix of health information and try and understand what is real. And yeah, that is a great advice. Thank you very much, stephen. It's been a pleasure speaking with you and I think we've you've prevented presented a lot of very important information for everyone. So thanks again and, yeah, we'll stay in touch, of course.

Speaker 2: 1:37:30

Of course, thanks for having me.