Stay Off My Operating Table

Ryan Cooley 168

• Dr. Philip Ovadia

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Dr. Ryan Cooley's journey from a heart attack survivor to a pioneer in metabolic health is nothing short of transformative. After following conventional medical advice and still suffering a heart attack, Dr. Cooley began questioning the lipid hypothesis and delving into how diet and lifestyle can influence genetic predispositions. With a special focus on insulin resistance and cardiac health, he shares his insights and personal experiences, challenging the prevailing norms and shedding light on new approaches to preventing heart disease.

In this episode, we dig into the complex relationship between insulin resistance, visceral fat, and cardiovascular diseases like atrial fibrillation. Dr. Cooley explains how fat accumulation around vital organs triggers inflammatory responses and arrhythmias, advocating for a focus on metabolic health over merely lowering LDL cholesterol levels. His personal and clinical observations provide a compelling argument for a more holistic approach to managing heart health, emphasizing the often-overlooked role of cardiac fat.

We explore the nuances of reversing insulin resistance and the difficulties of diagnosing ectopic fat, often invisible from the outside. Dr. Cooley shares his transition from a vegan diet to a keto vegetarian and nearly carnivore diet, leading to improved lipid profiles and overall heart health. The discussion extends to the importance of satiety, specific medical tests, and the future of cardiometabolic care, including plans for a clinic centered on lifestyle interventions. Tune in to learn how these insights can pave the way for better preventive measures in heart disease management.

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Theme Song : Rage Against
Written & Performed by Logan Gritton & Colin Gailey
(c) 2016 Mercury Retro Recordings

Any use of this intellectual property for text and data mining or computational analysis including as training material for artificial intelligence systems is strictly prohibited without express written consent from Dr. Philip Ovadia.

Speaker 1:

Hey, welcome folks. It's good to have you back. It's the Stay Off my Operating Table podcast with Dr Philip Ovadia, and we have a first today. Phil, I don't know if you realize this or not, but when I realized our guest is an electrophysiologist, I said to myself we've never had one of those on the show before, so I'm looking forward to it. For some personal reasons, let's go.

Speaker 2:

Yeah, definitely, so real excited to have Dr Ryan Cooley on with us today. I recently became aware of Ryan and his interest in metabolic health, as you mentioned. This is certainly the first time we'll go into what that is, but you know, it just really to me shows how this concept of metabolic health is spreading throughout all of the different areas of medicine, and I was very excited to hear him on another podcast and immediately reached out to get him on this podcast. Ryan, why don't you start just to give kind of your background, introduce yourself, and maybe you can explain to people what an electrophysiologist is and does. That will be a good way to get us started.

Speaker 3:

Awesome. Thanks, philip and Jack, for having me on. It's a pleasure to do this and, yeah, it's quite amazing how metabolic health and metabolic therapy has been spreading. Hopefully it spreads even more into a greater number of specialties within conventional medicine. I am a traditionally trained electrophysiologist, which means that I basically take care of heart rhythm problems, and I've been doing that for about 25 years now. I was in practice in Wisconsin for most of my career and then relocated out west. My wife and I kind of always wanted to come out west, to the mountains and less humidity, and so we moved to St George and then I eventually kind of settled with Intermountain Health up in Provo and currently living in Heber City, which is a very cool mountain town. So that's kind of where I'm at right now.

Speaker 3:

I think my journey into this really started about six years ago when I personally suffered a heart attack, and that was not all that surprising. To be honest, I have a very bad family history. That surprising. To be honest, I have a very bad family history. My father was 58 when he passed of heart disease and he had his first heart attack when he was 35. And when we go back to our family history dating back to the potato famine in Ireland. There's never been a male Cooley that's lived longer than 58. And every single one of them had early heart disease. A male Cooley that's lived longer than 58 and every single one of them had early, early heart disease, early heart attacks, wow.

Speaker 3:

So I was certainly, yeah, certainly aware of the problem from an early age and I enlisted the help of a preventative cardiologist somewhere in my late twenties around and maybe about age 30. And that's when I started having discussions about cardiovascular risk and my family history. At that time they didn't do LP little a testing but we certainly had the generic lipid panel that was available and LP little a is a independent risk factor for cardiovascular disease. It's a kind of a little LDL particle that has this lipoprotein A protein on it. That's its signature and it's been linked to increased risk of cardiovascular disease. Largely felt to be genetically determined, although my personal situation with that kind of refutes that a little bit, and I've seen it. I've seen it modified through diet, dietary measures in other, in other patients as well.

Speaker 1:

But I don't want to take it too far off yeah the rabbit trail, because your story, your personal story here is so compelling. I just you know, as phil warned, I ain't a scientist. Yeah, so I'll try to be fairly generic about this, but I'm blown away by 175 years of Cooley been not making it to 60. So clearly you're highly motivated.

Speaker 3:

Yeah, and I'm 58. So this is, you know, this is the year that I'm trying to beat the record, but it's been a little bit of a struggle but I think I think things are looking favorable for me. But early on I had a lipid panel that showed fairly unremarkable LDL cholesterol, but I had triglycerides that were a little bit on the high side not terribly high, 150, but I had a very low HDL, sometimes in the 20s, and my cardiologist at that time basically said that this was a genetic problem, that there really wasn't much I could do about it other than take a statin and try to live. At that time he called it a clean life, right Exercise, keep stress low, eat well, and that at that time it was. You know, it was the same. It's the same story we hear today, which is avoid saturated fat, eat lots of vegetables and fruits and whole grains, et cetera. And so I did that. I took a statin from age 30. And I, you know, I ate fairly clean, although I am a self-admitted sugar addict, so I didn't necessarily avoid sugar. I tried to avoid sugar and fat combinations and I was pretty good about it and I exercised quite regularly. I was a college athlete and continued to exercise throughout my life, still do that today.

Speaker 3:

And so when I show people my lipid parameters over the next 20 years, what is, I think, most striking is about my cases. It really sort of directly refutes the lipid hypothesis which basically states that LDL-C is causal in ASCVD and that is ASCVD, coronary heart disease Okay, and that is independent of context. So it doesn't matter what the context is, it doesn't matter what the nutritional context is. It doesn't matter what the context is. It doesn't matter what the nutritional context is, it just doesn't matter what the genetic context is. The higher your LDL-C, the greater your risk of coronary heart disease and the greater your risk of coronary events like heart attacks. That is the lipid hypothesis and my case refutes that.

Speaker 3:

And I think the problem in conventional medicine is they. You know I, I, when I'm on twitter and so forth, I, I get this banter back and forth that you know, outcomes are more important than anecdotes. You know n equal one cases are not important. We haven't. We have the totality of evidence that basically says that it's LDL Again, independent of context. And they use this totality of evidence argument. They use Mendelian randomization argument.

Speaker 3:

What's that Mendelian randomization are genetic studies that purport evidence of direct causality, because it's like self-randomization, you know. There's apparently yeah, apparently you're able to control for all confounders. And that's the problem with Mendelian randomization is there's a ton of assumptions in these genetic trials and there's also there also remains still a lot of confounders. So there also remains still a lot of confounders. For example, variants in LDL receptor often associate with genetic variants that affect coagulability and other potential biological processes that would have an influence on the risk of coronary heart disease and the progression of coronary heart disease. So there's just I just don't have a lot of confidence in MR because I think there's still a lot of confounders.

Speaker 2:

I'll just jump in and say I share your skepticism of the Mendelian randomization science. I really think it's in my mind. You know the statistical manipulation that goes into these studies and it's one of these examples of going in with a conclusion to a large enough data set and finding the data that supports your hypothesis. Yeah, exactly.

Speaker 3:

And it's not to say that they're not valuable. You know there's some value in those things but in those studies. But there are problems and those problems are not stated out front and they're just largely ignored. Ldl or ApoB, whatever you're looking at, apob is the whole cohort of potentially atherogenic particles. That's the signature of all those particles. When you have lifelong low ApoB, say in the 30s, ascbd would be an orphan disease. I've heard this time and time again orphan disease. I've heard this time and time again and I have all the records to show that my LDL and ApoB, which track pretty good, has been in the 30s and maybe 40s at times since I've been age 30.

Speaker 3:

And I had a heart attack at age 52. Luckily I, you know, was treated very rapidly and had a good outcome from that. But you know I've got pretty extensive ASCVD and it wasn't until I sort of, you know, once I had that event. I you know the reason. You know some people might ask why is he kind of starting to talk now about this? Why, you know, I'm just'm just starting my online social media presence now and I think it's taken me six years to kind of heal back everything that I was taught and unlearn and relearn. And I also really struggled with embarrassment. I mean I was what I thought was a fit cardiologist, electrophysiologist, and here I suffer a heart attack and I went through a tough time because I was embarrassed that this happened. And so now I'm opening up and kind of talking about my case because I think that I've kind of gotten through that and I think my case is an important. About my case, because I think that I've kind of gotten through that and I think my case is an important, very important case because and I don't think that I'm unique I know I now know, with the help of many people before me that are in this space and are talking about this stuff, I now know that this is a very prevalent problem which is dysfunctional metabolic systems, and this is biology 101. I mean, this is physiology, it's biology, and you know it's my view that medicine still is an art more than it is a science. And I just I struggle with people out there who belittle N equal one cases, that they're not important, that you have outcomes, trial data that make N equal one irrelevant, right, I mean it's.

Speaker 3:

You know, I had a little on Twitter recently, a little thread I was involved in where a cardiologist was reporting a case that they were involved with where there was a lot of risk factors in this particular patient and they had elevated LP, little a elevated LDL, and they were touting their success because, with a very high fiber diet, extremely low saturated fat diet, this particular patient and two drugs had a marked reduction in LDL, which to the now target, which is LDL in the 20s, 30s, 40s. And they were singing their praises because they got the LDL this low with two drugs and some dietary modification. And I said I kind of pushed back, I said where's the context here? You know what is the what in? What is the context for this lipid abnormality? And don't you think that's important? And they're like no, no, it doesn't matter, this person's risk relates to the very high LDL C that they were experiencing. And then when they finally disclosed some additional context, they couldn't understand that.

Speaker 3:

I said this patient is insulin resistant until proven otherwise. And they reported that the patient had a normal BMI, a normal A1c, and I still said this patient is insulin resistant until proven otherwise. You have to show me that they are not insulin resistant. They said the A1C is normal. And this is just everywhere. It's just pervasive that people don't understand that when you are only looking at glucose metrics you will miss insulin resistance.

Speaker 3:

And I see this in my patient population every single clinic. I have patients coming who have established coronary disease and have acquired arrhythmia, and I also have patients who come in with their first presentation of cardiovascular disease as arrhythmia Atrial fibrillation, for example, which is the most common arrhythmia we see, and when I mean a lot of them are already overtly insulin resistant. Either they have an A1C of six or they're frankly diabetic. So a lot of patients are like that already. And then you know that that is a big driver. We know from the atrial fibrillation literature that obese patients who are suffering from obesity, adiposity problems, body composition problems, that they have a high prevalence of atrial fibrillation. And when studies were done to evaluate the benefit of weight loss, you saw that there was a reduction in the AFib burden and a reduction in progression. In fact some people even had reversal and experimentally, when you look at that and you see fat excessive or ectopic fat, visceral and ectopic fat that fat actually penetrates into the atrial myocardium, completely disturbing and distorting the architecture of the atrium.

Speaker 1:

I think I know what you're saying now, but I want to try to get it into language for eighth graders. So what you're saying, I think, is that the connection between the insulin resistance and the heart arrhythmia is that the insulin resistance tends to lead towards some kind of additional body fat and some of the fat. Is that I'm assuming that's the ectopic fat is actually penetrating the muscle of the fat? Is that, I'm assuming that's the ectopic fat is actually penetrating the muscle of the heart? I realize there's probably some technical yeah, I mean there's.

Speaker 3:

You know, insulin resistance is a direct result of visceral adiposity, this personal fat threshold concept, where you have now fat being depoted into areas outside of the subcutaneous depot, and that includes the heart. For, you know, for diabetes, you have your twin twins.

Speaker 1:

The first time I've ever heard this.

Speaker 3:

Yeah, when you have your twin cycle hypothesis for diabetes, which is excessive fat in the liver and the pancreas and the heart. And if you're getting fat in the liver and the fat in the pancreas, you're probably getting fat around your heart. And so I think you have potentially two issues. You have the effect of being insulin resistant, which likely promotes inflammatory states, oxidative states. But you also have then, as insulin resistance being a marker of cardiac fat, which is secreting cytokines, which are inflammatory molecules that affect the development of scar tissue, you know, affecting the atrium fibrosis, we call it. And then you also have actual direct penetration of the atrial myocytes, the muscle cells in the atrium. And you know Philip knows this when you do open heart surgery, you look at the heart and you see where the fat is.

Speaker 3:

One of the areas where the fat's accumulating is around the pulmonary veins. These are the veins that attach to the left atrium. So you get all this fat accumulating around the pulmonary veins. Guess where atrial fibrillation arises? From the pulmonary veins? This is the yeah, this is the arrhythmic trigger of atrial fibrillation.

Speaker 1:

It's Whoa let me make sure I'm clear here. So the fat is what's triggering the arrhythmia, and the solution that has been offered, for I don't know how long, is drugs or some kind of mechanical device intervention rather than hey, let's get rid of the fat around the heart. Exactly, I'm not overstating this, am.

Speaker 2:

I.

Speaker 3:

You are not.

Speaker 2:

I mean, and I think you know what I would add is we just don't see the fat, right? No one, most physicians, don't think about that. And Ryan's right, as a surgeon, I see it all the time. You know, and this is just such an amazing conversation to have. Right, because we've talked so much on this program right, the clear relationship between insulin resistance and atherosclerotic heart disease. And you know, I do think that message is getting out there. Like Ryan said and like his story demonstrates, it's still not mainstream, it's still largely ignored by most of the cardiology community, but at least I see that starting to get into the conversation. But when we look at other forms of cardiovascular disease the arrhythmias, the irregular heart beats that Ryan deals with all the time there is really very little, if any discussion I've seen around insulin resistance playing a role in that, and yet it's something that I have been observing. I have a number of patients in my practice with AFib who they, you know, fix your metabolic health and the AFib improves, gets better, some cases goes away, and you know it. Just so I'm very excited to have Ryan on to talk about this and I definitely want to get into all these mechanisms and I think we maybe can also add the effects of insulin resistance on the autonomic nervous system is another reason that interacts with AFib.

Speaker 2:

But I also want to, at a high level, talk about your sort of black swan story and the. You know how it gets viewed, how it is viewed by the medical system. You know, in most scientific rigors, right, the black swan, the exception, right, this is what negates the hypothesis. Right, and in medicine, we tend to treat these black swans as just they're outliers. Right, you know, it's something, you know, genetics, whatever. You pull out of the air to explain it away and you say, but the theory still holds, right, the hypothesis still holds.

Speaker 2:

And in this case, the lipid hypothesis and cases like yourself, like so many others, that again, I see, you know they're, they're following the guidelines, they're being treated by the guidelines, their LDL cholesterol levels are low. They've been on these medications, these diets for decades. And yet, you know, from my perspective, I see them ending up on my operating table and we see them having the heart attacks. And again, we just look at the high level evidence. Right, we've been pursuing the lipid hypothesis as a, you know, societal treatment strategy.

Speaker 2:

When we look at the diet, when we look at the pharmaceutical interventions, we have been largely successful, right, people's LDL levels on a population level are lower than they have ever been here in the US and heart disease remains far and away the number one killer. And somehow you know medicine as a whole and many of my colleagues individually, and many of your colleagues individually, will just say you know people aren't listening or we need to do it harder. Well, just say you know people aren't listening or we need to do it harder. You know I've heard cardiologists talk about you know we should be putting teenagers on statins.

Speaker 3:

Right, we need to start earlier is the problem, and I just wanted to kind of get your perspective on that, now that you've obviously been through this personally but are also seeing it every day in, you know, talking with colleagues. Yeah, I mean, that's definitely the majority view that the reason that the statistics are so sobering the cardiovascular risk factor and cardiovascular disease projections based on consensus data and NHANES data is just sobering and the majority view is that we just haven't gotten the LDL low enough for long enough. Right. But the other view, which is the minority view, is that we're majoring in a minor and we're largely ignoring, because we're not trained to understand this and to help patients with this therapy. It's that the bigger driver is metabolic dysfunction and I struggle with it on a daily basis, trying to get my colleagues to understand this and to be interested in this, and I keep working at it.

Speaker 3:

I've given a number of grand rounds at my institution. Now I'm actually the chair of the cardiovascular department for the hospitals. I'm controlling the grand round schedule and trying to definitely change some of the focus of some of the talks, but it's a struggle. It's a big struggle. I think that you know what I see in my clinic and I test every almost every patient that I see with you know either pre-atrial fibrillation arrhythmias, hyperrelation arrhythmias, such as high-burden atrial extra beats or little runs of atrial tachycardia. I test them for insulin resistance and I do what's called a HOMA-IR, which is a fasting insulin and fasting glucose. As for me, the simplest screen and this is unpublished data yet, but I'm collecting this data and looking at the prevalence of insulin resistance diagnosed by HOMA-IR scores in an unselected atrial fibrillation population, and it's over 90%.

Speaker 1:

Dr Justin. Marchegiani Unpack that one for me, dr Peter Salgo. You lost me completely, dr Justin.

Speaker 3:

Marchegiani In my clinic I am basically taking everybody who either has atrial fibrillation or pre-clinical atrial fibrillation. So the way they stage atrial fibrillation now is in four stages. Stage one you have risk factors for the development of atrial fibrillation. Stage two you have risk factors and you have evidence of either structural or electrical remodeling, or what we call remodeling, which is basically change, which could be that on an echocardiogram your atrium is a little dilated that would be a structural remodel. Or on a heart monitor, for example, someone's complaining of heart palpitations.

Speaker 3:

You do a heart monitor and you see arrhythmias but they're not classified technically as atrial fibrillation. You might see a 20-second run of some fast atrial beating or you might just see a lot of atrial extra beats. That is what we call preclinical atrial fibrillation. It's evidence that electrical remodeling is occurring and that's again electrical remodeling is occurring, and that's again direct. That is related to this inflammatory response in the heart and the fat distorting the architecture which disturbs the progression of electrical impulse conduction through the atrium. The conduction through electrical impulse should propagate uniformly through that tissue. When you start getting little islands of scar tissue amongst healthy tissue, you start getting this very disturbed flow of electricity with the potential for wave breaks and then you get these re-entry psych circuits that are basic. That's basically what atrial fibrillation is. And so when we took, we've been taking this population and we've been doing FOMA-IR testing on them and we see over 90% of the population is insulin resistant to some degree 90% of the population who are, that's the people who are coming to see you already.

Speaker 3:

They're coming to see me for a symptom of possible atrial fibrillation, or perhaps they have a diagnosis already and they're looking for therapy.

Speaker 2:

Gotcha, and you know, as part of my workup it's let's uncover root cause, yeah, and this is, you know, perfectly in line with, you know, jerry Riven's work's work and Dr Kraft's work, showing that patients that showed up in their day with atherosclerotic cardiac disease again, more than 90% of them were found to be insulin resistant as well. You just have to test for it properly, and I would even make the argument that HOMA-IR probably misses some early insulin resistance. And if we really, you know, push this to the gold standard and did craft testing on all these people, you probably increase that number even higher. And yet, you know, as I said earlier, this is, I'm going to say, almost completely ignored in the EP community and still largely ignored in the, you know, atherosclerotic cardiology community and it just, it's kind of amazing. You know. You mentioned about, you know, giving grand rounds and trying to influence your colleagues.

Speaker 2:

You know I did a talk for the Low Carb USA meeting three years ago and I went back and looked at every study that I could find that around atherosclerotic heart disease that measured both insulin resistance and LDL cholesterol as risk factors and not a single study shows LDL cholesterol to be a bigger risk factor than insulin resistance. And you know, the totality of the evidence is that insulin resistance is probably a five to 10 times greater risk factor than LDL cholesterol. You know, and we get a lot of pushback, right, because oftentimes our discussions sort of get straw manned as we want to ignore LDL cholesterol, right, and I think what you and I are both trying to say is that, you know, ldl is contextual right, it's the environment that the LDL is in, not just the level of LDL, but beyond that, what we're trying to say is LDL clearly isn't the whole picture when it comes to heart disease. And you know, let's look at the big picture, right. The root cause insulin resistance. And again, I'd love to hear how that message has been received by your colleagues. You know, kind of you know what kind of pushback you get when you just try and say that insulin resistance is a big risk factor.

Speaker 3:

Yeah, I mean it's been different depending on where I've been. When I was down in St George, there was not a lot of acceptance of my views Up here, you know, in the Provo area with Intermountain. Intermountain's been excellent. They support a model of clinic work that gives us time to discuss these things with patients and to work through a lot of complicated issues, you know. So they actually cap our clinics so that we're not seeing too many patients, and so we get more than 10 minutes with our patients and I've got a really we're kind of a little bit of a fledgling cardiology group here.

Speaker 3:

We're only four or five years old at Utah Valley and I'm the first electrophysiologist for them, so we have five physicians now. We're growing. We're really growing a lot and everyone's been just awesome. They've been very open to the things that I talk about and in fact it's sometimes amazing to me because sometimes I get referrals from our cardiologists to manage lipids, to manage these primordial cardiovascular risks, and I'm starting to get patients actually coming to me. One of our cardiologists had aspirations to start a cardiometabolic clinic here at Utah Valley and so I was shocked and I was really happy about that and he and I are collaborating on that initiative. So in the not too distant future we'll have that. So they've been very receptive.

Speaker 2:

Yeah, that's great to hear and, like I said, you know, I do think the landscape is changing. You know, perhaps somewhat ironically, you know, the rise of the GLP-1 inhibitors, I think, or GLP-1 agonists, you know, has the fact that they have shown cardiovascular benefits even outside of weight loss, and it just points you straight towards, okay, they're improving insulin resistance. There's, you know, obviously that's a factor and of course you and I would would discuss that there may be better ways to improve insulin resistance than these pharmaceuticals be better ways to improve insulin resistance than these pharmaceuticals, but it at least starts us get, you know, I think it has helped to elevate the conversation around this. I wanted to go back actually to your personal story for a minute and just, I guess I wanted to really, you know, drill in a little bit on your transformation, right? So you realized that you were at risk early on.

Speaker 2:

You, of course, you know, being highly educated, being in the cardiology world, you know, had the resources right to all the best sort of options to manage this and it sounds like you were pretty aggressive about doing that and you follow all the advice and yet, you know, you still end up with a heart attack and, if I have the timing right. You know the whole sort of insulin resistance, metabolic health concept hadn't really reached you prior to that. So what was your thinking like at that time that you have the heart attack and maybe talk a little bit about that journey that got you to metabolic health? How'd you kind of discover the whole concept of insulin resistance and metabolic health, which doesn't really get talked about?

Speaker 3:

I went vegan right after the heart attack. I was looking at some sources like Esselstyn and Caldwell and still talking to my cardiology colleagues about my situation, and everyone was telling me that it was my LP, little a. When you look at my NMR profile of lipids, I had a classic type B LDL, so a preponderance of small dense LDL, although a preponderance of small dense LDL, although even though my LDL-C was not very, I mean, like I said, you know, without being statinized it was about 100. On statin, it was 30s 40s, a lot of small, proportionally small dense LDL. And the triglyceride HDL thing was just.

Speaker 3:

I didn't do my due diligence, I didn't do my own personal research and none of the cardiologists that I ever saw said anything about it, and so I carried on for several months as a vegan. This was whole food, plant-based vegan and when I had the heart attack I was 185 pounds. In college I was 150. So people always have to look at historical pattern right To understand the potential impact of weight and this personal fat threshold concept. And I lost some weight as a whole food plant-based eater. And then, through the encouragement of my wife and a friend, my friend Brett Smith, who I'm collaborating with on a podcast. He had gone through his own personal journey of 150 pounds of weight loss and was a low-carb, transitioning to carnivore advocate, and he was having discussions with me and trying to tell me that my veganism wasn't going to solve my problem. And so I went and saw a lipidologist a different lipidologist who did who tested me basically and said she right away looked at my history and all my lab work and said you're insulin resistant and I'm going to test you and show you that you are. And so I actually had a craft test and my fasting insulin was 16, but I flunked the. That was high by what I now consider the appropriate standard and I flunked the craft test. And so she convinced me to. She knew that I was still sensitive to the saturated fat issue because I hadn't at that time really done my research and dove into that deeply. So she said just do keto vegetarian. And so I kind of transitioned towards that.

Speaker 3:

And what happened then basically to make a long story short is that my lipid profile converted from type B to type A. My LDL did not go up as eating more saturated fat, although initially it wasn't a lot of saturated fat, it was still kind of keeping saturated fat restricted. But even as I liberated the saturated fat in my diet my LDL did not really go up. My ApoB actually went down and I started to kind of back off on the statin treatment. And then my insulin dropped to one. My LP little a amazingly went from 137 milligrams per deciliter which is moderately high, to 30, no 131 down to 37, which is a massive drop in LP little a, which is not felt to be responsive to anything it's. You know cardiology thinks it's just strictly genetic. You measure it one time, that's all you need to do is measure it once. And I've had multiple now CAC scans which did show some early progression from years one to three and then from years three to five. It's been stable. So no evidence by calcification of progression, despite eating a higher saturated fat, and now I'm essentially pretty much almost carnivore.

Speaker 3:

I do. I look at my diet almost strictly from the perspective of satiety and I love Marty Kendall's work on optimizing nutrition and the data that he's looking at and in terms of satiety you know nutrient leverage, protein leverage, diet quality. But my focus is really on satiety because for me, when my satiety and satisfaction is optimal, I don't overeat and I am much less vulnerable to succumbing to my addictions, and so that is strictly my focus, and so what I've learned is that fiber does help me. So I still eat, you know, things like raw cauliflower, and I do a lot of fermented foods like kimchi and kefir, but other than that, I'm pretty strictly animal-based and I eat the fats that come along, and I eat dairy full fat dairy as well. I'm kind of rambling on here. I forgot your original question.

Speaker 1:

I have a question. Our rather sizable audience is going to have people in it who have been diagnosed with some phase of heart arrhythmia and they're going to hear this and say, okay, what tests do I need to ask for? Yeah, it's what if these folks were in your clinic? What are the tests you'd put them on or you'd have them do in order to identify? I do where they are with this, yeah.

Speaker 3:

I try not to be overly complicated, to be honest with you, so I do just a few tests.

Speaker 3:

I still do A1C because I like to show people the limitation of A1C If they're coming into clinic and they're not already diagnosed as pre-diabetic by A1C or diabetic by A1C, I will get that.

Speaker 3:

I will get then fasting insulin and fasting glucose together for the HOMA-IR score and then I get an HSCRP as an inflammatory marker. Those are the basic things I get, and Philip had a great comment earlier that you may miss some people with just the HOMA-IR. So if I'm still very concerned about someone or some biomarker, some metric that is disturbing to me, I might go a little bit deeper and perhaps do an oral glucose tolerance test with insulin, the old craft test, because my focus is on diagnosing insulin resistance, which is always 100% associated with hyperinsulinemia too much insulin in circulation and that is then the focus of the therapy. So the end of the road for metabolic therapy is insulin sensitivity, which means normal insulin levels, is insulin sensitivity, which means normal insulin levels, and I will do whatever it takes to get people to understand that and to have that as the target. That is the target for me.

Speaker 1:

Right, it's not the heart rhythm problem less acute. And so let's find out why the hell you've got a heart rhythm problem less acute. And so let's find out why the hell you've got a heart rhythm problem. It's probably related to insulin resistance. And let's deal with the root cause.

Speaker 3:

Because I know that if we fix this, if we fix the underlying physiology, the broken biology, that they will improve Not only cardiovascularly but, as you all are aware you know, the risk of many things will go substantially down Cancers, alzheimer's, stroke, you know, coronary disease along with it and the prevalence of coronary disease in patients presenting with a primary rhythm problem is really high. Patients presenting with a primary rhythm problem is really high. So that's the other thing I do sometimes. I do often, as I test coronary artery disease, direct imaging. I'm not a big stress tester, I will do direct imaging. We have CAC scanning, we have CCTA, coronary CT angiography, with something called Clearly, which is an amazing AI-based software to really look at the presence of and the morphological characteristics of both hard and soft plaque.

Speaker 3:

So to kind of circle back to my personal story again, this lipidologist and a friend of mine were the ones that were critical in helping me get diagnosed and then I took it from there and I just dove into the literature trying to understand this metabolic dysfunction and I resolved it with diet alone. Resolved it with diet alone, 100% dietary resolution, remission. And again, you know my focus, you know for me and I think, for a lot of my patients really the patients that I see that do the best are ones that come along and follow the satiety concept. And it's funny, you know, one of the things I tell patients is I said look, if you want to heal yourself, ignore evidence-based medicine and ignore the guidelines.

Speaker 2:

That's pretty much. It Do the exact opposite almost, it seems, these days. What are you seeing in regards to the arrhythmias and EP issues? When you are reversing insulin resistance, they improve.

Speaker 3:

They definitely improve. And you know, when I was in my 30s and 40s, I was probably I was going through some pretty significant burnout, definitely in my 40s, and that burnout I now understand was really related to the fact that I didn't ever feel like I was really helping, helping people. You know I, we were prescribing pills and you know amiodarone and flecainide and these drugs for arrhythmia suppression, and we were getting into the, you know more and more of the ablation field for atrial fibrillation especially, and but. But patients continue to come back. You know, and it's the same story in cardiovascular disease, right, you know, you see it. You know patients are on statins, their LDLs are in the toilet, but they continue to come back with issues because that underlying root cause is not diagnosed and it's not dealt with and this is just pervasive.

Speaker 3:

But, yeah, they definitely improve and that's my first approach unless they're, you know, really not doing well and they still, you know, could benefit from a procedure such as an ablation. But it's always a message that, yes, we can take you and do ablation on you, but if you don't fix this root cause, you're going to be back in a couple of years. So it's really trying to get them to adopt this preventative mindset to help with progression, along with any therapy that modern medicine still might be able to deliver.

Speaker 1:

Let me ask a silly question, phil. You may have accidentally muted yourself. Question Phil, you may have accidentally muted yourself. My mom has been diagnosed with some arrhythmias. Looking at her physically, she's relatively slender. As somebody who's, at least externally, appears to be slender, can you tell anything about this particular kind of insulin resistance just by looking at them?

Speaker 3:

No, you can't. I mean, that's the problem with guidelines and these glucose-centric metrics is you're going to miss. And this is the new epidemic, I think, is this skinny fat, and you know we don't have great tools for diagnosing ectopic fat and you know it's hard. We have, no, we don't have great tools for diagnosing ectopic fat, and that is the problem, right? So you can't always look at somebody and make that diagnosis. I think you have to test, and this was the argument I had on that Twitter thread recently. I said you know, and you know, the argument that was thrown back to me was that there's no data that measuring HOMA-IR has any favorable impact on outcomes. And again, it was just outcomes are greater than anecdotes. And my response was are you crazy? Crazy?

Speaker 3:

We don't need an RCT to know that fixing broken biologies is going to have a favorable impact on outcomes. You have broken physiology here. Your cells are dysfunctional. Dysfunctional cells cause disease. We don't need an RCT for that. We need to get back to you know I've used the term terrain thinking before. Maybe you've heard this term which is the internal environment. This is what modern medicine is missing. This is the more medicine. We have to start thinking about medicine more holistically and broadly. And it's about, you know, homeostasis, which is creating the conditions for healing. And if you don't have homeostasis, your goal should be to get homeostasis right. Why would we need an RCT for that? This is the regulatory capture of modern medicine. We need, you know and I love Nick Norwitz's phrase evidence. Absence of evidence is not evidence of absence.

Speaker 3:

You know it's never, yeah, yeah, we never get the R, the other you know fault in that thinking right is.

Speaker 2:

You know, okay, this is a hypothesis, right, does it have merit being tested? You said you're gathering the data on your patients and, of course, yeah, it would be great, not that you would ever do this trial, but it would be great to have the trial. But you know, the point of medicine right is to progress. Like we're supposed to come up with new theories, we're supposed to observe a problem and, in this case, the problem being that we're doing a lousy job of treating heart disease disease and we're supposed to try and figure out how to solve that problem. And you know, as you said, it really just makes perfect sense. We have this biological you know biochemistry problem that we have demonstrated and let's see if fixing that problem, you know, fixes the you know fixes heart disease. Because you can certainly go back to 1970 and say there were no randomized controlled trials showing that manipulating LDL is going to have any effect on heart disease, and we can argue about the subsequent trials that were done. Maybe, but this is how hypotheses are generated and tested and in my mind it really comes down to this right, I've never seen a patient harmed by improving insulin resistance and I've never seen it and I'm unaware of.

Speaker 2:

You know a case report of it, right? So why not? Especially when we're talking about dietary interventions, right? I am really truly yet to see a patient harmed if they go on a low carb diet and improve their insulin resistance. Some patients it doesn't work. For some patients they can't adhere. But that, I think, is what should be guiding us, right? There's a problem, there's a mechanism for the problem that has been identified, and we have a way of addressing that mechanism that really doesn't appear to have any harm associated with it. So why not give it a try at least?

Speaker 3:

Yep A hundred percent agree.

Speaker 1:

I'm fascinated by this whole concept of fat around the heart penetrating the heart, causing arrhythmias, and I think this may be one of the most important just couple of sentences we've had in the history of this show. So I'm going to speak to the audience right now. Folks, there's a lot of you out there who've been diagnosed in some way, shape or form, with this. Take the steps necessary to find out whether or not you are, in fact, insulin resistant, and I'm sure Dr Cooley will have some more information available for us, possibly online. That'll help. Possibly online. That'll help. Phil, how do we wrap this up?

Speaker 2:

I guess I'd just like to hear what Ryan has planned for the future, where he sees, you know, kind of his path from here. I know many of us, you know, as we come to these realizations and we have to kind of figure out some different ways of participating in the medical system as it might be and, you know, trying to get this information to the people that need it. You know it sounds like you're in a pretty good place and have a supportive institution and are looking to build upon that. So I'd love to hear just kind of what your plans are for the future plans are for the future.

Speaker 3:

Yeah, I'm still, you know, still going to be doing my typical clinical work in electrophysiology and I still think that there's, you know, I still think there's value in, you know, providing some of the services that I do provide, especially in the area of ablation, but I definitely want to grow. You know my ability to help in the preventative sphere and you know our next project is this cardiometabolic clinic that I'm collaborating with, and I think that we intend to have a cardiometabolic program that is going to be 100% unique, because I think that most cardiometabolic programs that are popping up across the country are still, you know, focused on the clinical trial, pharmaceutical clinical trial data, and they're not. They're giving kind of lip service to lifestyle interventions, but it's just lip service, it's not a focus. The focus is on getting more people on more drugs for these programs, and so ours is going to be unique and my hope is that, if we can demonstrate some success, that we can make this a system initiative for the entire Intermountain, and so that's a big project for me.

Speaker 3:

I am starting to try to increase my online presence with a joint effort podcast. To increase my online presence with a joint effort podcast, it's Brett Smith and myself at it's, our handle is at the Metabocondriacs. So we just last I think it was last month we just initiated, we just put out our introductory podcast and it's kind of a slow thing because I do have a lot of other responsibilities and but we hope to kind of increase the output there okay you gotta spell metabocondriacs for me m-a-t-a-b-o c-h-o-n-d-r-i-a-c-s that's what I thought.

Speaker 1:

There's a band called the hypo, oh the hypo.

Speaker 3:

I love that.

Speaker 2:

Yeah, I love that title and definitely get it into the show notes. And very exciting to hear, and you know you're exactly right. The cardiometabolic concept is one that has been largely hijacked by pharmaceuticals, but I think there's a huge opportunity for us to build programs around, you know, effective lifestyle management directed at insulin resistance, and I love how you phrased it right. The target of the therapy is basically reducing the hyperinsulinemia, and that's what should guide us.

Speaker 3:

And, yeah, you know that this we we continue, I think to to suffer from the caloric concept of obesity, right, calories in, calories out. And I try to to send this message to to all the patients that I see that you know you can go hypocaloric, but if your insulin is 30, you're going to, you're going to really struggle. So you have to be thinking about how the body you know how the body is able to utilize the energy coming in and you can manipulate the energy. But if all you focus on is the energy and not the hormone, you will struggle. You have to focus on both and the first step is get your insulin low and then what you do after that will work, you know, with the energy intake.

Speaker 1:

Definitely, definitely so this has been a good one. So just you know from the Joe six pack cheap seats here. This has been really cool. Joe Sixpack cheap seats here, this has been really cool. It's kind of blindingly obvious now that I heard it stated, but literally never heard about it, never thought about it. Fat around the heart, triggering arrhythmias. All right, folks, thanks for joining us. This has been the stay off my operating table. Our guest has been Ryan. Dr Ryan Cooley. We'll provide links to his information in the show notes. Thanks for joining us. For Dr Philip Ovedia, we'll see you next time. Welcome back, folks. It's the stay off my operating table. I'm Jack Heald, joined by the man who fixes hearts, dr Philip Ovedia. Phil, who do you have for us today?

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Dr. Philip Ovadia

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Jack Heald

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