Dhru Purohit Show - Debunking Health Myths: Digging into the Truth About LDL Cholesterol, Heart Disease, & Keto Diet with Dave Feldman

Episode Date: March 4, 2024

The current thoughts around LDL cholesterol center on the fact that there is no scenario in which high LDL numbers could occur in healthy individuals. Traditionally, the belief is high levels of LDL can lead to a greater risk of cardiovascular disease regardless of metabolic health. Today’s guest is here to share his hypothesis and research on how higher cholesterol levels in metabolically fit individuals could be a physiological response rather than a pathological response that can lead to disease.  Today on The Dhru Purohit Show, Dhru sits down with Dave Feldman to discuss high levels of LDL in metabolically healthy individuals. Dave shares the current research on high LDL and cardiovascular disease in individuals eating a ketogenic diet. He also shares his personal approach to focusing on metabolic health and the key markers critical to overall health. Dave discusses the process and findings of the Oreo experiment conducted by his colleague and explains why this experiment further proves their hypothesis on how LDL particles move through the body.  Dave Feldman is a software and platform engineer, entrepreneur, and founder of the Citizen Science Foundation. Through a series of self-experiments and partnering with formal researchers, he has since published the "Lipid Energy Model," which may explain this phenomenon.  In this episode, Dhru and Dave dive into (audio version / Apple Subscriber version): Dave’s hypothesis on LDL (00:24 /00:24) Rethinking our approach to high LDL (2:17 / 2:17)  The research on high LDL and cardiovascular disease (10:00 / 6:48)  The Oreo experiment and what it shows about fat adaptation (17:23 / 13:45) The pushback to lean mass hyper responder (27:36 / 24:15)  Soft plaque versus hard plaque and the risk of cardiovascular disease (37:50 / 35:04)  Dave’s personal approach in focusing on overall metabolic health (51:42 / 48:30)  Fasting Insulin and Vitamin D (59:33 / 53:45)  Endothelial health and cardiovascular health (1:03:28 / 57:45)  The vegan’s twin study and the correlation to LDL (1:21:17 / 1:15:49) Dhru’s experience (1:32:17 / 1:26:36)  Also mentioned in this episode: Citizen Science Foundation  Oreo Cookie Treatment Nicolas Norwitz, PhD Twitter  This episode is brought to you by LMNT, Momentous, and Lumebox.  Right now, LMNT is offering my listeners a free sample pack with any purchase. Head over to DrinkLMNT.com/dhru today. Optimize your Omega-3 levels by choosing a quality fish oil made by and used by the best. Go to livemomentous.com and enter promo code DHRU to get 20% off any order.  Lumebox is offering my community $260 off their FDA-approved portable Red Light device! That's over 50% off! Go to thelumebox.com/dhru and get your Red Light device. Hosted on Acast. See acast.com/privacy for more information. Learn more about your ad choices. Visit megaphone.fm/adchoices

Dave, welcome to the podcast. A pleasure to have you here. You know, you have a pretty wild and somewhat shocking to some people hypothesis around LDL and LDL cholesterol, one that if proven to be true, could have the scientific community rethink the nuances around LDL cholesterol and it's linked to heart disease. So I'd love to start there. If you wouldn't mind sharing, what is this hypothesis? Well, cholesterol. that is, you know, being picked up in a blood test is often associated with cardiovascular disease. And that's why it's assumed that, generally speaking, the lower you can get it, the better. And the more likely it is that you'll have less heart disease.

And what happened to me is I went on a low carb diet. My cholesterol went up substantially. But I myself, I have no background in formal research. I'm actually a software engineer and was building platforms and code. But when this happened to me and my cholesterol went up, I had that fear that the cholesterol levels for as high as they were were going to lead me down the road of cardiovascular disease. And spoiler alert, I don't have a straight answer for that just yet. We'll kind of get a chance to go into how we're getting that information.

But yes, the hypothesis is the exact scenario I'm describing where I myself, who tend to be leaner and more metabolically healthy and saw my cholesterol go up from going on a ketogenic diet and becoming adapted to consuming fat, that actually the higher level of cholesterol may be physiological as opposed to pathological. I know there's two big words, but physiological meaning it may actually be a normal process that cholesterol is kind of a part of that means by which I'm moving fat around in my body versus pathological, which is to say that it's going to create an illness. And yes, obviously that's very controversial because modern medical science would say, no, there's no version of having high levels of LDL cholesterol, particularly the LDL,

which is the bad cholesterol, that could be considered healthy. You know, talk to us about what are the potential implications if your idea, your hypothesis, turns out to be true. How does it have us rethink how we approach this area of a blood marker, which is really connected to, you know, avoiding a downstream effect, which would be heart disease? Well, certainly it gets us to rethink the current prevailing hypothesis that all versions of high LDL cholesterol are necessarily bad. And I should qualify that this very specific way in which we're studying, it with people going on a ketogenic diet for which it seems to increase under the conditions

of being metabolically healthy, that's the one piece we're on right now. So I can't say if we do find people like me and my colleague Nick Norwitz, which I'm sure we'll get to talk to talk about here in a moment, that that alone would dispel the entire lipid hypothesis that, you know, this concept, that high LDL is bad no matter what the context. We're looking at the specific context and in this scenario, it may well be that if this doesn't increase the risk of heart disease, that the thing we are theorizing may be true, that it does have to do more with trafficking. It is important, though, to emphasize that this context isn't just the high levels of LDL cholesterol. You've probably heard of what's often called the good cholesterol, HDL cholesterol.

And there's another measurement you get in a lipid panel called triglycerides. Triglycerides are a measure of fat in the blood. That is usually lower in the profile we're looking at. So high LDL cholesterol coupled with high HDL cholesterol and low triglycerides, this triad, these three together are the triad we're interested in because the second two, HDL cholesterol being high, triglycerides being low, is typical for somebody who's healthy, particularly metabolically healthy. They tend to be able to handle the fuel inside their body really well.

And yes, this is the irony is that we don't really have a lot of studies on people who are metabolically healthy, but with very high levels of LDL cholesterol to see how much this does associate with having higher cardiovascular disease when their LDL is high. You know, it's an important point because largely when people go on a low carb diet, low-carb, whole-food diet is what we're talking about here. And in some cases, going on a ketogenic diet, which is even a step further, they see that a lot of their blood markers improve. Many areas of their health as markers improve. You mentioned a few of them. They noticed that their HDL would go up. They noticed that their triglycerides would come down. But the one area that always had

people scratch their head, including myself, would be that if you are otherwise lean and healthy and you guys have a BMI where you typically say that that number resides, we'll talk about that in a second, you know, if your LDL still goes up, there must be something wrong with this dietary approach. There must be something wrong with this dietary intervention. So the contrast for the audience that's listening is all of these incredible things are happening to your blood markers, but something must fundamentally be wrong with your approach and maybe the ketogenic diet in general or the low carb diet in general if your LDL is now not only increasing, but in some cases, you know, skyrocketing for some individuals who again are healthy and lean individuals. Is that a good

summary? Yeah, actually. And again, without having a lot of research on folks like these already, kind of in many ways almost starting from scratch, just in that there really hasn't been a lot of research, particularly in the context of the ketogenic diet. This episode is sponsored by Element. Our bodies are constantly using and losing water and minerals, like sodium and magnesium throughout the day, even when we sleep. Basically, most of us are dehydrating ourselves 24 hours a day,

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so you've got to make sure you go to drink element.com slash dh-R-U. This episode is brought you by Momentus. Taking care of your brain is as important as taking care of your body. One of the easiest things that you can do to keep your brain healthy is to supplement your daily diet with high-quality EPA and DHA. which is something I've been doing for years. EPA and DHA are the most important types of omega-3 fatty acids. They support cardiovascular health, improve muscle and joint recovery,

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So stay tuned. You're going to learn all about that. Talk to us why so many people in our audience, they listen to podcasts. They listen to experts that are out there like Peter Atia or whoever it might be. And they've heard that the research on LDL is pretty slam dunk, that there is a lot of data showing the correlation with high LDL and cardiovascular disease. What is the literature that exists out there right now? And how strong is that literature? Well, certainly somebody who's a traditional lipidologist would say it's extremely strong.

There's a 2017 EAS paper has a graphic. You've probably seen a lot of other people who have ever done any research or just looked for studies online might have seen, which shows three lines of evidence. It shows genetic evidence, which means if you're genetic evidence, which means if you're genetic, genetically born with high levels of LDL throughout your life, you tend to be more predisposed to higher association of cardiovascular disease. Interventional studies, so drug trials where they intervene to lower LDL, and those tend to have a lower association of cardiovascular events. And then there's observational that it tends to be folks who have lower levels of

LDL as observed with epidemiological data. They tend to have lower levels of cardiovascular events. But there's kind of a catch here. The catch is virtually all of these data across all of these lines of evidence. They are on populations that either partially or exclusively look at situations with those people who either have some form of acquired disease like metabolic syndrome or something like in the case with the genetic diseases I just mentioned, which is congenial, in that there's some dysfunction with lipid metabolism, some way in which they don't handle lipids or lipoproteins very well. In other words, it's a broken system.

It doesn't quite function properly. And that's kind of important because things like HDL cholesterol, the so-called good cholesterol, is actually intimately connected to LDL cholesterol. They're literally moving a lot of these cholesterol molecules between each other. And we actually go through that with the lip energy model, which we published, which kind of explains this phenomenon. And that's kind of important because if you're wanting to assess the totality of the evidence, folks like Peter Atia would say, look, the evidence across the board seems to agree. The catch is we have a major confounder that's shared among all of those different lines of evidence with this dysfunction in lipid metabolism.

We've needed to get a population like the ones we're talking about, the people have this triad, particularly folks like Nick Norwitz, where their LDL cholesterol is extremely high. And their HDL is extremely high, and the triglycerides are very low so that they're metabolically healthy. and who are, you know, as we study them, who are intentionally low to no risk factors otherwise, but seem to have a functional lipid metabolism. So it could be that their LDL is high for a functional metabolic reason. That's kind of important because now we're kind of looking into a new line of evidence that takes away that confounder. And I think that that's important for us to do, which is, you know, why we're doing a study right now out of UCLA for exactly that reason. We're looking at folks just like Nick, just like myself, and we're getting advanced heart scans

to find out if there is that association with risk. Is part of that being that if you look at the statistics, 88% 80 plus percent of Americans are metabolically unhealthy. Now, in all fairness, lumped into that could be individuals that have high LDL, but they have other issues as well. They're fasting insulin is high. They're fasting glucose is high. have, you know, other problems that are typically associated with being metabolically unhealthy.

So it's not just that they're LDLSI. So what you're saying is that even though there may be this association that is very clear in the literature on these large observational studies that individuals had have a higher LDL have higher risk of cardiovascular disease or cardiovascular events, it's the thing is that those individuals don't just have LDL. That's an issue. They have a plenty of other things because the population in general is metabolically unhealthy and is sick. So if you're studying a sick population, how much does this one marker matter? And maybe it matters a lot for them. And maybe it doesn't matter as much for individuals who are quite healthy.

That's how I understand it. Is that accurate? Yes. That's pretty accurate. I think it, I think maybe a good analogy might help to kind of bring home the, concept that something can both be causal, but not necessarily driving disease. And we'll use cars, for example. I would be correct in saying that car tires are part of the causal chain for car accidents. In fact, if we were to ban all car tires throughout the city, we would get less car

accidents. But on top of that, you would also get less people who might be saved at a hospital because they can't travel there in an ambulance because we banned all the car tires. So there's a tradeoff of sorts. But if I were to say, hey, we know because when we intervene and we take away car tires that there aren't car accidents, we can therefore feel confident that the car tires are causing car accidents. You would intuitively say, I'm not sure if that's exactly accurate. I think that there are other factors such as bad weather that can impact car accidents.

I think the drivers themselves and, you know, what state they're in, can. drive car accidents. What we really need is a test where we get people who are good drivers under good weather conditions and see if indeed the more car tires there are on the road, the more we're going to see car accidents. Does that make sense? That way you can kind of see how I'm saying something can both be part intrinsically of the causal pathway, but not necessarily the driver of it. No, that makes absolute sense. And I think that analogy is fantastic. Talk about or go back to what you mentioned earlier, which is there's just not a lot of data that had been out there and studies showcasing, is there some truth? Of course, getting to the full truth will take time and will take a lot of research that's there.

And that's why you said, I don't exactly have, you know, one answer on the subject, but I can give you clues based on what we're seeing that there are more threads to pull. pull on. So what research have you been involved in? And I think recently you guys put some stuff out there for the world to get a chance to see. So could you talk about that? Sure. So there's a couple things. One, I'd love to highlight my good friend collaborator, Nick Norwitz. He's a Harvard med student who, by the way, got his PhD right before going into Harvard med. He got his PhD at Oxford, very talented, has done an experiment that was intended, as he would concede, to draw headlines and attention to the lip energy model that we published. And what it was was he had two different interventions. The first was that he would consume Oreo cookies above and

beyond his existing ketogenic diet. He did this for a total of two weeks. And he wanted to see how much his already very high levels of LDL cholesterol when he's on keto, which hovers near 400, how much it would go down, as we would predict with the lip energy model. And indeed, in two weeks, he had shown that it had gone down substantially 70%. In fact, it was so substantial that they wanted to add a couple more days so that they could do this in triplicate himself and his physicians. And sure enough, it actually went further down with each successive day. So if I remember this correctly, I think it started around, say, 384 and went down to 111.

This is in, again, in just 16 days. This is because what we would posit with the Lip-energy model. I'm going to try not to get too geeky here is that when he's being powered by fat, like I was describing before, cholesterol ride shares in that process. It's existing in the same boats, if you will, that cure. around the fat that he's powered by. And the leaner you are, the more you have to move those boats around to keep resupplying and repleting your body stores of fat.

And when becoming carb adapted by adding more carbs in, you actually bring up your stores of stored glucose in the liver known as glycogen. And then the liver feels less need to traffic as many of the fatty acids. You're now powered technically a little less by fat. this case and therefore there's less need to move those boats around and therefore you end up with less LDL cholesterol now you put that up against of course the most popular cholesterol lowering drug which is a statin and i believe he was using a very powerful one crestor and i think at 20 milligrams which is a you know high dose for that power of statin and did that for a total of six

weeks. And at the nadir, which is the lowest point, its drop was substantially less. The first one with the Oreo cookies brought it 71% down. And I remember the exact number, but the statin brought it something in the neighborhood of 35% down. So of course, the headline is basically Oreo cookies brought his LDL cholesterol to twice as much lower than the statins did. And that was, was obviously very exciting. He's been doing such an excellent job of drawing further attention through that experiment to the lip energy model and our research. And I just, I really have to commend him that. That's probably going to be the most interesting thing I tell you during this podcast. It's kind of a big deal. And we just want to like kind of make sure everybody understands for a second

because there's a lot that's in there. On top of his ketogenic diet, his healthy low carb diet, that has worked well for him for years. And, you know, he feels this way. Not saying that it's the right thing for everybody else. We're just talking about Nick and his work. And you can follow Nick and Dave on Twitter, you know, X.com. We have their links in the show notes below. And they regularly share their experiments and the work that they're doing in the research.

So on top of his low carb diet, he added in Oreo cookies. Do you know how much he was having every day? I believe it was a two sleeves a day. Two sleeves a day. It's either one sleeve a day or was two sleeves a day. But it's important to emphasize. This was on top of his existing diet. So a lot of times people may assume that there was some drop in saturated fat to explain

the lower level of LDL. No, this was in addition. So if anything, it was a slight increase in saturated fat. Yeah. So already on top of his diet, already having saturated fat inside the diet, depending on how many servings, you know, this wound out to, you know, three cookies typically could be, you know, 25 grams of carbohydrates that are there and he's he's having a sleeve he's probably having two to three times that amount in in a serving that's there we can look that up exactly afterwards but

adding in these carbs which include per serving you know 14 grams of added sugar in a typical Oreo packet per serving and he was probably again having two to three times that much he showed that he could lower his LDL more than taking a statin. 71% on the Oreo cookies, 35%. And again, I've heard you share with folks who might be new to this and are unpacking this. It's not that you are trying to say, hey, we should all eat Oreo cookies and start adding them to our diet. That's not the goal here. The goal of this is to point out what?

What's the goal of this experiment? The goal is to draw attention to what we suspect. fact, as I mentioned earlier, is physiological, that this may in fact be a normal part of the process of our body handling fat adaptation. He, you know, his LDL cholesterol before he'd gone on a ketogenic diet, his LDL was closer to 90, which would be considered very ideal. And after going on a ketogenic diet, which he's used to great effect for efficacy for helping out with his all sort of colitis. It's been great, except that for as lean as he is, he fits this profile as we would expect it to be, and that his LDL is gone through the roof.

And so how does that get reversed? Is it really just that he's having that much more saturated fat? If you've seen interviews with him, you already know that he actually doesn't consume a lot of saturated fat, typical to most low carvers. His is more of a Mediterranean style. His primary source of fat is extra virgin olive oil much more than I would consume. And I think his average percentage of saturated fat for the fat source is something like 15% or less. So his LDL going up fits our model. We believe it's because there's more trafficking.

So what we're showing with the Oreo cookies is that it's really this repletion of the glycogen stores in the liver on top of, you know, a higher amount of insulin, of course, to some degree in the overconsumption. all of these factors can result in the reduction of the LDL cholesterol from this mechanism, from this larger mechanism we're talking about with the lepin energy model. And like I said, it's been great because it really has drawn a lot of attention to this research and to that model. What has, and the other item that I want to add in here is that, you know, the everybody would

agree pretty much on all sides of the dietary spectrum that. Oreo cookies with the amount of added sugar that they have. Some people may debate whether or not the excess level of carbohydrates that are there are good, neutral, or bad, right? But generally Oreo cookies are going to be seen as an ultra-processed food. Pretty much all health experts are going to agree. We want to minimize ultra-processed food, and we want to minimize above a certain degree. There's variations and maybe debates in this. We just don't want a lot of added sugar. I think the American Heart Association even says for people that not to have more than like 40 or 50 grams of added sugar a day. I think it's somewhere around that. I could be wrong. I'll double check.

So everybody agrees that eating a ton of Oreo cookies is not a good thing. And yet by doing this thing that was not a good thing, he could independently drive his LDL down, which puts into question, which is how does LDL in lean, healthy people actually transit through the body? And also, if this intervention works better as a statin, you know, what, all of a sudden we're going to start recommending to those individuals and that phenotype that they need to start having things like Oreo cookies or excess carbs or added sugar in the diet. And obviously, everybody would say that that's not correct. There's been a lot of, you know, interesting receivership of this experiment that's there. A lot of people that are in the different metabolic therapy camps. Recently, we've had individuals like Dr. Chris Palmer and a few individuals from the Metabolic

Mind Institute on the podcast talking about the role that ketogenic therapies and metabolic therapies can play in reversing mental health disorders, everything from schizophrenia to bipolar disorder and the brain energy model that they're exploring that's there, the brain. energy theory. And one of the biggest detractions that they've had for people saying is that, sure, maybe people's brains are getting temporary better on a ketogenic diet, but are you going to cause some other situation where they're going to have a heart attack in a few years? And a lot of them feel, you know, very kind of naturally upset about it. It's like I finally got my life back together and I'm not suffering from this extreme mental health condition.

There's got to be more to the story than all of a sudden the thing that's great. for my brain and actually helps my mitochondria repair is somehow, quote unquote, terrible for my heart if I'm generally otherwise lean and healthy as an individual. What pushback have you seen to this experiment? If you would have to stress test it from people who typically have said this lean mass hyper responder phenotype, that there's not too much to it and you guys are looking in the wrong direction, has there been push back from those individuals on this experiment that you've seen? We kind of anticipated that there would be some, there's no question, but to your larger point there, this is part of why we want to find any and all ways to get interest in this. In the last five weeks,

I want to say, there's a total of three papers that we've had dropped. And on top of those three papers, we've also had a presentation by our principal investigator at the Lundquist Institute for our match analysis, which I'd like to also chat with you about. But the reason I bring this up right now in totality is more of the talk right now is on the Oreo versus Staten experiment. And that's a credit to Nick Norwitz in that, yes, we just before that was a 41 randomized control trial meta-analysis. That's not gotten nearly as much play. But for which we would definitely hope that more of the people who are critics of the lip energy model would have looked at because it very much substantiates this leaner component, particularly as you get lower than, say, 25 BMI and the association of change

in LDL cholesterol, as would be predicted by the model. But again, doesn't get nearly as much chatter. It's not gotten nearly as much talk because it doesn't have something exciting and interesting like Oreo cookies somehow attached. Five and a half years ago, I did a similar experiment to demonstrate the model before I'd even connected with Nick. And it was the same thing, except that it was white bread and processed lean meat. And at that time, there wasn't as much awareness. The community wasn't quite as large as it is now.

And it didn't, that experiment didn't get as much play outside of the low-carb community. But it was the same general idea. which is just that we're choosing things you don't associate with health. You don't associate white bread with health. You don't associate Oreo cookies with health. Nick actually improved on it in many ways, including putting it up against a statin because that does carry a lot more weight and interest as it associates with LDL cholesterol.

But that's part of the reason for choosing it was that it gets that greater degree of interest. Ourselves, we'd love it if all of our papers got as much attention is the Oreo cookie experiment, particularly the coming match analysis. We'll find out because that's going to be published here soon. That's out of Lunkwist. That was the study that I got crowdfunded. And thanks to everybody in the community who's helped to make that happen. And for that, we're actually getting a lot of people like us, like Nick Noritz, like myself.

And we're actually scanning them with CT angiograms. And that match analysis that I'm describing, that was presented December 8th. And what Dr. Budolph showed was that when matched with this other group called Miami Heart, who had average levels of LDL, but otherwise were matched as one-to-one as possible with both demographics, with age, and many other risk factors, that the plaque levels were statistically, there was no statistical significance between the plaque levels. And that data is going to be very compelling as well. But same thing.

It doesn't get quite as much trafficking. It doesn't quite get as much interest. So I find we have to do both. I think we have to have some experiments like this one that Nick did. But at the same time, we have to do the good science and also get the risk data as well as to build out the mechanistic data. This episode is brought to you by Lombox. One of my favorite daily practices is using red light therapy. There are thousands of articles and studies published.

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Just go to the loombox.com slash D.HRU, Drew, that's me, to get your device and start stimulating your mitochondria today. That's the T-H-E-L-U-M-E-Box.com slash D-H-R-U. That's me to get $260 off this portable red light. light device that I recommend. You know, you mentioned that you guys did anticipate some pushback. What has been that if you would have to steal man the other side of things and when people are looking in, especially for this, you know, these individuals that are leaner and generally

have really good metabolic health. Well, actually not generally. They all have good metabolic health. If they're going to be in this lean mass hyper responder category, they have, you know, their BMI, you said was below 25? Generally, we find that it's not 100% of lean mass hypers responders are below 25. It just is very common. Yeah, that they're going to be below 25.

And the lower the BMI, the higher the response of increased LDL. Yeah, I would find myself in that category, even though I have familial hypercholestrolemia, family history of cholesterol. I'm in the 21 point something BMI, 21.2, 21.5, somewhere around there. And largely my metabolic health is all in the optimal range. I get my labs done every quarter through life force. I have a whole history and analysis of them. And the one that was just always seemed to be, you know, high. And in some cases, got worse. I'm not on a ketogenic diet, but I generally follow. I don't fear carbs. I'll include some white rice here and there, other things in a very targeted fat. but I would eat what would be called a low-carb diet and my LDL would continue to go higher and

higher and my APOB, which we'll talk about APOB as well, generally was always quite high. I don't have that historically as long as I as far back as I have my LDL. And, you know, I was concerned and I started seeking out information. My audience knows I've had a few of the cardiologists that I've worked with on here. And I have done some of these CT advanced scans. hands, one in particular, no affiliation that goes by the name clearly. And I've presented my results here on the podcast that shows that I had no hard plaque and the tiniest amount of soft plaque that was inside of there. So I digress a little bit. But if you had to steal a man the other side

in terms of sophisticated responses that you've seen back to these experiments and the studies that you're working on. What does the other side say about the threads that you're pulling on and the validity of them? So it's actually funny because I presented the steel man argument in advance in the announcement of the UCLA study. I was describing the one out of Lundquist. I said that our study would be pretty good at answering what I like to call the big magnitude question, but it wouldn't be very good in answering the small magnitude question. So you know how you brought up that, how strong is the evidence for those people who are pro LDL lowering?

And they would say that it's very widespread, that it's very consistent in how high your LDL is, or for that matter, how high your APOB lipoproteins are. That's the major protein that's a part of it, as you were mentioning from earlier. the faster you will develop plaque depending on how high it is and for how long. And the big magnitude question, as I like to call it, is, okay, so if we're looking at folks like we are in our cohort with the Lunkwist Institute, and their average LDL cholesterol is 272, well, that's in the very top 10% of the very top 1% of the general population. that's extremely high. And that's the average.

Our max level person, I believe was 582, I think, was their LDL cholesterol. So that's like at the very edge. Without question, the expectation is that at a population level, they will develop plaque rapidly. And that's because it's expected for this big magnitude of LDL exposure. they'll have a big magnitude of effect in rapid plaque progression. Now, in my announcement of the study, I said, okay, we'll at least get a chance to see that pretty quickly with these data. In fact, the study might even get closed down if Dr. Budoff is calling me, you know, at some point, says we have too many people showing up with advanced plaque at baseline with their first scan, right?

So as it turned out, no, we actually got to all of the first scans. And I probably should have mentioned this earlier. It's a longitudinal study, which is to say we're getting a scan for each participant at day zero and then another one at somewhere around day 365. So it's one year difference between the two. Well, the baseline first scan, the average, the amount of time these folks were on the diet. is around 4.7 years. So already half a decade at an LDL cholesterol, like I said, the top 10 of the top 1%.

So I feel like the big magnitude question is definitely getting addressed right now. And since we didn't see a very high amount of plaque, I would say that the steel man position is for people who still would be in favor of lowering LDL. They would say, okay, well, maybe metabolic health really. does have a strong impact on reducing your risk of high LDL resulting in higher cardiovascular disease, but you'd still be better off with lower LDL, with all else being the same, but your LDL is lower. And I'll readily concede that they could be right about that point. I don't know yet. Our study is not going to be good at detecting that if we're talking about a very small

amount of change in relative terms. The catch is that that's already a massive paradigm shift. Because right at this moment in time, the lipid hypothesis would posit that no, there's just no question. If you have high LDL, you were at a very severe risk for cardiovascular disease, full stop. At a population level, it doesn't matter. You will likely see a very rapid progression, even if everything else is in good shape. And that's why this is pretty exciting, because In a moment, literally this coming month, we'll have had everyone get their second scans. So we'll actually be able to do a comparison in the population. And the libid hypothesis would posit that we should see that rapid progression, given how high

their LDL levels are. I don't know yet what we'll see. And in the scan that you guys are running, it's looking at both hard plaque and soft plaque build up in the body. And is that correct? In the coronary arteries, yes, both calcified. and non-calsified plaque. And the reason that that's important for the audience, obviously a lot of people have heard of getting your CT scan,

getting your looking at hard plaque, calcified plaque. It's one of those tests that is recommended, you know, especially for individuals who hit around 40 men, you know, earlier sometimes, depending on their family history. And hard plaque and calcified plaque is part of it. But the reason that people are so excited and why people are excited, including myself, about, the study that you're doing is as better technology has come to the service to look at soft plaque, my understanding, and you correct me if I'm wrong, soft plaque is the plaque that actually can be more dangerous to a lot of individuals. You could go in and get a CT scan done. And generally, if you're not maybe severely overweight and you're not like a heavy drinker or other stuff,

you could come back with a very low score, but it could give you a false sense of reassurance because you could have very little calcified plaque, but you could have a lot of soft plaque in the arteries, which would increase your risk of cardiovascular disease. Is that correct in my understanding? That's correct. And the very test you're talking about is called a CAC, a coronary artery calcification test. Now, it is worth mentioning that a CAC of zero, you may have heard of the hashtag power of zero, a CAC of zero is pretty correlative. It doesn't mean that you don't have soft plaque, but there are now a lot of studies, including one that was out of Denmark that is still shocking me to this day as to just how tightly correlated a coronary artery calcification is to soft plaque.

To be sure, you can still have a large amount of soft plaque with the CAC of zero. It's just very, very unlikely. So it is true for the gold standard. I myself think, and many of my family members agree, to get something like a CT angiogram, as opposed to a CAC. And a Ct angiogram is like the one you mentioned with clearly. It's looking at both calcified and non-calcified plaque. And our major endpoint for this study is non-calcalsified.

Plac development. We actually specifically want to separate the two and see how much soft plaque is increased. To your point, yes, soft plaque is the more likely dangerous one, particularly if it has like a thin, fibrous cap at the top. It means that it can, it's vulnerable to rupture. And that's what you have to worry about is if it ruptures, it can, of course, release plaque into the bloodstream and that can create a mycardial infarction. And so, yeah, calcified is typically stabilized plaque. It can harden the arteries, of course, but you're not usually worried about a piece of calcification breaking off. It's usually the soft plaque that's a bit more concerning. Now, going back to your matching analysis that you guys are working on with the Miami Heart,

right? That's the, when you're referencing matching, that's the continuation of that work that you're doing there. Is that accurate? The match analysis was in addition to the existing study we're already doing that's longitudinal, we didn't know at the time that we started that there would be this other group that we could pull metabolically healthy folks from to do a match to actually look and find a group that matched ours so that it's like having a matched control. Got it. So in the first part that actually was published and put out there into the world, you found, as I understand it, you found that there was not an increased risk for people who had been, again, on these low-carb ketogenic diets for a period of time, there was no difference.

But did they have any additional extra protection because of their diet? Did they have less plaque in the arteries? You know, was there any way to know about that question? Well, that's actually one of the more interesting things. And I should correct one aspect of what you mentioned. It's not yet published. The abstract should be getting published here shortly. but Dr. Budoff, when he presented it, the data did become public.

It just hasn't yet been actually, I believe it's going to be published in metabolism, and we have another one that's going to be coming out. That's the full paper soon. But anyway, to your point, the, if you compare those two groups once the match analysis was done, what we were very interested in is even if there wasn't a statistically significant difference, given the size of both those groups, not being very large. Did we at least see a trend toward the direction of more plaque in our cohort with the very high LDL? And actually it was the opposite.

The trend favored our group more. Our group had less total people of their proportion that had a plaque at all. The majority had no plaque, zero plaque score. whereas the Miami Heart Group had a slight majority that did have a plaque score. There was only one in our cohort that had double digits in their total plaque score. And this is out of a total plaque score of 45. So really both groups were pretty healthy. But all of our group had single digit plaque scores, save one person who I think was at a 12.

But in the other group in Miami Heart, there actually were four people who had plaque scores and double digits. And if you compare the area under the curve, if you literally, are looking at just the total plaque amongst all the participants and compare it to the total plaque amongst all the participants in the other group. Ours actually had a lower area under the curve. Now, I always want to caveat that doesn't necessarily mean our group is doing better per se. Again, there's no statistically significant difference. But if the expectation per the lipid hypothesis that higher LDL should trend more towards

greater plaque development, you would have expected that. you would have expected that the Miami Heart Group would at least be trending in a better direction at a minimum. And that's not what we saw. You know, there's been a lot more awareness about APOB, right, a lipoprotein B. For those that are not as familiar with it, can you just talk about what it is? And where does that fit into the equation as another sort of part of a biomarker that is, that goes into the LDL story.

And what are your thoughts about how it fits into the equation over here? So I'm going to try to simplify this. And I'll let you be the layperson audience member. You correct me if I get two in the weeds. But I think I can pull this off. Are you ready? Yes. You can kind of think of these boats that I'm describing,

these lipoproteins as lipid-carrying proteins. And the major protein you hear about is APOB. And the boats that have APOB, they have exactly one copy of APOB. The best way to think of them is that they start big and their job is to get small. How do they get small? They get small by dropping off their lipid cargo. So they're meant to do this shipping job of getting a lot of lipids into circulation, dropping them off to your peripheral tissues all around.

There's all these docks, if you will, that the boats are docking with and they're dropping off their cargo. And in the process of them going from big to getting small, they actually connect a lot with another fleet. And that fleet has a major protein called APOA1, but you probably know it more by HDL. HDL is this other class of ship that you can say their job is to start small and to get big. And part of how they get big is they pick up the components that are getting dropped off by the APOB. And as they get bigger, they have more cargo on board, particularly cholesterol. And so that's why this process where things like triglycerides, which is the stored form of fat, which those APOB start out with, are getting dropped off rapidly. They rapidly increase the amount of HDL cholesterol.

That's why HDL tends to go up while triglycerides go down and vice versa. As somebody becomes metabolically less healthy, their HDL goes down, but their triglycerides go up. And we would posit this is a systemic failure. Those APOB lipoproteins packed full with triglycerides are failing to find anywhere to dock. There's no parking for fat in your fat cells. The fat cells are like, we don't have any more. storage. We don't have any more room. There's no tissues that want to oxidize that fat. They're like, what are you talking about? We've got more than enough. And so what do you have? You have this

combination of more VLDL, which is what they started out as before becoming LDL. You have more triglycerides. You have low HDL. All these things in combination. And that's why, Drew, this is why it's so important And to think of these things mechanistically, modern lipidology tries to pick each of these different components and then assign how much each of them applies risk in isolation. And the engineer in me is like, why would you do that? Why not look at this entire profile? Look at the whole scene that's out there in the bloodstream. And then from that, try to figure out how much there's a root card.

that's causing both this profile in these lipids and the atherosclerosis. So you were talking about insulin earlier. People who are hyperinsulinemic, now they've driven themselves to a point where their system is broken and they're not metabolizing these things at a high level. And therefore, you not only see these changes in their lipid profile, but you also see that they develop heart disease faster. But how much, how much are those two having? the same root cause that are causing both as opposed to one root cause that's causing a change in

lipids and then through various levels each of those lipids, you know, impact atherosclerosis directly. That's that's why, you know, understanding the lipid energy model, we hope, will better bring this all into view. When you think about your own health and regularly getting blood work, that was one of the big claims to fame is that you've claimed fame that you've claimed fame that you. you were known for in the beginning. You know, you're a software engineer by background. You're not a physician, a researcher in the field of coming from traditional research in the field of healthcare, having a PhD in that background or a master's. You were an individual, as you mentioned,

who went on this diet, low carb, ketogenic diet because you were convinced that this would help your health and you would feel better. And you did feel better. And you, I think there was a period of time in the early days, like you were testing your blood. Was it almost every day? You were testing your blood and like putting out the results? Yeah, there's a number of experiments where I tested my blood every day. And I'm talking blood draws where like I really went to LabCorp. But there was even a few experiments where I have something called a cardio check, which requires a bit more than a than a glucometer. You actually have to fill a capillary tube. But there's an experiment where I want to say it was maybe 28 days. I was. I was.

was taking my lipids six times a day. So when I woke up at nine, at 10, at 12, 2, 7, and right before I went to sleep, if memory serves. But that alone already provided enormous data because, again, a lot of how they currently approach lipids is they think it doesn't change that fast. But I would argue it definitely does. definitely changes quite a bit. And especially if you're using it metabolically, especially if you're fat adapted and you need to make use of it. So, yeah, that was, I would argue that a lot of the lipid energy model was taught to me through these experiments.

Like I didn't, there's a lot that I learned from the textbooks, from, you know, having a PDF copy of clinical lipidology. But nowhere near as having some high. hypotheses that I could just test and test easily because I had access to these devices, because I made connections with people who I could get these wide spectrum blood tests with Lab Corp, for example, that turned out to be very meaningful. It really helped out a lot. Well, the reason that I brought this up was that how do you think about when it comes to your own health, of course, right? This is you sharing your story. This isn't medical advice to

anybody out there in the world. How do you think about your levels? Do you do you think about your levels? Do you generally think of, do you still, first of all, regularly test your, you know, get your blood drawn and have a history of your markers? And when it comes to these categories of things like LDL, APOB, are there things that you pay attention to? I'm sure you do just out of the fact that you're just interested in this space as a whole. But do you have any thresholds or are you paying attention to the to the numbers at all or do you generally feel look if my metabolic health is in a good position i personally again this is your personal thought i'm not too worried about the fluctuations that might happen include including those those individual two markers you know going up higher what are

what is your sense when it comes to your own health and your own biomarkers for me personally i feel as though I'm doing my due diligence in that, like you, I've got a CT angiogram. I've actually had two. I've had a total of three CACs and two CT angiograms, but to be fair, Ct Angiograms, but to be fair, CT angiogram includes a CAC. You probably already know this. The first pass they make is to check on your calcification. So when I say that, the reason I bring this forward is, regardless of what's happening

within my blood, nothing beats actual detection of the disease itself. I don't, you're going to have a tough time convincing me that anything is as important as actually looking at the geography of the heart. So if I know where that's at and I'm feeling good about it, then I'm not as concerned as I might be in looking at, particularly a biomarker, a blood biomarker in isolation. Now, what's the next layer, I guess you can say, of risk concern for me that I am looking for? it's inflammatory markers. My favorite, which most people already know about, is C-reactive protein. It's a very high sensitivity, non-specific inflammatory marker, and it's really good. Now, to be sure, you can have false positives, but you almost never get a false negative,

or at least I find in what I'm doing. If it's low, if it's like under one, I'm feeling pretty good because it's usually when it's well above one, especially, then at that point I want to investigate further. Inflammation is, you know, heart disease especially is an inflammatory disease. And what I like about inflammatory markers is it at least kind of gives you a sense of where the body feels it's at. It's kind of like knowing if the emergency services are getting called out. And so in that sense, it's something that I think everyone needs to be mindful of.

But again, I'll just mention real quick. You can't have false positives. For example, don't work out right before your blood test because you are, in fact, inflaming your body. That's literally part of the point, right? But I have had my, in fact, to prove this, I have, I think I've taken something over in the neighborhood of 110 C-reactive protein tests total. But a few of those times, I intentionally got them following a half marathon.

And that's when I've seen them at the highest. I've had it as high as 52 once, 38 once and 52 once, which was after, you know, pretty brutal half marathons where I, you know, set personal records. And an ideal rule, would you recommend that people, if they're going to go in and get these tests done and include these inflammatory markers like C-reactive protein, they should just like, you know, get the blood work done early and they haven't like worked out at all that day. Is that like an ideal recommendation?

Definitely. Now, there's something else that I'd like to draw attention to, which is I do think there, in being in this space, I've definitely come to find that there are. a lot of over-exercisers. It's something we were worried about with our study, that some of the lean mass hypers we'd get might be overexercisers. And by that, I mean, folks who just don't give themselves enough time for recovery. Some people get really addicted.

There are runners. There's one I just talked to recently who loves to run 10 miles a day. And as long as your body can handle that, it's fine. But he's exactly the person who I said, hey, you may want to get blood work the next morning. just to confirm inflammatory markers aren't high. Otherwise, it may be you're not giving yourself enough time to recover, and there's just too much of a backlog of repair

that your inflammatory response is trying to work with, your immune response is trying to work with. So I think inflammation is very important. I know it gets a bad rap. People talk about it like it's the bad guy, but it's really not the bad guy. It's true. There are things like autoimmune,

where it is more the bad guy. But generally speaking, inflammation is the process of healing. We die. without it. We need inflammation to some extent. And so you want to be sure that your body succeeds at the inflammation the same way you want to be sure it succeeds at lipid delivery, for example. And yeah, so outside of that, other markers are the typical ones, CBC. But as far as lipids go, I'm much more interested in HDL and triglycerides than I am, say, LDL or APOB or LDLP, for example. Any other associative markers, you know, that you feel that are important as a part of, even if they're not directly connected, they might be an indirect item that are important when it comes to our metabolic health, our heart health, you know, are you paying attention to, you know, vitamin D, any other markers that are there that you are, would say are on your top list when it comes.

of this topic and category that we're talking about. Well, the other that I would put as part of the big three is insulin itself, fasted insulin. If you're fasting insulin levels are elevated, that that's concerning. I've had many conversations with family members about that. Again, fasted. For those folks who say, hey, you don't have to be on a ketogenic diet, but sure, your insulin might go up and having carbohydrates if you're on a carbcentric diet. I know plenty of people who are on a carbcentric diet.

they're doing fine, they're metabolically healthy, but they, like my low carb friends, would have a low fasted insulin level. So maybe the insulin under the curve might even be a bit higher, but in the morning, their insulin levels are low. You want your insulin levels low. Let me put it a different way. There's no good reason for your one major anabolic hormone insulin to be elevated after 12 hours of doing nothing.

If you've slept overnight, you've not worked out, you've not eaten, there's no reason why that hormone should be high. So I call that the big three in that if I were to get three tests, I'd get a lipid panel, I'd get C-reactive protein, I'd get fasting insulin. Vitamin D, I'm kind of glad you brought that up. Vitamin D is a pretty serious issue. And we all know why. We all know.

It's because we're spending way too much time indoors. Of course, it's better if people can just intentionally take more time to get outdoors. Yes, you can dose up to some degree. One of the interesting things about learning about lipid delivery, particularly in things like supplements, is that it can be a challenge for things like megadoses to some degree. There's throughout our, throughout our intestines, our interocytes. Those are the cells that line. They're kind of like the, you know, the fingers, if you will, that line, the intestinal track. And you may already know this.

supplements kind of are a little hit or miss on the degree with which they can absorb, especially if they're in a high concentration. So the one thing I would advise for people who are doing that is just try to always eat it with food, especially if it's a fat soluble vitamin. Vitamin D is fat soluble. So ideally you have it with food so that your stomach acids can get moving and so forth. But I myself, living in Las Vegas, I do like intentionally try to take you know, 45 minutes to an hour of walking or just trying to even be outside or even just working outside in the backyard. Vitamin D is very, very vital.

It's extremely vital to your, to the nuclei of your cells just to, you know, do their general transcription work. But it is true. We just, we do not get as much outside time as a, as a species anymore. One of the cardiologists that I work with, who we've had here on the podcast, represents, his name is Dr. Michael Twyman, a really nice sweet guy, does the personalized approach to cardiology and looks at all aspects of things. One of the theories that he puts forward and presented to our audience is that, you know, these, we talk a lot about diet, we talk about

LDL, we talk about APOB. Of course, there's good reasons. And we We've highlighted a lot of those good reasons. An area that we don't talk about as much that he believes is an important part of cardiovascular disease is the health of our endothelial lining. And the theory that he put out there is that there are some major sort of lifestyle behaviors that we have in our modern world where our endothelial health, the single cell lining that lines our arteries. and when that lining is disrupted by inflammation, it creates almost a sort of pothole in the street that things can get caught in. And when we think about our lipids, our lipids are floating around and they're neither good nor bad, so to speak.

We might think of them as being elevated, but they're neither good nor bad, but that these lipid particles could get caught in these potholes and these divvits. And when we asked them, what are some of the top things that you believe are damaging the endothelial lining and the endothelial, I always mispronounce it, but glycolyx, glycoelics. Glycogelics. What is damaging that? The list of a few things that he mentioned is, of course, chronic inflammation when you're, you know, these markers are, you know, lifted. And there's a lot of debates about, you know, different things that are driving chronic inflammation. But of course, definitely ultra-processed foods are a big part of that, a diet that is, you know, very high pharmaceutical levels of sugar, which unfortunately is a lot of people's diet in America with over 65 to 68 percent of Americans, you know, getting a huge amount of sugar in their diet.

But he also added in a few other things, you know, excessive drinking, and there might be certain populations that don't do as well with alcohol, not getting photobiomodulation, which is basically not having exposure to healthy sunlight, not getting your morning sunlight in the morning, which is helpful for your mitochondria, not getting your evening sunlight, and then maybe a handful of other things, like not having healthy levels of nitric oxide inside of the body, largely because of a sedentary lifestyle as well as having ultra-processed foods. What have you come across as, you know, truly, I mean this in the highest compliment. As an amateur professional, you have to put those two things together. You're an amateur professional citizen researcher

who's in this field. What have you found out or thought of? And do you think that there's any true to that when it comes to the endothelial lining and its role in cardiovascular disease. Yeah, so this is actually an area that I'm quite obsessed with. I did a lecture recently on a process called transytosis, which we'll get into in a second. But I need a little bit of license because I am going to have to kind of get in the weeds because this is an area that I really, I'm genuinely excited about. First of all, odds are everybody who's thinking of endothelial layer, which is the layer of cells that line our vessel walls,

particularly around the arteries. Odds are, whatever your construct is, it's off. Let me try to reconstruct it for you. So, yes, you have, you start out with a one-cell layer set of endothelial cells, typically called the endothelium. And that over time will actually increase in something called DIT or diffuse intimal thickening. So you actually end up with more cells on top. And there's some debate as to why that happens.

But there's something else that's happening all the time with everybody constantly. And it's that they're getting injured and they constantly need repair. That's just happening all the time. If you're born with a disease that results in you producing less anti-influenced, inflammatory factors towards clotting. You'll end up with millions of clots like right away. And a lot of those people never make it to birth because there's just they can't, they can't have the antagonistic opposing anti-inflammatory part of the existing clotting

cascade. So think of it a bit like shingles on a roof. You know, the shingles just constantly need some re-roofing. And that's fine. This gets us back to the immune response. You have immune cells. Almost half of your blood are cells devoted to the immune response. Platelets, neutrophils, but the one that we're going to be really interested is something called monocytes. And the reason why is because when there's damage that is done to endothelial cells, there are levels of complexity. And the easiest level is something called. first primary hemostasis. Hemosis, blood, stasis is control, right? Hemosstasis. And that just needs one platelet or a few platelets for what's known as a platelet plug.

They just, they're coming by, they adhere. And it's kind of like, no problem. We got a Band-Aid on it. That's all we needed. Past that is something called secondary hemostasis, and already it's much more complex. Now you actually need to get red blood cells involved, and you need to build a clot to close that breach, right? But here's something that's important to bear in mind.

The injury, the injury, or a cell, an endothelial cell getting in trouble on its own in some fashion, they release the inflammazons. They release the chemicals that call inflammation toward them. They're a site of inflammation. So now immune cells are attracted by design. They're attracted to that site of inflammation. And they have to first make sure there's no hemorrhaging through that breach. They have to cover it.

That's the first important part. But then there's the second important part that brings us back around to this process of plaque development. And that's what's happening underneath. So underneath, if you've got a site of inflammation, it's pretty serious. then part of the, there's a bunch of things, a lot of things I'm not going to cover. There's one thing we're very interested in, which is those monocytes. Those are cells that actually get stopped. There's a process called VCAM.

You don't need to remember that, but they're slowed down, like a bunch of speed bumps. And they're brought in between these junction gaps between endothelial cells so that they can differentiate into macro phages. Macro is big, phages eat. And they're like giant amoebas that work for us. us. They get into that space underneath the endothelial cells, that subintimal space. And guess what? They are a big component of the plaques that we find, right? And so what the current present hypothesis is, is that LDL particles get somehow into that space, macrophages

come and they consume it. And then they kind of can't help themselves. They just stay there. They never go anywhere. But one of the first questions I asked when I was learning about all this is why? Macrophages are actually very mobile. Like I said, they're like amoebas. They're quickly grabbing all of the bad stuff that's there and they clear it out. And they're good at it. They're very good at clearing it out. But if you go into a plaque, it's necrotic. Necotic means that there's dead macrophages, dead macrophages that do have cholesterol inside them. But why? Why did they die. And I'm like a detective going, come on, guys, these machines, they, they run great under normal circumstances. Why aren't they going anywhere? And that's why I had to understand more of the

physiology of that space, that area. So the way that you described it back to me, I would already have a bunch of complaints. Here's why. That glycochalics, those are like long stalks and they're like fur. They're like fur that are on top of that, that bilayer that is the endothelial cell, right? So, LDO particles are 22.5 nanometers in size. They're not busting right through that fur. But even if they could, underneath that fur is the bilayer. That's 5 to 10 nanometers in width. underneath that is the cell itself with a cytoskeleton and organelles and all of that.

So you'd have to believe that they bust through the fur, through the bilayer, in and around all of those organelles without turning them to Swiss cheese, and then still have enough force to bust through the other side of the other bi layer and into the subintable space. So already just learning that basic amount of physiology, I was like, this doesn't actually make a lot of sense to me. Now, the junction gaps opening up at a site of inflammation. Again, the first thing is the inflammation. The second thing is the response, which includes endothelial cells intentionally separating out so that the monocyte could differentiate in and become a macrophage. That makes sense. Now, those junction gaps are larger.

They're originally 5 to 10 nanometers with proteins going in between them like a zipper. There's no way that that was going to just squeeze through. Now, that's one way LDL particles can come through. But guess what? There's another one. It's very important. Cells, endothelial cells undergoing inflammation. It's now recognized that they have a higher amount of transcytosis, trans being transport,

cytosis being a process of the cell. So in a controlled fashion, endothelial cells, hear me when I say this, endothelial cells are binding to non-modified LDLDLB. particles at a higher rate and pulling them through endothelial cells to the subintimal space down below. I think that's no accident. I think LDL particles are participants in the innate immune response. I know that's controversial to say that. But I've said a lot of things that are controversial that would have been my hypotheses up until this point, and I'm getting less and less afraid to just put those hypotheses out there.

I'll emphasize that, right? But this brings me back to the question of whether inflammation is causing LDO particles to go into the subintimal space. Technically, yes. But what's causing the inflammation? In particular, what's causing it at that threshold, at such a threshold that it never regains control. And so if you've got things like, say, high blood pressure, well, that's a lot easier to answer because now it's mechanical.

If you've got a site of inflammation and you never and you actually are environmentally preventing, you're preventing those immune cells from ever getting a good level of control over that environment in the sub-intimal space, then it makes sense to me that the plaque is going to continue to grow. Right, because the more complex the injury, the more difficult it is for them to get to a degree of stabilization. Getting back to the rougher analogy, right? I'm in Las Vegas. It'd be pretty easy for me to fix my roof right now. But imagine if there was like a category four storm that was just going around the clock. Well, I would start trying to get out the duct tape and the plastic and try to just, you know, that to me is what calcification is. That's why you find plaques at areas for which there's greater sheer stress is it's more difficult for things like macrophages to have the same level of control in places like that for mechanical stress reasons. It makes total sense. It's why, by the way, I think you find people like runners who will have, like, say, an occlusion in just the LAD, right?

Just the weddome maker. But they won't have it throughout the rest of the vascular system. but then you get somebody who has who was born with a genetic disease of dysfunction and lipid metabolism such that their own immune cells, their own macrophages, can't metabolize lipids or lipoproteins very well, and they have it all over the place. The clues are right there, in my opinion. Sorry, I think I really went on a bit of a monologue there, but this is, the engineer in me loves this part of it because that's much easier to kind of understand and work with.

And yet that's the more controversial area because of how certain everybody in lipidology feels that LDL is the true root cause. Well, we've had a lot of certainty throughout the history of medicine and society. And ideas have upended and they've always started off with a group of individuals who are willing to question things and say that, hey, we may not have the whole story, but there's something here worth pulling on. And that's what you, Nick, and the rest of the. individuals that you're working with and the community that you've helped put together are all getting a chance to do. Just one thing that you said that I'm just trying to make sure I connected the dots, right? Because, you know, I haven't spent nearly as much time in this area as you have. Part of what I heard you say that I'm that I'm extracting out is that you believe that LDL,

or do you believe, rather, that LDL and these lipids are actually an important part of the sort of, you know, plaster fixing process, right? They're an important part of like kind of the healing process. Is that kind of what I gathered from one section that you were sharing? Or did I completely mess that up? Yes. Let me let me just say a qualified yes. It's a bit more, you know, I mentioned earlier the car tires and the car accidents.

If you take steps to remove LDL particles from the equation, then I believe you'll end up with less relative. incidence of cardiovascular disease or at least less development of plaque on a net if you get to large scale numbers, right? Because you're kind of removing that part of the cascade. But to be fair, I think the same thing about macrophages themselves. I think there are other components of the immune response that you could inhibit. And you'll end up with less potential of plaque formation. The reason I want to bring that to the front, though, is obviously I think highly of the natural body's immune response. It's a lot of the process of atherosclerosis itself.

So I don't feel it's as certain as to what the tradeoff is for folks who are metabolically healthy. It may well be that metabolically healthy folks who really lower their LDL and do nothing else but lower their LDL, have a reduction in cardiovascular events without a tradeoff of some other kind, without there, for example, being other things that are associated with a robust immune response that might or might not get affected. I don't want to put a hypothesis out there for that, other than I'm interested. I'm interested in us studying it because it's possible that there is. It's possible that there's a tradeoff. I'm not asserting it, but it would explain why it is that folks who have very low levels of LDL, associationally tend to have lower lifespans.

It's associational data as all understandably qualify. But if LDL were only pathogenic, if it only caused cardiovascular disease and that there was no tradeoff in its lack of presence, then you would expect it'd be like smoking, right? That people who were lucky enough to be born smoking no cigarettes a day, where the rest of us were born smoking in pack a day. they would live longer than the rest of us. And I haven't actually seen any data that shows that. Even people born with PCSK-9 loss of function, that's a genetic disease, that's the opposite

of ph, you're born with very low levels. I mean, we're talking like 30 milligrams per deciliter your entire life. They don't live longer than the average of their population. But you would think that they would, right, if there was no trade-off at all. because, again, cardiovascular disease is the number one killer. And that's not what we see. Again, all the same caveats. It's observational data.

Observational data is not great at proving causation. But it is good at knocking down claims of causation because the data should align with something that's being claimed as a cause. That makes sense. Super clear. while I have you here, just a few areas that I want to get your sort of thoughts on as we sort of extrapolate out the potential sort of implications of this and how the average person who's listening here and is trying to make sense of how they eat, what they eat, how they approach things, the lifestyle they live. So would love for you to get a chance to comment on because something else just as your Oreos experiment, Nick's Oreos experiment, has made a lot of headlines and garnered a lot of attention. in a really great way to help ask a lot of questions about LDL. There's been other things that have also been in the news on this topic of LDL,

and one of them is the Vegan Twins Study and the Associated Netflix documentary whose title I'm blanking on right now. But that's been in the news a bunch. For those that are not following, I'm sure you've seen people talk about it, but if you haven't, there was some Stanford. researchers that basically took twins and one of one group of them was put on an omnivore, you know, diet. They could eat vegetables, but they could eat, you know, meat as well.

And then the other group was basically put on a vegan diet and it ate only a plant-based diet. And I believe it was eight weeks, somewhere around there, six to eight weeks that they were on these respective protocols. And the reason that the study was getting a lot of attention, is because there was a significant drop in LDL in the individuals who are following the plant-based approach. So the headlines and the documentary, you know, we're really touting that this is why a plant-based diet makes sense for a lot of people, because we want LDL. And of course,

you already talked about the big observational data that's out there, which is large in volume with LDL and cardiovascular disease. But what is your take on? the vegan twin study. I don't know if you watched a documentary or not. Just because even though we've talked about themes that are going to be part of your answer, it's nice for the audience to sort of hear your perception of that study and what it means and what it doesn't mean. Well, in full disclosure, I hadn't actually watched. I've watched a few videos, including Nick.

He has a great summarizing video. Shout out to Nick on his. It was actually pretty viral, too, because I think he hit a lot of great touch points. A lot of times somebody does such a good summary video and you weren't specifically attracted to watching something that you're like, oh, I think that's probably pretty good. And I won't judge it too harshly unless I actually do watch it all. But I will say that this is a commonality. It's common that if somebody goes from a low carb ketogenic diet over to a more plant-based vegan diet, there are a couple things that my expectation is would result in lower LDL cholesterol. Per lipid-erangee model, again, probably higher relative carbohydrate intake.

And if that's the case, if you're powered more by carbs, if you're powered less by fat, probably you're going to see a change in your LDL cholesterol. Again, kind of depends on how lean and metabolically healthy you are. The other component is fiber. It is true that generally speaking, the more you're consuming fiber, especially for things like gastricemiting, you know, the use of bile acid, it creates more demand on the liver to take up more LDL particles. What did kind of fascinating me is, and correct me if I'm wrong, I think the drop was just like

16 milligrams per deciliter. It was like just barely over statistical significance if my memory serves. And that I, that I was kind of, you know, it impresses me that that ends up becoming the big headline because that's the thing I keep coming around to is when I started on this, I didn't actually realize how many things are really built. on the lipid hypothesis that are built on LDL, and for that matter, how much people see it as basically the disease itself, that if you have higher LDL, it's as good as if you already have heart disease. It's often referred to as cardiovascular health, just your LDL level,

is your cardiovascular health, as though they're congruent, that they're the same thing. And that's kind of important because, for example, with the study that we're doing out of lunkist. They don't just have high LDL. They have high LDL because many of them are carnivore. Some of them are, you know, extremely high fat, for example. So you have folks who are typically on diets very high in saturated fat, very high in red meat, very high in animal protein. All of these things are getting vilified a lot. And for that matter, typically are low in fiber. And will we see that corresponding expectation met of rapid onset of cardiovascular disease? We're about to find out.

So in a roundabout way, our study is kind of, it's kind of hitting lots of notes at the same time. Obviously, there's not just the high LDL. It's that they're on a diet that's checking all the boxes for what not to do. Yeah, I'm pulling it up over here. I believe if this article is accurate from CBS News, which covered the study, It was 22 vegans in total. The LDL cholesterol drop was 14 milligrams per deciliter. Oh, 14.

Which was more than a 10% drop. But if we go back to the Oreo experiment, you know, how much of a drop came from Nick's own experience just with being on Oreos, right? What was the number again, if you don't mind mention? It was, if I'm not mistaken, it's 384 down to 111. but the total percent of the drop was 71 percent through almost three-fourths of his LDL wiped out in 16 days so I don't know oh sorry go ahead no I was just going to say so yeah it's both Nick and I if we were taking our lipids if I was doing what I was describing earlier let's say I was using my cardio check and I was just checking my lipids throughout the day it absolutely

exceeds 14 milligrams per deciliter just in the course of the day going up and down But then again, I wouldn't be surprised if that's going to be the case for many of us who are fat adapted. So theoretically speaking, if Nick's experiment was extrapolated out and you could find, you know, a group of twins that were fit this model of lean mass hyper responders, you could actually make an entire documentary and study of giving them Oreos. and you'd expect that one group, which was the control, which was eating a traditional ketogenic or low-carb diet, and the other group, which was same diet, but was given a sleeve or two sleeves of Oreo a day, you'd expect the headlines to go gangbusters because you'd see probably on average a 50%, 60%, 70% drop in LDL that would be there. If we would extrapolate it out, we would see something like that.

That's the hypothesis, and that's why you guys were doing the experiment, which, number one, is that accurate? Not, is that accurate? We don't know until that was done, but that's at least the theory that would be there. And number two, it sort of puts into question, the idea that a 10% drop in LDL just in itself, without necessarily looking at the actual level of hard plaque and soft plaque in the body means much of anything. It could mean, and I think this is why I really appreciate your work, because part of what

you're saying is that if you're not healthy as an individual and you look more like metabolically unhealthy American and you're eating kind of like a standard American diet, then an increase in LDL probably is and most likely is going to be problematic. for you just based on the amount of observational data. We don't know maybe fully. That's not the part that you guys are looking into, but that's kind of a little bit of what I'm hearing you say. But if you are a healthy individual,

then maybe that drop in LDL doesn't mean anything. And in fact, we can actually get it to drop a lot higher if we just fed you a shit ton of Oreos. I think what I would say is I don't know on that last part. I genuinely don't know. Here's the challenge. The challenge is for me the way that I would want studies to be conducted overall is I'm a big fan of transparency.

All of the papers that we've done, we've released the code and the data as we published it. I would love if more studies were done in the same fashion. Unfortunately, a lot of pharmaceutical studies, the data is proprietary and there's not quite as much access. There's not quite as much ability to do. analyses, but I'd love to do subgroup analyses at least to help build on hypotheses like that. You know, what populations have the most benefit from various interventions, whatever they are?

And that gets to the larger arc of your question is if there's some degree of LDL levels that are truly physiological, they are just, they are part of a process of either being fat adapted or being carb adapted and that that won't translate to cardiovascular disease risk. Let's find out because there are a lot of folks who are on a ketogenic diet, not for ethical reasons, but for medical ones like Nick. Nick has, Nick has been using the geogenic diet to work with his ulcerative colitis and it's just been a godsend. And I know so many people who have his story across multiple various ailments, such as having epileptic, such as type 1 diabetics and so forth, they have everything going for them except this one thing.

And that's why we need to know, right? So once we have that, once we have that data in hand, at least to be able to say it for those folks who are metabolically healthy, that would be the first step to us getting a better sense of this more complex version at a minimum of what we think we understand today. That's the one other thing I'll just mention. I think I always also underestimated how much we, I think, as a species, we really like a simple problem that turns out to have a simple solution. And so in a way that's, if you look back, that's how medicine has been. It's, for a long time, we were pretty attached to the body makes too much blood. And that's why therapeutic bloodletting is so great for all these various ways of curing

diseases and it took us a long time to get over the possibility that no actually maybe the body is pretty good about its production of blood and maintaining blood pressure and so forth. What do you do? Sometimes it just takes a while. So we'd love to get your perspective, right? You're not a medical doctor. I'm not asking for medical advice, but, you know, just as I'm navigating my own relationship with these areas and I'm just.

as confused as anybody else trying to talk to experts like yourself and other people who are looking at this, getting all the different angles and markers to be a little bit more educated, you know, in terms of how I approach things. So I did my, you know, clearly scan. I saw that there was basically non-existent, soft plaque and hard plaque that was there. It looked extremely clean, at least from the individuals that, you know, had interpreted for me. And my brother-in-law also took a look. He's a cardiologist who's in this field as well. Shout out to Dr. Neil Patel. And I'm sort of looking at things and I'm taking everybody's information.

And I'm hearing people, experts that are out there, they're saying, look, even if you feel healthy and everything else is, you know, good, we just don't know the answer to a lot of these things. We may not know the answer. So with an APOB that is elevated, I believe that, you know, three. four years ago when I was doing a little bit more of, it wasn't a true ketogenic diet, but it was a much higher fat diet than I was used to eating. I think my APOB was like somewhere in the high, almost like right under like 200, somewhere around there, like 180, something like that.

Then I got a little bit spooked and I started sort of cutting out some added saturated fat in my diet, moving towards more leaner, you know, cuts of meat. And naturally, it sort of kind of came down, but still not being fat, you know, not being fearful of fat, you know, having plenty of fat that was out there, but definitely watching how much saturated fat was coming into the body. And then it came down to about 124, went back up to 144, And all along the time, my LDL was around like 250 to 18 at its lowest. It came down to 167. And I was chatting with the cardiologist plural that I was working with. And I have a few genetic. I had some advanced genetic testing done. And I saw that I had a few of the genetic, I don't know exactly how to say them, snips, markers, I don't know, genes.

that are associated with and connected to, you know, familial hyper cholesterolemia. I'm a hyper reabsorber is what I was told. I don't know if I got that right, but that's some of what I was told. It's not that I'm a hyper producer, but I'm a hyper reabsorber. So one of the recommendations that was given to me personally, again, this is my interaction with my medical team was, look, you're doing a lot of things that are right. You're getting your morning sunlight. You're doing high intensity interval training, which has, you know, not every single day,

but you're including, you know, one or two of those workouts. You're getting strength training in. You know, you might be taking some supplements that could be beneficial, like aged garlic extract. You know, there's some studies that are there. And you got the clearly scan done and you don't have any, you know, soft plaque or little to no soft plaque that's there. But if we want to ensure if you are thinking about rolling the dice with your own health, you might want to think about having something like a Zetamide. For those that are not familiar, pharmaceutical intervention, which, as I understand, is related to the reabsorption of cholesterol and lipids inside of the body and has shown an impact on reducing your LDL. So I started that.

You know, I took a Zetamide and I asked around and generally I saw that, you know, there's always potential side effects that were there, but that it was comparatively to some of the concerns that people have about statins and other. the things, it seemed to be pretty mild to, you know, not really anything strong that I was personally worrying about. And my LDL did come down. It dropped from in a matter of a few months of me just being on Zetamide. I think it came from like 200 down to like 102. And my APOB went from like 144 down to like 86. And I'm due for a test actually next week. So I'll get my latest numbers. now be about four or five months that I've been on that. I am just, you know, trying to make the decision for myself, you know, and I guess, you know, if you have any comments on that, right, I'm not generally worried about, you know, the more that I learn, and especially me fitting into

this, you know, phenotype of a lean mass hyper responder, the more that I learn. And because I got my clearly scanned done and I don't see hard plaque and I don't see soft plaque that's there. And because I'm interested in longevity, I just turned 41 last year. I sort of like, okay, cool. Like, I guess I'll be on this. But is there? But then I'm also worried about like dropping my LDL too low that's there, right? Because that's something that you mentioned. So that's what I'm navigating. Do you have any commentary on what I'm navigating as an individual? Again, not medical advice, not anything. You know, do you have any commentary on what I'm navigating? So I'm probably going to give you a pretty unsatisfying answer. That's okay. I'm all good with the unsatisfactory answer. I want the truth, right? I want

the truthful answer that's there of how you feel about things. Well, it's a little, it's a little more than that. So when I was first entering the space, I thought it would be like the culture I come from with engineering, which is that we are firing off hypotheses everywhere. We're just, we're excited to chat about the thing that we're into. And while my profile, my social media profile was relatively low, that was fine. As my social media profile has increased, in particular as I've taken on more research partners who themselves are cardiologists, who are lipidologists, and so forth, I have to be more mindful of things, anything that I could say that could be taken as individual medical advice.

You'd think that I could just say, listen, don't take anything I say as medical advice. I'm not a medical professional, et cetera, blah, blah, blah. But I do find that even in spite of that, there is that potential risk. So I'm going to kind of make you. You don't want to take your research, right? That's right. Right. But at the same time, I do want to draw attention to that being kind of a problem because

science is very much about building hypotheses, discussing them openly, you know, working through what you think is going on. the day and age of information and this technology sharing and social media, what we're doing right now, there shouldn't be that level of reluctance, or at least there should be that expectation the caveat is baked in. So with all that said, here's what I can tell you is going on with our existing lean mass hypersponder Facebook groups, which you mentioned, you're like a member. It seems as though that is the most popular intervention for those folks who are seeking

to lower their LDL, they seem to, seem to, it's anecdotal, respond the best to having anzademite, that the reduction in absorption as a means by which to get to lower levels appears to be tolerated well compared to others. And if you were to probably take a poll, that's my guess, is insetamide in particular is probably one of the most used. I myself, again, I've got a kind of caveat, I don't know. I will add one more thing, though, on the concern for being too low from having crunched those data myself with R and so forth, I'm usually referring to, at least of my own crunch data, it's usually something in the lowest quartile or quintile.

And again, it's observational. If a lipidologist were in the room, who's very pro-LDO lowering, they would rightly point out, hey, some amount of that, you know, could be reverse causation, which is a fair point, except that it seems to go across all time scales. So there's not a time scale. Even if you censor out the first like three, even five years, you still have people who, if they're at the lowest level, 20 years earlier, they're still going to be more likely to die.

But those are usually at very low levels. There's usually at levels like, say, you know, less than 70, less than 60, something like that. And again, it's observational. I think if you were to stratify by metabolic health, there would be a lot of equalization across the board. This is why, like, we want to always think, or at least I would say, I always want to think in terms of these lipid profiles as resulting from something more than they are driving something. That's so far still my hypothesis. No, that's super helpful. And I appreciate we need you to be cautious in your languaging because you are moving forward important.

research and one way or another, we're going to continue to, you and your group are going to continue to pull on this thread. And that's just going to be interesting. And it's going to bring up great questions. Probably a lot of questions in the beginning, more so than immediate answers, but those questions are an important part of scientific discovery. And I want to thank you and your team for being a part of that and all the incredible people that you work with. And Nick, who we mentioned, we're going to link to all those individuals below. Dave, as we wind down over here. Any final thoughts that you want to leave our audience with and how they can participate? If they're curious about this and they want to be a part of the movement, you know, you mentioned

you crowd fund a lot of these studies that you've been now getting a chance to get into, where do you want to send our audience to? So final thoughts and then where people can follow you. Sure. And thanks for the opportunity on doing the plug. We have the Citizen Science Foundation. That's the 501C3 bona fide public charity that I founded. We have a legitimate 0% admin overhead. Literally none of us take any money, save some amount that goes towards like, say, credit card processing or other third-party transaction fees. If people want to donate, they can go to citizen sciencefoundation.org to donate directly

or even better, come join us in Las Vegas. Maybe you'll get a chance to come on over. In March 15th and 16th, we have a fundraiser that's basically a conference. We have a lot of big names coming like Dom Di Agostino, Nick Norwitz himself will come. We have Dr. Budoff, her principal investigator. He's going to be giving the keynote. And it's going to be a great time. It'll be a lot of fun.

And it's for a good cause. Your donation is your ticket in. As far as on social media, you can find me under real Dave Feldman. X.com slash Twitter slash Real Dave Feldman. Same thing for my YouTube channel. Same thing for Instagram. But I'm more active on Twitter in particular myself. And I hope everyone continues to stay curious.

You know, if there's anything that I'm proud of beyond the research that we're doing ourselves, I love whenever I find that people are bringing their unique insights from coming outside of formal research that actually helps out research because I myself have gotten and a lot of the ideas that have helped to build the lip energy model for me from other folks who themselves aren't lipidologists. So don't underestimate your ability to work out new things that we all need to know. Well, Dave, thank you so much for having the courage to put yourself out there, even though we have so much history in medical history and other fields too.

but importantly in medicine that the outsider's idea that was at least willing to question the status quo, if not directly, indirectly often led to the contribution of important work that changed our ideas about foundational things that we thought were true. And I know you got a lot of pushback. In fact, you know, I won't name the guest by name, but I brought your name up and the lean mass hyper responder to an individual who was on the podcast in the early days. And, uh, they kind of just laugh me off, the fact that I even would acknowledge it as if it was a thing worth addressing. And this individual who was well-intentioned and, you know, kind of came from the world of plant-based eating, you know, they even intentionally went out of their way to kind

of share a clip out there on social media of just showcasing how much they knew about something and how it was done in a tasteful way, but it really was to highlight just how mis-examination. informed and kind of when they started realize the interview was going off track when I started bringing up these questions about their thoughts, which I thought were genuine questions. And I still think are. And nonetheless, I'm sure you've gotten a lot of pushback over the years and people even just saying, who do you think you are? Well, I'm thankful that you didn't let that stop you or anybody else that you get a chance

to work with because this is an important topic. And we need to keep on digging to get to the truth of the matter. So thank you for your work in that space. Yeah, and thank you so much for having me on, Drew. Hi, everyone, Drew here. Two quick things. Number one, thank you so much for listening to this podcast. If you haven't already, subscribe, just hit the subscribe button on your favorite podcast app.

And by the way, if you love this episode, it would mean the world to me. And it's the number one thing that you can do to support this podcast is share it with a friend. Share with a friend who would benefit from listening. Number two, before I go, I just had to tell you about something that I've been working on, I'm super excited about. It's my weekly newsletter and it's called Try This. Every Friday, yes, every Friday, 52 weeks a year, I send out an easy to digest protocol of simple steps that you or anyone you love can follow to optimize your own health. We cover everything from nutrition to mindset to metabolic health, sleep, community, longevity, and so much more.

If you want to get on this email list, which is, by the way, free and get my weekly step-by-step protocols for whole body health and optimization, click the link in the show notes that's called Try This or just go to Drew Perot.com. That's D-H-R-U-P-U-R-O-H-I-T dot com and click on the tab that says try this.