Transcription
Is having high LDL cholesterol going to cause you to develop plaque in your coronary arteries faster? Is having a high APOB going to cause you to have a heart attack sooner? I have a special guest today that I think uh is going to help clear up these uh seemingly eternal questions. At least for the last few decades, those have been the questions. Today I have the honor and pleasure of once again having the esteemed Dave Felman. Hello Dave. Welcome back.
>> Hey Ken, how are you doing >> son? I'm great. It's a pleasure to chat with you again. I know you've got some new information to unpack for everyone. Uh I was just thinking how many years has it been since you and I first met on the first low carb cruise that I ever went on. when you were talking about uh the LDL particle being like a little UPS truck that picked stuff up and dropped stuff off >> and and drove around and and did lots of lots of things. One of which was carried cholesterol and I remember thinking this this seems really important. And I I feel like this is going to lead us somewhere in the future that's an actually that's going to be very useful for people in in order for them to understand their overall risk of having a heart attack, stroke, and other morbidities. Um just give us a super quick introduction because I think most people know who you are now and and what you've been up to lately.
>> Yeah, so I'm going to speedrun this part. Obviously, I'm a an engineer who went on a ketogenic diet like so many that are probably watching this right now. I saw my cholesterol go up and also like so many you're watching this right now, I had a bunch of friends and family that did not see their cholesterol go up. And so, I became obsessed and started developing what is now termed the lipid energy model. Uh you can check our published papers on that at cholesterolcode.compapers. And that is the mechanistic reason that I believe our cholesterol goes up. But that's not the main reason I'm here today. The other main thing that I think is more pressing for all of us is the same thing that got me obsessed, which is is it harmful? Is it going to turn out to be the case that if you go on a ketogenic diet and your cholesterol increases, even if it might be for what we think is a greater trafficking of fat and those people are leaner and more metabolically healthy, does that mean that there's a higher risk? And so the lately is really hard to say lately because it's been what it's been since 2019. I got on a Houston stage and said to the world, "Hey, I'm uh founding this um this public charity to help raise money to help us study this. Let's recruit a bunch of people like me and like so many people you know, Ken, who have seen this cholesterol increase and then actually scan their hearts. Scan their coronary arteries that surround the hearts with some high resolution scans called CT angiograms. Do it at the beginning and then do it again a year later and look to see how much the plaque has changed in this population. And uh that's where we're at now. took a long time, but we're finally at a point where we have all four analyses in for these scans that have been completed. Really completed about a year and a half ago.
I love it. I love it. I can't wait to unpack that. But first, I want to I want to relay two facts for anybody who might be new to the keto carnivore LDL apo heart attack risk lipid heart hypothesis issue. So first of all uh let's talk about LDLC and its function. So a lot of people think that LDLC LDL cholesterol is only in the human blood just to give us heart attacks and strokes and that you want that to be as low as humanly possible pharmaceutically possible. And so first I want to just remind everybody or teach you depending on where you're at on the learning curve that LDL cholesterol is a normal particle to have in your blood supply. It is a natural evolutionarily appropriate. We have tr billions to trillions in any given second. And the LDL cholesterol molecule does hundreds and hundreds of things, beneficial things, good things in the human body, many of which I opine that we haven't even discovered yet. Give me a quick blur. Do you do you agree with that? Do you think there are things that LDL traffics and does that we don't we don't even know about because we we stopped studying it? We villainized it and then we started prescribing medicines to get it as low as possible. Do you think that's possible or or likely true?
>> I can definitely help you out in that the first thing to learn about LDL is that it typically doesn't start as LDL. It starts as VLDLDL. So for lay people out there, it starts filled up with cargo. So getting back, right? It's and it's not just got cholesterol in it. It's got triglycerides. You usually hear triglycerides in a bad way, but if you're powered by fat, that's a that's a fuel. That's a fuel source, but it also has fat soluble vitamins A, D, E, and K. All of that is packaged into these VLDLDLs that your body ships around. And what you could say is that the job of this big, you know, container is to start big and get small. It's supposed to drop that cargo off around throughout the body. So yeah, I realize that there may be some debate and some controversy with regard to its final form as an LDL, but when it starts out as a VLDLDL, there's just no question that it's its cargo being delivered successfully is a big part of the story. And what you tend to find is in people who have problems, that's why the triglyceride level becomes so associated with bad things is if there's a problem in delivering those important lipids that we need throughout the body, that's the sign. And uh I I by the way I I got your your most recent edition on the book with um blood work. So I'm excited to labs. Yes.
>> Read it. I don't know if you knew this but uh we we happen to to both be interested in blood work.
>> Absolutely. Absolutely. And now and then the second part that I want everybody to know is my personal experience my my view of the anecdotal evidence when somebody adopts a high a high highfat low carb either keto keto or carnivore about onethird of the people who adopt that diet and stick to it their cholesterol their LDL in total actually go down about onethird of people their LDL cholesterol and their total cholesterol stay about the same and then about onethird of people's LDL cholesterol and total cholesterol go up and then about 1 to 5% of people I'm I'm it's still I can't it's it's a little cloudy 1 to 5% of people they have a marked elevation in total cholesterol and LDL cholesterol and that's one of the the diagnostic criteria that you might be a lean mass hyperresponder and there are other uh diagnostic criteria for that which is not not officially recognized by the American Heart Association yet or any other regulatory body. That's been my just over, you know, what 15 years now of recommending ketogenic diets. Is that what the research seems to be bearing out as far as the 1/3 and then 1 to 5%. Is that what you guys see as well?
>> Well, we're actually published on this and this brings us back. Listen, here's the good news. Here's the good news for anybody who's watching right now. If you're taking on keto because you're overweight, we h we've published for a meta analysis on 41 randomized control trials that have at least one or more arms for the ketogenic diet. And for people who have a BMI of above 25, if it's say 35 and above, your LDL cholesterol typically goes down as you're on your way to greater metabolic health. If you're a BMI of 25 to 35, it typically hardly changes. It's mostly for those people who are 25 and below, especially leaner, that are going to see the marked increase in cholesterol. And dude, the one to 5% you're talking about, that's like our good friend Nick Norwoods. He's very lean, very active. That's the prototypical lean mass hypersponder. So to really emphasize the reason why it's a more recent phenomenon and why we didn't see it as often in like the age of Atkins is because mostly those folks who were taking on a low carb diet then were were people who actually were just trying to lose weight. Only more recently do you have people like Nick who are treating his ulcerative colitis or you have more people who are treating now metabolic diseases of the mind that we're seeing more and more efficacy for. Those are the ones who tend to see this. So to be fair, if you're concerned that your cholesterol might increase but you're looking to lose weight, it's probably more likely than not that your cholesterol will not increase substantially. Again, we're just playing the odds here. Yep. And the the epidemiological research is is very clear that having type 2 diabetes, having metabolic syndrome, being severely obese, having very high blood pressure, those are much much provably bigger and more dangerous risk factors for heart attack than having uh an elevated LDL cholesterol. And so the research is quite clear on that, especially in women, but I think that's applicable to men as well since they're the same species and contain 99.999% the same DNA. I think that probably applies to men as well. So, uh, we've got that out of the way. Now, oh, I wanted you to explain also before we dive into this. A lot of people have heard about the CAC score and they know that that's a a very quick CAT scan, very low in radiation, just takes a few minutes and that gives you a kind of a a measured calculated score of how much uh calcified plaque are in your heart arteries. And then there's the the CT angiogram or a CTA. And I know you guys I think we're recording data from both these. give break down what's the difference and then why is the CTA an even better way to look at plaque in the coronary arteries.
>> Yeah. So a CAC a coronary artery calcification scan is something where you go through through a CT scanner and it does not have any contrast die. We'll talk about in that in a moment. It's actually something for which uh it's very easy and it has a very low dose of radiation about uh one and a half times that of a mammogram. It's a very good scan. I have to tell you I've gotten more bullish the more I've seen the data. It closely correlates with the CTO, which we'll talk about in a moment. Um, the only thing that some people bring up is that it is still possible to have a low amount of calcification, which is the primary thing it's detecting, um, and yet have higher soft plaque than non-calcified plaque. That said, the odds are pretty low. Calcifi calcified plaque tends to be very correlative to soft plaque in general. It's not always the case, but in general. Okay. So, what's a CT angagram? Well, CT androgram is actually a CAC and in a second pass a much more highresolution scan that includes contrast die. So you now have two passes. You have the first pass where they get a CAC. It's almost like it's, you know, baked into the combo, right? And they need to do that so that they can find out how much calcification you already have if if you have any. If you do, it's important because they then determine how much of a dose of radiation they need to use for the next scan. And the next scan has many more rotations and and slices, if you will. And that's a higher resolution. A CT angagram is a high resolution scan. And they use something called a contrast die, which they'll they'll wire into your your hand. It injects some dye. And what's happening is that dye uh fills up your lumens or at least lights up your lumens so that they can be seen by the scanner. In the case of a CT angagram, there's a little bit more risk with the contrast die, but it's still relatively low. I want to say it's maybe one in 10,000 for possibly some kidney issues. Um but then there's a bit more radiation, but the radiation dosage has come way down in recent years. It used to be something like I want to say 20 millisevers. I've had two CT andrograms. They were two millisecevers each and huge improvement. I was actually a radiologic technologist before I went to medical school. So I'm very u familiar with the severs and the rads and the other measures of radiation. And back back in those days, a CT angog was an ungodly amount of radiation, just like a CT of the abdomen or chest because it's so dense. You had to get through that. But I know that they keep improving the image receptor part of it so that they can use yet less and less and less radiation. Um, and so that that that's really important to understand. And a CAC can only see those calcified or hard plaque that contains lots of calcium. And a CT angagram is the first pass is a CAC. Then the second pass, it can also see soft plaque. In some of the some of the machines, it can actually see signs of inflammation. Uh it can see signs of of intimal damage in the very best newest latest versions. But it it it gives you much much less radiation. And let's I want to talk about that and then uh talk about one other thing and then I'm gonna let you jump in. So a lot of people are like well I don't want all that radiation and that's absolutely valid. You should always question is the benefit of this scan is the benefits I will receive the diagnostic information. Is that going to be worth this amount of radiation? And you should always ask that question of your doctor before when the when a scan is ordered. You should always ask that question. But just rest assured that most doctors won't order a scan like this unless the diagnostic information that we're going to glean from that is worth the radiation that you're going to be subjected to. There are always risks with every single thing you do, right? But you want the benefit to outweigh the risk. And so that's the thing. Now, I want to say this, Dave, because a lot of people who are new to low carb, keto, carnivore, they're like, you know, I it's it it freaks them out, Dave. Just to be honest, it freaks them out that you and I and everybody else in this space are constantly talking about CAC scans, LDL cholesterol, APOB, uh, heart disease risk, and it because it feels like somebody just coming into this space. They've come to improve their mental health or a skin condition, gut condition, joint condition, lose weight, reverse type two diabetes, but they're like, "This must be super dangerous because all these people talk about is their heart arteries and heart attack risk and and and calcification." And I I just want people to understand, if you're new to this, there's a reason for that, okay? It's because we all are very very interested in helping you achieve your optimal health. That's our goal. We we obviously none of us want to cause you to have a heart attack. Now, in the very early days of keto, many many authoritative cardiologists and lipidologists and other people basically put out there on social media to the public that if you do keto, you're literally a ticking time bomb. You're going to have an early heart attack. You're going to die. You're going to have a stroke. Blah blah blah blah blah. And so now, first of all, they seeded the public consciousness with that belief right off the bat. That's number one. And number two, people who are not following any diet, just eating whatever, not going to the doctor, of course, they don't talk about CAC scans because they don't give a damn about their health. That's why they're just doing whatever, right? So, they've never had a CAC. They've never heard of a CAC. They don't know anything about that. And then the implication with plant-based diets or vegan diets, vegetarian diets, is that they are super super heart-healthy, right? So why would a vegan cardiologist, why would he even think about getting a CAC scan if you were vegan, vegetarian, plant-based? Well, that'd be that'd be a waste of money and you'd be getting radiation for no reason because they believe in their hearts. Not they don't know in their minds. They believe in their heart that this is the heart healthiest, safest diet you can eat. So, they just don't check these tests. They don't talk about them. They don't tell you maybe we should get a CAC because they just know you're on the right path. Even though I think they're completely wrong, upside down, and backwards. But I just wanted newcomers to understand that's why, first of all, out of an abundance of caution, Dave and I and others in this field have been saying, get your CAC check. It's not because we secretly believe keto is going to kill you. That's not it at all. I secretly think keto is going to save you and Dave is secretly trying to prove with research and data that keto is going to save you. And so that's why you you hear so much more talk about all that stuff in the keto, ketoore, carnivore community, even the low carb community than you do in the plant-based, vegan, vegetarian, Mediterranean communities because those doctors falsely in my opinion believe that the diet they're recommending is improving your heart health. And so I I eventually would like to see a head-to-head study of of 500 vegans and 500 carnivores who just started the diet. Let's follow follow those two cohorts for one year, two years, three years, and see what their CAC score does. That's just my personal when I when I hit the lottery, that's going to be the first study that I fund. Okay, Dave, now you've got some updates for us and I've babbled long enough. I'm just going to give you the floor and let let you explain to everybody what the updates are, why they should care, and then I'll jump in with questions from either our audience, which let me remind everybody, this was filmed in front of our live private community.
>> They actually have the uh they have the right and and and the obligation to ask questions from our our guests. And there, you know, we have lots of different people on this channel. And so if you'd like to be able to ask your own questions in the future, consider becoming a private uh PhD community member. Okay, Dave, the floor is yours. What's the latest?
>> Well, actually, I I did want to capitalize on that last point you were making in that I have I've never felt stronger on the value of doing imaging. So, it doesn't even matter what diet I'm on or that my family is on. If there's a concern, I mean, nothing beats the physical detection of the disease. itself. So, we're just lucky that we're in an age right now where the radiation levels are as low as it is. Just one last time, a CAC is only about a mammogram and a half of radiation. So, just for reference, keep that in mind when you're thinking about this,
>> which is a very very low amount. I think that's probably less than a a chest X-ray.
>> I think Well, no, I think a chest X-ray is less. I think it's a 0.6 millisecevers last. Just a little more than a than a standard two view chest X-ray.
>> Yeah.
>> Y
>> So, yes. Um I didn't So, I've been having a little problem getting a PowerPoint working on my computer coming up to this, but I can I can speak to the slides that are in front of me. The last time that we had done ketoCTA, it's worth emphasizing, we had two of the analyses of the four that we ultimately end up with. Now the first two was what's known as a semiquantitative and the other is a quantitative by a company called clearly. That's the April 7th paper uh from about four months ago. Now the semiquantitative is is actually when the cardiologists themselves are using software they're looking through and they're they're capturing it. And that was uh looking not only really good, but on top of that, when we were filming the documentary, that's actually what's throughout the documentary. Now, there was an additional analysis called the Clearly analysis, and that's from the company Clearly, and it agreed in the two major findings that we have in the April 7th paper. The first is that plaque predicts plaque. the likelihood that you'll have future plaque progression was associated with whether you had plaque at the baseline scan. So when participants had uh plaque in the baseline scan, it was more likely they would have more plaque progression in the future. Now again, not it's it's not a guarantee, but it's a commonality. The second was that there's actually no association between LDL or APOB and the progression of plaque. Not at all. And this included in both the semiquantitative and the clearly data sets. Now that said, I do want to emphasize that there was a difference between the two with regard to the degree of plaque progression. There was enough of a separation that we wanted to look into it a little bit closer with the company. clearly and a lot of that's actually still in negotiations which has been um something that I presented on when I was describing this data from before but I think that's an important thing to draw attention to because only now and like I want to say the last three weeks um was I able to present and because all four analyses were in heart flow is the third analysis that came in that's a quantitative data set like clearly and Q angio is in fact the pre-specified methodology of this study that took the longest because it's the most labor intensive. It took around two to three hours per scan. Dr. Budof and his team had gotten that completion. So when I say I have results, it's going to sound like I have a lot of different results, but in truth, these are all four analyses looking at the same 200 scans. That part, that part's important. Think of each of these as kind of like a different lens, right?
>> Yep. So with that said there is the there is the actual uh prespecified endpoint itself. The prespecified endpoint is for the non-calcified plaque volume percentage change percentage change and what we reported from before I believe is 80.6 six for clearly which was part of what kind of got me interested in understanding what had happened and why we wanted to do the quality control pass. Uh for heart flow it's 6.3%. Cohortwide and for Qangio it's 39.8%. Now why I want to add some additional context is obviously Ken you can tell those are very different from each other. The reason for that is the we when we were choosing the percent change of non-calified plaque volume it was in 2019 2020 and that was when a lot of longitudinal studies were using cohorts that typically were not very healthy and low in plaque. So a percent change in non-calified plaque volume was actually fairly common but it was losing ground to what now the industry is more interested in which is known as percent atheroma volume. So don't worry if these terms are getting kind of lost on you. What's more what's of greater relevance is beyond this percent change in non-calified plaque volume non-calcified plaque being the non-calcification. We go into these other metrics. But before I do, let me explain why having a low level of plaque makes it more difficult. Because the lower you go, the more you've got error rate, the more you've got machine level changes that can make things seem more more outsized when comparing one to the next. Do you have a kitchen scale at home there, Ken?
>> I have a I have a bathroom scale. We don't weigh stuff in the kitchen. We just cook it and eat it.
>> Oh, there you go. All right. So, if I grabbed, say, four uh bathroom scales from um Walmart down the road from you and you weighed yourself, you probably expect that they would agree with each other a lot. However, let's say that we do you have any animals there? Any small animals?
>> Chicken, sheep, cows, dogs, peacocks now. Yes, lots of animals.
>> Okay. Okay. So, let's say we grab a uh a chicken and then we weigh them on the the uh bathroom scale, right? Do you think that there would be a greater variability between those scales with the chicken compared to you, Ken?
>> I think that probably the heavier the thing you're weighing, you would expect to see a greater variability in the result would be my Well, actually, no. I think I'm going to reverse that. I think there'd be more variability with the chicken than with me. Yeah, I think that's true. Yeah.
>> And that's and that's the irony. The irony is our prespecified endpoint was a bit confounded by the fact that we didn't anticipate so many of our cohort would have such low levels of baseline plaque. I guess you could say it's a good problem for us to have, right? But needless to say,
>> needless to say, not all of them did. There were some who had higher levels of baseline plaque, but that's also important information because we can see what happens with them. And now I can get into the other metrics beyond that one. Now, as I'm sure you probably had in your own conversations, your own presentations, there's a big difference between the one we just talked about, which is a relative change versus an absolute. Would you be interested in the absolute change in plaque from
>> Absolutely. Yes, absolutely. And let me let me let me preface this. I want everybody to understand because we're always having new people come to the channel. The people in this cohort were eating a very highfat, very low carbohydrate diet for how many years on average, Dave? So when he says that their their CAC scores were so low that it was messing with the variability of of being able to tell if there how much progression there had been. These people had been eating high fat, lots of animal fat, lots of cholesterol, very low carbohydrate. They were none of them were vegan or vegetarian for what four years before
>> four and a half years. So understand that if keto if if ketovore if carnivore if these highfat low carb diets were so dangerous these people been eating that for four and a half years and in I think the majority of them their CAC score was so low that it was messing with the variability parameters that that they were trying to do to judge if there had been progression. Is that accurate?
>> Yeah. To be fair, we're not looking just at CAC. We're also looking at soft plaque. But the majority had a CC of zero at baseline. The majority.
>> After 4 and a half years of highfat, lots of coconut oil, lots of of beef butter, bacon and eggs, beef tallow, butter, bacon grease, these people, the majority had a zero CAC.
>> That's correct. Yes.
>> the
>> interesting
>> and and to be fair like it's again we'll get to the those who had it higher levels but would that be expected especially for a middle-aged population and for half a decade at these levels the average LDL for our cohort was 254 milligrams per deciliter which of course is very high for the average now pretty soon we'll get into the spread but hold that thought here's The absolute change in plaque volume now from the April 7th paper it was 18.8 8 which millimeters cubed was the year-over-year that was something that I was wondering about and is also something that we're talking about with clearly but both heart flow and Qangio the successor analyses done by different teams different technologies both came in at 5.5 millime cubed and 5.6 6 mm cubed. They're less than a third of what Clearly was, but importantly they actually agreed with each other and that was something that we were very interested in. That's that's the non-calcified plaque volume absolute change in plaque. Now there's something called the total plaque volume that includes both the non-calcified plaque and the calcified plaque together. Right? So what do we see? Well, in the case of clearly it's 23.3 mm cubed change, but heart flow had 5.5 mm cubed and Qangio 6.6. Once again, very close to each other. But now I want to get to that one that I was talking about earlier. Percent atheroma volume pav. How much did they agree or disagree in this case? Well, in the case of clearly, as we reported in April 7th, it was 0.8, 8, which did surprise me again because the baseline was 1.6. So going from 1.6 up 50% seemed a bit unusual because the average age of our cohort was 55 years of age. So middle age and we just happened to catch them by the
>> 55 is not middle age. What are you talking about?
>> Oh, yeah, fair enough. Fair enough. But then heart flow and Qangio came in and those are 0.3 and 0.2 respectively. So in in both cases basically all of the metrics that I've just told you they all came in low for heartflow and Qangio but not as much in clearly. And that's why we're especially interested because in the case of clearly when we brought this to their attention when when uh citizen science foundation got the raw anonymized data I did go ahead and reach out to them to say there's there's a a report that I can't share but that we've engaged a formal process with but in sharing that with them they agreed that we should go ahead and do a quality control pass. Um, unfortunately they've they've shifted gears since then and so now we're kind of in a little bit more of a formal process. But the bottom line is we want to get all of these analyses confirmed or disisconfirmed for their validity. And thus far, not just these two quantitative analyses, but also the semi-quantitative one that I mentioned from a little bit earlier. All three of those agree on what is cohortwide a lower level of plaque. Again, for the cohort. Now, I want to throw on the brakes for just a second. I want to bring it back to the progressors. Just as I would expect in any cohort of, sorry to say it, middle-aged population, particularly mostly male, you are going to find some rapid progressors. I would expect this in a population of vegans. I would expect it in a population of athletes. I would expect it in a population of people even on a cholesterol-lowering medication. you tend to have it tends to be heterogeneous. Some people often have rapidly progressing heart disease and just don't know it at all. And it's worth taking a moment to be responsible and emphasize that we did have a fraction. It's not a lot. It's I want to say it's somewhere in the neighborhood of like six or seven of the total of 100 that I'm happy they got imaging because they could also understand better where they're at. Now that said,
>> that said, I want to draw attention to something else. We also had regression. We also had in both heart flow and Qangio double-digit number of folks, not a majority, but a sizable fraction that saw less plaque in their second scan than their first. Yes,
>> I'll responsibly say that cohortwide there was an increase even if it's very small increase. But the fact that we have regressors at these levels of LDL and AOB B was of course very exciting for us.
>> Yeah. And let me let me just let me restate that and you tell me if I get this wrong. So there were there was a small minority of participants in the study who were eating a very highfat low carb diet whose CAC uh progressed and but there was actually twice as many in the same cohort also eating highfat low carb keto carnivore who their CAC score regressed or got lower. Uh you you said about 10% of people their score actually went down about 5% it went up. Is that accurate? And they were all eating a very highfat diet.
>> I what what I would rather emphasize is that cohort wide there was an increase most of the increase is very small increase of those who did see an increase. Yep.
>> There were some who I who would be qualified as rapid progressors and the ones who would be considered rapid progressors see a plaque level comparable to what I was explaining just now with clearly where there's like say a 50% year-over-year. That's why seeing it cohortwide was a bit surprising to me. I that's why I want I was excited that we were going to have other analyses. Now, would it have been predicted that we even would have um I believe it was 15 in the cubangio set and I believe 33 in the heart flow set that would have lower plaque in the second scan than they did in the first. No question that wouldn't have been predicted. And
>> and the two scans were roughly a year apart.
>> Correct. So,
>> so you said in one of the the analyses it was 30% because there's 100 people in the cohort.
>> Yeah.
>> 30% of those people
>> it went down in one of the one of the analysis.
>> Yes. Now, I I have one more thing to say to
>> be intellectually honest. You know how we were just talking about the scales, right?
>> Yep.
>> I would not be surprised if some amount of that is statistical noise at those low levels.
>> Absolutely. But also to be intellectually honest that goes both directions, right?
>> Exactly right. That's exactly.
>> Some amount of the low progression could be regression. Some amount of the low regression could be progression. The larger more interesting thing is, hey, is it so low that it's difficult for a good proportion of our people to even measure a change in plaque? That's exciting in and of itself. That's I think so newsworthy and and I'm I'm so appreciative that we finally get a chance to see that.
>> Oh, I love that. And so there's a lot of silence around the research that you've been doing because if if somebody just like recently just earlier this week there was a study that's like oh a ketogenic diet causes you to age uh your aging to accelerate. It causes inflammation. It causes this that and the other. And there were several different large websites that shared that out everywhere. I think Science Alert, um I think that Science Daily, there was five or six of them that I go to to look at research and you know, and then in the third paragraph, you find out that was a mouse study. It's like, oh, okay. So, in mice, I whatever ketogenic diet they've designed for the mice, which every time I look at the actual diet they're feeding them, it's still a high carb diet. They just add canola oil or something to the diet to make it keto. But this was a mouse study and they didn't lead with mouse study shows. Of course, they just they they let everybody believe, oh, this is a study in people. But yeah, and so I see any little mouse study. I think they could do a cricket study about keto and it would it would literally make the New York Times about how keto is going to kill you, right? But you guys have you guys have had you have years of data in human beings eating a very highfat ketogenic diet and yet none of the science uh study finds that I don't I haven't seen any of y'all's research blasted on their front page. It's very odd to me, right? And then the second thing that I'm increasingly seeing and saying is that if researchers who believe that a plant-based diet is the heart-healthiest diet, right? You know, there's a huge cohort of cardiologists and nutritionists and dieticians who believe that in their heart of hearts. If they truly believe that, there's a million people around the earth right now eating a carnivore diet. And there's many probably 10 million using a ketogenic diet to improve their health. You would think that of all the cohorts that you could study, you definitely wouldn't want to do a study on on mice because there's millions of people eating keto and carnivore right now. Why are you still doing mouse studies? Does do you get my point? And then if you truly if you you know you're a PhD at Lomol Linda University in California and you just wanted to just shut down the meat heavy keto keto carnivore people like I'm sick and tired of the all their misinformation. I'm just going to reach out to a hundred of these people eating meat heavy keto or keto carnivore and I'm going to study them because I know I'm going to compare them do two cohorts. one that's eating highfat keto carnivore, one that's eating lowfat vegan, and we're just going to follow them for a year because you guys have been you're doing this. You're following people for a year. This is a doable study in human beings, not in crickets or mice. Would that I mean that would clearly shut the carnivores up and shut the keto people up if in fact the these diets were causing just ravaging rampaging heart disease. Does that make sense, Dave? Like that would be the population you would want to study. In fact, I think that's the reason you chose this population to study was because they were de demonstrably eating this diet with huge amounts of fat and very low very low amounts of fiber and carbohydrates. And you're like, "This is this is the cohort right here. If if if this is true, if keto's going to kill you, this is the population to study." Correct.
>> Well, yeah. But it's even more than that. You didn't have to specifically have a designated diet. You just had to have the high LDL. So importantly, Ken, what is it about saturated fat, for example, that is considered so harmful? It's the presumption that it'll increase your LDL. Beyond increasing your LDL, what is harmful about saturated fat?
>> Nothing that I can detect. But what would the what would a what would a vegan researcher say?
>> I so I've I've actually asked this exact question many times because so much is built on top of the lipid hypothesis to push back at the ketogenic diet. And to be fair to be fair if indeed the lipid hypothesis is true we have the perfect population to study to find out if there's a direct signal. Now, it is worth, by the way, emphasizing because this you kind of gave me the perfect segue. What happened following the April 7th paper, I think was was a great level set for the kind of winds that we're looking at. So, when we did the match analysis, which is before we had the longitudinal data, you remember the match analysis, we had our cohorts baseline scans compared to another study called Miami Heart. And when you compared the two, they were statistically no different. In fact, ours trended slightly better in spite of the fact that our cohort had over twice as much LDL than the Miami heart matched control. Right now, Ken, how much coverage did we get with that match analysis? How right? So,
>> I did not see it on study finds. I did not see it on Eureka. I did not see it anywhere. And that's that's my point. You guys are studying the premier cohort that if if eating lots of saturated fat caused heart disease, if having a very high LDL cholesterol, if that truly was causitive of heart disease, then your cohort that you're studying, that's everybody should want access to that cohort. Everybody should be talking about that cohort. Everybody should be crunching the numbers from that. Everybody should be reporting that because this is the the premier cohort that should just prove be like literally uh the the makers of Zokor, Lipitor, Crestor, they should be literally throwing millions of dollars at you saying we want to study your cohort because we think that that that they're going to prove the lipid heart hypothesis beyond a shadow of a doubt and then our profits are going to increase even more. But I hear nothing from from the plant-based plant believing researchers. I hear nothing from the statin makers, the PCSK9 makers. They they seem to not be interested at all in your cohort, which and I I think everybody watching this, you ought to just think silence speaks volumes in my experience, just in human nature in general. If if you really don't want something discussed, then you don't bring it up. That's just wise to not bring up something that's going to disprove your point. So I would opine and of course Dave can't say this because he's being very diplomatic and very academic and I applaud him for that. But I can say this. I think this reveals this lack of interest from the plant-based researchers and the plant-based dieticians and from the statin and PCSK9 makers. The complete lack of any interest whatsoever in Dave's research and Dave's study. I think that silence speaks volumes and I'll let you, the educated, common sense listening audience, I'll let you decide what their silence is actually saying.
>> Sorry, Dave.
>> No, I I I couldn't agree more. And to to everybody who's watching, I definitely implore you to listen to whoever is on either side who continues to engage the data, who continues to maintain the dialogue. Both Nick and I kind of, you know, it's a three-man band because uh but Adrian's actually busy doing a lot of real clinical work and so forth. Nick and I tend to be a bit more on the spokesman side of things. We are active and interested in engaging, including being challenged. But getting back to exactly what you just now talked about, Ken, hardly any coverage on the match analysis. When the April 7th paper got released, it's interesting. there was a narrative that kind of got held on to that required you know m maintaining attention to one piece but ignoring another. So the interest being on the clearly analysis even at the expense of the semiquantitative but at the same time ignoring another key thing that I've mentioned a few times now but I'm going to repeat it one more one more time there is no association between LDL and plaque progression in our data anywhere and when I say that I mean it's not in any subgroup analysis like those rapid progressors there's no association between LDL and APOB with them for the regressors there's no association between LDL and AOB. There it's only been the plaque that actually tends to be the most predictive of future plaque, which again brings us back to the value of actually finding out for yourself if you're worried. And that's what's so powerful. Well, a lot of that attention came in the April 7th paper. Now that I've now that I've actually presented, it's preliminary to be fair, but I presented the new data that I shared with you just now from three weeks ago. I reached out to many of these same folks that I've I've cultivated good relationships with, but who actually are concerned about this research and the silence is back. There's not the there's not the engagement. There's even there's even three individuals who I think I have a good rapport with who were in my presentation that includes uh Nutrition Made Simple Gil. I always know he's good with his name, but also Lane
>> I know. Yeah, I know you're talking about Yep. He's very intelligent guy. He's an MD, PhD.
>> I think he got a degree in nutrition. Very intelligent, but he obviously has a bias of thinking that plant-based is best. Uh, and I've actually he interviewed me on his channel and we agreed to disagree and I think I did okay on that interview. But but I just want to be clear, you and I both acknowledge that he Gil is super intelligent. He is very well educated, very articulate. He understands the literature better than the average MD MD does for sure. And uh yeah, I I respect his academic acumen, but I think that he's blinded by his current paradigm.
>> Well, I I sorry, just to finish off the list, uh Wayne Norton, and Simon Hill, all three of those I've had many conversations.
>> Commenting I'll pass commenting on the second person who I think is not worthy of mention. Uh, and then Simon, I think also very very intelligent, loves to read the research and try to try to make sense of it.
>> But I, but you know, I'll just let me let me take it a step further just for for I now have a podcast. You know, it's an in-person podcast. Let me just make the offer right now. I'll fly any of these three great gentlemen to have a sit down long form conversation with me in my studio and and I'll I'll buy them a dinner of their choice. Wow.
>> On the evening after, right?
>> Plant-based only.
>> It could be plant-based. I'll I'll go with it if if that's where we got to go. No matter what, it's about keeping this conversation going because we've got to be getting to the real answers. We got to be getting to the truth. So, getting back to what I advise everybody who's watching this now,
>> pay attention to who remains engaged, who cares about understanding everything that's happening and working with the data
That we have. You know, I I'm so proud of my team because up until the April 7th paper, we just had a lot of things that just kept rolling and flowing, but I felt like we had a few missteps in our initial roll out for the April 7th paper. But I appreciate the fact that we owned it and carried it.
However, at the same time, you've got to kind of count on the same thing from the other side, right? If there's misses, one of the biggest misses, frankly, is the lack of that that construct I was just describing. Kind of the emphasis of trying to think that um the clearly data might be all that matters and dismissing that association. That's part of the lipid hypothesis doesn't compute. It doesn't work. That's got to be something you've got to be willing to engage on and accept challenge on. And that's part of what makes this a bit of a a difficult situation, but at the same time kind of illuminating. You know, we we've come to really understand what kind of headwind we're against.
You know, you mentioned the the keto study. Let's just call it what it is. It's very fashionable, right, to take down keto right now, especially in the nutrition space. It sure >> it moves a lot of clicks. It gets a lot of eyes. >> Sure. there just doesn't seem to be the same. >> Let me just let me interject, Dave. Not only does it get lots of clicks and lots of people who tried keto and it didn't work or whatever or their mama tried it, then she, you know, had had some bad outcome because humans are not bulletproof regardless of what diet they're eating. And so they're they're piling on. But it also supports the industry narrative. That's that's the part that I want everybody to understand. When a when a when a plant-based cardiologist or a plant-based dietician says, "Well, obviously keto is going to give you a heart attack, there's this new mouse study that proves it." they are they're either patting their nest u ensuring future collegial working relationships with the pharmaceutical companies and the regulatory bodies the American Heart Association and others or they are uh at least solidifying their position that hey I am on the home team here I am part of you guys I am I should be accepted into the fold because I also said out loud on social media that keto will kill you.
And I think I think that there's not only is their own personal paradigm currently blinding them to what's increasingly becoming the obvious truth based on you guys research, but they're also you don't I mean it just imagine if you're out in the wilderness and you're in a party of a hundred people and you know what they're about to do is obviously wrong, but your only option is to disagree with them and then be kicked out of that and party and then be alone in the wilderness. That's how many of these cardiologists and dieticians and nutritionists, I'm sure that's how they feel. It's like, wow, gosh, this research keeps coming out showing that there is zero association between very high levels of LDL cholesterol and coronary artery plaque progression. And there's also zero association between very high levels of APOB and coronary artery plaque progression. There's literally no association whatsoever. How can that be? So you can just put yourself in their shoes. They have ba basically bet and based their entire career that the lipid heart lipid heart hypothesis is correct. That eating lots of saturated fat raises your LDL and that a high LDL will cause your plaque to progress and will cause you to have a heart attack sooner rather than later. And therefore, you need to take a medication that will lower your LDL cholesterol. And that that lowering of the LDL cholesterol is the thing that is protecting you from having coronary artery uh calcium progression and a heart attack, right? And because I I every day I have somebody reach out and say, "Well, my cardiologist said that if I'll take this highdose uh zokore lip crestor that that will stop my CAC progression." And I'm like, "But did they explain how it will do that?" Because I'm still looking for that in the literature. And then based on uh you know, Felwin Felman and Norwitz and my my my other uh good friend, I h I don't see how that happens. How does it happen? what's the mechanism for that? And of course, they have no answer and their doctor never explains that in any detail.
>> Now, I'll do I'll do the due diligence thing. Th thing number one, I know if some of my colleagues were here, they would they would say in the circumstance where you are a rapid progressor, >> then they themselves, this isn't me, but what they would say is then you should consider taking steps. And I know many low carb doctors would say and that includes taking steps on uh various interventions that might also reduce LDL. The the other piece is if I'm wanting to be as good a scientist as I can, I'll give room for it's possible that years later there may be some association that emerges, >> right? >> And in the case of uh our cohort, this has been kind of known for some time. We're in the process of getting five-year scans approved and through an IRB and that would start. So, in other words, there would be literally a five-year gap between their first scan and scans that would start uh next year. So, for example, somebody who got their scan in October of 2021 would get their second scan in October 2026 or sorry, their third scan in October 2026. And therefore that would be very golden data really data unlike anything you've ever seen in imaging before because again they've been at 4.5 year average nearly half a decade and then you add another half decade >> and again I want to be a good scientist. It's possible an association emerges >> but would I would I bet that the lipid hypothesis just kind of snaps into place? That's that to me feels like a stretch, right? >> Yeah. It's >> it's possible that there's some association that emerges, but again I'm having a tough time here because I've seen these numbers. I've actually looked at it and I don't want to get too much into the gig zone with you, but I'll just say that we know that the same the thing I talked about at the very beginning, the reason why a lot of people their LDL goes down when they're when they're working with their obesity and they're coming back to something healthier, even if they don't become lean, why their LDL goes down is it gets back to that failed trafficking of fat, right? those triglycerides when they're coming down there's less of that traffic jam that I believe is upstream from the reason you have higher LDL. So this gets to the heart of causality itself is the higher LDL that we see in metabolically unwell populations is that association with atheroscerosis have the same root cause. That's why we always need to do this Ken. We always needed to study people who are metabolically healthy and who may in fact have higher LDL because they're trafficking more fat to see if that's the true common denominator. We always had to do this and now here we are. We're doing it.
>> Yep. I love that. Now, I want to ask a question that uh you as a trying to be a good scientist, you're going to be like, "Yeah, that's that's a little dicey to talk about." But this is a question that all common sense people will understand. And let me preface it by saying this. Anybody watching this, you've been to your doctor and you started keto to lose weight or reverse type two diabetes, whatever your your goal was, or carnivore, and your LDL cholesterol went up. Did your doctor say, "Gosh, you know that there's a tiny increased risk that you might this might cause a heart attack. We probably need to get you at least consider getting you on a statin just to lower that LDL." Or was your doctor inflammatory about it? Were they almost was it almost like a scare tactic? Did your doctor become emotional like, "Oh crap, you're a walking heart attack. We've got to get you on Crestor right now. The highest dose we can do or repatha or prow." Did your doctor get emotional? And then if if god forbid you said, "Yeah, I don't I don't really want to take that." Did Did they become even more emotional like physically emotionally upset? So, what I'm I'm getting at is is you would think when a doctor becomes emotional about something that it must be super super dangerous, Dave, right? You know, like if a doctor saw a toddler juggling knives, you know, the doctor be like, "Holy crap, you've got to stop juggling those knives, 2-year-old, it's going to stab you in the the the cranium, right?" Of course, yes, that makes sense. You you should get upset and rush to try to save that situation. That makes sense. So you've been following these people with these very high LDLs uh for four and a half years. >> How many people in this cohort, this is 100 people, give or take. How many people have had a heart attack in the four four and a half years? >> Now I'm again I'm going to try to be a good scientist. To the best of my knowledge, none of them. >> Yeah. To the best of my knowledge, there's not been an what's called an AE or adverse event that's been recorded. Now I want to be fair. the period of time of our study is that one year. So, it's possible that somebody may have had one that's outside of the the span of time of our event. >> But, if I were to get the five-year uh extension, I would actually want it to be reported. I'd want it to be back channel because the >> as you get a larger and larger number of people, a statistician wouldn't say, "What are the odds of X happening?" They would say, "What are the odds of it not happening?" Just like >> when somebody goes, "Oh, I found an anecdote of, you know, a vegan that got a heart attack, >> right? >> I would be a good scientist and say, "What are the odds >> given how many vegans there are and given how and I'd say the same thing to somebody saying that with a carnivore?" Right. >> Exactly. And my point is is two my point is twofold. First, to the patients, if if your doctor's getting emotional like you're juggling knives, then the risk must be super high. It must be 10%, 20%, maybe 30%, right? It must be a huge risk or they wouldn't get so emotional trying to get you on that crest. That's my point for the patients. But then for the doctors, for the health care providers that watch this, and there's thousands that do, are you shocked that that not a single one of this 100 people has had a heart attack that's been documented and they've been following these people very closely? Does that change your view? Like, well, gosh, I would have I mean, you as a healthc care provider watching this or a dietitian, what would you have guessed the percentage was over four and a half years of a a cohort of 100 people having a heart attack? There should be at least one, right? I if if the risk that you've been relaying to your clients and patients is really truly that big of a risk, there should have been five or 10 people who had a heart attack by now. Because keep in mind, these people's LDL cholesterol is super high. like spooky high, scarily high, but not a single one's had a heart attack. So, I want the patients to take a breath and understand, yeah, maybe it's not as high of a risk because Dave is, you know, he's being a good scientist and well, maybe there's a risk we haven't uncovered yet. Maybe a fiveyear study, a 10 year, 15 year, maybe we'll find it at some point. Haven't found it yet. But for the health care providers and dietitians and nutritionists, that's who I really want to hear this. You need to reassess how you're voicing this to your clients and patients. The risk is not whatever magical number you thought in your head 10% 20 30 40 50% for people with this very very high LDL cholesterol. It obviously cannot be that high. Now we can't say how high it is because it's just a hundred people and we've just been following them for four and a half years. Right, Dave? But we can say, well, it's probably not 50% since not a single person has had a heart attack in four and a half years.
>> I I do want to, you know, you are actually opening up. >> Be a good scientist. That's okay. >> No, no, no. I I'm actually going to sound almost like I'm going the opposite direction, but I do want to call out an inconsistency. You've literally watched this in real time. When we were originally talking about lean mass hyperresponders before the study was getting started, there was a lot of push back as to how high risk they are on social media. You saw it. What happened when we were announcing the study, when we were putting it forward, we had a lot of the same voices. You know who you are. A lot of the same voices who said this won't tell us anything. This not that there's people with skyhigh LDL. takes decades for them to develop cardiovascular disease. And I and I said, "But wait a sec. What if what if a lot of them are, you know, our age? What if you've got a lot of people have existing plaque at baseline?" And I was stunned at just how many of the same folks who said, "This is this is of enormous urgency. You need to be doing something now." would simultaneously hold the position that we need to have not even just years but decades to actually see a difference in a CTO in in an imaging study. We're not even talking about events. We're talking about actual verifiable changes in plaque levels. So, I I say this with love in my heart, but I I want more people to really think about if somebody walks into the office and they have the eligibility criteria of our study, right? So, they have low cardiovascular risk factors across the board, they have high HDL, they have low triglycerides, but their LDL is 190 or higher, right? What is the standard of care? My understanding is the standard of care is that they should be on the highest tolerated dose statin. Consideration, right? >> 100%. >> Okay. That right there is already worthy of study to find out if indeed they are exhibiting the risk that Brown and Goldstein were seeing from 50 years ago. We have See, so this brings me back to the spread. This brings me back to the spread. A lot of people were thinking we're in like this narrow band of how much the LDL would like it's just above 190. Actually, we had about 17 that were below the 190 because that was the qualifier. So, sure enough, people's lipids can change. So, we had 17 that were below. >> We had a whole lot that were above, including we had six that were qualifiably at homozygous FH levels. This is the one in a million genetic disease where their LDL was 400 and higher. So bringing it back to the work of Brown and Goldstein, the ones who who won the Nobel Prize for discovering the the LDL receptor and you know foundational to limit hypothesis. The children they were looking at had very high levels of LDL. And the only time you'd see humans with levels of high LDL this high were if they had that impairment in genetic metabolism. And now we have lean mass hypersponders in our study who have LDL levels comparable to those that Brown and Goldstein were looking at. Of course, you would expect you would expect to see some progression in plaque given that Brown and Goldstein were seeing it in a matter of a few years. In a matter of a few years. >> Right. Right. And right that was that was what they reported is that we're seeing this increase almost yeartoear but now it seems that uh the plant-based people are holding these two inurous things. First of all uh your study I think there were several that spoke out and said well the the ethics board shouldn't even approve this study. This is dangerous. >> But yet at the same time they said oh well it's going to take decades. You can't study this for three years, 5 years, seven years. That's not going to show anything. But yet, it was unethical to perform the study. How can you hold those two inongruities in the same human brain at the same time? I'm unclear how that's possible, but they were somehow able to do it. And I think many continue to hold that in their in the same human brain at the same time. Um, one one more question. And I know you and Adrian and Nick are you guys are studying this particular question, but also you guys are constantly brainstorming and trying to figure out and and think about this kind of circumspectly. If it's not the very high levels of LDL, if it's not the very high APOB, we've known for years in in medicine, if you if you read your literature, that we've known that statins have an anti-inflammatory effect. And many uh healthc care providers opine that that's actually how they reduce your risk of having a coronary event if they do at all that it's probably the anti-inflammatory part of that. Which we could we could do with lowd dose cultine or lowd dose aspirin or lowd dose ibuprofen without all of the side effects that can come with the statin. What is causing the progression in these in these rapid progressors? If it's not the high LDL and not the high APO, this is just theoretical we're talking now. What what are you guys with your three very large brains put together talking about this over a a keto coffee or a steak? What do you think it is? What is it that's causing this rapid progression? Well, >> in in some >> I can only I can only speak to myself for those and again I take it outside of diet or even LDL per se. First of all, I I'm a believer that plaque is not instantaneously shifting gears. So for example, let's say that Ken you were not living the best life right up until let's say age 52, right? that right at age 52, you went into what we would magically know right now as the perfect protocol, perfect diet, perfect lifestyle, etc. Do I think right then all plaque progression would just instantly halt and possibly even regress? I don't think that. Once you learn more about the immune response, you learn things like inflammation is a process. At the sightes of inflammation, there's work the immune response has to do. There's the coagulation cascade. There's the um there's the uh macrofasages that have to get in and actually perform. Not even just things like hemostasis, which is just kind of stabilizing things. There's something called ephroytosis, which is really fascinating if you can take some time to get into it. Then you have things that are really fantastic about the human body such as if somebody has a deep olusion. You can sometimes find it depending on their own health status that their body will actually make it's called neovascularization will actually bypass it. Right. >> Yep. >> Okay. All these things take time. And the problem is that that freeway that is the 60,000 miles of our vascule never closes >> ever. >> It has to stay open at all times. So it's a very the engineer in me is excited about how complicated this problem is, right? But you think about construction that's off to the side of the road that you're in and the town that you're in. That's a lot of what's going on inside of your arteries. And the reason the coronary arteries are special is unlike almost anywhere else in your body. It's where a lot of the highest pressure is and it's on a muscle that's conforming and shifting. So imagine I like to use roofers, right? Like if I was roofing my own house right up here, putting the shingles in would be a piece of cake. But imagine I'm out in the Florida Keys off the edge and the hurricanes going. I'm trying to like get the It's tough. It's tough to reconstruct tissue in that area. It's a very deep and difficult problem. So, I don't know, Ken, if there isn't some degree of that that's going to be related to diet and lifestyle, things they're doing. I think I've talked to you about this before. I'm concerned about people like say overex exercisers because I believe a lot of the progression especially rapid progression that we see is underrecognized lack of recovery. So if you don't have enough fasting if you don't have enough sleep and if you don't prioritize recovery from things like exercise, like stress, I think those all contribute not to just the progression independently, but the lack of repair. That's my Dave theory. >> I don't think that's everything, but I think that's a larger proportion than people probably give it credit for. You need to let your body heal itself. And it's actually really good at it if you give it a shot. I totally agree with that and I I love that you left the door open that there might be other things that we don't even know about because if people listen to me they know that I believe that back in the 30s 40s and 50s when pharmaceuticals were becoming popular basically all scientists stopped studying how the body actually naturally heals. They stopped studying all that. Everybody wanted to study pharmaceuticals so they could get a patent and make a million dollars. And that's human nature. It is what it is. But uh this has been just fascinating and I love having these conversations with you. I'm going to give you the floor now. Anything we didn't cover that you really want to cover? Uh any anything that we didn't talk about that needs to be talked about and then at the end tell everybody where they can find you.
>> Yeah. I just uh I want again I want want to once again thank everybody for their help. I mean this is as grassroots as it gets. I mean quite literally this is I'll concede. I thought it was going to be shorter span of time that it would take to do this. But uh that said, the data has been so exciting and this process has been so exciting and the journey has been great and as you know the documentary is all going to be the better for it. It's quite a story. Uh so I just want to just personally thank each and everybody who's watching this right now who's helped us make every single milestone. I also want to give a special shout out to the Bazookis. They've been very very supportive. not just in uh the funding with this study but also with the filming itself >> and um with uh with incidentally these uh last analyses too which we we managed to get everything together and uh open up so much of this data too for everyone else to look at. So >> yeah, the Bazooki group is making the world a healthier and a better place on the daily. I I I can't thank them enough for all the work they're doing and the the funding that they're giving for research just like this. I love I love what they're doing. >> Yeah. Um people can find me I'm probably most active on XT Twitter, Real Dave Feldman. You can also check out my YouTube channel, Real Dave Feldman, as well. And start a podcast. I'm going to try to rope you over here. >> Yeah. Oh, I'm definitely coming. We're gonna come to Vegas and we we'll have a steak with you, Dave. Don't worry. And we're going to do that podcast as soon as farm life permits. And I let's let's close by I want you to cordially uh diplomatically invite the three people you had mentioned earlier. >> You can use my my uh video here as a platform just to to politely invite them to have a conversation with you. Call their names and we're not we're not being mean. We just really want to have want this conversation to happen. So, who are the three people you'd love to fly at your on your dime? I think you said uh to interview to have a discussion with them about this issue. >> No, listen, I part part of why I identified these three gentlemen is I've had many great conversations both public and private. I appreciate a lot of their opinions. Um and yes, one of them can be a little bit more rambunctious than the others, but um that that would be Gil Cavado. I hope I'm saying it correctly. Simon Hill and Lane Norton, all three of which have made uh have made videos on the keto study. I'd love to chat with them about their analysis because I do have a a bit of cordial push back, but by the same token, I'd love to entertain theirs. And sure, I'd love to. As I mentioned, the podcast is supported by Own Your Labs and Own Your Labs on their dime. We'd be happy to fly them out so that we could have a nice long form conversation right here in Vegas and I'll get their meal afterwards. We'll we'll have a nice dinner. So, I think it'd be great. Listen, we've got to have more conversations. We've got to be able to engage each other to make this real. Otherwise, it's just going to continue to be as tribalistically distant as it has been. And nutrition of all place, health of all places should be where we try to find more common ground. >> Totally agree. I love everything about what you said. Thank you, Dave, so much for doing this. Uh if any of you guys uh would like early access to interviews like this and the ability to ask questions, please consider becoming a tribe member. We're actually closed right now for new tribe members because we're re revamping, but as soon as we open back up membership, we'd love to have you. Thank you so much, Dave Filman, uh, for what you do. Don't stop doing it. I know you won't. You don't need me to say that. Thank you, Dave. Have a great one. >> Thanks for having me, Ken. >> Byebye.