Cardiologist Reacts to BREAKING Cholesterol Research: "Data Challenges Dogma"

What you're about to hear is a conversation between myself and Dr. Aseem Malhotra, a famous consultant cardiologist and close friend of Robert F. Kennedy Jr., who himself has been tapped for a position in the new administration. I note that up front to call out the elephant in the room. Our conversation is going to be centered around data that colleagues and I have just published around LDL cholesterol and heart disease that will be controversial. Actually be published tomorrow morning as I record this, but it's gonna make big waves. Now if you haven't seen the video covering those new data, please do so before or after watching this conversation. Now the last thing I'm gonna say before we start the conversation is that science and people have something in common. It's often the most controversial samples that are the most poorly understood. So please keep an open mind. And now for the conversation. Dr. Maholtra, thank you for taking the time to speak with me. I want to get right into it. I know you read our new paper which releases tomorrow morning to the public. What was your reaction to reading the paper?

It was fascinating, Nick Norwitz. I mean, really great work what you've done. I think for me also, it seems consistent with what we already appear to know. At the very least, there needs to be a big question mark around the original understanding dogma on LDL cholesterol being a significant risk factor of heart disease, especially as you've pointed out, in people who are otherwise metabolically healthy. And when you bring that into the equation, you've then got to ask yourself whether or not it is truly an independent risk factor for heart disease. William Craft-Helly, co-director of Framingham, 1996, actually said, looking at— going back over Framingham data, LDL cholesterol, unless it was above 300 milligrams per deciliter or 7.8 millimoles per liter, depending on which country you're in and what units you use, it had essentially no value in isolation in predicting heart disease. So it's very consistent with what we already know, Nick. I think that's why it's, it's such a good paper.

Thank you. But would you agree with this? You just mentioned LDL in isolation. But I don't think we've actually had a population of people up until this point who as a population isolate LDL as a risk factor because we have generally in the population metabolic dysfunction as a background, or we look towards familial hypercholesterolemia and it's talked about as if it was just high LDL, but I'm sure you'd agree like FH is a lot more. Also, the etiology matters, the cause, like if you're born with with very high LDL because you have a broken lipid receptor. That's very different than a metabolic response.

You're absolutely right. So I think there's two points to be made there. So the first one, in reference to what you said, yes, this is the first time I think this has been studied in this way. But interestingly, David Diamond and Paul Mason, I don't know if you read that paper, they did a review of looking at statin trials, specifically what they found in subgroup analysis of both primary and secondary prevention statin trials, which is very interesting. Was that those subgroups that had normal triglycerides and HDL got no benefit whatsoever from the statin, which is interesting, but also on FH. So I was involved in some research looking at FH with a number of international scientists, and this is an interesting one. So the big headline for FH, and these are people I manage, by the way, so I'll give you some examples of what I found in my clinical practice, which also seems to be consistent with the research. Is that in people with FH, 70% of women, okay, unselected, and 50% of men with FH, right, genetically high cholesterol, will not develop premature heart disease. So the question then is, is there any factors that differentiate those ones that do develop heart disease versus the ones that don't? When you look at the LDL, they're the same. So LDL isn't the differentiating factor. They're obviously very high in both of them, but it's not the differentiating factor. What is the differentiating factors? Well, insulin resistance, so type 2 diabetes, hypertension, smoking, obviously, um, lipoprotein, lipoprotein little a, and fibrinogen. So I've had many patients come to me, some of them by the way are probably lean mass hyperresponders, right, in their 50s, but some of them are true FHs. And I look at their insulin resistance markers and I, we go through the history, I say, listen, actually you don't appear to be at high risk. These people are fit and active, but they've been scared by their doctor that their cholesterol LDL is so high, like 250, 300, like, and similar to the people in your study. And, uh, they literally think that, you know, they've got the fear of death put into them, and, but they're a bit reluctant, they're a bit skeptical, and they want to get a second opinion. So what do I do? I organize CT coronary angiograms for them, and more often than not, they come back completely normal. Which means that it just reinforces that for them, these people, some of these with FH, especially females, that if cholesterol is a problem for them, LDL is a problem for them, by your mid-50s, late 50s, early 60s, you will see some degree of atherosclerosis and there is nothing there, Nick. Nothing.

Yeah. No, my mom falls into that category. She's MD, PhD, and she's had high cholesterol all her life, but when she went low carb, it went even higher. So lean mass hyperresponder on top of congenitally high LDL. Probably 160s, 200 LDL most of her life. And then she became a lean mass hyper-responder several years ago. LDLs in the 400s. She's having her 60th birthday actually 2 days. Today's April 6th. Her 60th is on April 8th. Happy birthday, Mom. But she wanted to know whether or not she should go on a statin. I said, just like, get cardiac imaging. You're a physician, you know, you know what this means. Get a CCTA, zero plaque score, no plaque. And that made the decision for her. So, you know, the high-level truth I think that we agree on is when you look at risk factors like LDL and ApoB, even if you consider them a risk factor, it's very context dependent. And to have a myopic focus on that is problematic.

Well, yeah, that's true. I agree. And I think the other thing to add in, which is another layer to trying to really question whether or not LDL is an independent risk factor of heart disease, and then the degree of which it is. So, you know, is it a major risk factor? Is it a minor risk factor? And myself, and in 2021— I always get the year wrong— 2021, in BMJ Evidence-Based Medicine, myself, Robert Dubroff, and Michel Delorge-Girardot, second author, we did a systematic review which has now been corrected to a review for some reason because there was a bit of backlash. But we really looked at all the randomized controlled trials looking at statins, the PCSK9 inhibitor drugs, which are very potent lowers of LDL cholesterol. And ezetimibe. And it was about 35 randomized controlled trials to answer this question: is there a consistent relationship between the reduction in LDL cholesterol, Nick, and reduction in cardiovascular events? Because you got to look at the other side, right? Because one is, okay, you've got a biomarker that's got some association with disease, again, context dependent. The next question is, does lowering it make any difference? And we found there was no consistent relationship, even from industry-sponsored trials where the data is usually not independently verified. So, when you— and then your paper now is so good, so strong, so helpful that it really reinforces this message. Of course, one of the things I want to ask you, which was interesting, of course, one of the limitations is this one year. Okay? Yes. But my understanding reading the paper is that the people enrolled had had their LDL levels quite high, at least over 200, right, for a period of several years. Is that correct?

Yeah. So the precursor paper to this was a baseline study where we had a matched population, the Miami Heart. And what we did is we compared plaque levels in those two populations. Now, at baseline, the average age of the participants was about 55 in the keto group, and they had been keto for 4.7 years on average.

Right.

At the end of this study, it's 5.7 on average. This, we were looking at a 1-year, you know, ah, study, but we still did look at about, you know, 5 years after they started keto and their LDL jumped, how do they compare to a matched population who is generally healthy? And what we actually found was there was no increase in plaque in the keto group versus the people with LDLs that were— I think the average levels at the baseline were 277 for the keto group and 123 for Miami Heart, right? And that works out to about 700 milligrams per deciliter a year exposure. Actually, the lean mass hyperresponders were trending to have less plaque. It was a non-significant difference, but there was a trend towards less plaque in the lean mass hyperresponders. So So by the end of the study, 5.7 years on average, everyone at least 2 years keto.

Yeah, that's fascinating. I mean, that adds, I think, another layer that it's a reasonably medium term, you know, that you haven't seen any significant increase in LDL.

Yeah. And I would say, yeah, with the high resolution CT angiography we have now, 1 year is pretty standard. I mean, our PI Matthew Budoff is an expert in cardiac imaging and like He said this is an appropriate timeframe based on what other people do, based on the modern technology. The fact of the matter is, of course we want to follow them for 2 years, 5 years, but like, we don't have a time machine. So check back with me in 2030 and we'll have more data. These are where the data stand right now. And I think, yes, they're preliminary, but they're pretty reassuring. But I also want to be respectful of your time and I have a few more questions I definitely want to hit. You're a cardiologist, so you obviously know many cardiologists. How would they most cardiologists react to the idea, now the evidence-based idea, that lean metabolically healthy insulin-sensitive people on a ketogenic diet with LDLs of 200, 300, 400, 500 or more might not actually be a high-risk group for cardiovascular disease? How would they react cognitively, emotionally?

Well, it's a really good question. I can tell you that they probably, first of all, just part of human nature, their initial reaction would be one of skepticism. They won't want to believe it. These things take time. I've even seen that. I thought there's been great progress in the shifting of the paradigm of heart disease away from focusing on LDL cholesterol, in part because of some of the work I've been doing and getting a lot of publicity on over the years. But recently what I found, Nick, and this is really important for the context of what we are up against in terms of the narrative, that's why your paper's important, is why it's so important that we get coverage on this. I'm sure it's going to do very well. It's going to get a lot of, certainly, alt media, and hopefully some mainstream media will react to it and amplify the message. But what's happened in the last couple of years is I've noticed there's been almost a reemergence of an obsession and an extra fear around cholesterol. And I suspect that's also because of the non-statin new cholesterol-lowering drugs that are getting pushed because they're very lucrative. Drug industry spend a lot of money on them. So what I've been finding, and this is, and the reason I find this is actually from my interaction with patients who come to me from second, for a second opinion, or even reading letters from other reputed cardiologists in America. I have a lot of patients in the US and in the UK where there is almost a reinforcement of this cholesterol hypothesis. Like as in, you know, unless you get your cholesterol down, you are gonna have a heart attack soon, you're gonna die. There's a lot of misinformation, unfortunately, Nick, within the minds of cardiologists. And this is still based upon, to a large degree as well, the focus on the management saying if you get your LDL as low as possible, you are massively reducing the risk of a cardiovascular event.

Yeah, I have an interesting assessment of that, and I want to see your reaction to it. I think that's going to backfire very strongly. We have this you, you, you just alluded to it, lower is better mantra, like really focusing on getting LDL cholesterol and ApoB lower and lower and lower. And I think it is a reaction to alternative points of view on the pathogenesis of heart disease, risk factors that are important, whether or not people need to be treated. And I don't think any self-respecting individual could stand behind the statement lower is better as an umbrella statement. Better with respect to what cardiovascular outcomes? How are you lowering it? Because that's important. But my impression is Conventionalists might want to push a conservative narrative because they don't want people, you know, seeing an inch and taking a mile. But what I think is happening, I want to see if you agree, is people, even if they don't understand the depths of metabolism and cardiovascular health and atherosclerosis pathophysiology, most people can tell when they're being patronized too. And when you project a message of lower is better, that's all you need to know, here's a medication, people get pissed off and they react. And what's more, I think a lot of conventional outlets, including cardiovascular journals, are destroying their credibility and the credibility of the associated medical establishment by putting out what are effectively propaganda pieces that can be very easily explained. So I can give specific examples, but for example, did you see the, the, what was it in JAMA Cardiology that there was that cardiovascular imaging report of the man with the yellow nodules on carnivore?

No, I didn't see that. That's interesting.

I'll send it to you. So it's a brief report and they present a case of a man in his 40s. That is the entirety of the patient's description. They don't give his actual age. They don't give any genetic, family, or other history. And then they say he had been on a carnivore diet for 8 months, eating, get this, 9 pounds of meat cheese and butter per day. Per day. And the senior, the first author went on mainstream media news and doubled down on that narrative that that was the dietary intake. And then they said he had basically cholesterol oozing out of his skin and they showed some xanthomas or whatever, right? Yeah. And it was just, it read like a Monty Python skit. It was behind a paywall. So people just kind of assumed maybe there was more details. I looked at it, I posted literally the whole thing on social media. I emailed the journal. I emailed the first author. I even said to the first author, if you actually have data on this patient and want to do a more comprehensive report, I will help you write it. I will do the legwork. And if you want to get genetic testing, I will pay for it at my expense. No response.

Yeah.

And that's a pattern. There are more papers like that. And I just think they see that and then they're like, why would I trust JAMA Cardiology? That's what you're right.

I think, I think there are two other aspects to add in in terms of the reaction. Which we have to acknowledge, just head up, just to understand the psychology, but also the barriers to the truth. One is most cardiologists, most doctors have no training or understanding of lifestyle interventions to prevent and manage heart disease. Okay? Zero. So you give a man a hammer and every problem is a nail, right? So for them, their only approach to see a high LDL, which again, they don't fully understand the data on, is because they're just following guidelines and a narrative that's being pushed through propaganda, right? Is that they think they've got this drug and you take this drug. The second issue is, and this is the second barrier to them maybe speaking out, even the ones that do realize there may be an issue, they would be very reluctant to go against what their peers and what the guidelines are telling them because they know that that is gonna be potentially threatening to their career. And I say this as someone, as an example of being in this space for almost 15 years. As soon as I wrote in the BMJ in 2013 that saturated fat doesn't cause heart disease, we've overestimated, I didn't say completely overestimated cholesterol as a risk factor. We've overmedicated people on statins, right? We should be pushing low-carb diets, right? Hit all those in one 800, you know, commentary piece that got peer-reviewed and press released. Became a big news story. I've had relentless threats to my career ever since then. I've lost 3 jobs. I went, I carried on with the campaigning, but that was what happens. So you've got people, one, that don't understand it. Two, if they do understand it, are they going to speak out? So, but listen, the truth is the truth. And incrementally over time, this ripple effect, and the more and more of this sort of research that gets out there, and the more advocates we have, Nick, powerful advocates like yourself, like Dave Feldman, right? Like others like Malcolm Kendrick in the space and Ofer Ravskov. The more people that speak out and articulate this with the scientific evidence, as you say, the harder it's going to be for them to maintain this, this false paradigm.

Yeah, I mean, I'm reassured, like, I don't need everybody to agree with me, but I think there is this idea that all of mainstream medicine and all like clinicians are pushing forward one particular narrative. And I can tell you, and I'm sure you could tell my audience, like on the back end, like when I go around and talk to my peers at HMS, Harvard Medical School, and like residents and talk to them about the research, they're not like, oh no, everybody needs a statin. They're like, oh, this is interesting. Like, I want to learn more. So when you kind of like remove the filter of social media, I think a lot of people are generally curious and open-minded because most people just want to help their patients.

Nick, you're right. But I think that's a very good point. And I find the same happens when I give talks and lectures to doctors, usually primary care physicians or non-cardiologists, very open-minded and they find it interesting. Not necessarily the same with cardiologists, but it's a bit—

yeah, you would know better than me on that. All right. My next question for you is, do you think you can reverse heart disease? And I want to frame this in the context of in our paper, we had 6 people, despite their extremely high LDL, have a decrease in total plaque score and one with a decrease in non-calcified plaque volume as measured by the CCTA. Now, even though 6 out of 100 or 1 out of 100 is not, you know, a high percentage, the fact that potentially we could have regression of plaque despite those levels, do you think that could be generalizable given underlying physiology? And do you think you can reverse heart disease?

Absolutely, yes. And I'll tell you that not even that we can, we know it happens. So the question is, what is the best— what is the mechanism? Or what are the mechanisms of how it happens and what is the best management plan in general for people and obviously context dependent. So the first thing to say is if you start from an understanding, and people can look up this paper in 2017, I'm sure you're aware of it. Saturated fat does not clog the arteries. Heart disease is a chronic inflammatory condition that can be improved by lifestyle changes, right? So that was me, Rita Redberg, Pascal Meyer, BMJ, British Journal of Sports Medicine. So if you start from the understanding that the best explanation for heart disease is insulin resistance combined with chronic inflammation, right? Then of course, theoretically, anything you do to combat insulin resistance and chronic inflammation will at the very least stop the progression of heart disease, but also potentially reverse it, understanding that it's a dynamic process. We were led to believe for many, many years that it was a gradual accumulation of plaque over time and it was fixed and it would just increase. But we now know that isn't true. The best data I've seen, but also the angiograms I've seen with my own eyes, Nick, was in India. A cardiologist, cardiologist called Satish Gupta, he did a study called the Mount Abu Open Heart Trial, which was essentially a single-center prospective observational study where he took Several hundred patients. Okay, this is really interesting. I mean, this is, it's mind-blowing actually. What he did and what I saw myself and what were in his results is mind-blowing. So he took several hundred patients who had at least moderate to severe obstructive coronary artery disease. That means the stenosis was at least 50 to 70%. Okay, they were high risk. For whatever reason, they didn't want to have a bypass or a stent. They wanted to manage through alternative means. He put them through a healthy lifestyle program. Okay, you ready for it? Low fat, high fiber, 50 grams a day vegetarian diet, 2 30-minute brisk walks a day, and something called Raj Yoga meditation for 40 minutes a day. Okay. And he put them on this lifestyle plan, and then he repeated their angiograms 2 years later, like gold standard coronary invasive angiogram, right? Completed their angiograms 2 years later. On an average, the reduction in the stenosis was about 18 to 20%. So 70 became 50, 50 became 30, for example, which is huge, huge change in the plaque, right? And of course, events were reduced as well. And then he did his own analysis of what was it, what was the independent factor or factors behind reversal? And it wasn't the diet, it wasn't the exercise. The only independent factor for reversal was actually the meditation, 40 minutes of meditation a day. Is there an explanation for this? Yes, we know that chronic stress as an attributable risk for heart disease is now thought to be equivalent to smoking 20 cigarettes a day or being diabetic or hypertensive. And we know the mechanism through chronic inflammation and through increasing clotting factors. So potentially that was what— so the reason why this is fascinating is I think all these things played a role. And my personal view is, and this is my hypothesis, that if one was to pick a diet that is likely to be the most effective for insulin resistance and chronic inflammation, it's going to be a low-carb or ketogenic diet with anti-inflammatory components in the food. And I'm very happy for people to contradict this or find a better way. But at the moment, I seem to think, looking at the literature, as a general default, a low-carb or ketogenic Mediterranean diet seems to be, in my view, the best dietary approach for this. So that needs to be then tested. But I think that the other component is stress reduction. And I'd be curious, of course, I don't know if whether it's something you can look into, is that the patients, your participants in your particular study. Yeah. I'm wondering what else they were doing other than the diet in terms of lifestyle.

I mean, I think for the most part the population tends to be pretty active, but we don't have, to my awareness, like detailed lifestyle assessments.

Yeah.

So it would be interesting to take a survey of that small population, which we could do post hoc, those 6 people, and see if they were doing anything that made them stand out. But just to kind of summarize your last point, when, you know, another way to frame this is when we're learning, you know, in our first year at Harvard Med about risk factors for cardiovascular disease, really you're saying maybe they should have on their bullet points, all right, LDL, ApoB, insulin resistance in the medical school itself. Yeah, I don't know. Probably I joke about it, but I mean, you, you can probably empathize. One of the worst hits I've taken to my health has been as a function of medical training, which I'm not even a medical resident right now. I'm finishing up my 4th year of medical school, but it is just ironic that the training load almost requires you to martyr yourself in terms of your lifestyle. And yeah, the reason I raise that is because I think it can create an underlying bias about the value of lifestyle and medicine when you can't live it yourself just because of the training that's required.

Very true, very true. And that's actually something that still exists, um, within medicine. You know, I remember during the pandemic, uh, when the whole thing was happening with COVID and there was data coming out and it looked pretty consistent that poor metabolic health was also a risk factor for poor COVID outcomes. That was then proven later on. For example, you had hypertension, you were 34 more times more likely to be hospitalized or die from COVID than if you were metabolically healthy, right? Yeah. So, and you look at— then diabetes, obesity, all those things. And I remember there was a situation in the middle of the pandemic, early 2020 or mid-2020, where one of the teaching hospitals in the UK— I don't know if you remember this, it was a big social media thing, BMJ even wrote about it— one of the teaching hospitals in the UK were very proud to announce that they were getting free Krispy Kreme donuts, like 1,000 Krispy Kreme donuts for the staff. Now, the point is it's not just that, and I obviously objected to it, and I, you know, I made a fuss on social media. There was a huge you know, back and forth backlash, you know, lots of people joining in. And one of the things that was really interesting to observe is a lot of these doctors who found it funny that I was saying that why this is not setting a good example in the middle of the BC epidemic, but also you're probably going to make the risk, your risk of COVID outcomes worse if you are. And we actually do have data showing that the people that had very high glucose levels with type 2, for example, or even non-diabetics who came to hospital with high glucose had worse outcomes. So There's definitely some evidence for that, but in general, it wasn't sending a good message. People were responding like jokingly, like as if diet had no— they were being very explicit. I mean, I'm talking about people who are diabetologists and endocrinologists. They're thinking that diet has no role to play in disease or very little role to play in disease. I mean, that is the mindset. That's what we're up against.

No, no, no free Krispy Kremes to incentivize immunization. It's like Setting aside your opinion on social distancing, whatever, the pathophysiology is clear. The risk factors are clear. Poor glycemic control, insulin resistance, diabetes are high risk factors for poor outcomes. The fact that you would incentivize people to get an immunization by giving away free donuts, it's such a dysfunctional— like, it's— I don't see how people can see that and think that that's okay. So what we would need obviously is like a cultural shift where everybody sees that every healthcare practitioner sees and is like, this is not appropriate. It, it just not. But speaking about junk food, I wanted to ask your opinion on this in case you hadn't heard of it. You know, let me frame this as you are a firebrand of sorts. You've definitely gotten your name out there. Don't have trouble putting your opinions out there, which I think is great as, as a general point. I, I am new to the scene, new to the social media scene. I've only been putting effort into social media for about like a year and a bit. And my emergence was we were doing this research. This is now our like 11th paper on this topic, but people weren't talking about it. They're like, where's the data? I'm like, I've shown you like 12 times the meta-analysis of RCTs and that we've done on this particular topic. Like you are ignoring entirely. So I wanted to force a conversation. So do you know what I did at the beginning of 2024?

Is this to the Oreo cookies? Yes. Yeah, tell me a little bit more about that, because I remember just— I, I superficially saw, saw the— what was happening, but it was fascinating.

I was just like, look, first of all, I don't have many resources at the time. I was like a 27-year-old, you know, medical student. But I'm like, but I really want to force this conversation. How can I do it? So I'm like, all right, what do I have? I have brands, an Oxford PhD, I have a Harvard Medical School, and I have social media. I'm not big on social media, but can I design an experiment that is so provocative everyone will have to talk about it? And so based on my understanding of the lipid energy model, which is the idea behind the lean mass hyperresponders, this population of people, low carb, high LDL, the leaner you are, the higher your LDL. That is a graphic of the mechanism. We have paper that I'll post in the video notes. Put that aside. The physiology, as I understood it, would predict that I could reverse my high LDL by just adding carbs to my diet. It didn't have to be a swap. It could be a pure addition of carbs. It could be any carbs too. So I'm like, what is the most viral-worthy source of carbohydrates? And I'm like, I think Oreo cookies. I can't think of something that's like, has a better brand for just being delicious, unhealthy than Oreo cookies. So I designed a crossover experiment where I eat My baseline diet, I'd lock it in for 2 weeks, get lipid tests, then eat Oreo cookies for about 2 weeks. The dose was 12 cookies per day, which is about 100 grams of carbs. Add it to my diet. Diet was locked in. This was not a swap. Then do a washout period to reset and go on 20 milligrams of Crestor for 6 weeks. The statin phase was longer because I wanted to give it, you know, a fair shot. And I went for the gorilla dose of 20 milligrams. I will also note the senior author on the paper is a two-author paper, me and Professor William Cromwell. I don't know if you know him, but he's a lipidologist, over 30 years experience. I chose him because he's very open-minded, but he's also has relationships to people that are relevant in the space. He trained Thomas Dayspring in lipids, who's obviously very close to Peter Attia. So anyway, he gave me input on how to design it. That's how we decided on the 20 milligrams of Crestor for 6 weeks anyway. I executed on the study and the punchline was the Oreo cookies were twice as powerful as the statin at reducing my LDL. The Oreo cookies dropped my LDL by 71% from 384 to 111 in 16 days. The reason it was 16 days, not exactly 2 weeks, 14 days, is because the drop was so dramatic at 14 days and we were doing weekly tests. So that was only the second.

What was actually, what was the mechanism of the drop? I'm curious because the diet, because in general, like high sugar, high carb diets will give you high small dense LDL that increases LDL. So how come it dropped? I'm curious what was actually dropped it.

Our understanding of the physiology of these matters—

Do you see the oil wonders?

No, no, no. So when you go low carb and you're very lean, you release more free fatty acids even than someone with obesity or diabetes. And the spillover of the fatty acids goes to the liver and then there's recirculation whereby your liver exports more large VLDL.

Right, right, right.

And then there's a really rapid turnover of the VLDL So your baseline starting LDL was actually quite high compared to most people? Yes, on a ketogenic diet. Although I will note, when I eat a standard American diet before I went keto, my LDL is about 90. Like, my LDL at baseline on a—

And what was it only on keto? So are you a lean mass hyper-responder then yourself?

Yes. So my LDL fluctuates between 250 and 566.

Okay, that makes sense. Okay, now I understand. Now it makes sense.

I want to move on because I want to be respectful of your time. My final questions for you. One—

Nick, one quick question though before you answer. Sorry, we can put this in. What happened to your triglycerides and HDL when you ate the Oreo cookies?

So that's really interesting. HDL, because of— it's complicated and I know you have like 2 minutes left, so I'll skip over that— was stable. I think over time if I continued, it would've dropped. That's the prediction. Yeah. The triglycerides went— were stable or went down. Most people wouldn't think our model predicts that, but it actually does. Because in the acute setting, 2 weeks, I remained insulin sensitive. You don't get metabolic syndrome in 2 weeks. What happened was the relative hyperinsulinemia while being insulin sensitive was probably triggering my lipoprotein lipase to be more active. So the fat had been cleared out of my blood from the diet when I did a fasting test. So what's going to happen is the lipoprotein lipase is going to pull extra triglycerides out of the VLDL.

So I would—

my triglycerides go down and they did.

Over the longer term, it would've gone up though, obviously. Yeah.

As I accumulated like fat in my liver became insulin resistant, but it was all predictive with the model. Now I, I generally rail against short-term studies, but short-term studies can be useful when you're testing dynamic systems, which is what this is. Okay.

Yeah. Great. Go on.

I want to jump into a couple more questions. One, you are good friends with RFK Jr. Do you, one, think he'll see this paper, listen to this conversation, And if he does, what do you predict his reaction will be?

Listen, I think first of all, he's obviously an extremely busy man doing lots of stuff at the moment, really important things. Um, given the fact that I am closely aligned with him and, uh, I can communicate with him on a regular basis, part of this will definitely be part of the bigger picture. I'm sure he will come across, um, his, uh, you know, uh, he will be aware of it. For sure. We'll make sure that happens. And in general, and with a, with, with a broader perspective, also looking at shifting our current approach to preventing and managing heart disease, for sure. And this is 100% part of the story.

Excellent. And with my last question I want to ask, is there anything I should have asked you that I haven't? Anything you want to say to my audience?

No, I think people just need to be— keep an open mind and realize that— and have a think about how they receive medical information and the fact that most stories in the mainstream media do not actually fulfill criteria for accuracy, especially if they are sponsored by very powerful vested interests. So I think, yeah, just keep an open mind. That's all I would say.

Fantastic. Well, thank you so much for your time. To my audience, links to the papers and associated videos are going to be down below with more information. Thanks so much for taking the time, and I look forward to this hitting the news streams tomorrow.

Awesome.

Thanks so much.