Nick Norwitz Has Total Cholesterol of 700 — So Why Zero Plaque? – TFP #030 | Nick Norwitz MD PhD

I just want to point out my dad had 99% occlusion of his L when he was 44 and I have an LP delay near 200.

Right. So by all accounts, by all accounts, I should be a walking corpse.

So plot twist three is I have been running a natural experiment for 7 years with a cholesterol of 700, LDL 500s to see does this cause plaque accumulation in my arteries, and there's going to be objective data that I can't fake. So that's going to be plot twist three.

That is actually a dangerous perspective because you can overmedicate people, and I think that's happening. My opinion, I would happily debate it with Peter.

Well, part of the challenge, and I was just chatting with a mutual friend of ours a little before this podcast started. Part of the challenge is that there's not as much of a proactive interest in studying folks who are metabolically healthy with high levels of LDL.

Because I think the democratization of information is the death knell of a paternalistic medical system. And in their death throes, there are certain, let's call it a minority to be generous, paternalistic doctors who adhere to that old model who, in defense of the paternalistic medical system, just get more arrogant and paternalistic, which is just accelerating their own demise in irrelevance. That's my hot take.

So I don't care what somebody says about a note. I've did a blinded crossover trial on myself. This clearly impacted me. Oh, also my creatine kinase has been up on statins, too. So, there's an objective biomarker of muscle damage.

Hi, everyone. Coincidentally, just as I was about to release this podcast, I had to insert this because we just published a paper. It's a very special paper. It's entitled "Seven Years of LDL Cholesterol Above 700 Milligrams Per Deciliter Without Coronary Atherosclerosis." I call it special because the subject of the paper is our guest in this podcast, my very good friend and co-author, Nick Noritz, who has been living with extraordinary high LDL cholesterol and recently underwent a 7-year follow-up coronary CT angiography. The results are no detectable levels of plaque, soft or calcified. Definitely check out the paper and share it on social media.

Also, Nick just returned from Oxford University where he lectured on lean mass hypersponders, and he informed me that the talk went extremely well and it was received, uh, very positively by the academic community. So, we'll have much more to say on that in time, but I'm just very excited to report that lean mass hypersponder research is increasingly entering the mainstream scientific conversation in a very positive way.

So, without further ado, tell me who you are and what you do.

Oh, wow. You know, it's funny. You think I'd have an answer to this question. I actually get this question all the time from my friends and family, and I don't have an answer yet. Sometimes I say entrepreneur. Sometimes I say metabolic health educator. There's so many things up in the air.

Um, among other things.

Mhm. I'm a close friend of Dave Elvin. I'm guessing everybody listening probably knows who so I am. But, um, uh, how would you describe what I do? Gosh.

I don't even know. I mean, certainly I would say, uh, an entrepreneur and science communicator if I had to keep it down to a few words. But you're exactly right. You, you, you have so many things going on. But definitely you have stepped full-time into science communication, and, uh, if I may say, you're killing it.

I'm having a fun time. I'm in, maybe this is a good time to, I haven't sat down and done an audit with someone of like my past year in my life because, um, I mean, listening, people listening might know this, so I apologize if it's redundant, but like from my earliest memory, I have thought about a very conventional path in science and medicine. For those who don't know, like it was my path, you could say set for me, not beginning in like college when I was premed, but from my earliest living memories. For context, both my parents were MD/PhDs. Um, my dad now has an MBA. My parents have like affiliations with all the top universities in the world. But this is what we talked about at the dinner table was science and medicine. I was playing around with five-syllable words when I was like five. Um, and then as I grew up, it was the default. So, it's something that I thought about from middle school through high school through college through my PhD through med school. Um, and I'm 30 now, and a year ago was graduating med school, which was supposed to be the jumping-off point of like really starting a career in academic medicine. And I put all the, you know, blood, sweat, and tear equity into that path, and at the last moment, I'm like, you know, maybe this isn't for me. And I kind of, I guess, took a leap at the end of May in 2025, which is less than a year ago now, to explore this brave new world that we're in with respect to a lot of opportunities ahead of me, um, or open to me with respect to research, with respect to business building, with respect to teaching. Um, the last year's gone by in a blur, but it's been a blast.

Yeah. When you say this maybe this wasn't for me, I mean, you're still very much entrenched in medical research, in medicine, and discussion on patients and efficacy and so forth. What do you mean specifically?

Yeah. I mean, if I'm being completely vulnerable, um, when you grow up in the culture in which I grew up, and then you're going to school with like everybody around you who holds medicine as the highest ideal, you do idolize it. And there's this idea that there's nothing nobler than to be a healthcare worker, to be a physician, and like serve patients, and that it's a calling. It's not just a career. It's a calling. It's like the only thing you're built to do. Um, and I think the hard part about medical school for me was never feeling like I had that calling fully. Um, and not sure how to grapple with that because there's a little bit of shame involved in that, if you can imagine, right? It's the thing to do. It's like, it really is noble to the degree to which a lot of doctors will sacrifice themselves, you know, for their patients. And I saw my parents do it, like, I mean, and at least for one of my parents, like, it really was sacrificing everything, including their health, for their patients. And I see some of my friends do it. Uh, my girlfriend's a surgical resident. How hard she works is like unbelievable. And I think they can get through it because it truly is a calling. And it was hard for me to reconcile internally that like it wasn't what got me up and made me happy. I remember some very, um, vivid memories in medical school when I was like, you know, maybe rounds started at 6, I'd be up at 4:30 and like I'd have the newest Nature paper on my mind. I'm like, this is incredible. I want to like think about this Nature paper, how to communicate it to people, how to get people excited about it. And I'd have that in my mind as I went to rounds, and I'm rounding on patients, and I'd literally have, I remember this one instance, I had the paper folded up in my back pocket, and I'm doing a physical exam, um, on a kid, and I realized my mind is on that paper, and I felt so riddled with guilt because, of course, the patient in the room deserves all my attention, and I want to be the person that like, I am here with you. This is my purpose to provide care for you one-on-one. And I just found it wasn't the thing that got me up and excited in the morning.

And the more and more I thought about it, the more I came to realize, you know, medicine and science are evolving. And now in the information ecosystem, I think we're going to need people on the team of medicine who are the communicators. So I did not go down a conventional medical path. I didn't even apply to residency, which is a very conscious choice, as I could have, which means I'm never going to be, at least my my ambition is not to be a standard clinician prescribing medications, but someone who's like, I have a decent amount of background in academia, you know, even if I don't know what it's like to be a standard clinician day in and day out, I think the broader team of medicine, as the sport of medicine evolves, needs people to be like, "Look, full-time, I'm going to be reading the science and communicating it to you because clinicians do not have the time to do that." Um, so that's that's been my problem.

Like it's, I get what you're saying, and I've heard this before from other people, especially medical professionals, is that that's what they stepped into it to do. A lot of people do step into medicine to ultimately get the MD and then they've got, you know, this additional clinician perspective, right? But coming from the engineer side of things, I'm thinking, okay, the problem is it doesn't sound like it scales. You know, I'm coming from the world of, you know, watching Steve Jobs building those first Apple computers out of their garage and selling them doesn't scale, right? They could have still been doing that up until the point where it became obsolete or they ultimately find the ways in which they can, you know, mass it out a bit more. Well, in the case of science communication, do we, do we have a problem with regard to enough people knowing what they can do to improve their health outcomes so that they don't become patients, for example, or that if they are patients, that they know what steps they can take to improve their health in ways they may not have otherwise heard, even from other medical professionals? I think many people who are watching this right now would already have a strong opinion. I do. I have a strong opinion on that right now.

Yeah. I mean, there are so many levels to this. It's hard to like even put into words, let alone a few hour podcast. I could talk about this for like dozens and dozens of hours. Where do I want to go with this? We're talking about empowerment of patients, right? Empowering patients with information. There's the superficial level, which is like you go to your doctor's office, you have how much ever time you have. Maybe you have a half hour, maybe it's a long doctor's appointment, right? And you can start to talk about things to get informed on your own care, to be a participant in it. But that presumes the doctor has the knowledge, which they probably don't about a lot of things, not because they're lazy, anything from it. And on one level, it's because they don't have the time to read the literature. On the other level, it's because of the culture of medicine and the infrastructure and incentive structures that have been built up around it to spotlight some things and not others.

So, you know, my favorite example of this was the human control trial on, um, atorvastatin and GLP-1s. So, to catch people up, there was a paper that came out in a top science journal, Cell Metabolism, and it was a controlled human trial showing that, um, one of the most prescribed drugs and one of the most profitable of all time, atorvastatin, which is like lower GLP-1s in humans by a lot. Like it was a very obvious signal, and nobody knew about it. Like I went around Harvard hospitals asking cardiologists, have you heard about this? Have you heard about this? Nobody knew about it. That's not them being lazy. To some extent, I mean, I guess by definition, it's ignorant. But the question then comes up in my mind, why? Like, why didn't they know about it? It's not like it came across their desk and they're like, I don't want to see it. It was never elevated in the first place. And the reason it wasn't elevated in the first place is because of the business models and incentive structures that are like built around the medical system, which handicaps what clinicians actually know. Now, the beautiful thing about this is in the information age, with the democratization of information, the patients can find out. But how are they going to find out? And I think that's where we need people in the broader medical ecosystem to say, "Hey, I'm not going to be your your prescriber, per se. I'm going to be the person who's like, I'm going to be up to date in the literature. My incentive is to gather the most compelling, interesting information and platform it and communicate it to you. At the end of the day, you can do whatever you want. This is your health journey. Like, you make the decisions whether to listen to me, whether to listen to someone else, whether to accept your doctor's recommendation or not. But I think in a world that's moving away from a paternalistic medical system, we need people in medicine saying, 'Hey, I'm the patient empowerer, effectively.'"

Um, I think there's a, I think there may be some debate as to how much the world is moving away from a paternalistic medical system, right? I think it, I think it, here's the funny thing. Let me first ask, why do you say that?

I say that because what's one of the most common complaints you and I hear from folks? It's what they're feeling is a push by their doctor to do a particular thing. Right? Now, make no mistake, there are so many times where a patient should be listening to their doctor who's giving them very, uh, well-advised advice, right? That's that's very educated, for which they have unique insights, but is that 100% across the board? Are there times in which a doctor is perhaps pressing a patient to do something for which they themselves may not be perfectly informed? Right? Now, again, we're acknowledging doctors are humans. All medical professionals are human. But is there a degree with which there's a kind of expectation that at least some doctors, perhaps even well-meaning doctors, have toward, "Hey, this is my, this is my role to play in your life to enforce you to follow this advice that I'm going to put forward in a very strong fashion?" Right? So the reason I asked that question is because

I'm trying to say it so delicately.

There's a, there's a discrepancy between what I think medicine wants to be. Let's say medicine as dictated by the old guard wants to be, and what people will tolerate. So this is all what the, the patient is at the end of the day in charge of everything, whether they are compliant with therapy or not, whether they go to their doctor or not. So they, as a population, dictate what medicine will be. And if the expectation is the doctor is omniscient and I need to listen to the doctor, which is how it's been, then yeah, a paternalistic medical system can exist. If the expectation from the broad patient population is, "We're not going to tolerate this. Like, you are supposed to be the guide and the teacher and the partner, not like the judge, jury, and executioner," then the medical system has to change. And I think more and more patients are realizing that, yeah, it's their right to be informed, to be part of the conversation, in fact, to be driving the conversation with an informed guide. And the patient population isn't going to tolerate increasingly a paternalistic medical system. And here's where things get interesting because I think what's happening is I think the democratization of information is the death knell of a paternalistic medical system. And in their death throes, there are certain, let's call it a minority to be generous, paternalistic doctors who adhere to that old model who, in defense of the paternalistic medical system, just get more arrogant and paternalistic, which is just accelerating their own demise in irrelevance. That's my hot take. But I think that we're seeing this in real time.

No, I, I agree. Agree. I do feel like we're seeing it in real time, especially on social media. Th this this podcast, The Feldman Protocol, you know, its origin. It it goes back to what's covered in the film, The Cholesterol Code, by the way, which you should see, by the way. So, we're we're going to try to turn this around really quickly so that it gets out. But, um, definitely, uh, where we're ultimately working our way around to is not only the film, the documentary that covers our story, but particularly that covers, uh, this research that's based on. But it, it is meant to fulfill this very, it's good, it's good that we started in this arc because it's meant to get back to this kind of patient empowerment, right? Because in the film, it covers these personal stories of people who are like, "Oh my gosh, this diet, ketogenic diet for me in particular, proves to have this great benefit for this illness that I'm working with." Ah, but then there's this one thing. It's the cholesterol levels, right?

Obviously, one area for which there is some very strong opinions is what you should do about your cholesterol, particularly if it's very high. And as I think you and I do as best as we can, we try not to emphasize that we have all the answers. It's not the worst thing in the world though to say that there may not be all the answers to questions like this, which is why we do the research. I think people underestimate how comforting it is as a patient to hear those words. "We don't know." And I think I agree.

At least in prior generations of physicians, that was like a taboo thing to say. Like, you project confidence. If you don't project confidence, people aren't going to listen to you. You are knowledgeable. You are confident, and you're going to tell them what's up. But I think people also have good BS detectors. And so when you can level with someone like, "Look, you're like, this is what I learned, and you're not fitting the population and the rules that I learned. So, we're going to have to figure out something creative. And like, look, we might not get it the first time. I'm in this with you, though, and we're going to figure it out." Like, that goes a long way. And it's not said enough. It's It's tougher to have a conversation just in general as a human. It's tougher to have a conversation when somebody's seeking out advice to say, "Here's what I think. My confidence level isn't at 100%, though. Here's what I think. Here's what's, here's what my hunch is, but I'm not actually totally sure about that. Also, I would advise you to continue looking to other people, too. I continue to, I would suggest that you take more ownership of this than what I can provide you right now because it's true. Doctors are put in that position a lot. And it's not to be fair to them, it's not fair to them, right? Like that's the irony."

What do you mean it's not fair to them? It's not, it's not fair for the patient or the doctor to put the, the doctor in a role of omniscient, in in the role of somebody who does have all the answers.

Well, who's who's appointed them in that position? Because I would say historically doctors have tried to paint themselves in that position.

I think it's a little from column A and a little from column B. I think that patients do to some extent say, "I want to give you that power. I, I trust you, Nick Norwitz, to be the sole per," I mean, they they may not say it exactly the way I'm saying it right now, but they're they're going, "I just want a person who I trust to give me the one answer that I can then just kind of take and run with it. I want the cliff's notes, right?"

But is that trust default, or is it built? Again, I think it's not easy. I think we are wired, and I've talked about this a lot on the podcast before. I think we are wired to want simple answers. And we're wanting our problems to be simple, too. We like a simple problem. Oh, is there a simple answer? Oh, is it a pill? Great. Wait, are there any side effects? Oh, only rarely. Even better. Good. Good. I can finally get on to the other things that are in my life that I want to put more of my effort and concentration into. Maybe. I guess the question is, whose responsibility is it to rewrite that narrative and have people immerse in the pleasure of grappling with complexities? And this is something that I don't know if it's just how I'm wired, and and you as well. I mean, I know you well enough to know you're wired like this, or is it something that's learned to be like, this is a big problem. This is a complex thing. You can't really dumb it down, or you can only dumb it down so far. But that's cool. Like grappling with these complexities and being a little bit confused doesn't need to be an unpleasant or burdensome process. It can actually be really enjoyable. And so, how do you flip the switch in someone's mind to go from, "Please just give it to me straight, tell me what to do, I want it simple," to like, "I want to grapple with the hard problems because personalized healthcare is always going to be difficult. And I think it's ignorant to say that it can be made simple." So, how do you enjoy the process of dealing with the complexities, balancing at the same time that, look, the stakes are high, it's your health, but you can also like, in some way, parse that from the exercise of going about dealing with the problems? Maybe this is just like how I figured out how to cope with it. I mean, my background, for people who don't know, like at one point in time, I was very, very sick, and I've always been like someone who's dealt with problems by just obsessively focusing on how to fix them. And for me, that was therapeutic. Like, I would, I had a big medical problem, and I'm like, I am putting all my energy into solving this. Like, I'm reading the papers. I'm like, you know, trying to puzzle things together. On the one hand, usually I could solve the problem, and on the other, just that focus for me was like, I enjoyed the process. So I could have like.

And help me remember this. Were you, were you misdiagnosed?

Yeah, in one case, I was misdiagnosed.

Right. And so, so again, we're getting back to that that issue, right? Is the, um, something coming across confidently like, "We figured out what it is." It's a diagnosis is supposed to be that it's, here's the answer to the question, and it should be delivered in such a way that, well, this is about how much we think it's this.

Yeah. I mean, think about it as a multiple choice test. Say you're taking a multiple choice test, Dave, and you have a question, and there's like A, B, C, D, and you have to choose one, and you're just looking at the answers like, "None of these are right. None of them are right. I don't know what to say. There's not an option from all the options you're giving me that is correct." How do you answer that question? So that, like, I've been in that bucket, and you've been in that bucket. That was the start of your journey where you're like, "This thing's happened to me. Here are the possible things that it could be based on what medicine knows, and none of them are right." What do you do then?

That's the whole point is for me like.

"I don't know" needs to be an E.

I know.

You've got to be, you've got to be able to say, "This literally this happened." Um, a couple days ago, so I have a family member has a medical thing that they're dealing with. I didn't, and I was the one person that they thought, "Oh, well, they would probably know." And I literally didn't even have a good like starting point relative to other things. And, um, you know, as it turns out, it resolved itself a couple days later, but it's, I, I was comfortable just saying, "I have no idea. I have no clue."

Yeah.

So, since the last time you'd been on with what is still the record longest podcast.

Although we had this echo that ruined it.

What's? Yes. We like recorded for over six hours, right? And then there was like a, I have a very booming voice, and for whatever the acoustics, it was just like my mic was echoing.

It's why I keep, it's why I keep checking the levels so closely. I want to be sure that we don't have it again. So this will be a fun thing to to share with the audience. I'm, I'm getting ready to launch the podcast, and my intent, my intent was my intent at that time was to launch it in probably about June of last year. However, some stuff happened. We may get around to that in a moment. But I did, and was chatting with you, I did genuinely want you to actually be the first podcast that I launched with. Now, to be fair, um, I ultimately ended up launching with Cynthia Thurlo. She, I did record with her before yours, but I thought it'd be fun to have literally the first splash be, uh, Nick Norwitz. However, we had this technical issue. Indeed, as you said, you have a booming voice. It was either, by the way, we had the mics arranged, or I don't know what the thing. I'm new to podcasting. It picked up your voice, got picked up by my microphone. That's why it's going to be so embarrassing if this proved to happen again, but I'm pretty sure, I'm pretty sure by the settings that were okay. Anyway, that echo issue ended up being something where we involved, I want to say four or five different sound engineers. People were trying to work it, and at the end of the day, if you go back to that episode, I think it's the second episode, but you can hear it a little bit.

It's listenable.

It's listenable.

But also, like, it was also like happening at like a key time in our conversation, like a.

I know, I know.

Anyway.

But, um.

Live and learn, but.

I'm glad it happened with me and not someone else, you know, when you have like a technical issue with a guest, this happened to me where like, like, DCR will like die, and you're like, this is the most mortifying thing to have to tell someone. I mean, I don't care, I'm your friend, I'm just going to sit and talk with you anyway. So.

Right.

No biggie.

Well, that's the thing. If if it happened to me on a podcast, I'd be like, "Okay, it's fine." It's just that it's true. That podcast was foundational in so many respects. And that's why it was kind of cool that we could do this where. So, at the time that we're recording this, we're going to be doing a screening of Cholesterol Code in two and a half hours, I want to say.

Yeah, I know. Boston, Boston Commons, AMC.

Yeah. I used to go to that theater all the time as a kid.

Okay. It's like right on the Boston Common. So, if people know like the area, there's this big green space, very famous, and there's one theater on it. And I mean, I'm remember like going up the escalators that we're going to be going up, watching just like Shrek and stuff. So, it's going to be in the same theater. It'll be fun.

And so, the, is it a little exciting that you're about to go see yourself on the big screen? You've already seen it, but still in that theater.

Yeah. It connects. Well, also with, I mean, this is my hometown, so like people are going to be showing up, like my sister's boyfriend, my girlfriend. It's going to be a very interesting thing. I mean, also the person in the movie, I mean, in some ways I'm the same person, and in other ways I'm a very different person because it was filmed when I was.

I was a second year, I was a second year med student. Like, there are people in my life, like, I mean, the person that's probably like the biggest part of my life right now, my girlfriend, we've been together 2 and a half years, and I was thinking about this as we're going to see the movie. I'm like, all the bits from the movie are before you met me.

Yeah.

Like, we didn't even know each other then. My life has changed so much in those that time. You know the story about when I first watched the movie premiere, and there's a scene of me that I won't spoil, but I'm doing something, and everybody in the theater is like, "Oh my god, is he going to do it? Is he going to do it?" And I'm sitting there like, "Is it going to do it? Is it going to do it?" Because I don't remember. And I'm like, and then I did. I'm like, "Oh, this is mortifying. Why did I do this? This is embarrassing." But, um, it's, it's a good time capsule. But it is, it is me from a different stage in my life. I think my only social media at that point in time was Twitter, and I had like 5,000 followers, and I was like in the midst of medical school core rotations, and I'm just like, "Okay, there's this little like film. They're coming with a camera. This is kind of cool. Let me go shopping. They'll come around." And then lo and behold, what our lives have become, what this has become. I mean, it sounds like what's been, it came out the night of April 16th, and now what is it? April 28th, 29th?

20. And so it's been like 12, 13 days.

And it's blowing up.

It's so, it's exceeding, genuinely exceeding, exceeding all of my expectations, exceeding all of my expectations. Uh, ironically, except for one. I was trying to rally a lot of interest around it, get a lot of people excited. Uh, obviously, it's very, it's very advantageous if people leave their honest review because, as I was hoping, most people's honest review has been on the positive side. However, um, the aggregator thinks we're the victims of our own success. My intent was for it to be so popular that Amazon would then take it and make it part of their major catalog so it'd be available to watch for free.

It is in the UK, right?

It is in the UK.

And it's number six in.

Oh, that's right. It's gotten to number six, at least last week.

And what? That's not overall, is it?

Over. Well.

In movies and documentaries.

In documentaries. I, I'm not sure if it's overall movies, but.

I was like, you can't, that's not possible for an academic. But six in documentaries is nuts, on Amazon Prime in the UK.

Because that's up against multi-million dollar super documentaries, right? Like it's crazy.

It, but it is really, like, I will say that's not like a, a luck shot. Like, it's that good. Yeah, that's, well, that was that's part of what I was saying to the team is after all, after after it's all said and done, if you just have really good content that carries the day, it always will, right? You, you and I are big MCU fans.

Not to take this into a totally different direction, but I am bringing it around to the quality of the content.

MCU all through the Infinity War saga. Pretty solid. The worst of the movies might have been like Thor 2, right?

I was going to say Thor 2: The Dark World, definitely.

Oh boy, don't even bring up Thor since the Infinity War.

Ragnarok was good, and then Taika.

Ragnarok was.

Love and Thunder, and I was, it was a sad moment.

Yeah.

You can't take a movie with Chris Hemsworth and Christian Bale.

I know.

And Christian Bale. Okay, sidebar. Sorry, everybody. That movie where they have Christian Bale, who played Batman, and a bunch of other amazing characters, playing Gorr the God Butcher. Literally, if you don't know his name, it's Gorr the God Butcher, and he's supposed to be an ultra baddy. At no time do you see him butcher one god.

You, the whole movie.

Except for the origin, except for when the first.

Uh, no, you don't even see it on, you don't even see it on, um, on film. You just see like a cutaway, and then a head roll.

Nothing. I'm like, oh, come on. Anyway. All right.

Anyway, anyway. So, no, wait. The film itself, Cholesterol Code.

And again, I'm, I'm just passing a bunch of the accolades on to Jen Eisenhard and Tim Hadzor.

You were one of the writers.

Yeah, but I mean, my my writing, I'll take a lot of credit with regard to the technical. Pretty much a lot of what Jen was writing was based on what she's seen me discuss. So, it's almost like having a super ghostwriter, per se.

And that a lot of my narration is a lot of her making a, you, you know me. I like a long-form podcast so that I can be long-form.

Yeah.

How do you get something to be nice and tight and concise to the way that that movie takes it? You have Jen Eisenheart writing your words. Now, the technical, that's where we had to put in a lot of work because it took a lot of back and forth and a lot of trying to figure out how we could show things graphically that are just enough but not too much, because you can lose an audience real quick. I just, um, I just watched a, um, somebody had sent me a video. Doesn't have a lot of views, and don't need to go into it too much, but sure enough, it was one that was critiquing, but from the other side of the fence. There's somebody who's very pro keto, pro carnivore. They're going, "You're going to lose credibility by not getting into the Randall cycle and getting into the thyroid and so forth." And I'm like, "No, I'm going to lose the whole audience."

We, we cannot put a scientific lecture into a movie. We're going to lose everyone.

It was very, very like, I, of all the people who want the deep science, I'm going to be like, in my heart, watching it with that lens, even if I know the practicality. And I was like, pretty satisfied. I wasn't like, this misrepresented the science in a grossly simplistic way, and at the same time, I'm like, I know that I can recommend this to like, some cousin.

And they're going to watch it, not having any interest in cholesterol, be like, "Damn, this was an enjoyable watch. I like this. I was moved." And like, that is an amazing line that, uh, Jen and you and the team walked.

For context, I did nothing. I got, I showed up and got filmed.

For a couple days. Everybody's like, "Nick, you're in a movie." Like, I remember it was, I remember there was a moment where I'm like, "Oh, this is big." When Adrian was coming up and they sent out a film crew so that you, they could film you, me, and Adrian having one meal, and they set everything up. I'm like, "You sent out a film crew so we could have lunch together because we're going to have lunch anyway." And that's just the level of production and commitment and then taking hundreds and hundreds of hours of stuff and making it into an hour 44 minute, I think.

Yeah. There's so much that's left on the cutting room floor. But it, it, that that lunch was actually quite amazing. That some of the best lines in the movie come from that lunch from the.

Science frat.

Yeah.

The hazing process wasn't over.

It continued for many years to come.

Yeah.

We're still continuing.

It. Uh, anyway, yes, obligatory pitch. If you haven't already, don't be the last person on the block to to watch a movie. What are the best ways that people, by the way, I was not asked to ask this, can like support it? Like, where specifically do they go? I know there's like technicalities like IMDb and like.

Yeah.

Like, what is the the thing to do?

Yeah, it's true. Actually, there's so there's watching it on Amazon if they want to take a moment to go to the web.

It's very easy to, you know, give it a rating, give it a review. Again, an honest one. But also, there's IMDb, for example. They, a lot of people look there for ratings. And I think we're actually, I mean, I, I don't want to get ahead of myself, but it's looking pretty good over on IMDb at the moment. But as always, you know, honest review, if you're hearing anything from me here, it helps to, it helps the film for people to be genuine and honest. It, it would, it would look weird. It would look strange if it was just like 100%, you know, practically copy-paste statements or something like that. I want people to share what they really felt, good and bad, all together.

I mean, overall, I was reading some of the reviews, they're all, I mean, they're vast majority, like 98% were five-star reviews.

And a lot of, like, they're all glowing, but they're all diverse. Like, they're all honest reviews.

Yeah. It was funny, I was on, um, Dr. Bosa's channel yesterday live, and I thought there was like some cons, she had some concern about like reviews not getting posted. So, she's like telling her audience, and I want to go caution people, guys. She's like, "Don't write a too good review because then it will be like flagged as fake and get suppressed." Like, "Wait, wait, no, no. You can write a nice review. It should be honest, but like, I think it's probably just a lag time when they get posted." I'm like, "You don't need to make it like a mediocre review to get posted. Just be clear."

Yeah. Just broadly.

Whatever's in your heart, write that, right?

Unless it's black. So the other part that I want to come around to is the, something happened this week which was kind of fascinating. There was an article that was released by, uh, it was on Peter's channel, but it was written by Thomas Daypring and the research team, and also Peter Attia.

Yeah.

Which was kind of a giant treatise of.

Just a larger broad attack on our research on the lean mass hyperresponder phenotype. And, uh, I think was interested in The Cholesterol Code because.

It was all about The Cholesterol Code.

Yeah. Because in, in effect, there's it's an interesting circumstance that we're in where the research is garnering enough attention that almost everyone's talking about it, seemingly almost reluctantly, right? Where I have a different take.

I think Peter like is very happy to have this moment.

Because I think it.

I think it's a a topic of relevance where maybe in a trying time for certain individuals, they can garner points. Uh, fair enough. And but to to that extent, I am appreciating the fact that it's it's bucketing it a number of points that I've wanted to address. Anyway, we're now, we're now at a point where we have the preprint of the the paper up, which it's under submission right now, and the film has been released. So now we can have much more in-depth conversations. And my hope is more things like this. I would love for people who have these kinds of critiques to sit down like we're doing right now and show up to discuss it.

So I, I want to get on that point because I think whether it's Peter writing about us or us responding to Peter, there's a tendency to have it come off as like siloed and snippy. So I, before we even get into some of the points, and I will have some things to say, and I think you will as well. What I want people to reflect on is rather than saying who is right and wrong, like ask the question, well, who is willing to just have an authentic open conversation about it?

Right.

Because we always have been. And so I think it's very conspicuous when someone like dodges and avoids collaboration and communication at every turn. I've even communicated with Peter about having him be an author on LMHR related things in the past. I can give some more detail on that that I feel happy to. Um, I just want people to think about in that in the abstract, and even like set aside cholesterol, just in scientific discourse where there are two differing points of like points of view, you know, the data are relevant, but also like, I think it is a telltale sign about like, if one side's being like, "Hey, anytime, anywhere, live, recorded, whatever, let's just have a conversation openly, non-defensively," and the other side is just going to be like, "Let me make some points and then like, go away. I don't want to talk to you." And then it's extra conspicuous when there's levels of hypocrisy, like behind the scenes, they're saying that they're not informed enough on this topic to comment, which Peter did via Bob Kaplan when I asked him about the Journal of Clinical Epidemiology editorial. Again, we can get into that. Um, or would they just make errors in physiology that they don't own up to? The first one that came to my radar was from your 2018 podcast with Peter,

where he makes an error, um, around, um, LDL receptors on the endothelium. And the interesting thing about that is not the mistake. Anybody can make a mistake, but the confidence with which he made the mistake, and then the audacity to do like an autopsy on that interview and fact-check it, but not correct his own errors when that was not only just like a little slip of the tongue, but that derailed the conversation down a whole different track. I've seen people on Twitter use Grok and Chat GPT to say, "How would this conversation have played out if Peter had corrected his error in the moment or not made that error?" It would have been a different discussion. So, it's just like, who's being authentic and is actually like, really trying to grapple with these ideas? And we can go piece by piece with Peter's, um, attempted rebuttal, but I think it was just sadly misinformed and very clear that he didn't want to engage with the ideas or present anything else as an alternative to explain the phenomenon we're seeing. I'm honestly, and, and I've chatted with our mutual friend Austin Ditzky about this quite a bit. I'm kind of happy for there to be not just this article, but also the way by which it's framing a lot of the common arguments that come up at the same time. So, in a way, it's, it's kind of like a, almost a checklist of the common things people like to say. So, for example, the, I, I try to say this in a way that's meant to be, um, in an effort towards nuance, that there may be a lipid hypothesis, as in higher LDL causes, in a dose-dependent response, higher and higher atherosclerosis. There may be a version of the lipid hypothesis that's not that simple that does allow for greater nuance. And that's my attempt towards saying, if you don't put yourself in a position of having to defend only the most simplistic version, then there's probably a much more defensible position. Now, I'm not going to steal man that in the moment. What I will say is it is going to be difficult to defend just the simplistic version of the lipid hypothesis that it is the central driver, if indeed we find that lean mass hyperresponders, and more and more of our research continues to show that there's no association with LDL or ApoB and the progression of atherosclerosis. And that's not only what this article got into, but that's a lot of what the back and forth online has been about, particularly since this study started.

Yeah, I keep on saying this. I don't know if your audience has heard it. They probably have. So, I apologize if I sound like a broken record, but I think the most abused term in cardiology that Peter himself, I think, abuses is causality. Because there's this idea, we say central driver, that like it often comes back to this idea of causality where LDL, or more correctly, ApoB, um, containing lipoproteins are causal in atherosclerosis. And there's a legitimate argument to be made there where there are necessary dominoes in the causal cascade. In that sense, they are causal. And that gets conflated with the idea of important. And those two things could not be more different. In fact, I found it hilarious when I listened back to your, um, podcast with Peter from 2018, where he tries to explain necessary, sufficient, and causal. And he uses oxygen and fire. Oxygen being necessary and causal for, uh, for fire being atherosclerosis. You understand the irony of that analogy? Because then if you apply the layer in the whole idea.

Of well, lower is better to lower risk. Yes, lower oxygen, all else being equal, is better for risk of fire. So if we lower the oxygen in my environment to zero, my risk of my lungs spontaneously busting into flames from me breathing would be technically reduced. I'd also suffocate and die. Right?

So oxygen can be causal. It doesn't mean you want to eliminate the variable. And you can go through all those examples. And I know it's an extreme analogy, but it's an analogy that makes an accurate point, which is you can say LDL is part of the causal cascade. And also say it should not take up all the oxygen in the room. Pardon mixing metaphors, nor that it is necessary or even responsible to treat when it's high in all circumstances without any additional nuance needed. That is actually a dangerous perspective because you can overmedicate people and I think that's happening. My opinion, I would happily debate it with Peter.

Well, part of the challenge, and I was just chatting with a mutual friend of ours a little before this podcast started. Part of the challenge is that there's not as much of a proactive interest in studying folks who are metabolically healthy with high levels of LDL. You know what I'm gonna... People who are just listening can't see how my my face just like went into this like Grinch-est grin. You know that like like a meme where like that's ear to ear. You know what I'm thinking about, right? So there there's a commentary yesterday. I had a thread, um, which was actually ironically about me taking lipid-lowering medications, in this case, not statin. We can get into that, um, because people will be surprised. I'm not all that dogmatic on not lowering LDL. Put that aside. They commented that my argument that statins don't have as much benefit in metabolically healthy people was weak because, I think the phrasing was, "being metabolically healthy isn't a stable state, and those people who are metabolically healthy can develop obesity and diabetes." Therefore, the implication was, "You should treat the metabolically healthy person with a statin in case they develop diabetes and obesity later."

And then you and I came to the same like analogy, which is immediately like, "Will you treat people who are perfectly healthy with chemotherapy in case they get cancer?" Like, obviously not. But the mental acrobatics people go through. Because I do want to insert this, because it is true, all of us, just pure nature, you have some amount of cancerous cells inside your body. Now, whether or not it actually metastasizes in a way that's even detectable or becomes problematic is a whole another topic. But in theory, you could have prophylactic chemotherapy, right? You could have just a little bit of chemo just to help keep it down, right? But to your larger point, you you cannot start with the assumption that the benefit outweighs the costs, particularly if you're not studying the population in question. You can't just extrapolate from all of these studies that we do for folks that may have... I mean, there may be a stronger case that can be made for a certain population to have benefit from a certain intervention, a certain drug, but why then do you just immediately assume that it can be extended out to everyone else?

And there are like huge signals here that are really relevant to population health. We respect it. We'll just focus on statins as an example that like, you be a... I am astonished that they don't get taught in medical school. I'll give you an example. So, we already went through the GLP-1 statin example. Like, I'm like, "Okay, that's weird." Here's another one. Statins tend to harm women more than men. Now, for one of the most prescribed drugs on the planet, and women being half the population, I'd be like, "I feel like something about that is relevant to teach training doctors, maybe." And it never even gets brought up. But there's a higher risk of muscle pain and damage and new onset diabetes, uh, in women treated with statins.

Now, the reason this is so interesting is not just as an abstract point, but once you understand the physiology, you can actually go like, "There are ways to attenuate the risk." So, if you'll indulge me in in like a quick extra scientific diatribe. The mechanism appears to have to do... I think it was a Nature Communications paper. I'm going to send you the link to put in the the show notes, but with, um, X chromosome dosage. So, as people might know, women have two X chromosomes, men have one X chromosome and a dinky little Y chromosome. And generally, what happens is, women have that extra extra chromosome and a lot of the genes get suppressed. Um, it's called X inactivation, but not all the genes do, which means about 15 or 20% of genes on the X chromosome, women have a higher dose of those genes and those gene products than men. And in this particular case, what it appears is there's one gene that has to do with omega-3 fatty acid synthesis. And the way the higher gene dose in women interacts with statins actually leads to a suppression of omega-3, in particular DHA levels, in women. And you end up finding in women who have statin-induced increases in blood sugar, there's an inverse association between how much DHA, the omega-3, drops and how much blood sugar goes up.

And where I'm getting with this is, even if we say, "You know, said woman needs to be on a statin," understanding this physiology means, "Well, there's a solution. Just give her a fish oil pill and you can improve her blood sugar." In preclinical models, this works. Like, they they model it out in animals. Now, if somebody's asking, "Why hasn't the definitive randomized control trial been done?" I'm like, "Well, yeah, why hasn't it been done? It freaking should be done. You could help tens of millions of people." So the fact that it hasn't been done is an abomination and a reflection of what our priority system is and what our incentive structures are in terms of uplifting and pursuing knowledge to help people. The compass of medicine does not point towards the patient, and we need to find a way to realign that, which is why I think public education is so important. But I think that example is like really striking because it's, "Why is it an offense to bring up data like those?" They seem so medically relevant, and as soon as you bring them up, people like, "Well, you're fear-mongering around statins." I'm like, "No, this is really, really relevant information. Why is it scary to you?"

I I know what the typical answer is. I know because you're on the same online space that I am.

They're going to say, "Yes, sometimes there's side effects, right? But it's very rare. You could look to the CT meta-analyses, which will insist that it's extremely, extremely rare for there to be side effects." And the common refrain is, and this is me trying to steal man their position, common refrain is, "And if there are side effects, then, you know, you could... there's multiple kinds of statins, right? You just go, you switch to a different statin, or you take a drug that handles those particular side effects." I don't even think that warrants a response because also that's not how like that's not how it's actually executed. Generally, if this this happens, people are just like more or less brushed under the rug.

Well, this this this gets around to another thing that I do get a bit vocal on myself, which is that there's there's also this push toward, uh, emphasizing the nocebo effect, which...

You know what I just... About that.

Yeah. I Yes, because we're going to the same place. It's in our minds. But I'll concede something, which is that, you know, that I'm very careful about trying to avoid any discussion on treatment because I re... genuinely, I really do believe it's my job to get the research or to talk about the research and not get involved in, um, you know, when people want to ask about what they should do, or, you know, that's between you and your doctor. I will... I will say, though, that I really dislike, really vehemently dislike, the suggestion, even the discussion of this concept of the nocebo effect, because of the fact that, I mean, it's literally the definition of gaslighting, right? Is this... this is probably in your head. I don't feel like that should be something that that is assumed ever, and it's a frustration of mine that this could be. And and unfortunately, I think the reason this maybe activates me a bit more is I've also had a family member for which this was kind of pushed on that person, and they were... they they don't read the literature. They're not talking to the internet. They literally take every pill prescribed to them. And then when they were feeling these effects, it wasn't even something that they thought of the statin first. They actually thought it was other things first, and then eventually came around to the statin, and then only after discontinuing use with the statin figured out that that's what it is. Now, again, I want to be fair and say, I'm sure the the doctor would say, "Well, there's other things you could have taken." But the problem was is that's not what they were told initially.

Right. What they were told initially is, "You're probably just listening to, you know, the fearmongers online and that kind of stuff." And then they showed him a a paper that basically is trying to emphasize this case that it's the nocebo effect and suggesting that they need to white-knuckle through it. I hate even talking about this anecdote, but it really just has weighed on me for a long time. I mean, it gets to the idea that even if the nocebo effect is a phenomenon, it is it? And it is like, is that your default assumption with people? And and and why can't there be an honest discussion about side effects, not just symptomatic ones? Like, I I think my on the scope of things that worry me about certain medications, let's take, not take, we're talking about statins, myalgia is the least of my like concerns. There are so many things going on under the scenes where we don't even know the full biochemical relevance. You don't feel diabetes coming on if your blood sugar is coming up because you're a woman and there's something going on with this gene interaction with the statins or DHA is going down, your blood sugar is going up. You don't feel that. The suppression of GLP-1, like you don't feel that. And what are the long-term effects? Because we're not really like the cumulative negative impact of what that could mean on a person over decades, especially a metabolically healthy person. We don't fully understand.

So, it's not even me making a claim of, "This means X." It is, "We have not ruled out that this is not incredibly biologically important." So why should a pharmaceutical be presumed innocent until proven guilty in a study that no one wants to conduct? Or can? Particularly when it's the reverse nearly 100% of the time when it has to when it comes to diet, it's assumed over and over again. I don't know if this is sustainable. I don't know if it's going to be good long-term. How many times when I was coming into the low-carb space, I would hear over and over again that it's too high in protein and that that's going to be very hard on the kidneys. Right? I I haven't heard that forever, but that was a claim made on a regular basis. And how often is it that we're talking about the sustainability of a diet, but we don't talk about the sustainability of a drug, particularly if the drug is being assumed to work beyond what the trial periods are?

So, let's talk about, uh, working out when on a statin, because as, because as I understand, you've got some fresh data of your own on this.

So, I I did a, um, a a blinded crossover experiment of atorvastatin 80 mgs versus a placebo. I actually first asked my doctor, "Can they prescribe me a placebo?" Which I feel like doctors should be like, "No, we don't do that." I'm like, "All right, now I have to go through the rigmarole of creating my own placebo," which is surprisingly difficult. I had to like source the closest placebo pill I could, and even then there was like markings on the pill, so I had to like shave them off and like it was a whole thing. Um, long story short is I I had came up with an objective exercise performance metric, which was, um, time, um, on a, a sprint series on a vertical ski erg. And I will just tell you, like, the statins obliterated my performance. Like, it just like tanked it. Uh, and it was a very real effect. This wasn't, you know, it when you feel it. So I don't care what somebody says about a, like, I've did a blinded crossover trial on myself. This clearly impacted me. Oh, also my creatine kinase has been up on statins too. So there's an objective biomarker of muscle damage. I've had, uh, Josh Wageman on, who himself conceded that he, I'm not, I don't want to put words in his mouth. I believe he said either he said on the podcast or he said on the book that athletes often report this exact problem, that it annihilates their workout.

Um, this, this is again, it can't be said enough, and I think we try to do our best to emphasize whenever discussing any downsides to a drug, particularly a drug that's going to be discussed a lot that has to do with cholesterol lowering, uh, like statins, that we're bringing this up for the awareness aspect, right? Not because there's a value judgment being made, because it gets back to the nuance and the complexity of understanding it for herself.

Well, let's prove that point, because I can prove that point with, um, recent content I had come out earlier this week in my newsletter, but also the video that I'll be dropping in two days, which spoiler alert is, I'm taking cholesterol-lowering medications. And there's actually three plot twists here. The first plot twist is, I'm doing it. And the second plot twist is, why? Basically, the point is, why am I doing it? Because I came across new literature about benefits of a particular biomolecule or two that actually had nothing to do with cholesterol. So, just to take a step back, when we as humans name a molecule, be it like an enzyme, GSK3 beta, which has now many functions, dumbly named, but like in Alzheimer's disease, or a molecule like this is a cholesterol-lowering drug, the drug don't care. The drug, the molecule, whatever it is, it doesn't care what you labeled it. It's going to do its biological thing, which can have a lot of different effects.

So, one paper in particular that I found really interesting was, um, on ezetimibe, which is what people like consider a kind of sidekick cholesterol-lowering drug that acts in the gut. Um, and and to be clear, this paper wasn't looking for benefits of cholesterol-lowering drugs like ezetimibe. It was looking at, basically, it was starting from the premise that neurodegenerative diseases, including Alzheimer's disease, Parkinson's, and others, a a core hallmark of them is that proteins misfold in the brain, terrible origami in your brain, that sets off a cascade of events that leads to neurodegeneration. So think about like amyloid, tau tangles, hallmarks of Alzheimer's disease are effectively this misfolding.

Um, now, there's an interesting interaction between two proteins. They're boring names. One's called 14-3-3. Um, one's called hexokinase. 14-3-3, I did know of before, because it is, um, well known to be involved in something called Creutzfeldt-Jakob disease, which is a very debilitating, uh, I think it's a prion disease that like kills you in a year with like terrible dementia. I think the one-year survival rate's like 30%.

Gez. But I remember learning about it in med school, like on like some flashcard that's going to come up on some esoteric exam because you never see it. But anyway, that's where I knew about it. But that aside, the idea is these two proteins can interact in a pathological way. The one protein actually supposed to be on the mitochondria, and it pops off, and that can set across a cascade of events that leads to brain decay, increased amyloid, increased tau. And so what they did was like, "Oh, huh, what if we can interrupt this interaction between these two proteins? So they don't come together and this cascade doesn't get set off?" So they just go screen a bunch of molecules. It's like, "What do we have that's FDA approved that might interfere?" Ezetimibe popped up. Completely coincidentally. This isn't even about cholesterol. It's a cholesterol coincidence. This molecule has this completely different nature, like Bruce Wayne and Batman. This is the Batman face. The Bruce Wayne face is the cholesterol face. The Batman face is the stuff it's doing in the brain face.

And what they found was, at least in cell culture models, so take that with a grain of salt, that ezetimibe reduced amyloid buildup, reduced tau buildup, increased autophagy, so cellular recycling, by 40%. And then they did like, um, a patient case chart review, and it was like an eight-fold lower risk for patients taking ezetimibe for Alzheimer's disease. Now, I that's something that is particularly of interest to me, and based on those data alone, and let me be clear, those are not perfect data, but they're interesting. I'm like, "Oh, here's something that I can get access to that, based on the balance of data I've seen, I think might have more net benefit for me that I'm willing to have a little bit of a risk on, particularly for the brain." Now, if my cholesterol goes down, fine. Like, I'm not dogmatically trying to live with high cholesterol for the sake of it. But that was a new element in a personal calculus of, "Is this choice of net benefit to me, Nick Norwood, as an overall system?" Turns out, most people bucket this as a quote-unquote cholesterol medication. I don't care what people call it. Is it going to help me?

And and and the reason I bring this up as an example is you're talking about, we're talking about surfacing information. We can do it both ways. And we have been doing it both ways. Obviously, only one way gets elevated, and you can see this in the response to frequency. So, like, when you do, or I did the other day, like say a rebuttal to Peter Attia's commentary trying to defend cholesterol code and Lima response, everybody gets all up in a tizzy and tries to defend "lower is better." And then literally, I'm I'm signaling, "Hey, something's going to come out tomorrow you might find surprising." And I post my LDL and ApoB. Dropping. These are graphs from my health records. 56%. Both LDL and ApoB. And all the detractors just like ghost away from it. It's a very selective attention.

No. Yeah. No, I agree. I I wonder how much people will be interested in what you do with your LDL levels until you're ultimately going to release your next scan, because that's coming, right?

So, importantly, I I mentioned there were three plot twists in the video I'll drop Friday. You'll see how I set it up. It's plot twist one: taking cholesterol-lowering medications. Is a... my primarily I was going to take bempedoic acid, but my insurance declined it.

Yeah. Yes.

Which is just comedic. We'll set that aside. The insurance said I didn't qualify for this cholesterol medication even though I failed a statin. Like, "Yeah, no, your LDL of what, 574 doesn't qual..." Anyway.

Yeah. Like, basically, basically if Nick with an LDL of like five...

74.

574. Let's say cuts it in half, right? Let's say you're down to, let's say you're down to around 300, and you're going back to the insurance company, you're going with one medication. I got to 300. Should I go ahead and have a second one with bempedoic acid? And they go, "No, we're not going to cover that." No. Anyway, we... insurance issues aside. So, plot twist one: the medication. Plot twist two: is why, which has nothing to do with cholesterol. It's just, I guess, call it the flex of me saying, "Look, I've always said I'm not dogmatic on these issues, and I never have been. I've never been trying to defend high LDL is good, you should have it. I've just been like, look, cost-benefit analysis of the whole system, and I haven't had any side effects." Um, I guess brief aside, because people ask, can cause some GI upset sometimes, especially if we're on a higher fat diet. When I tried it the first time a couple years ago, I did have GI upset. This time I started at a very lower dose, so five milligrams with food, and then after two weeks, brought it up to 10 with food. That seems to make it without any side effects.

Now, a tough question.

Do you feel comforted by the fact that your LDL is lower, even if that wasn't the reason that you were doing?

So, here's why I don't want to answer that. Plot twist three.

So, wait, wait. I'll get back to your question.

Okay.

Plot twist three was...

I have... I didn't start this, um, until after I got my seven-year, six years, eight months, and one day, if you want the exact coronary CT angiography with expert-guided quant, like expert-guided read and AI-guided quantification down to plaque levels of the lowest millimeter cubed. And I just want to be clear, like, after talking to the chief medical officer of the company that was doing the scan, Reed, which is HeartFlow, and also just observing some current discussions on social media about people also in their 30s who have prioritized having low LDL, who even they have measurable plaque, on the order of 60 millimeters cubed. You know, one might one would expect, given my levels, I would have a lot of plaque. So, plot twist three is, I have been running a natural experiment for seven years with a cholesterol of 700, LDL 500s, to see, does this cause plaque accumulation in my arteries? And there's going to be objective data that I can't fake. So that's going to be plot twist three. I'm going to release all the information when all the data are in hands and I've dotted my eyes and crossed my tees. People can kind of guess, um, what this might be. But the reason I don't want to answer your question...

No, I I think I can help you here. So, so it sounds like there there are two very plausible reasons why you may not want to answer the question. The first, given what you just said, is that your scan will indeed confirm that you do have plaque. You have a decent amount of plaque, and therefore you might be reconsidering your position. That would be one plausible explanation, right?

Yeah.

That you're going to give. The second plausible explanation, and I'm going to be like, "It's the second one because I can't give a secret," but go ahead.

I know. It's like I was trying to help you out. I'm not even going to mention the second one now. So, I'll just...

People can read between the lines. Let's just say...

Okay, let me, let me back up and say, and and Dave can validate this from when I got, this is the second scan I'll be getting at seven years. The first scan I got was at around two years, right?

And I told you when I was getting that scan, I'm like, "Whatever the data are, I'm going to share them." You said, and I and I'm going to vouch for what you're saying. You said to me in private. I I said, or literally I was saying this in private. I was saying, "Just so you know, having existing disease, um, with what you dealt with before, is also potentially an aggravator because inflammation is..."

Terribly inflamed.

"...highly relevant towards atherosclerotic cardiovascular disease." And you said then, to your credit, and I can so appreciate this, is you said, "Whatever the data is, the data are," or you said, "The data are, whatever the data are, the data are."

The point being is that...

You were intent on publishing whatever your scan was. And this was, and I just have to also vouch for how responsible this is. You didn't end up with sky-high levels of LDL cholesterol, becoming lean mass hyper-responder, and then just said, "Eh, I'll check in seven years." You said, "I'd like to check now," right?

Well, the degree of exposure I have is like really astronomical. It's comparable to Brown and Goldstein in your first scan in the two and a half years, right? Right. When we when we published the case study, we even had, um, a a case study for a baby that was like less than a year who had homozygous FH.

Who had very advanced plaque.

It was less than a year old.

Right.

I'll also say my first scan didn't have AI-guided quantification because this was five years ago.

Ah, it's true.

So, it was it was semi-semi-quantitative. So, like, you know, there could have been plaque there that got that just wasn't picked up because there wasn't the resolution. Now we have more technology, and again, like, there are people around my age with measurable plaque that they're reporting out on social media, and I have manifold more exposure than them. So, but but to really tie a bow on it, it's not that, set aside LDL for a sec. It's not that there's a cardiovascular risk factor at very high levels for which you're being blasé about. You did get a scan not too far into that level of exposure to that.

About two years in. Yes. And I will say my CAD-RADS score then was zero, which is not with AI-guided quantification. Now I'll have, um, quantification down to the lowest millimeter cubed. And if anybody's like, "Well, maybe he's projected genetically." I just want to point out my dad had 99% occlusion of his LAD when he was 44, and I have an LP(a) near 200.

Right. So...

By all accounts.

By all accounts, I should be a walking corpse.

Yeah.

So, we'll find out. So, bottom line is, without Dave revealing what the second possibility was, although we didn't like discuss this beforehand, so you guys can be between the lines. Um, I I will release all the information. I will release it in time, but I want to have it in the appropriate package. There's a, um, there's a point I I want to put forward. I I say this online a lot of times. People tag me with their quote-unquote success story of being lean mass hyper-responder for a long time, not having any plaque. They get their CT angiogram and they go, "Look at this." However, I've also been tagged where somebody's going, "Ah, it turns out I have heart disease." Right? I'm not retweeting either one. There's an issue with anecdotes in general, but there is relevance to us, literally the trio that's researching this in real time, and you being of the three of us, the person who has the homozygous FH levels. So, you're not just any anecdote. Your name's on the papers. And that is why it deserves some degree of special consideration, particularly given we did the case report from before.

Yeah. I mean, when I, I never intended to have a social media presence, not really. I started like tweeting like anybody, like I had an account and I started sharing some things about myself. Um, and then it kind of took on its own life. If I could go back and put the genie back in the bottle, would I? I would say probably not, but it would be something that I thought a lot more about before I did it. But the fact of the matter is, like, people know me. People know like what my levels are. Like, it gets discussed. I mean, I came up on Rogan. I came up on Mark Hyman was discussing my LDL levels with Huberman. Remember Andrew responding, what Mark said something to the effect of like, "His LDL is like 500," and Andrew's like, "They're like that now? What?" And I'm like, "Oh god, I need more context." But bottom line is, the genie is out of the bottle. So I think the only responsible thing to do is like, look, I'm going to update you.

Right.

And you can take it with a grain of salt in either direction. Um...

And I give, I give credit to anybody who, if they make their medical information public knowledge, they follow it all the way through, right? They continue to make it. I... This is one of This is one of the things I don't like when there's more of an effort to, uh, take somebody down on health information or personal information that they don't make part of their own story that they want to make public. But if they make it public, then it's there.

Well, there's one additional element that I'll I'll come clean about, which is I never want to withhold information that I might think is relevant to good-faith actors, but there are other actors who I know will misuse confidences. I remember one in particular interaction early on where basically I was explaining my personal rationale for why I was eating a ketogenic diet, which had precipitated my very high LDL levels. Now, this person, um, themselves is a healthcare provider, and I confided them, like, "Try to, like, level, look, this is a complicated decision for me." They ended up really abusing that confidence to the extent that they were making memes about me. I think you know what I'm referring to. I don't even need to mention the person's name. And it wasn't that, like, the memes even hurt my feelings. Like, this is just immature and stupid. But I'm like, people have different motives. And I've become a little bit more anticipatory about like how someone might take something and skew it for their own purposes. And I hate to have to think like that. I wish you could be like, "Yeah, here's all the stuff. Here's my genetic code. I don't care." But now I know what people will go digging for and how they will use it to create a false narrative. And and I'm ten times worse than you are on that because I'm always... I hate there's literally a a portion of my brain that anticipates the ways people can take something genuinely out of context in a way that's unfortunately just not good faith. I mean, it's it's hard to see it any other way.

Do you think they do it unaware of the impact? Do you think they do it because they think they're somehow doing good?

Oh, yeah. They think they're doing good. No, I think I think there's not 100% of the people who are doing it are doing 100%. But there's a, there's a person we know between us, you'll know immediately who I'm talking about, but who themselves have conceded when they've been acting in a way that could be considered bad faith, but from their perspective, it's for the benefit of their patients and for the world at large. Right. And what do, what else do you call it but motivated reasoning to the extent to where they're just, they're... It sucks because it would be easier for us to just think of them as villainous, that they're just trying to to hurt us because they're bad people, right? They're deluded. Like, and and and I want to be very, like, clear on that. Okay. Tangenting. I know we're talking about the same person. I don't, I don't want to mention the person's name. But in this particular circumstance, and not just with this person, but with other people, the rebuttal I often get, and you already alluded to it, like, you know, it's in, it's for the sake of my patients, is this allusion to clinical experience. And I want to unpack that a little bit. The idea of like, "Well, you know, I treat patients every day. I know what it's like to be a care provider for many decades, and I have wisdom from that." Because that is like a fail-safe rebuttal in academic medicine. It is a very much respect your elders hierarchy. You respect the senior clinicians. The more years someone has under their belt, you respect that. And it's a very complicated thing, I think, because on the one hand, there are insights to be gained from just being a care provider for a long time. You see a lot, you learn a lot. I get that. There's also a danger because just because you're sitting there in a room with a patient prescribing medications and providing healthcare doesn't mean you're actually providing good care. And I think sometimes clinical experience gets manipulated into a shield. Meaning, "I don't have to contend with new data. I don't have to contend with new ideas. I've been doing this for a long time, and it seems to work based on my perspective," which obviously could be confirmation bias. And it ends up acting as an excuse to, "I can say and do whatever I want because I know what it's like to provide, like, I have the prescription pad in hand, and that gives me the authority." And it's a difficult thing for me to navigate as just, given even my age, because I know I know who's watching, and I know how much it irks most physicians to have someone younger push back against someone senior and say, "Look, I get you've been doing this for a long time. I don't think you're doing a good job. I don't think your reasoning here is sound, and I'm not going to give you a pass because you've been doing this a long time. We're talking about specific issues, and you need to answer the questions and contend with the data." So many times, including with this individual, there's been like a topic of data. New paper comes out. Here are my methodological qualms. And the rebuttal is, "Sit in your seat and listen to me because I've been doing this a while." Complete dodge of the data. And I think that is inexcusable. I think clinical experience has a lot of value, but it often is actually just confirmation bias and ego being labeled as clinical experience.

I don't... The issue that I, and I still very much have it, it's one we kind of alluded to from earlier, is the play on emotion. Right? So the issue is that you don't have to treat a patient who is dealing with XYZ issue.

Have they...

Like I do. Like I do, because they were taking bad advice that you give. Right. That's often how it's framed. That's my... This came up on a phone call, and it was the most glorious moment for me because I don't think they realized the way they posed it, but effectively they were like, "My patients coming in and asking me these really hard questions because of information they got from you, and they won't listen." I'm like, "You so I'm more compelling than you, and you're ineffective as a teacher in the clinical set." I'm like, "This was..."

Just the way that you framed it. They won't listen. And they, but, but the patient, it was literally the words, "The patient's asking hard questions."

Right.

And I'm like, "Great. Answer them if you're competent to. And if you can't give good answers, that's on you. Be a better teacher. Know the data better." Like, that's not on me. Everything I'm saying, I say precisely, and I can defend. If I'm shining the spotlight in somewhere you don't want it to be shown, and now your patient's asking you hard questions, you need to be the more compelling person. You have a direct line to them. So you should be... Don't get pissy with me because your patients don't want to listen to you because you're not making good arguments. Like, yeah, there's a, there's a distinction to be, there's a distinction to be made in that if your patient's coming in, they're going, "Well, I hear Jupiter's in retrograde, so I'm supposed to not get surgery on Tuesday." Right? That's an understandable hard question for which you can say, "I don't know that that's going to have a big effect on your treatment." And frankly, I'm not going to take the time to learn astrology to better answer what it is that you're bringing to my attention. Right? However, if the patient comes in and says, "Wait a sec, why haven't I been getting regular testing of my insulin? I now have and found out that I have very high fasting insulin levels, and I think that might be relevant towards potential cardiovascular disease, right? Given a number of things that that Nick's been saying or Dave's been saying or so forth." And they don't have a, they don't have an answer to that question. I would hope that they would get curious to to look more at Joseph Kraft and Dr. Dr. Bernstein and all of these other resources for which you could get a better sense of what that's the time. If there's that's that's the true CME. Right. Right.

Well, in addition, there's so many layers on this because in addition, like these particular people who will not be named, we've also given them opportunities to like have discussions with us. I'm like, "Refer your patient to the chat that we had so you can lay out your points and have your like gripes heard." And like, "No, no, I don't want to do that."

Yeah.

Well, again, this is where I feel like social media, I know it's a bit cliché to state it this way, and I've said a few times offline before here, but it's the sense that they like to throw rocks from the sideline.

Yeah. It's the, it's the social media is kind of one of the best ways to air out grievances but not feel that you're as accountable for it because you can't be here like you and I are now where I can ask you a question, have a follow-up question, you can challenge me on beliefs that I have, right? Um, and that, to to that extent, we have a lot more capability. I was trying, it's funny, I was trying to think of something that you and I disagree on, and I think most of whatever comes comes to mind has been food-related. Was it, Was it Kobe Jack cheese that you didn't like? Or I think that might be Siobhan. What is it?

I'm not a Brie person. I'm a, uh, I like like stinky cheeses like Roquefort. I don't, I'm not against Kobe Jack.

We agree. Well, what about broccoli and omelets?

Broccoli and omelets? Oh, yes, we disagree. You know, wait, backstory here. I once made Dave an omelet, and he's like, "This is the best omelet ever."

It legitimately was the best omelet I'd ever eaten. And then he came back to my place, and I made him the same omelet, but I had a little bit of like leftover broccoli, and I put it in, and his face. It like made all the difference. I'm sorry. I just... It wasn't as... It was like I was poisoning you.

Yeah. I... It was. And I was trying to... Okay. So, also your girlfriend was there, and I was trying to...

Picked up on it. You look like a 12-year-old who...

Well, I was trying to be like, "Good. I'm like, 'Yummy.'" Anyway, uh, it was an omelet that includes capers, which I had never thought of before. It's freaking delicious. And...

I I had like an anchovy oil that I fried it in. And Dave loves salt. So, it's just like the salt and the salt and the salt. Salty cheese, capers, anchovies...

More more salt. So, Dave likes salt.

Yeah. I was trying to basically, what was happening just now is I was trying to reach for an example of something we disagree on. Frankly, we just agree on a lot on the science side. Um, the things we disagree on are on things that we are not and should not be talking about publicly. But, um, the point being is that that's what that's what's great about an in-person forum. It's, it's very... All of my debates that I've had. So I've had three people on who have been very pro-LDL lowering, right? Chris Masterjohn, mutual friend of both of ours. Uh, Alex Leaf, um, and Greg Moshé, Moshé, I hope I'm saying that correctly. All three of them, I had on. All three of them were pro-LDL lowering. And sure enough, when you have an in-person conversation, it benefits everybody. It only benefits the two of us, but also benefits the audience because a lot of times when you have like this amount of engagement, they can actually see how much you have in common. A lot of times the nuance unfolds a lot better. But then those places for which you have disagreements almost necessarily have to become less cartoonish, less one-dimensional, because they just, they don't hold up to scrutiny.

Yeah. I mean, often it's less a matter of actually like brute, like head-on disagreements as much as it is, because of my background, I want to shine the spotlight in a particular place.

Right?

There actually might be a lot of like agreement, but this happens in my media all the time. People are like, "Well, why aren't you writing articles on all the potential benefits of statins through pleiotropy?" I'm like, "Well, because where I want to shine the spotlight is where I don't think it gets shown." So, yes, my personal intellectual ecosystem is biased in this way, in a very conscious manner, because I feel like I need to balance out an overall ecosystem intellectually.

Because like I think other things are getting too much play, and other people might have different, like, like focuses. So, sometimes I get a rebuttal be like, "What about this thing?" I'm like, "I agree. This is a different point." Like, let me ask you a direct question. Are you anti-statin?

No, not at all.

Follow-up question. Are you sure you're not anti-statin?

Why are you... I mean, I I think that they are... I've prescribed them blindly. I think that they have more effects, both both positive and negative, that people don't appreciate. In fact, it's interesting, if you go to look at the association between, um, the magnitude with which LDL is lowered with a statin and improvements in outcomes, which there are, the R-squared is like 0.0 to 0.1. The association is abysmal. And the way I interpret that is like, well, statins also can have beneficial effects on the endothelium, on inflammation. So if you have metabolic syndrome and obesity and, you know, like a dysfunctional endothelium, you could have been having like protective, you know, endothelial effects, increase nitric oxide, decrease inflammation. Sure, that could carry a net benefit in a person. And then also the thoughtfulness of coupling with other things. Okay, can you offset the GLP-1 effect? Yeah, take a TUDCA or UDCA. Okay, you're a woman. Maybe stick some fish oil with that and a CoQ. Like, you can put it together in a stack that's quite thoughtful and could have a positive overall effect on a patient. In fact, I have this conversation with my girlfriend quite a lot because, I mean, she's brilliant, and she does like digest a lot of my information, and importantly, she likes to challenge me. She likes arguing, and she has a very, very different patient population than me. Like, the patients that are coming to her like aren't that scientifically literate. Probably most of them have obesity, class one or class two metabolic syndrome, high blood pressure. And she's like, "Should I not prescribe these patients statins?" I'm like, "Honestly, this is like a, like a very select population, and I'm trying to provide information more broadly, including to people who are scientifically literate who are digesting my content, and on balance, probably healthier." So it does depend on who the patient is. It's not black and white. So no, I'm not anti-statin.

So, so to capitalize on what you just said. So, in a population that has, say, class one, class two obesity, would you speculate that it's more likely that they would get benefit from statin than say, those that are more athletic, the population that's following you?

I mean, I would say that's probably not the best singular triage metric. However, at a population level, yes.

Okay. So you're not anti-statin.

Never have been.

Are you sure you're not anti-statin? Sorry, I'm laying it on. Actually, I changed my mind. You've convinced me, Dave.

I I'm going to also mention this, if you don't mind, which is that I have been in private group chats and email chains for which you have, uh, effectively endorsed for that individual case. Do you mind? Because I'll edit this out if you don't want me to.

But I, but I'm basically, I'm backing up the case that not that I'm necessarily pro-statin or anti-statin. Again, I try to stay out of the treatment decisions. My opinion, I want to keep as far off there as possible. But for people who are who are specifying it towards people I know, like you, who are very vocal on the topic and are trying to approach in a nuance way, they often try to paint you into this binary that you must therefore be anti-statin because you're bringing up what should be things everybody can discuss openly, right? There are side effects with every drug. To what degree that is something that's meant to be an individual choice, but for hopefully we're well informed on.

Yeah.

Right. But you cannot just simply assume it could only be beneficial. You can't do it. I feel like the entire medical world is sometimes gaslighting me. I'm like, basically my...

Position is, hey, statins are a hammer. Some people are nails. Some people are pickle jars. And everybody's running around with a hammer being like, "Nail, nail, nail, pickle jar, smash." And I'm like, "You know, you could use a can opener. It's an option." And they're like, "Now you're anti-hammer." I'm like, "All right, whatever."

So, tell me about the uh, you're wanting to try bempedoic acid, but you haven't tried it yet. Is that right?

Or you have. I tried it before when I had other insurance. Now, my insurance doesn't want to cover it. So, I'm just like, but when you tried it, it wasn't for the purpose of an experiment.

It was, I was just collecting. Well, it wasn't like a, "I'm going to report on this and see what the side effects were." It was just collecting data. I said, "I do this for six weeks. I wonder what it's going to do to my lipids." Just out of curiosity. I mean, people are like, "Why?" Whenever I do an experiment, they're like, "Why are you going to, why would you do this to yourself?" I'm like, "Like sardines." I'm like, "I've done worse."

Or I did, um, I'm doing one with like Redat True Tide and I'm like, "Why would you do this to yourself? You're already thin." I'm like, "I'm not trying to lose weight, but I want to get the data." I've done worse. Like I've done, or like it's, it's four weeks of something if it's not going to actually make me like problematically sick. Just collecting data.

So, um, yeah, but it was a very, the thing that got me interested in it was there was an interesting paper out. Technically, it actually comes out, I think it's Cell Metabolism. It's Cell Metabolism, um, May 2026. So things go to, to online before they go to print, but the print issue is going to come out next month. But it was showing that, um, people who don't know bempedoic acid, brand name, it's kind of thought of as like a sort of like a statin, but it's called a prodrug, meaning it's inactive until it gets to the liver where it's, it gets activated. So the benefit is it's not going to like affect your muscles or other organs like statins might. So it's like a liver-specific statin. However, they discovered that even in the prodrug form, it has a second nature like a zetami. These drugs do more than one thing. And it, um, serves as what's known as a PPAR alpha activator. PPAR alpha is an important, um, transcription regulator with a lot of broad effects, including, we're circling back to brain health in, um, amyloidogenic processing. It's not clear. I don't think there are any good data, and if anybody can find it and surfaces that'd be great, on whether or not bempedoic acid actually crosses into the brain, potential implications for various metabolic diseases, uh, including Alzheimer's. I won't get into the nitty-gritty. People can read my Substack article on that or watch the video that I have coming out Friday, May 1st, which is in two days, which is, I can't believe it's May already.

So anyway, bottom line is, like, I'm like you. I'm just curious about how these things interact with the body from all angles. So something new comes out and I'm like, "Wow, this is a benefit I didn't know about." I'm excited to talk about it. I'm not like on the train of, "Let me fear-monger about the negative side effects of X, Y, and Z." It just so happens that a lot of really interesting information about statins doesn't get surfaced, like what we talked about in GLP1s or what we talked about with, um, like, you know, the X chromosome interaction. I'm like, "That is cool science, and people want to know about it." And it's a little bit of a pat on the back and proof people want to know about it.

You know what happened after that Cell Metabolism paper coverage?

Oh yeah, with the GLP1.

Yeah.

Yeah. So this was a paper that came out in 2024. I think it was February, and like, nobody had heard about it, and then I cover it. I think it was late 2025 and into 2026, and right after I cover it, it goes from obscurity to Cell Metabolism's most read list. And then Peter Attia did a letter on it right after, without mentioning you. So everybody, I was so confused because everybody's like, "This letter came out, Peter, and people like, Peter Attia is responding to you, Nick." I'm like, "Did he name me?" They're like, "No, but it's so obviously you. It couldn't be anybody else."

I will sidebar on that. We didn't even get back to his his current letter. But what pissed me off about that letter was the entire thing was trying to debunk this GLP1 study. I think he did a pretty piss-poor job, to be honest. Like, some of the things he was trying to do, like, "Oh, well, the absolute decrease is small if you compare it to postprandial spikes in response to carbs." I'm like, "That's such a stupid comparing a postprandial spike to carbs and GLP1 to the reduction in the fasting level. You know you can't do that." But that aside, the key graph is Figure 1H from this paper. It's she et al. in Cell Metabolism. And if you go to Figure 1H, Y-axis, GLP1, X-axis time, zero to 16 weeks, there's a big fat red line going down at a 45-degree angle. And a six-year-old could be like, "Ooh, red line go down." It is very obvious what's happening. And so what he does is, remember panel 1H? He shows Figure 1 and clips out 1H. He has the analogous figure in the same format for how much LDL goes down, and then just like this one's been clipped out. The only relevant piece to his whole argument has been cropped out of the figure.

Talk about people like, again, circling back to what I said earlier. It's not about who's, well, it's partly about who's right and wrong. If somebody isn't willing to have a genuine conversation, stand up, defend their points to the opposition, and actually try to understand the opposition's points, which he never sincerely has, that is a telltale sign. I think I, I will capitalize just for a moment, and then we should probably wrap up.

Yeah. Uh, yes. Then flash forward to what, a few days ago, when this article got dropped. I wasn't mentioned. You weren't mentioned. Adrien Sodto, who actually, you know, is lead author on the paper, you both of you were co-lead authors on it. Instead, in order to address us, he used the organization, the Citizen Science Foundation, the CSF.

It's worse than that.

The CSF was discussed as though it was the entity making claims, making assertions, and so forth.

Didn't he like me? He mentioned you like by an aside, something about like, he didn't say Dave Feldman, but like an engineer's maybe? Maybe, maybe I'm misquoting that. Maybe I was just me reading it, but I tie CSF so closely to you, and I think people do.

Bottom line is, let me get to what I was trying to say. It's a very verbose article, and the whole lead point, or like, there's this framing that it makes it feel like it's some esoteric group of renegades, the CSF, this that and the other, making claims. And if you know the backstory, it's so embarrassing for Peter. Like, if, take the lipid energy model, he's trying to debunk the lipid energy model. He's making mistakes left and right. Like his whole thing is about like low triglycerides debunking the energy model. Like, this is comical. But that aside, he fails to mention that his past head of research, Peter Attia's own past head of research, jumped ship with him to be an author on that paper. And when I asked Peter, did he want to collaborate on something? He said, "No, don't ask me. I'm not the expert. Ask Ronald Krauss, who has now collaborated on us with multiple things. There are multiple esteemed cardiologists, lipidologists involved in it." And he very clearly tried to cast it as just some renegade group of nobodies rather than acknowledging, you know, my past head of research jumped on. People that I've recommended the team to go seek out, they jumped on. You know, it, it is an article written with the air of, "I am the authority," even though he's basically all but admitted he is not the authority on this topic, and then he's not willing to engage to discuss the ideas that he's again messing up on. I just, it, it's a bad look for him. And I do have to speculate, and let me be very clear, I'm speculating why now. Now, one argument, and this might be the entire story, is the movie dropped, and the movie is making waves. And if that's the case, great. I'm glad the movie is making waves. I'm glad he's giving oxygen to it. Please keep doing that. I'd love that. The less favorable interpretation, and let me just say this is just like an alternative possibility. It is conspicuous to me that he had you on in 2018. It's been eight years over which there's been an incredible amount of opportunity to engage, including multiple papers dropping. I think something like a dozen papers we have now, including us trying to reach out to him via his team, him commenting he didn't want to engage. Now, given some recent events when, let's just say his reach and influence might have been a little bit destabilized, he comes out. Now, I'm not going to say if that was any part of the motivation, but if I'm, if I'm just like putting on my strategy hat, this would be a good topic to attack now since the, based on the conventional point of view, it's an easy win for him. Maybe I'm wrong. Well, again, I'm, I'm, I'm, I'm the motivations here are tangential.

Yeah, to the extent to where there's just intellectual discussion to be had, I definitely welcome it. We'll see what happens. Okay, I ask this of every guest. I, I almost laugh when I do it with you, which is, how do people find you? But the way I want to say it is, how do people not trip over you? You're, you have so much con, you are a fire hose of content blasting out into the internet. Um, but seriously, how do people find you?

Well, the nice thing about being named Nick Norwitz is there's like no other Nick Norwitz on the planet. It's perfect. It's, there's no. So, Google Nick Norwitz on any platform except for TikTok. I'll never be on TikTok.

You said that about Instagram.

That's true. I might, but I might have to eat my hat on that one. But, um, in all seriousness, my, you know, I'm on Instagram, I'm on Twitter. My biggest platform is YouTube. I think I'm about to cross a million subs, which would be exciting. And Dave has just seen it, but I now have a new space to build out a studio. So all your investment in me is going to be invested into building out an awesome studio. We're going to level up our game. I'm expanding my team. It's awesome. A lot of the financing from that, I'll be honest, comes from my Substack, which is Stay Curious Metabolism on the Substack.

Which is fantastic. It's, well, it's where I have like no overhead, no filter, like I can jump on the newest Nature paper, get it right out. Um, I've been doing that like more rigorously for a year. I'm really proud. It is now number two top selling overall in science globally. Not rising, like the overall list. Um, and it, it has only gone up. Usually we're number one in Rising Science, and it's just the best thing. It's so much fun. I can cover whatever the heck I want, and the audience is so freaking engaged. Um, and the premium members of that channel, it's like eight bucks a month for, it averages out to like 67 cents per premium letter. So I think pretty decent value.

It's like it's like a magazine. I mean, you, you, it's not like you just throw in some words. It's actually very well-constructed articles. I think it's, I think it's fantastic content.

I just, I have fun with it. It's, it's where I get to do like a lot of the things that won't even make it to YouTube at this point. Um, but like something new comes out and I'm just like, "This is awesome. I want to cover it." I'm getting a little bit more into the peptide world. So there's going to be some more of that content coming out. I'm very interested in, uh, some in particular. Um, but really anything that captures my attention in human health. So it's an evolving ecosystem and, um, I'm just having fun with it. So, yeah, the Substack and my YouTube channel and anywhere and everywhere else. Um, thanks. Well, thanks for jumping on this special mobile episode. We've, we got a screening to get to. So, we do.

All right. Cheers.

Perfect.