I Interrogate a Cardiologist | Dr. Bret Scher on Cholesterol, Heart Disease & Alzheimer’s

If you're going to use this as causal for LDL and heart disease, then how could you ignore LDL and Alzheimer's disease?

There was a human controlled trial showing that statins massively reduced GLP-1 hormone levels in humans.

You absolutely cannot ignore blood pressure. You cannot ignore inflammation. You cannot ignore metabolic dysfunction and blood sugar.

What actually irked me and surprised me is the lack of curiosity in the results.

One, it was fascination. Two, it was frustration. And three, it was like, okay, I mean, we got to start talking about this, right?

Everyone, I'm thrilled to welcome Dr. Bret Scher to the channel. For most of you, this is a man who needs no introduction, but I'm going to give one anyway. Dr. Bret Scher is a double board-certified cardiologist and lipidologist with over 20 years of clinical experience. He's been practicing medicine basically as long as I've been alive. In other words, he also serves as the medical director for both The Metabolic Mind Group and the Bazooki Group, where he's helping to lead some truly groundbreaking initiatives in the mental and metabolic health space. I promise we're gonna get into all of that in part 2 of this interview. But first, I wanna kick things off by picking Dr. Scher's brain, his cardiologist brain, broadly, and then more specifically about some hot new studies. So Brett, welcome to the channel. It's very nice to have you here.

Oh, Nick, Thank you. It's a pleasure to be here. I'm always glad to chat with you. Yeah, I love curious minds, man, and you've got one of the most curious out there, which is great.

I appreciate it. I was also just telling Brett, um, before we started, as I was developing questions for this interview, it occurred to me that Brett conducted my first ever social media interview way back when, years ago, uh, and I was just starting medical school. So this is, I think we've had a couple conversations since then, but this is the first time I'm hosting you, so I feel very honored and lucky to have you here and thank you for helping me with my start.

As I mean, I can take like total credit for your, all your success and blame.

It's a two-sided coin there.

Maybe I don't want that. Hang on, lemme rethink that.

A little troll maker. Anyway, I'm gonna start with something kind of broad, but something I think people will be interested in your perspective as a cardiologist. There's this caricature, particularly in the metabolic health space of the modern cardiologist who basically just measures their patient's LDL bad cholesterol, or maybe if they're a little bit more advanced, ApoB, and and then if it's high, just prescribes them a statin or other lipid-lowering medication. I'm curious, as a cardiologist, to what extent do you think this caricature accurately reflects modern cardiology practices?

Pretty accurate. Pretty accurate. And I wouldn't just stop with cardiology. I mean, primary care too. And the way medicine is structured is very much around getting these numbers into the normal range. And there's a lot of emphasis on educating about it on, you know, whether it's pharmaceutical-sponsored education, which much of it is, but even beyond that, you know, financial incentives for big group practices by X number of people with LDL above a certain number are on a statin. You have to check that box. Your medical practice administrators have to check that box. You know, you get your lab result back. And if your LDL is above, I think like 130, it comes back red as abnormal. No context, nothing about the patient, just that is a red value and an abnormal value. So just the way the system is set up is very much geared towards treat any elevated LDL. The assumption is the treatment is completely benign. That is a very generalized assumption within medicine that it's a benign treatment, so there's no harm. And you might be doing them a favor, so you might as well treat it. And there's also this belief in cardiology, certainly, and in medicine that lower is better, period. So I think that character is pretty, pretty accurate. Now, I would say unfortunately, because although I certainly don't say LDL is, you know, meaningless, I think LDL still is important, but it really has to be in, in a broader context of cardiac risk. And I don't believe the treatment is completely benign and harmless. So when you take it from a different perspective, you would approach things differently. But I think in en masse that you're, you're right about that character and that perspective.

I wasn't even trying to say right or wrong. I wanted to know if it's an accurate characterization. I'm almost surprised to hear you say it is because I know you as a pretty like moderate and honest guy. You're not just gonna characterize your average cardiologist like that for the sake of it. But I wanna unpack a few things you said, starting with the term incentive structure. You use that term and I really love that term because I think in social media there's a villain that is generated, like somebody's trying to do something, um, you know, maleficent. Actually, I don't even know if that's a word or if that's just a character. Either way, point being malicious, I should say. But it's more complex than that. It really is about like ecosystems, exposures, and incentive structures, the financial ones you mentioned, or even just like how people look at the lab report, that alarming red without putting it in the further context of, you know, a patient's history, other markers. In fact, I always found it interesting when I was going through medical school, when I went to like endocrinology clinics or to work with endocrinologists or hormone doctors, the first thing they always told you as a medical student, like Endocrinology 101, there is no normal lab. There's only appropriate or inappropriate for the context. And so I always found it interesting bouncing back between endocrinology and cardiology that it's not treated like that. You know, with LDL and ApoB, there is, there are these heuristics of lower is better. So now I wanna unpack that a little more with you. What do cardiologists mean when they say lower ApoB is better?

Like specifically, what do they mean when they say that? Well, I mean, the belief that LDL or ApoB is causal for cardiovascular disease, and therefore if you can lower it, then you are by definition reducing their absolute risk of developing cardiovascular disease, and therefore you should lower it. That's sort of the, the belief. And you look at paper after paper after paper that's published that uses the words LDL or ApoB is causal for cardiovascular disease. So there's, there's a belief when you read that, that therefore you can eliminate or significantly reduce the risk of heart disease by lowering ApoB. And, you know, we can talk about all the different literature that either supports or refutes that, but regardless, I think that is the most common belief in medicine today about ApoB and LDL.

I want to double-click on now another word, which is causal. People use this word a lot and it's grossly misused in my opinion. And I don't mean misused as in like correlation doesn't equal causation. That's too easy. I'm talking about the value placed on the word causal. To give a little bit of context, one person in particular, and I'll just name them because it's a prominent person and their opinion is well known, is Peter Attia. He talks a lot about causality and ApoB and other people as well.

Most of the day, on some level, I sit around thinking about causality.

A confusion point for people is I think they equate causality with importance. So everything you just said about the literature showing LDL and ApoB is causal for cardiovascular disease, like, that can be true and at the same time doesn't necessitate treatment of the biomarker. Because to your point earlier, intervention can have consequences. So it can be true, lower is better, provided you wrap the context around that lower is better for this particular outcome and also not considering the off-target effects of the intervention. My basic question for you is, one, is ApoB or LDL particles causal in cardiovascular disease? And two, do you think causal should be equated with importance?

Yeah, so I mean, I, I hate the word, I think because it's been misused and misinterpreted and misunderstood. I think a better way to discuss it is LDL involved in the process of developing vascular disease? And the answer is yes, it is involved. Is it by itself the cause of vascular disease? I would say no, it is not. Now, if you ask somebody when they use the word causal, do you mean it by itself is the one and only cause of vascular disease? They would say, probably say no if you ask them that question. But how they approach it seems to reflect that the belief is yes. So I think there's a little bit of a disconnect there. So I, like you, would rather use the term importance or, you know, where is it in relation to other factors? And because you absolutely cannot ignore blood pressure, you cannot ignore inflammation, you cannot ignore metabolic dysfunction and blood sugar, you know, what's happening on the microscopic level with the glycocalyx and all these different things that have absolutely nothing to do with LDL, they are all still very critically involved in the, in the process of vascular disease. So, we like things to be simple, you know, have to admit that. We like simple messages, we like simple guidelines, you know, make things easy, defensible, and quick. Whereas the discussion of what truly is involved in vascular disease and how do you prioritize the treatment of the different potential causes is not easy, it's not quick, and it can be, I guess you could say, harder to defend because you don't have these large 100,000-person blanket-type studies to necessarily fall back on. But that individual patient that you're talking to and working with may not be represented in that 100,000-person study, right? So you like nuance, you like the details. I do too. But for population-based medicine, it's very challenging.

I wanna transition to talking about pharmacotherapy medications and their potential negative effects. But before we get that, I want— I kind of already, I'm setting this up because I know what your answer's gonna be based on what you already said, but I'm setting up another question. My first question is, do you believe it's possible for a patient to have very high LDL and ApoB and be at low risk for cardiovascular disease?

Yeah. And the answer is clearly yes. I mean, it's clearly yes because there, you know, not everybody with heterozygous familial hypercholesterolemia and LDL in the 200s gets heart disease. Right. So there are clearly— there's a subset of people who have very high LDL and don't get heart disease. Now, is that population more likely to get heart disease than those who don't have the genetic mutation? The answer is also clearly yes, but we treat it as an absolute. Okay. So that means everybody with an LDL above this level is at higher risk. And it's clearly not right. All populations like this are are heterogeneous. But again, if you believe the treatment is totally benign, then the approach is, what's the harm in treating them? So of course we should treat them to lower the risk. Or you say, well, why don't we dig a little bit deeper to see if they truly are at a higher risk or not? Because we know not everybody with that lipid profile is, is going to develop heart disease. So why or why not? And that, that's the level of question and curiosity that really doesn't exist right now, or doesn't exist pervasively enough because it's more complicated. You know, if you've got 5 or 10 minutes for your patient and you're not gonna see them again for another year, and imaging, you know, is limited in terms of the options from their insurance carrier. Okay. I can see you've kind of got your hands tied, but that doesn't make it the right way to practice medicine or the best thing for that patient.

Yeah. I wanna lean into this a little bit more to parse something that I don't think often gets parsed, which is the scientific and academic answer, which you just gave. And you know, I, I, is one I would give and I think is pretty straightforward. Obviously you can have high LDL and not heart disease because there are people with high LDL that don't have heart disease. And then there's the clinical and personal element, and that gets a lot more complicated because the question is, okay, we know that you can have high LDL and not have heart disease. But we also don't know with precision why. And your heart health is not something you want to gamble with. So it becomes personal. It affects me. My LDL runs in the 500s. My mother, you know, when I'm having these conversations with my own mom, like, I want her to be doing the responsible thing. And there's things we know and there's things we don't know. So when, you know, she's going to figure out if she's going to be on pharmacotherapy for her LDL of, say, 400 plus, it becomes a very difficult calculus because I have reason to think she probably is at lower risk. At the same time, I don't want to make a wrong call. And so what you end up with, and this is what we're going to, I think, get to in the conversation, is a very difficult individual choice. Because effectively what you're doing is you're trying to make a decision with a risk-benefit analysis that includes big unknowns on both sides. What's the risk of not treating? Unknown. What's the risk of treating? Actually, a lot of unknowns. There are known side effects of medications, we'll talk about some, but there's also big unknowns and we're gonna talk about those as well. I'm gonna, right, but the medications, I wanna give you a true response.

Sorry to interrupt for a second, but I, cuz I think that's a really important point because if you approach it as, well, the risk of not treating is heart attack and death and the risk of treating is muscle aches, that's an easy choice if you paint it with that broad of a brush, right? And that, I think that's what. I, I'm speaking for a lot of other, other people in medicine, but I think that's what I see. Like that is how they paint the picture. And so there, it's kind of an easy decision when you look at it like that, but I don't think that's necessarily the way to look at it. Right, right.

So we'll actually talk about some known side effects of more popular medications, say statins, but I'm gonna jump ahead in my interview plan because we're already kind of talking about these unknown unknowns and I find those particularly interesting. Let's talk about a medication that is not a statin or return to statins, but PCSK9 inhibitors. These are kind of the bazookas of the lipidology world. I'm statin intolerant for various reasons, so I was considering at one point with my lipidologist and cardiologist starting a PCSK9 inhibitor. Now being me, looking holistically at my risk, one thing that jumped out at me was the study. I'm gonna talk about the study. It relates PCSK9 to Alzheimer's disease, but to lay the groundwork for that, we need to talk about Mendelian randomization. Can you explain at a very high level for us what this is and why it's of consequence? To the lipidology world right now?

Yeah. So, yeah, really important because a lot of studies refer to this. So Mendelian, the word Mendelian basically referring to like genetics, randomization. And this is where it gets kind of confusing. Randomization is— it's sort of like the assumption that these people are randomized for this study, but there's obviously no randomization that goes on. What, what this type of research does is it looks for people who have a specific genetic mutation. And the assumption is that that mutation is really going to affect sort of one thing that you can track over time, and it's basically random who gets it and who doesn't. So it's not like studies where someone chooses to do something or someone, you know, chooses to get their LDL treated or not, or chooses a lifestyle that affects their LDL. There was no choice in this matter. So the assumption is it's going to affect the population randomly. So you're not going to have those, um, confounding variables basically. But again, one of the problems is sort of the assumption is it's going to affect one thing and one thing only. So I think where you're going is there are Mendelian randomization studies that show people having mutation for various different reasons, and it could be in a PCSK9 mutation where they have very low LDL for their life, basically from birth, and not by anything they did. It was just a mutation.. And the assumption is the only thing that was affected was that LDL, and therefore we can see exactly what is the cause of— or sorry, what is the effect of low LDL without confounding variables.

Yeah. So just to reinforce what you said and how I understand the methodology is, because you can't really do a lifelong randomized controlled trial for a single biomarker, people assume, okay, at the population level, The confounding lifestyle variables are gonna wash out and there's nature's genetic randomizer for a particular trait. And the reason this methodology is so consequential now is it's because it's what a lot of cardiologists and influencers lean on to reinforce this idea of ApoB is causal, LDL is causal. This is always what's referred to as like, this is the, you know, proof of the causality.

There is no ambiguity that ApoB is causally related to atherosclerosis. You know, how can I tell you that? I can tell you that looking at all of the clinical trial literature, all of the epidemiologic literature, and perhaps even most importantly, the Mendelian randomizations.

I don't need to get into my concerns, caveats around the methodology, and I think the problematic assumptions. However, if you're using Mendelian randomization as the gold standard for causality, you do need to apply that standard across Mendelian randomization studies as relate to, you know, lipids. So one really interesting study that jumped out to me was one where they looked at Mendelian randomization effects of a lower PCSK9. And PCSK9 again is this protein that if you inhibit it, it helps reduce LDL and ApoB. So there's a whole class of drugs that is targeting reducing PCSK9, but this study showed— and I'll show the graph on screen for the audience. Indeed, lower PCSK9 appears to reduce various cardiovascular outcomes. But people will be seeing right now is a very conspicuous dot way on the right, which it represents increased risk, and it's for Alzheimer's disease. It was showing a 2.43 hazards ratio of— for Alzheimer's disease and PCSK9 inhibition. So this graph, this very simple graph, is showing the point that you and I, I think were making earlier, which is, yeah, lower is better, quote unquote, specifically for cardiovascular risk. But if you're targeting this protein, it's also predicting, quote unquote, causally that you're increasing your Alzheimer's disease risk. I am not claiming this is the be-all end-all proof that PCSK9 inhibitors, say, increase Alzheimer's disease risk. What I am saying is I think there's a double standard. And two, this at least has to go to the category of the unknown risks because we don't have 50-year studies on metabolically healthy people taking just PCSK9 inhibitors. We don't, and we probably won't. So my question to you is, one, do you find those data compelling? I know you saw them before we did the interview. And two, how do you enter this into a conversation with a patient who might be considering taking this medication? Yeah.

Yeah.

So there's a lot to unpack there. The first being, well, one point to point out for this study too is that, you know, cardiovascular events were lower but not zero, right? So LDL was very low, um, with, with the natural PCSK9 inhibition and cardiovascular events were low but not zero. But second, yeah, if you're going to use this as causal for LDL and heart disease, then how could you then ignore LDL and Alzheimer's disease? You can't promote the findings of a study you agree with and ignore the findings of the study you don't agree with either. You know, it's the same methodology. There was nothing else in there to, to really impact the change. If you believe there's nothing that can impact the change between LDL and heart disease, then you have to believe there's nothing that's going to impact LDL and Alzheimer's disease. So I think if you have to interpret the study the same way for both. Now, again, I don't necessarily believe these are the end-all be-all studies, but if you do, You have to approach it both ways. The second part of your question though is a little more challenging. How do you introduce this into a conversation with, with patients? And you know, the easy answer is, well, it's all individualized. You have to treat each— everybody's an individual, which is absolutely true, but that doesn't tell anybody how to do it. I think one of the things I do is I try and put people in buckets, like what is your biggest risk from what we know about your health and what is your biggest concern? What are those buckets, right? You can— some people come to me like, look, my dad had Alzheimer's and that was just an awful 2 decades of life. I want to prevent that at all costs, right? Or somebody could say, look, my— everybody in my family has had a heart attack in their 40s and 50s. I know I'm at risk for that. I want to prevent that at all costs. It's not always so black and white, but those are black and white examples to then say, okay, Well, look, this medication shows there could be an increased risk of Alzheimer's disease. There's some risk of lowering LDL and dementia. It's not the greatest evidence, but it's— there is some suggestion. Since that's your biggest fear, we're staying away from that. But if somebody has, you know, they're 40 and they've got a calcium score of 800 and they have a family history of heart disease, we're going to double down on everything to lower your heart disease risk, knowing that there might be some potential adverse effects. But what is your risk-benefit ratio? So it all comes down to that. And then of course, what is your metabolic health? What is your inflammation? What is your lifestyle? All those things have to play into it. But I guess that's my general approach is putting people into buckets of what their workup shows is their higher risk, but also what is their biggest concern personally.

I really want to emphasize, I think, something that some people might miss that is really unique about your response, which was You know, we talk about risk-benefit analyses, we talk about wrapping context around a patient, but there are two dimensions to that, which you pointed out. There are the other metabolic factors. So you look at the lab sheet, what's the HDL, what's the triglycerides, what are the inflammatory markers? That's all informative. But also, what does the patient care about? What are they scared about? What really matters to them? And that is a huge part of the conversation that I think gets overlooked. I can tell you, having gone through medical school very recently, I mean, I graduated like 4 or 5 months ago. There's a lot of talk among this generation of physicians about patient-centered care, about, you know, letting the patient be a partner, not like just a client. That's a nice thing to say. It's a nice virtue signal. It's a lot harder to execute. And in my experience with, uh, you know, more senior clinicians, it's not something I always see executed well. It's something that is talked about a lot. But when it comes down to it, there's still a lot of patronization and paternalism because there's this whole idea of, you know, informed consent. You give the risk-benefit, you know, and then help make somebody make a decision. But I think my impression after working with, you know, being a patient to a lot of physicians myself, there's still the air of, you know, we can't really give somebody all the data and trust they can understand it. So I'm going to kind of skew them towards what I want them to do. And I, I don't mean that as a harsh judgment. It's just like an observation of the way things are. And so I just wanted to reflect on your response because I really heard you highlighting the, you know, there's the metabolic context, family history context, and then having the patient is an actual partner in the decision-making of the risk-benefit analysis. So I wanted to commend you for that. Now I wanted to talk about maybe some more concrete data moving beyond Mendelian randomizations to actual human-controlled trial. I know there was a study that came out in Cell Metabolism last year that came to both our attention. We've both done independent content on it, on statins and their effect on GLP-1s. So at a very high level, there was a human controlled trial showing that statins massively reduce GLP-1 hormone levels in humans. The graph was so obvious that I think a 7-year-old could understand what's going on. What was your reaction upon getting this paper in your hands?

Well, first, I think you're being modest. You said it came to both of our attention and only came to my attention because of you, because of the content you produced. And, and that's part of the problem, as you said in your content, like this is a year-old study that is on nobody's radar screen. And how is that even possible? So my first response was a little bit of surprise, as was yours, that, you know, maybe yours wasn't surprise, actually, maybe yours was. More understanding, maybe ulterior motives. But mine was, was like a little bit of surprise and frustration that this hadn't been brought up. But secondly, it was kind of just super interesting, right? Like, we, we know this concept of statins increasing the risk of insulin resistance and type 2 diabetes. That's probably— I don't know, is that new? Maybe 5 years ago, 10 years ago or something, that has been in discussion but previously not mentioned at all, right? So the same sort of concept. Like, the data was, was kind of there under the radar screen but not mentioned. Okay, so first we had to mention and recognize that it can increase insulin resistance and diabetes and, and pre-diabetes, but now we have a potential mechanism of reducing GLP-1 levels in an era where everybody's starting to take GLP-1 drugs. So it's, it's super fascinating, sort of the dichotomy there about giving us a mechanism. And then the study was really elegant the way they looked at then the microbiome and ursodeoxycholic acid and the relationship there. And one, it was fascination. Two, it was frustration. And three, it was like, okay, I mean, we got to start talking about this. So that's why I made some content to sort of amplify the content you made as well.

You asked us, or you implied maybe I wasn't shocked. I'll tell you what I wasn't shocked about. I wasn't shocked that I kind of feigned shock that this wasn't being talked about. And part of me was surprised because it is just like, this is a major journal. Cell Metabolism is a major journal. This is a human trial showing that the most profitable drug class in history, in fact, the particular statin they used was atorvastatin, which Lipitor, which I think is the most prescribed specific statin, if I'm correct, massively lowers GLP-1 levels in humans. So right there, like you said, you have like this awkward paradox metabolic tug of war. Most profitable drug class in history, lowering levels of the hormone that is now mimicked by the Triamterese drug class in history. That's kind of interesting. But what irked me, what actually irked me and surprised me is the lack of curiosity in the results because the mechanism in understanding the mechanism, like you said, we kind of already know statins can increase insulin resistance and diabetes risk. This study identifies a mechanism, but in understanding the mechanism, we open the door to solutions. So literally in this study, there was a pilot trial saying, hey, You just supplement back some bile acids and it reversed the effects. Think about all the patients. I think 1 in 4 adults over 40 are using statins for secondary prevention, could be helped by that kind of knowledge. So this is a matter of patients who just aren't getting the best care because there's not curiosity in this topic, and then there's not follow-up. So this is what really bothered me was the kickback by some, the statement that Oh, it was just a 40-person trial. So why are you making a big deal out of it? That is precisely why I'm making a big deal out of it. First of all, anybody who tells you a study should be judged on its end value doesn't know what they're talking about, doesn't understand statistics. But second of all, you mentioned earlier incentive structures. This is a perfect example. You have a strong signal in a human-controlled trial showing that this medication has these negative effects, that it can be reversed with simple supplementation. So if the incentive structures were geared toward actually helping patient care, what would you do? You do a bigger trial and then make it standard of care. The reason that hasn't been done is because nobody makes a buck off doing that trial. So it comes back to—

Yeah, you could patent UDCA. You better believe that trial would have happened. Absolutely. Yeah.

So it's a matter of like I've made this statement before, but I really wanna emphasize that term evidence-based care. It sounds great. It's a great virtue signal. Before I started medical school, I was all about quote unquote evidence-based care. But then I had, you know, my experience and something worked for me that wasn't quote unquote evidence-based. And I realized evidence-based care by no means means the best care because evidence-based care just means you check certain boxes that you could check. Because there was the infrastructure and incentive structure in place to do the studies to get those boxes checked. So often the most effective medicine isn't quote unquote evidence-based because the studies just haven't been done because there isn't a business model wrapped around the studies. Do you have anything to add to that or things you'd like?

Yeah, so just an analogy here. I'm in California, so here in California we have, I think it's Prop 65 that has to have a warning on everything that has something potentially cancerous. So this warning is on everything, like absolutely everything. So it's become absolutely meaningless because it's— it doesn't really have a certain threshold that is meaningful for the cancer risk. So everywhere you go, you see, you know, Proposition 65 cancer warning. So it's meaningless. That's— I would say the same thing for evidence-based, because you could say basing something off of the weakest, lowest quality evidence is quote unquote evidence-based. And that is a true statement. But what does it actually mean for the quality of the evidence? And like you're saying, the holes of where the evidence exists or doesn't exist is enormous. And so saying evidence-based doesn't always mean what you think it means. So yeah, absolutely right.

I want to get on to talking more broadly about metabolic health in part 2 of our discussion. But before we wrap up, this discussion of lipids and cardiology, I wanted to ask you just broadly, is there some— like, how do you feel about the future of cardiology? Are you pessimistic? Are you optimistic?

I think I have to break that down into two parts.

Okay.

Because cardiology is very broad, right? If I'm having a heart attack, if I need a heart valve replaced, if I get an infection in my heart and have severe heart failure, there is nowhere in the world I would rather be than right here in the United States with our cardiovascular care, the stents, the transplants, the defibrillators, the medications for severe heart failure, the TAVRs, and unbelievable what we can do with that type of technology and skill from the cardiologist. So when you say, am I optimistic about cardiology, that division of cardiology, absolutely. Prevention, different story. Am I optimistic? I don't, I don't know that I am necessarily for prevention of cardiology, but I hope that there will be more of a discussion, I mean, of metabolic health, of, you know, multiple risk factors, of a broader risk profile, and get out of this LDL and ApoB as the number one focus, and really talk more about metabolic health, about lifestyle interventions that can actually have beneficial impacts and that people can do and sustain and give you the results of metabolic health that you want. I want to be optimistic that we're moving that direction. I think cardiology is probably going to be one of the slowest to move in that direction, um, unfortunately. But at their core, I believe doctors want to help patients. Doctors want their patients to get better. Sometimes they get beaten down with the system and it's harder for them to focus on that. And I get that. I was in that system, and that's why I'm no longer in that system. I'm practicing in a completely different way now. Um, but at their core, they want to help their patients. So when they get their eyes opened enough that this is a way that they can help their patients, I think they adopt.

Maybe then I can ask a follow-up and maybe a better question that is more pertinent to the audience. The way I asked it was, are you optimistic about cardiology? I kind of was leaning towards conventional, like mainstream, but one of the really beautiful things I think we both agree about the modern era is access to information, uh, including via social media, which obviously has its downsides, but it has great benefits as well. And I think One of the things people grapple with, even I grapple with, is like, how do you as a patient walk the line and use your doctor as your partner? So put more directly, what advice do you have for listeners who are thinking critically about their own case, want to advocate for themselves, but don't want to alienate their physician, their conventional physician? How do they approach the conversation with their doctor?

Yeah, and that's a very broad question that, that can be difficult to answer. But the way, the way I like to do it is to find a way to reassure your doctor that you want to engage with them as like a health partner. I want you to help me get healthier, but also sort of going back to what we talked about before, being clear about what your concerns are, right? Not just what the lab sheet says, not just what the tests say. But what you feel and believe and your concerns. And to vocalize that and say, look, I understand that there are risks based on my workup, but here's what I feel and what my concerns are, and I want those to be equally valuable. The other thing is, if you want to potentially suggest a course of action different than what your doctor wants to suggest, is to phrase it as a— in a way where, again, you get them to be a partner with you and say, okay, I hear you. All of this is like just Communication 101, whether it's with a spouse or with a coworker or whatever, right? Reflect back. I hear you. I understand your reasoning for wanting to do this, but I want to try this, and I'm hoping you will help me make sure I can do this safely and effectively. And we will give this a trial for 3 months, 6 weeks, 6 months, whatever. It's a trial, and I want you to work with me And I'm counting on you to help make sure I'm safe, right? Things like this to help engage them and make them feel like they're still part of your, of your care. So that's my general advice. And for some it works great and for some it may not work, but I think that's a helpful approach.

That was a great response. And I also feel very validated because it's generally the way I go about things. Like I'm talking with one physician now about doing a medication trial as an experiment, like you said, like I want you to work with me. You have an idea, let's just collect some data on me. And the themes that keep coming up are like communication, partnership, and then authentic curiosity on both ends. You should deserve to have your physician curious about you and your needs and your concerns. And then also like, so like honestly be open to, you know, input from your physician. So excellent response. Before we get onto part 2, just to wrap up part 1, where can people follow you and find more about what you're doing?

Yeah, well, thanks. Well, I think as we're gonna get into in, in part 2, most of my work right now is gonna be at Metabolic Mind and also Coalition for Metabolic Health, which is something that is pretty new as of the recording of this. So both of those sites online, and then my cardiology practice at lowcarbcardiologist.com. So those 3 sites, you know, I'm on X, I'm on LinkedIn a tiny bit, and Yeah. So those are the kind of the places to find me.

Awesome. Well, thank you so much for giving your cardiology wisdom to us here in part 1. Everybody should come back for part 2 where we're gonna talk about Brett's journey beyond the field of cardiology to talk about metabolic mind, mental health, and some really cool new studies and initiatives. So come back for part 2.