Transcription
Today, we're going to talk about statins. And yep, I know we'll get people on both sides of this fence. Everybody wanting to throw rocks. And we'll also get accused of sitting on the fence. But the reality is, and there's also going to be a lot of people that say, "Well, just make a choice. Pro-statins, anti-statins." At the end of the day, reality is just a little bit more complicated than that.
Uh, there are times when statins make sense. Unfortunately, I think the vast majority of statin prescriptions are inappropriate, and we'll get into that today. Why that's the case. I'll just give you a quick couple of examples though. For example, uh, most women uh that are on statins, uh, some of the large standard researchers in the country agree with me that are inappropriately on statins. Why? Because some of the data indicating that they have risk, some of that evidence comes from NHANES, the National Health and Nutrition Examination Survey. But that information is routinely up to a decade or more old. So it shows higher risk for women than they currently have. And doctors see risk, cardiovascular risk, and tend to just think, okay, put them on a statin. That's also the wrong thing to do.
Now, there's a lot of debate on YouTube about statins and LDL causing cardiovascular risk. And you see the opposite side of that debate, especially with the low-carb community. Uh, they say it's all metabolic disease. We lean more towards that direction, by the way. Um, but they say a lot of people say it's no LDL. Um, and so therefore, you should never take statins. There's other reasons for getting into that debate as well. Um, we only use statins for plaque development. And guess what? The other side, the side of this debate that says, "Oh, you should only use, you know, just get an LDL and, uh, if it's high, take a statin." That group is not following their own standards. The standards committees for the American Heart Association, American Cardiology, uh, uh, conferences have said, look, if you have zero plaque, you do not need a statin. And so, those of you that are statin haters and you want to have this debate with your doc, you can use that as part of your debate.
Now, we have with us, uh, one of my favorite team members. It's Dr. Bernardo Mesa. Bernie has a very, very interesting history for, uh, for our work. Uh, he's, in part, you might say, a recovered, uh, big pharma guy. He used to work for big pharma. Did a lot of research for them. Um, and is very, uh, very aware of the narratives that you see with big pharma. He has, um, as I said, recovered from that position. I'm not sure how deep he ever was in that position. Bernie's more of a scientist than than a politician, and, uh, is not a lazy doc at all. So he doesn't do single synapse. He agrees with us that lifestyle is far, far more important than any kind than any medication or supplement, but that there are times for medications and supplements. Uh, Bernie gives a lot of our presentations when we need to dig into the science. We have weekly meetings of our clinical team, and usually the person that's leading with the science is Bernie. Bernie's also got a couple of other, uh, background points that are very, very helpful for us. He's, uh, he's been a bodybuilder in the past. And as many of you know, if you've watched many of our videos, we focus on muscle maintenance and muscle growth as we go into these 40s, 50s, 60s, those years of increasing metabolic resistance and, uh, anabolic resistance. So Bernie's, uh, got some background in helping, uh, improve and keep those muscles that are so important, our biggest safety valve against, uh, increasing metabolic disease. I'm yaking on too long. Jesus is probably over there twiddling his thumbs, and so is Bernie. So let's bring Bernie on and, uh, talk for a few minutes about statins, the good, the bad, and the ugly.
>> Hey everyone. Hi, Dr. Brewer.
>> Thank you for the.
>> Great. And you?
>> Good.
>> Thank you for that introduction. So, thank you for having me on the show.
>> I'm glad to have it. Uh, we're going to be doing some, as you know, we're going to be doing some series where we get more of our coaches on the on the show like this because you, you guys are interacting more and more with the patients. We're, uh, driving more and more, uh, health behavior and unlike, uh, you know, we're, we have been sort of like standard medicine where the tail wags the dog. The tail in this case being prescriptions and seeing a prescription level provider. But the dog, the real body of the dog, the real important part is healthy lifestyles. So, we're wanting to get this series where you and the other health coaches are getting onto the channel so people can start seeing your face, hear your voice, understand where a little bit more about you.
>> Yeah. So patients can start picking their favorites.
>> That's right.
>> Nice. Great. So, where do we start, Dr. Brewer? Could should we start about should we start about talking how did we get here in the first place in terms of why do we use statins so much?
>> Yeah, let me, let me give a couple of comments about that at a very, very high level, and if you can, um, maybe you can start filling in with, um, some of the studies that we've talked about. I'll go back to, um, oh, the name, a couple of the, the Wascop study, the West of Scotland trial that was long ago, what, 30 years ago, and, um, the Jupiter trials. Those were some of the trials that demonstrated early on that, uh, people that studied, uh, participants that were on statins had fewer events. Events meaning had fewer heart attacks, had fewer strokes. There was just no question about that. And so the LDL statin side of the debate, uh, among doctors said, "Look, this is great. It's very simple. It's very easy. And it decreases cardiovascular risk. There's no question. Just give it." And it's sort of like what happens now with the glipizide. Once you get a drug class that's really, really good, really effective at something, it gets way overused, and then the, the trend becomes, let's beat on that drug class. So, you had these studies that came out. There were a couple of studies that came out in in Great Britain, in the UK. Uh, one was, it was between the British Medical Journal and The Lancet, and those two journals started, I can't remember which was which, I think it was The Lancet that was posting, uh, evidence indicating, um, risk associated with, uh, statins. And what you began to see, those that evidence became very popular, and what you began to see was huge numbers of people coming off of statins in droves. Now, from, you might be surprised to hear me say, since I would say most statin prescriptions are wrong and inappropriate, that exodus from statins that started, what was that, 20 years ago?
>> Mhm. That was, I, I'm very convinced it resulted in a lot of deaths, a lot of heart attacks, a lot of events because a lot of people that needed to be on statins came off too. Now, uh, we'll talk again a little bit about, um, the relative value of, of, um, lifestyle versus medications, including statins. We'll have to repeat that several times during the video because some people will dive in, hear a few minutes, make some comments, and move on. Uh, we'll always say lifestyle is far, far more important. That's why we focus on it. But you have, but back to the, to the, um, this debate between The Lancet and the British Medical Journal. So then the British Medical Journal, seeing all these people coming off of statins, uh, developed a group, uh, it wasn't the journal, there was a large government group of experts looking at, uh, statins. I can't remember the name of the group, but it was something like the statins safety trial group or something like that, and they looked at it, and they, uh, those activities led to a couple of the studies that you're going to talk about today in terms of nocebo. Bottom line was, hate to say it, hate and hate to give it away. Well, let me just not give it away. We'll talk, we'll let you talk about the nocebo trials in a few minutes. Why don't you take over for a minute?
>> Thank you, Dr. Brewer. So, let's start with why do we use statins so much to begin with? So it all started when doctors started noticing that when people had LDL increased, they used to have more heart attacks, strokes, and even deaths. So that in research is known as an association. It's not necessarily caused by the LDL. So then they started treating people with niacin, which was the first anti-cholesterol medication, should we call it. Um, then they discovered that the red yeast rice supplement that we see many patients use is actually lovastatin. It's just purified, isolated, and then converted into a medication. So the problem with the lovastatin is was that the half-life is very short and used to produce a lot of side effects. So we've come a long way since then, and we now have a lot of statins, and that's why the research has been pulling us to the narrative of, okay, this statin produced 30% less relative risk than the other one. But when we look at the numbers, it's really just a .5 or 1% difference of the absolute risk. So, uh, in simple terms, it means that they are enhancing the benefits that they found with one statin over the other just for marketing purposes. So go ahead.
>> Can I jump in and argue with that for a second?
>> Please, please do.
>> You're talking about the relative versus absolute risk, right?
>> Yes, sir.
>> So, um, you know, that is a narrative. You clearly hear it with David Diamond. Um, a huge portion of his content has been, uh, that that's marketing purposes. Um, and I have a different perspective on it, a little bit more nuanced perspective. I think, um, I, I don't think that that's unreal. You know, I think if you take a hundred people and 10 of these people have cardiovascular risk, uh, those 10 people are no longer thinking of themselves as, as the other nine. They're thinking of themselves as, I got cardiovascular risk. What are the things that will decrease my risk? So, I think it's a little bit too, and I've, uh, gone out with content on that too, taking the other side of that debate with, uh, Dr. Diamond. So, I don't think that relative risk is simply a marketing term.
>> There's no question it benefits big pharma in terms of the facts and the outcomes, but it's more than just marketing. Uh, we work, as you know, we work with people that have cardiovascular risk all day, every day,
>> and, uh, dozens of them every week. And,
>> these people want to minimize their risk. They're not putting themselves in the class of a teenager who has no plaque.
>> Yeah. The difference between statins are real. For example, we are known to use mainly two of them, um, rosuvastatin and one new one called pravastatin, and it's mainly because they don't produce any side effects, especially towards diabetes. Uh, we don't, they don't push di, uh, diabetes, they don't push patients towards diabetes, so I think that's a real difference. But the way I've seen statins differentiate themselves is on the relative risk towards specific endpoints, and not always is, um, cardiovascular death or heart attack or stroke. It's mainly, how much does one statin reduce LDL versus the other? So that was the reason for my marketing comment. Now, when they, when people started noticing that even if they controlled for diabetes, blood pressure, and even cholesterol, why were they still dying? Well, that's where the residual risk comes in. The residual risk is something that makes us have events that is not attributed to the diseases that we're treating. So that's where inflammation started to come along as a topic of discussion. And not many years ago, a study was published called CANTOS. And what it did was it used a monoclonal antibody that they normally use for inflammatory diseases, right? Lupus, etc. And they used it,
>> arthritis.
>> I'm sorry, Dr. Brewer.
>> Juvenile female arthritis, a very, very unusual rare type of inflammatory arthritis that hits kids.
>> Yep. Thank you for the, for the comment, Dr. Brewer. So basically, this study was the first study in terms of cardiovascular trials that aimed to reduce inflammation to reduce mortality. And even though it didn't reduce mortality because it was a short trial in comparison to more long-term trials, it did however reduce the number of events of cardiovascular events, especially heart attacks on people who just had a heart attack on the six months prior to joining the study. So what it did was it proved to us that inflammation was a player all along, and we just didn't see it. So that's where the inflammation conversation started, and then that opened the door for much cheaper medications like colchicine to establish a benefit as well, reducing inflammation in people with stable coronary artery disease. So, um, having said all of that, this is used, these medications are used as standard of care. So what does that mean? It assumes that the doctor already exhausted every other possible way of treating the diseases in the first place, aka lifestyle, nutrition, exercise, sleep. Studies assume that doctors have a very deep conversation about these topics. However, in reality, we know this is not the case. So, what doctors normally do is just titrate all medications as high as they can go because the guidelines say so. So, well, yeah, I've, I've rambled for a few minutes now, so I want to see if you have any comments about what we discussed, Dr. Brewer.
>> Well, thanks, Bernie. Yes, I do. You know, I'm so glad you brought up the information about inflammation. Information about inflammation, cardiovascular inflammation. You know, most docs, myself included, had a very, very difficult time making that leap from saying, "Oh, it's LDL causing this problem," to saying, "There's inflammation that's causing the issue." And, you know, the CANTOS trial that you just discussed, the one of the first ones showing inflammation and decreasing inflammation with that, uh, medication you mentioned, canakinumab. That CANTOS trial was done by the principal investigator was a fellow named Paul Ridker. Now, when you go back 20 years, Paul Ridker and his friend Gavin Blake at Harvard were the first guys to notice, and you go back to a couple of other studies that I've already mentioned, the Wascops trial, the Jupiter trial. What they noticed was whether the LDL was elevated or low, if the study participant was on a statin, they had fewer events. So Ridker and Blake started thinking, you know, maybe it's not, it certainly doesn't appear to be LDL level. Maybe it's not LDL causing the risk. And maybe these statins are not, uh, having their impact on preventing heart attacks because of they're lowering LDL. Maybe they're doing something else. And sure enough, at that point in time, there was no evidence to clarify that it was inflammation. They made a guess and then they began to research it. And over the next couple of decades, it became very, very clear, and that led to Paul Ridker doing a host of studies. He looked at, um, the gout medicine that you and I just described. He got a, a positive impact from that, decreased events. He actually, uh, ended up going back a year or two later with canakinumab, which he used in the CANTOS trials, and did get an indication from the FDA to use it for cardiovascular, um, uh, prevention. And as you know, uh, you and I use that gout medication today, as long as well as people on both sides of this LDL debate. Yes. And people who want to try to find gaps or limitations on the colchicine study might say, well, colchicine was added on top of standard of care. So meaning they really had, um, their statin treatment, blood pressure, diabetes medications, and on top of that, the colchicine. However, as you said, Dr. Brewer, you and I know colchicine can be very effective to target chronic inflammation derived specifically from cardiovascular causes. So, we've had, we've gone down this path in terms of understanding inflammation. Let's go back and talk for a few minutes about why is everybody so afraid of statins anyway? What, what were the, what was it that The Lancet was bringing up? What were some of the other groups that were bringing up? Uh, you know, if you've ever watched any video on YouTube other than this one about this topic, you already know muscle pain, uh, diabetes, brain fog. Those are the biggest ones. But we're going to talk in just a minute, I think you're going to cover some of what we call the nocebo trials, some of those trials showing, um, that these side effects aren't nearly as as common as people think they are. However, I have a major problem with the next step in progression that happens with doctors being aware of the nocebo trials. Doctors tend to ignore statin side effects, and they're real. You shouldn't ignore them. They are very real. You mentioned, for example, a few minutes ago, um, that rosuvastatin and pravastatin don't cause any side effects. Well, I would, I would differ. I'd back up. You know where I'm going with this. High-dose rosuvastatin clearly does. It causes progression into, uh, diabetes. It causes muscle pain. It causes those things that we're talking about. But the lower doses that we use really do not. Now, um, the, the big side effect that I haven't mentioned yet is rhabdomyolysis. Yes, it's muscle pain, but it's muscle pain to the point that it's, uh, it's destroying the muscle. That, uh, some proteins from the destroyed muscle can hit the kidney and actually destroy the kidneys as well. So, these are real, very big, uh, side effects. They're not totally made up. There's no question there's a bunch of fear around them. Um, and so, why don't you talk a little bit more about the, uh, the fear, the nocebo trials, what that means, and then let's go back and put those together with, well, what do you do next? Because there is a way through this. It's not a quandary.
>> Okay, Dr. Brewer. So yes, you said, um, low-dose statins really are very well tolerated by our patients. And when I said they have no side effects, I meant versus the placebo arm, which is what we should compare it to when we do a clinical study. So, as you guys probably know, the statins block a specific enzyme on the liver, right? That it inhibits the liver from producing more cholesterol, more LDL. So, the problem is this enzyme is not specific to the liver. It's, it's present on the brain. It's present on muscles, on joints. So that's one of the theories that, uh, scientists have come up with that explains the pain and the symptoms that patients feel when they use a statin. However, some other scientists wanted to really put that to a test. They wanted to know if the patients were reacting specifically to a statin or they were reacting towards taking a pill in general. So that was the premise for the SAMSON trial. The SAMSON trial is a small trial. It's 60 people that were studied, and it was a one-year, uh, three-arm crossover trial. So what does that mean? It means that we had the population divided into three groups, and all of those three groups were going to use statins, placebo, or no treatment at all during one year. So the overall study lasted for three years, but people were required to have a full year's worth of data. This study was published in 2021. It involved adults over 65 years of age who had specifically stopped taking statins within two weeks of having started them because of the side effects. The, the statin that was used was atorvastatin 20 milligrams daily. Now, we don't like atorvastatin at our clinic because it has a higher incidence of side effects and also it, it is one of those statins that pushes patients towards diabetes. So, we don't really like that, but it's all we've got for this study. Now, the patients tracked their symptoms with a daily app. Okay? They had to track their symptoms daily on an app. And the outcomes that were evaluated were the self-reported symptom intensity, the rate of discontinuation, and the quantification of the nocebo effect. Now, what is nocebo? You've certainly heard about the placebo effect, which is a benefit that we're feeling from doing something, specifically taking a pill, and attributing the benefits or the results of that intervention to the pill, even if that pill was only sugar. Okay? Now, because there's a placebo effect, there's also a nocebo effect, which is the feeling that the medication or pill that I'm taking is actually making me feel worse, even if the pill was just containing plain sugar. So that's what basically a nocebo study is. So what did the scientists find in these, in this study? So they found out that the symptoms were higher when people were, when people were taking a pill, independently if it was a statin or placebo. And not only that, the behavior of the reports, the patients actually reported the same intensity of side effects as the arm that was actually using the statin. Almost identical curves. I think we can put that curve on post, but so we can show it on the screen. But it was basically lines that behaved exactly the same over a three-month period. Okay? The initiation of symptoms, the, the ups and downs were almost identical, even though patients were using placebo and statins. So that really makes us think, was it really the statin producing the side effects, or was our own perception of what the statins can do to us that made us feel that? So what do you think, Dr. Brewer?
>> I think it's clear. I, I think there's clearly a boatload of evidence, and that's a, and that's a big chunk of it, that indicates there is a lot of fear with statins. And at the end of the day, um, doctors can argue with fear all they want, but, you know, it's sort of like what we know, you know, from what you learn from doing a YouTube channel. People react and they make decisions based on emotions. So, uh, that, you know, if you're a doctor and you're trying to help the patient, and you're, you need to think, you need to think through this. The patient is a human being, and they are very much, uh, motivated by emotion, in this case, by fear, and fear of side effects. And to just deny it or, uh, ignore those emotions is really the wrong thing to do.
>> Mhm. Yes. And us in the clinic have developed protocols based on your knowledge and experience, Dr. Brewer, that involves using statins halfway. So basically using it at a low dose, and even at studies have shown that even rosuvastatin 10 milligrams once a week significantly reduces LDL and other markers of cholesterol. So I think the main reason, I think our goal is to exhaust every single intervention related to lifestyle. So nutrition, exercise, sleep, toxin avoidance, and community support. But if that doesn't work, how do we counter aging and genetics? Right? That's the difference within our own patient populations. Why some of them develop more plaque than others at the same age, even if they are doing the same exact lifestyle. So that's where some studies we've reviewed in our practice come into play. Basically trying out different protocols, rosuvastatin once a week, three times a week, and patients overall really tolerate them well. Don't you think, Dr. Brewer?
>> Oh, there's no question. You know, one of the things I love about, uh, working with you, Bernie, is your knowledge. You know the space very, very well. And sort of because you do, I love to debate with you. One of the things that I would debate is I'd go back to. One thing I won't debate was the comment about this, um, this monster that's following us and getting closer and closer. It's called aging. Growing old is not for sissies. You know, you're, you're still a young man, and so is Jesus. And sometimes Fred and I, who are both old men, love to give you guys a hard time because again, uh, you haven't dealt personally with the problems that we've dealt with. But unlike most men your age, you deal with this on a daily basis. You work with it. So, you have really good knowledge in it. But I still would, uh, would debate something that you said a minute ago about, you said something about we do a halfway with statins. I would say no, it's not halfway at all. It's a totally different perspective on statins. So to your point about what we do, we, uh, like the standards committees on, on the, you know, the American Heart Association and others. We do not, uh, we don't recommend people that have no plaque to use a statin. We recommend lifestyle all the time and we focus on it. Uh, we only use statins in people that have already proven that they have gone through periods of cardiovascular inflammation. And our goal is usually not to lower LDL. In fact, I can't remember the last time that I recommended lowering LDL. The, uh, what I recommend lowering is inflammation, which gets back to that 30-year-old story about that started with Paul Ridker and Gavin Blake noticing that, hey, you know, most people are given these things to decrease LDL levels, but it, that doesn't appear to be what's actually going on here.
>> Exactly, Dr. Brewer. No one is talking about the pleiotropic effects of the statins, and preventive medicine has been a pioneer on this topic. What are pleiotropic effects? Are basically things that we found out the medication does which wasn't really the main purpose. Best example in the market, Viagra. It was supposed to be a blood pressure medication, and now we all know what, what it does. So the statins also have pleiotropic effects, especially the reduction of inflammation. So we know it reduces inflammation because it brings down the C-reactive protein and other markers we use in our practice. Um, it stabilizes plaque. So what, what's really allowing LDL and other particles to get inside the artery wall is the inflammation. So if we reduce this, the inflammation around the plaque buildup, then the particles have a harder time getting inside, and that's why we really use the statins for.
>> It is true. Now, speaking of LDL levels, as you know, you work with me all the, all the time with patients, and we have a lot of patients that have unique high levels of LDLs, the familial hypercholesterolemia patients who have a genetic predisposition for this, and the lean mass hyperresponders. At the end of the day, um, I, we do think that LDL levels do matter, and there's an inflammatory marker called LP-PLA2, but we do think it matters. The problem is we don't think it's clear enough yet how much it does. So the patients that we bring in, or they come in to us that have one of those two genetic variations, um, we make sure that they know the science, they know the evidence, they know the science, they know what's known and what isn't known, and can support them. A lot of them choose to say, "Yeah, I would like to lower my LDL." Uh, up until about three or four years ago, most of them did. About three or four years ago, with all this information about lean mass hyperresponder and all this pushback you see on LDL versus metabolic disease, you see a lot more people now saying, you know what, I'm familiar with all of that. I'm not quite as concerned about lowering my LDL, but I would like to make sure that I manage my inflammation. And again, although all, most of the conversation on this show is about statins and LDL, the reality is most of our conversation always gets back to lifestyle.
>> Correct.
>> Yes. And we do have developed, uh, very specific protocols tailored for every single type of patient with different, uh, levels of mobility. And many of them come just about to jump off the cliff, and you have to literally bring them back because they're so afraid. They think, like, they talk to the cardiologist, and they think they're going to die.
>> Yeah. That's a, it's a really, really good point. We do get people that come in to us quite often that are panicked about one thing or another. For example, I went to, I had, um, I got a calcium score and it came back over a thousand. For, I had, my doc wanted to do a stress test, and then he took me in to do a CT angio, and he wanted to do a stent or a bypass, and the doc told me that I have zero flow in the artery of my heart, or I've got something in the widowmaker, the L, and one of the, the biggest first roles we have to play is to again, uh, help that person deal with their emotion, the fear that they have, because they're looking at, they think they're looking at life and death. And the reality is they're not in nearly as much risk as they think they are based on those interactions. They go for, they'll go low carb, and their LDL will shoot up, and then their doctor will say, "Well, you're killing yourself with that diet." And the evidence is not, does not support that.
>> Yeah, there's definitely a need, uh, to train current and future doctors about cholesterol behavior, about genetics, about lean mass hyperresponders. Not everything is fixed with a statin. And well, that brings me to our final study for today, the LoDoCo2 study. So this study answers the question, well, how else can we treat inflammation on a cardiovascular patient if it has plaque, stable plaque, but it has plaque, but he has plaque? So the LoDoCo2 study basically used also a medication normally used by autoimmune patients, um, or patients with autoimmune diseases to try to reduce that residual inflammation. And what they managed was just that. They managed to reduce the composite endpoint called MACE, major adverse cardiac events, mainly heart attack, stroke, and cardiovascular death, significantly versus the arm that wasn't using low-dose colchicine. So, colchicine is really a game-changer because it's a very cheap medication, known by the community, by the medical community, many, many years ago. So we actually use it in our practice in on specific situations, but many of them rely on patients not tolerating statins. So also a medication I learned with you is bempedoic acid, which I like to call the statins without side effects. Because remember, remember when I mentioned the statins block an enzyme that is not specific to the liver, because it's on the brain and muscles and joints? Well,
>> Bempedoic
>> I'm sorry.
>> acid.
>> HMG-CoA reductase.
>> Yes, sir. That's that same one. Well, bempedoic acid blocks another enzyme involved in cholesterol production that is only present on the liver. So that's theoretically why it has less side effects. But the reduction on LDL and inflammatory markers are identical. So we might hear a lot of bempedoic acid in the next few years, especially in cardiovascular event reduction.
>> It's a really good point, and I, I had forgotten that about bempedoic acid and the mechanism. So thanks for reminding me. While I'm thinking and while we're talking geek speak right now, there's a couple of things that, uh, that you brought up that I wanted to help people with memory on. One is the pleiotropic. You know, that's a, that's pleiotropic is a side effect. A pleiotropic effect, there's a side effect, not the original effect. The way to remember that, and you were talking about that with statins. Statins, the original effect was to lower LDL. But the side effect is what we use it for, uh, lowering inflammation. Those of us who have heard of anything of the constellations, you may remember the constellation, the Pleiades. That's the seven sisters. So as you see, that's a, it's a Greek root word meaning many or extra. You also mentioned the LoDoCo trial, and that came from a mashup of a couple of words too, three words in fact, low-dose colchicine. So the LoDoCo trial is a low-dose colchicine trial, and yes, we do use low-dose colchicine for people that have inflammation. We recommend it. We have, because of the increasing awareness of colchicine these days, a lot of people come in asking for it, and yep, we, um, we do use it.
>> Yes, Dr. Brewer. So I think we're running out of time. So what would our main points be for today?
>> From my perspective, again, it gets back to the same thing. Number one, uh, statins became a victim of their own success. And they're not perfect. They do cause problems, but again, because they became so successful, people begin to look for the downsides of them. And there's no question they are not perfect. They do have their downsides, up to and including death. So they're not, they're not totally harmless drugs, unfortunately. Um, they got, they got overused, and they're still being overused. They're being used as an easy button for docs. You know, insurance, medical insurance has a, some good sides to it. It helps people pay for their healthcare. On the other hand, once you actually get into the meat grinder aspect of how it works, medical insurance wants to make sure that a doctor actually does something before they pay the doctor. Education is not easy for an insurance company to, um, to document. So they start looking at things like, well, did you give them a statin? Did you give them a prescription? Did you give them a statin? Docs, on the meanwhile, are getting paid less and less and less per visit. So they need to see more and more patients in the day. So they create a treadmill for themselves and their patients. You come in at this point, you're getting an average of six to eight minutes with your doctor, and that is not, I mean, you and I have talked about this, statins, this one issue for an hour. Six minutes is just totally inadequate for seeing a patient, but that's what the medical industry, the, uh, insurance industry has created. And, um, so then that just watersheds back down to something like statins, which were very successful at helping prevent cardiovascular diseases. Doctors have said, "Hey, it's an easy button. Let me just look for LDL and give a statin." Unfortunately, we've ended up in a bad place. And as you know, good medicine involves stepping back, talking to the patient, doing what the original standards committee said, doing a significant deep dive into the different types of risks of cardiovascular disease, not just taking an LDL, a cholesterol level, and prescribing a medication, statin or otherwise. So, um, that's what we do for a living. You know, we're sort of a voice in the wilderness out there saying, "Hey, let's get back to the originals of medicine, which is lifestyle and helping the patient understand the lifestyle that actually drives good health." Yep. There are times when statins can help. There are times when other medications can help. There are times when supplements can help, but it takes a little bit more knowledge than just getting a lab test and reacting to it. That's mouth.
>> Exactly right. Exactly right, Dr. Brewer. So, there you go, folks. If you want a clinical practice that takes care of you, that discusses things with you, just not tells you to take things, and that actually knows how to explain and help you develop sustainable habits in the long term, uh, you should talk to us. And if you want Dr. Bernie on your visit, you can tell Tracy that you can ask for me.
>> We got a plug for Bernie there.
>> Yeah.
>> There we go.
>> Well, thank you very much for having me, Dr. Brewer. It was wonderful. I really appreciate it.
>> On Bernie.