[ 00:00:00 ]Welcome to the Dr. Gabrielle Lyon Show, where evidence-based information meets innovation and practical application for everyone. Today, I sit down with Christy Ballantyne, MD. He’s an internationally renowned expert on lipids, atherosclerosis, and heart disease prevention. He’s the chief of cardiovascular research and the director of cardiometabolic disease prevention at Baylor College of Medicine. He’s in the top 1% of the most cited investigators; he has over 800-plus journal publications in the areas of atherosclerosis, lipids, and inflammation. His research has led to the approval of, get this, two biomarkers for cardiovascular risk prediction, and he has played a prominent role in the development and approval of new lipid-lowering therapies. Dr. Christy Ballantyne is the current president of the National Lipid Association. He is an absolute unicorn, and what you’re about to listen to is someone who is an expert with decades of experience in clinical practice and basic science genetic research. This is a highly scientific episode, so if you are a provider or if you are someone who is interested in lipids, this show is for you. Please sit down with me with Dr. Christy Ballantyne.

[ 00:01:30 ] Dr. Christy Ballantyne, thank you so much for coming on the show. Current president of the National Lipid Association, just an incredible researcher and academic. Welcome to the show. My pleasure. Now, we are going to talk about all things cardiovascular-related and cardiometabolic health, which seems to be the buzzword now. But before we do, tell me, why cardiology? So, you know, a lot of things that we end up doing in our lives, some of the antecedents begin before we were born, actually, because genetics plays a big part in all of our lives. I never knew my grandfather because he died of a stroke, and I never knew my grandmother because she died of a stroke. And when I was a junior in high school, my father had a heart attack.

[ 00:02:17 ] So, he had atypical symptoms, went into the hospital, was not in the ICU. But had a cardiac arrest, and he was very lucky that my mother was in the room, ran out, grabbed somebody, and resuscitated him. So, I had an interest in cardiology beginning, you know, I’m sure because of my father’s event with it. But there is, the family histories are really important. So, everyone needs to know their family history because there is likely things you may have inherited with that. And another thing is, if you look at the, the families, it’s actually the people who died at the youngest ages were women, not with men. My aunt, my father survived, but his sister did not. The first day she had symptoms was the last day she was alive.

[ 00:03:06 ] The first day she had symptoms was the last day that she was alive. Right. She lived on a ranch in Arizona and was always taking care of her husband. And then she had symptoms, you know, did not get into care soon enough. And unfortunately, my older brother, who was incredibly bright, but really kind of focused more on alternative approaches to medicine, the first day he had symptoms was the last day he was alive. Ah, that’s really significant. And I, I also really like that you said, alternative practices, because oftentimes, listen, there are certain things that can be treated with alternative means. And then there are very particular metabolic challenges that cannot and should not. Correct. So, this is where genetics plays a big role.

[ 00:03:53 ] We can talk more about that, but it is something also, we’re knowing what the symptoms are. And then, you know, if you have a bad family history, if you have symptoms, it’s better to get it checked out immediately. So, if your chest pressure, chest tightness, shortness of breath, just don’t feel right, and you know you have a family history, it’s easy to go into some of the local ERs. They get a quick EKG, blood test, and they’ll rapidly send you home if there’s nothing wrong. If there’s something wrong, if there’s something wrong, then sometimes you go straight to the cath lab. But I do think that knowledge is power. That’s why you’re doing this podcast. That’s right. For it. And it’s important that people understand it’s, it’s women and men, both.

[ 00:04:36 ] And my mother’s she, her mother died when she was young. How old? She was probably about eight or nine years old. And so, and her mother had a stroke. Hypertension treatment wasn’t, people didn’t treat it well back then. They were Greek immigrants. And she probably hadn’t seen a doctor. Or something. I don’t know quite why she had the stroke at such a young age. But it is, just because sometimes women think they’re protected. But actually, more women die from cardiovascular disease than from cancer. More women die from cardiovascular disease. What, do we know some of those numbers? How many women are dying from cardiovascular disease versus cancer? So it’s the number one cause of death for women. Now, what happens is women tend to be older.

[ 00:05:20 ] So people say, well, I don’t have to worry about it when I’m young. But unfortunately, there’s, and this is when we bring up this cardiometabolic concept. There’s been a change in some of the risk factors for cardiovascular disease. So, you know, when, when I, when I first started, you typically saw someone who, they maybe were a heavy smoker, very high cholesterol, and frequently thin. Uh, and now what we’re seeing is, unfortunately, younger people with the epidemic, obesity, they get insulin resistance at a young age. Many get diabetes at a young age, teenagers, 20 years old. So by the time they’re 40, they’ve had diabetes for 20 years. And now you’re seeing young men and women coming in the hospital in their 40s, having heart attacks who were not smokers, uh, didn’t necessarily have a terribly high cholesterol.

[ 00:06:15 ] So it’s, so this is one of the reasons we talked about cardiometabolic, because it turns out that, obesity, diabetes, triggers inflammation, other different processes that can also lead to the same events, heart attacks and strokes, as very high cholesterol or cigarette smoke. You know, it’s really fascinating. It’s also, you know, you mentioned, um, and I have a question that no one, I think, has been able to answer, except I think you’re going to be able to answer this question. And it’s a very simple question. The numbers for cardiovascular disease deaths, when someone goes into the hospital, and let’s say they die of natural causes and their heart stops, what goes on the death certificate? Does that get counted towards, um, does that get counted as a cardiovascular event? Not necessarily.

[ 00:07:07 ] So, I think this is one of the things that, uh, and this is a more nuanced question, but when we look at clinical trials, so there’s lots of studies that are done looking at how can you reduce heart attacks and strokes and cardiovascular deaths, it’s important to look at cardiovascular death, but also total mortality, because a lot of times we don’t know exactly how someone dies. I used to work in emergency rooms, and when somebody brought somebody in and they were dead, and I had to sign their birth certificate, I didn’t spend a lot of time thinking about that. I mean, they were already dead. So, you know, what did they have cancer? Okay, I put cancer. Maybe they had a heart attack, but when someone’s dead, there’s not a lot of medical investigation that goes on.

[ 00:07:53 ] So we don’t frequently know unless they died in the hospital, and even then sometimes in the hospital we don’t know. So I do think it’s, you know, your question as to, do we know exactly why people die on these, when we see these statistics, we know more or less, but there’s going to be some gray areas. Yeah. And the reason I ask is because I always, you know, I’m trying to think, is cardiovascular, we know that there’s cardiovascular disease, and then there’ll be, you know, the CDC will publish, um, a ranking of causes of death. And I always think to myself, okay, well, people seem to live with cardiovascular disease for long periods of time, and are those numbers accurate? Is it truly the leading cause of death, or is it how it’s being reported?

[ 00:08:35 ] And it’s just out of curiosity. Yeah, so I think it’s in between cardiovascular disease and cancer. What happens is, now that we’ve gotten better with cancer, now there are people that end up living longer, they’re dying from cardiovascular disease. So those two are your major two threats. One thing about cardiovascular disease is that in addition to death, there’s a whole quality of life issue. And there is with cancer, too. But, you know, if someone has heart failure, if someone’s had a stroke, if you’ve had angina and you can’t do your activities, quality of life is very impaired. And so that’s an important issue. We want to live longer, but we want to have robust lives. And the other one that comes up is, you know, one of the hats I wear is we’re the core laboratory for the atherosclerosis risk and community study.

[ 00:09:26 ] So this was a study of middle-aged people when it started, but it started in 1987. How long have you been in practice? How long have you been in practice? I’ve been in practice. I joined the faculty. I took over the Eric Lab in 1997, and I joined the faculty in 1988. 1988. And to be fair, you’re a cardiologist, but you also, you know, have a lab in, is it translational genetics? So we have a this study, the Eric study was 16,000 people, and they’ve been followed. But now, of course, they’re quite old. And it’s turned into a study that’s looking at neurocognitive changes. And one of the things that, there’s an appropriate, so people are very concerned about Alzheimer’s disease. Because Alzheimer’s hits earlier in life, in your 50s and 60s.

[ 00:10:21 ] But as you’re getting into the 70s and 80s, what we’re seeing is a lot of the dementia, cognitive decline, looks to be more of a vascular, and maybe sometimes mixed with Alzheimer’s. But there is a very important aspect, is that the biggest predictor of dementia in middle age, diabetes. Second, hypertension. Third, high cholesterol. So, and those are all cardiovascular risk factors. So I think this is one of the things that comes up, is a cardiovascular health is important in terms of both the quantity of life and the quality of life, including mental function, and including, you know, other things. I mean, if you just imagine sexual function, that’s also vascular health. When people talk about impotence, you know, for men, and we’re talking about really dealing with blood flow, endothelial function, and the drugs that work there have that effect.

[ 00:11:18 ] So it’s, it’s a big aspect of really, you know, both quality and quantity of life. If you were to think about what your legacy is to be, and what information you want to really impart upon people, what is so important and critical for cardiovascular and or, I don’t know, should we say cardio metabolic health? Because that seems to be with 70% of adults are either overweight or obese. What would you tell them? What would be the top three things that they should know about cardiovascular? Well, so I, I think the thing is most people will die of either cardiovascular disease or cancer. We have the knowledge to prevent 75%, 80% of the cardiovascular deaths and to reduce pain and suffering and quality of life there.

[ 00:12:06 ] You know, with cancer, it’s a little more challenging. Yes, we know smoking cessation, but a lot of the cancers now we’re seeing, for example, why are younger people having more colon cancer? I mean, there’s, it’s something in the food or the diet. We don’t understand a lot of what causes cancers, which some of it’s harder to prevent with it. Certainly, a risk factor would be obesity. So, obesity is an important one. You know, and I’ll tell you, so for example, in addition to cardiovascular disease in my family, I had lymphoma when I was in my forties. And so one of the things that came up after that was when talking, and no one knows why you get lymphoma, you know, it could be pesticides, there’s environmental things.

[ 00:12:49 ] But talking to my oncologist, he said, ‘ask him’, well, what can I do for, you know, stopping a recurrence? He said, ‘well, it looks like the people who do the best are the people who exercise.’ And that’s probably something that you’d like to hear about. No, we don’t. We’re not interested in exercise on this podcast. But after, you know, after the okay, let’s see. And I forgot, my mother’s side, it’s all diabetes. My father ended up getting diabetes later. So I’ve got diabetes. I already had coronary calcium when I was 39 years old. And then I have cancer. I said, you know, and I’d always exercised some, but I’m like, okay, if it’s going to make a difference, I need to get really serious about this.

[ 00:13:28 ] And so I do think it’s, the lifestyle is a huge part of cardiovascular disease. And it’s an even bigger part of healthy aging. So I do think, you know, I know your focus on nutrition and exercise. That is our fundamental behavioral changes that we all need to work on. We’ve fortunately, we’ve got fantastic medications. And this is where the genetics is really important. Because if you’ve got bad genes, and many, many, many of us do have bad genes, there’s something you can do about it now. And people understand like in sports. And I always use the example, I think you’re new to Houston, but Jose Altuve, have you heard of him? No, am I, should I? So, yeah. So Jose Altuve is a baseball player. Okay. And, you know, he plays for the Astros.

[ 00:14:16 ] And when he was first tried out for the major leagues in Venezuela, they sent him home. They said, look, you’re too short. You’ll never play baseball. Just forget about it. Height is genetic. And when people understand that, like a height, they say, okay, he came back the next day. That’s because the scout said, ‘You got to watch him play.’ So if you have bad genes, looks like height or something in sports, what do you do? Try harder, play smarter. So it’s, it’s the same thing in life. If you’ve got bad genes, you’ve got to play smarter. So diet and exercise are important for everybody, but not forever. I mean, for everybody, but it might not move the needle for those. So, but it’s still, if you don’t do it, it’s even worse, right?

[ 00:14:57 ] So if you have a gene for familial hypercholesterolemia, even with a great diet, you won’t normalize it. But if you have a terrible diet and then you get obese and get diabetes, you’re in a really bad place. So the issue is, but playing smarter is I do the lifestyle and then find out more. Do you need a medication? Do you need your, what about your blood pressure? So these are the things, you know, if you get, so I think the most important message is, is it’s a preventable and treatable disorder. And if you’ve had a heart attack, you can, there are things you can do to not have another one. And when we think about lifestyle, let’s talk about exercise. What are some of the key components to exercise?

[ 00:15:41 ] So this is one thing, uh, I think you, if you look at the residents who are rotating or working with it, they always have a little note. They say, well, we’d like you to exercise. And they always put in there. I want you to walk 30 minutes, five times a week; that’s wonderful. That’s a great start. But I mean, that’s not exercise. I mean, that’s, that’s, that’s moving a little bit. Because the funny thing is, and they, then they say, ‘And you should get 10,000 steps.’ And so they always ask me, ‘Do you know how long it takes to get 10,000 steps?’ Can you get 10,000 steps in five minutes? In 30 minutes? And of course, you can’t.

[ 00:16:16 ] I mean, unless you’re running at it, you know-you have to really be running fast to get 10,000 steps in 30 minutes. So, you know, exercise to me ends up being, is it, you know, I, I try to get an hour a day of exercise, you know, and 10,000 steps. Cause sometimes if I’m doing resistance work, it may not be as many steps, but then I’ll, I’ll walk more. Uh, steps are great for vascular health. I mean, you know, if you help sustaining it, that’s very good. But I think you, you also need in particular as you get older, uh, you know, it’s, uh, like if your car gets old, it takes more, you know, get them a lot of more maintenance, you know?

[ 00:16:57 ] So I, and I think some of the data on healthy aging and cognition, I think exercise is doing even more than just the vascular. I think it’s doing some other things in terms of brain function that are really important for maintaining, uh, uh, you know, cognitive health. I, I absolutely agree with you. Um, thank you to Timeline Nutrition for sponsoring this episode of this show; Timeline makes Mito pure, which is one of the most thoroughly researched products that I have come across in over a decade, peer-reviewed, published science. This is where it gets really interesting for those following a muscle-centric lifestyle. When you increase the health of mitochondria, you improve muscle function and overall wellness in adults. 40 plus timeline, which makes your lithium a has been shown to increase muscle strength and endurance without changing activity.

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[ 00:20:22 ] It is a mix of electrolytes, and it comes in a cute, easy-to-travel-with packet. For me, that means no more dehydration headaches or muscle cramps. Now let’s talk winter for a second. Winter is one of my favorite times of year because Element releases its special flavors. Which, by the way, I stock up on for the year, which include their chocolate melody, chocolate mint, chocolate chai, chocolate raspberry. Holy cow! Have you tried these flavors? I guarantee you will never go back. Sometimes I mix it with coffee. Sometimes I mix it with hot cocoa or have it alone. Now don’t forget to hydrate in the cold. Winter activities also require water and electrolytes. Element has offered my community a free Element tea sample pack.

[ 00:21:09 ] So, you can get your money back with any order when they purchase through my custom URL, which is DrinkLMNT. com/ slash DrLion. And basically it’s totally risk-free. If you don’t like it, you can get your money back. But I know that you will. And especially with winter coming, get after these chocolate melodies. That’s DrinkLMNT. com/ slash DrLion. When you talk about exercise, and we talk about walking resistance training, would you say that walking is enough? How do we begin to think about taking care of skeletal muscle health? So I think this is really a critical issue, particularly. So it’s a funny thing, you know, when I’m seeing younger patients versus older patients, some of the older patients are like, ‘Well, I walk.’ And that’s great.

[ 00:22:04 ] Younger people tend to go to the gym more, but it’s even more important as you’re getting older. So when you hit menopause, when people are getting into their 60s and 70s, 80s, the issue that comes up is now we’re worried about basically quality of life, healthy aging, and things like insulin resistance, diabetes. You know, we get into things. Why? Why do we have these issues? Well, we know muscle is critical in terms of glucose uptake, but also mitochondrial function. And, you know, one of the things that comes up is, and, you know, balance. People fall. Well, walking is good, but, you know, you can do core exercise. There’s balance exercises. You can do a lot of things where you’re actually using coordination, strength. There’s an issue of free weights versus machines.

[ 00:22:54 ] There’s using bands. There’s, I work in a little trampoline thing where you’re having to balance at the same time you’re doing weight. So using, think about all the things your brain is having to do when you’re exercising. But I do think is that walking is great. It’s a strange thing sometimes where a lot of physicians are like, well, we can’t expect patients to do more than that. That’s a, I think that’s a, the wrong message. It’s, it’s completely the wrong message. And I think we need to lead by example. But the other thing is, if you really want optimal health, we put people on five or six drugs. That’s a lot of medications to take with it. And if you, if they were really exercising and eating a better diet, we can reduce the amount of drugs.

[ 00:23:39 ] So I think we want to give people guidance as what is optimal and encourage them to do whatever they can. But there’s no sense acting like optimal is walking 30 minutes, five times a week. It is not optimal. We don’t use, you know, five milligrams of low lovastatin, which was the first stat anymore. I mean, people used to, but we’d say, well, that’s not, that’s not that effective. So why are we recommending something that we know is it’s beneficial, but it’s not really optimal. It’s not the most effective way to, to, to prevent things or treat things. And what role do you think resistance training has, whether it’s machines or free weights? Essential. I think you, I mean, there’s what you, you know, the issue that comes up is as you age, you lose muscle mass.

[ 00:24:27 ] So you either are going to lose your strength. You know, it really is just a use it or lose it, a thing. So this is why it takes, it may, may take a little more time as you get older, because you may have to warm up more and then build up and do a lot more reps instead of doing real heavy weights, depending upon if you want to avoid injuries, but it’s still highly beneficial. In fact, the benefits are probably even greater as you get older. They’re there, they’re all along, but I think it’s even more necessary. You know, you also mentioned diet. And I think that, especially in the lipid space, this is highly, I don’t, I don’t know if it’s highly controversial or contentious, but in the nutrition space, people will say, well, don’t eat saturated fat because saturated fat is going to somehow translate to blood saturated fat, or don’t eat cholesterol because that’s going to increase your blood level, cholesterol.

[ 00:25:28 ] But the conversation really, you know, in my opinion, should be around total caloric intake and carbohydrates. So, I agree with you completely that total caloric intake is the real issue. And where is most of that coming from? It’s coming from carbohydrates. I mean, people tend to eat, I mean, if you take a look at, some of it’s fat, but it’s like potato chips. What people do is, there was a nice meeting all of a sudden, they were talking about highly processed foods. Where you can, in nature, you’re not going to find lots of carbs with lots of fat and salt, all in one thing like a potato chip. But, you know, food scientists studied what foods people like to eat. And in fact, which ones would they keep selecting over and over again?

[ 00:26:19 ] So, it’s almost like, you know, drug addiction that developing highly processed foods, which have very high caloric density, and which stimulate the brain and, you know, and you feel good. So, temporarily, you don’t feel; you feel bad afterwards, but it’s; there is this issue of people eating, because they’re; most of the eating we see, you know, in clinic, we always get; you know, weight, lipids, blood pressure. Somebody comes in, their numbers are off, their weight is up; what’s going on? Well, there’s, you know, stress; there’s job, there’s family; someone’s ill, and people turn to food, and they turn to the wrong foods, and then they usually quit exercising. And if you do just the opposite, if you increase exercising, you’ll handle stress far better, and maybe make better selections on your food.

[ 00:27:11 ] I think, you know, foundation therapy is is nutrition, lifestyle, and things like smoking, drinking your calories, particularly alcohol, sweetened beverages. Your brain doesn’t even sense, you know, that you’re full. So, you don’t; people can take in a huge number of calories with sweetened beverages. And have you, and yes, absolutely, and I think that that’s one of the reasons why we’re seeing such an increase in obesity, people are drinking their calories. Have you thought much about the recommendation or any of the dietary guidelines from a cardiovascular standpoint? So, they chose this number of 10% or less, your calories should come from saturated fat; not exactly sure the evidence behind that, because it doesn’t seem to be solid. And then, of course, cholesterol was in the guidelines, which they ended up taking out, I believe, in 2000, or 2010, or 2015.

[ 00:28:04 ] Do you get asked a lot about the dietary impact? So, I see a number of patients; now, it’s interesting. So, responses to, for example, someone goes on the keto diet; some people have a beautiful response, everything gets better. They’re; they lose weight, their glucose goes down, blood pressure goes down. Some people have what I call almost a paradoxical response, where their cholesterol goes way up, and their LDL goes way up. Now, and so, this is this, you know, lean hyper-responder issue. So, that concerns me, when I see that. And, it’s, it’s challenging, because some of the people are very young, and very fit. And, and I don’t know exactly how much, and it’s not easy to assess that, because when people are young, the imaging modalities are not as good, they’re not as useful, in terms of that.

[ 00:29:03 ] Would that be a C, would that be a clearly scan, or a hard and soft plaque scan? Yeah, so you can end up doing CT angiography, and then there’s some approaches towards looking at soft plaque, and things like that. There are different companies focusing in this area. And more people are getting that, and it’s reassuring, and I; the other one I like for women is; still we do chronic ultrasounds, and there’s a lot of criticism, but if you have a good, this is not one for vascular surgery, this is a screening test, to look at thickening, and specifically for plaque. So they get to scan the bulb, and if you do that test, there’s no radiation.

[ 00:29:41 ] So, in terms of women, comparing doing a chest CT, where there’s some radiation, a lot of my younger patients, I’ll get a baseline, see where we stand, in terms of making decisions, do we need a statin or not? There’s always the issue, in terms of younger people, when do you start? And sometimes, if it’s clearly genetic, like familial hypercholesterolemia, and with an LDL of 230 or 240, and a family history, we don’t have to worry, we don’t need any imaging test, we can start. You would start them on a statin, as opposed to say, azetamide. So, and that’s the other one that comes up is, there’s not enough utilization of combination therapy. So it’s interesting, in blood pressure, I mean, this will really show you how deep.

[ 00:30:24 ] When I was a resident at UT Southwestern, and they taught us that you start with one drug, you dose it up to the top dose, and only then do you start the second drug. So can you imagine a diuretic, like hydrochlorothiazide? So we did 25, then 50, then 50 twice a day. Oh my gosh. That would just kill quality of life too. So everybody had, you know, they had all kinds of hypokalemia, and metabolic alkalosis, so it was like, okay, this. People relapse pretty quickly, and then it’s like beta blockers to huge doses, clonidine. I mean, terrible drugs, at terrible dosages. And then they said, wait a second, why don’t we just go to combination therapy? We use a low dose of two drugs; you get control faster with fewer side effects.

[ 00:31:13 ] So, I think there has been, this is the case with the azetamide you mentioned: You can use azetamide with a low dose of statin, and get the same as the highest dose of the statin, without the muscle problems, without the insulin resistance. I mean, statins are fantastic drugs, but when you go to the top dose, the top dose is there for a reason. It’s because the dose above that, led to unacceptable side effects. Rosuvastatin, we did the trials there; we were studying 80 milligrams, but at 80 milligrams, we had some cases of rhabdomyolysis, and then they noticed that it was nonlinear pharmacokinetics, so that some people suddenly shot with very high levels, and it turns out East Asians were problematic. So they reduced the dose to the top dose, to 40 milligrams.

[ 00:32:04 ] So in general, you might say, well, if the top dose is there for a reason, you’re probably safest at the dose below that. And there’s a logic to that, which is pretty reasonable. So why do we go all the way to the top dose? Before we add ezetimibe? I don’t think it makes any sense. You can add in, and if someone’s afraid of side effects from a statin, add it to a low dose. And that blocks cholesterol absorption also. Yes. And you know, I don’t want to let you off the hook on the nutritional science part, the saturated fat and cholesterol, because I’m sure people are asking, and you know, on social media, you’ll hear people say, ‘LDL cholesterol doesn’t matter.’ Right. It can be as high as you want it to, it doesn’t matter.

[ 00:32:49 ] I’m curious as to what your thoughts are that. And I recognize that we’re going to cover LDL cholesterol, ApoB, Lp(a). It’s not simply just one marker, but. So, and that’s one of the things that comes up is LDL cholesterol. LDL cholesterol does matter, but so do all the other things. So if someone, you know, ends up having low blood pressure, excellent body composition, they exercise on a regular basis, which is also giving vascular health. They don’t smoke. They don’t vape. They don’t do cocaine. They don’t do some things that are adverse vasoactive. No family history. Everyone lives to be a hundred years old. You know, I don’t know. I mean, I’m not, is it ideal? No, but is it harmful for this person? There’s sometimes, and we see older people who have high cholesterol.

[ 00:33:41 ] They’re seven years old. They got a zero calcium. And they’re having someone said they, you know, they’re having, they’re having side effects. Well, you know, maybe you don’t need a statin. So frequently we end up trying to help people to understand, do you really have to be aggressive? Or sometimes you can say, ‘Look, your health is good. Everything else is perfect. You have this one factor and I’d like to lower it a little bit, but if it’s causing problems with your lifestyle, it’s not worth; it’s not worth it. The risk benefits aren’t there. What would your cutoff number be for something where you’re thinking, ‘Okay, if we were to just take a hypothetical patient, is it fair to take a lean mass hyper-responder?

[ 00:34:23 ] Or should we just take an individual who comes in with, you know, LDL cholesterol of 250? So every patient, I try to look at the total picture.’ So we always look at all the traditional things. What’s the age? And sex makes a difference in terms of, and for women also, you know, when women, you need to also take a look at things. We call them risk-enhancing factors. If someone was pregnant, did you have hypertension during pregnancy? Did you get impaired fasting glucose? Did you get diabetes? If you had preeclampsia, we know that you’re increased cardiovascular risk. If someone has polycystic ovary syndrome, increased cardiovascular risk. That’s interesting. Is that from, is that just related to insulin resistance? Related to insulin resistance. Yeah.

[ 00:35:11 ] So there are some things that you can also be getting that are, and then you then think you’re measuring lipoprotein A, HSC or P for inflammation. You might look at that. If they’re at appropriate age, I get a coronary calcium score, sometimes like an ultrasound. And then if there’s a bad family history, we were also looking at genetic testing for people, looking at beyond the traditional genes sometime. And would that be a GBS insight, something like that? We happen to be using them because we’re doing projects with them to try to get better understanding of their polygenic risk scores. You laugh. Is that because there’s another? No, no, there are many different; I’m just laughing because we happen to, you know, we’re doing some research with them, and it.

[ 00:35:55 ] So, we’ve been using GBS a lot for it. I think it’s particularly in the area of high triglycerides. They have an interesting panel. And when you are thinking about risk stratification, so there’s not an absolute; so it’s not just one number. There’s not one number. Basically, is what you’re saying. So, it’s very myopic to say LDL cholesterol at this number, is unacceptable. Is that fair to say? Or would you say, listen, this is 300. This is a risk for pancreatitis. Well, if an LDL is 300, I’m worried no matter what. So are there numbers? I think when we get into 190, we start thinking genetic for it. For some people though, 130 could be high. So it depends upon the individual. You know, it’s a continuous variable.

[ 00:36:36 ] In medicine, we like to have, make things dichotomous. We want to have a cut point. Yes, we do. I would like an algorithm, but life is not like that. You know, I mean, it’s basically so it ends up is you need to put that variable in with a bunch of other variables. You know, when I tell people like lipoprotein A is important. And can you explain, so before we move on, because I, we have to talk about LP little a, I will say we’ve been measuring that in clinic since we started. And I’m glad to hear that. That’s very valuable. The LDL cholesterol, there is a certain number where you, so, I think the next question is at what percentage will that, if it’s dietary related, could you modify that by 20%?

[ 00:37:24 ] Do we know, is there a certain percentage that we can move the needle? You know, so you can, for some people are diet and lifestyle sensitive. And I’ve had some people have drastic changes and you can go to extreme diets. I would say Dean Ornish. So Dean Ornish went to Baylor Medical, Baylor College of Medicine. And you know, he goes in with-if you go with a vegetarian diet with extremely low fat, basically low cholesterol. Now he also had meditation, exercise, weight loss. They lost weight in his program. So there were a lot of things going on in that program. I’m also curious as to the quality of the weight loss, how they were able to maintain their skeletal muscle mass. So I know they didn’t do that-that they didn’t lose that much weight, but it was, they were doing yoga.

[ 00:38:10 ] It was part of the program. Which actually will, which is beneficial. Yeah. So that was also part of one of the, one of the things that was with, with the program. And he showed some benefits, but it’s, it’s in general, those types of diets are hard to maintain. I think we have lots of information that the Mediterranean diet, which includes more fat, but a lot of it’s monounsaturated. It’s things like olive oil, but I mean, we talk about healthy fats, omega-3 fatty acids. So it’s not necessarily the fat. It has also to do with the quality of the foods that have the fat. So I do think that someone’s eating a lot of high saturated fat. Trans fats are clearly bad. Do they still allow those in the diet?

[ 00:38:52 ] They’re not supposed to be. Yeah. I think that they’re not even, they’re not supposed to be allowed, but you know, the issue that comes up is that it would be something also, like if you take something like ghee, which is a, you know, particularly the way it’s done and where they just keep heating and heating and heating it. So you’re probably doing a lot of modifications. And having, you know, if you have oxy steroids, if you can, you can probably make foods more unhealthy sometimes than if you’re eating something that’s more in a, you know, like in a natural state. So. So would you say that maybe. So, so some people can have big drops, but in general, it’s hard to modify your level of LDL.

[ 00:39:32 ] So, usually if someone, wait, wait, can you say that again? So, in general, it’s pretty hard to modify your level of LDL cholesterol, regardless of by diet, by diet, by diet. So triglycerides is a completely different story. Okay. Triglycerides, you can modify tremendously, but LDL, you might, some people might get a 20% reduction. That would be considered great. That would be considered amazing. And it doesn’t always happen. And it’s more likely going to be five or 10% is what you’ve seen. And, and there are things that we used to use for, you know, increasing soluble fiber. There were things that you can do. Does that make a difference? Five to 10%, you can get in that five to 10%.

[ 00:40:12 ] Now there was a, there was a Canadian who looked at the combination of diet and adding some of the, some of these other things we talked about. And he could show that if people really worked at it, they got around 25%. And that was using some basically nutritional things that to, to, to compliment your changes in diet. And the, would you say that the LDL cholesterol, is typically at a genetic set point and the body, if you, the body will make a certain amount of cholesterol. So much more so than triglycerides in terms of it’s, it’s much harder to modify by you. It doesn’t mean it’s not worth the efforts. Cause I do think it is worth, worth having a healthier diet, but triglycerides, we can see dramatic changes.

[ 00:41:01 ] I mean, someone can go from, you know, 5,000 down to 200 with changes in lifestyle. And that can happen within 10 days. It can happen in a week. Where do you like to see triglycerides? Ideally. So we talked about less than 150 being desirable, nor was normal, but desirable optimal be less than a hundred. Absolutely agree with you. And when you are looking at your patients, is there, when you count, do you guys counsel on diet? Do you talk about diet? So we do. We, my clinic, used to be run by a dietician and she just retired. Unfortunately, you know, like a year and a half ago, that was nice. Because we would, she would do the same thing for that. And it turns out also, she was really good at getting more information.

[ 00:41:50 ] Sometimes people don’t tell the physician everything. And then when they get out, someone asks questions, and all of a sudden they’ll say, ‘I didn’t really understand what he was saying.’ Can you help me? The triglyceride numbers we see, I worked on some of this, some of the early studies with, with Dr. Donald Lehman out of the University of Illinois. And when we reduced total carbohydrates to one thirty or less, we would see a drop and we; it would nor, it would completely. So 130 grams of carbs or less would completely normalize their triglycerides. Yeah. So what ends up happening is it’s, it’s a, when everybody comes in with high triglycerides, I give ’em like a quick, cause I asked them, okay, what are triglycerides?

[ 00:42:35 ] So people have heard of cholesterol and they’ve heard of the bad cholesterol, LDL cholesterol, the good cholesterol, HDL cholesterol, which really isn’t good cholesterol, right? It’s not, it ends up being, we call it not harmful. I would say, and not harmful. And unfortunately, the better number would have been the non-HDL cholesterol. Cause that’s, it turns out your LDL cholesterol is usually calculated. What’s measured is total cholesterol, triglycerides and HDL cholesterol. And they use the, the derivation, the respite calculation called the Friedwald equation, which has been, wasn’t that good if you had a high triglyceride or low HDL. So that’s been replaced by other numbers now, at least by some of the labs, but with it, but basically you can do something simple. If you subtract the HDL cholesterol from the total cholesterol, everything else is bad.

[ 00:43:25 ] And, and unfortunately, it’s not HDL cholesterol that doesn’t sound very threatening. I mean, how can a non-HDL cholesterol, that’s really the number that should be looked at. Oh, really? In terms of negative outcomes? Well, in terms of atherogenic cholesterol, in terms of atherogenic, it should have been called atherogenic cholesterol or something like that. The non-HDL, the non-HDL cholesterol, which has an extremely high correlation with APOB 100. Okay. So let’s break this down because we have clinicians and we have lay people. So, so, so when you get your lipid panel, it’ll show total cholesterol, triglycerides, LDL cholesterol, and HDL cholesterol. If the LDL cholesterol is high, that’s bad. But as you point out, if the triglycerides are high, that’s also bad. And many times people get false reassurance. They may see their triglycerides 250.

[ 00:44:17 ] They say, oh gee, my LDL is only 100. But if their HDL is 35, and then they see what the, if you were to look, usually it means that if you subtract the total HDL from the total cholesterol, they have a high level of non-HDL cholesterol. Now, what’s happening in your blood is that cholesterol and triglycerides are not soluble in an aqueous solution. You put fat with water, it floats. So they’re being packaged in these particles. And the LDL particles are particularly bad, but those particles carrying triglycerides, they’re called VLDL and VLDL remnants, IDL, they also contain cholesterol. And they’re also harmful. So, when you see a high triglyceride, you should be looking at all of the bad cholesterol, the atherogenic cholesterol. And that’s one reason why, yes, ApoB is better than LDL cholesterol, but so is non-HDL cholesterol.

[ 00:45:13 ] Non-HDL cholesterol. When you think about non-HDL cholesterol, what you’re saying is that that is atherogenic. And what that means is that causes plaque deposit. When someone hears atherogenic and why it would be bad. So that’s thinking of that, that’s the cholesterol that can be built up in the plaque and the arterial wall. And we know that in the, if you look in the atheroma, so when we talk about atherosclerosis, that means there’s atheroma. Atheroma has macrophages and they have cholesterol crystals. And where is that? The atheroma? It’s in the arterial wall. In the arterial wall. So, and that’s from data from going back from Anichkov, who was looking at foamy macrophages. So we call them foam cells. So, now one other approach is to measure ApoB100 because there’s an one ApoB molecule in each LDL particle.

[ 00:46:09 ] And in those triglycerides particles, there’s no ApoB in HDL. So you can measure. There’s no ApoB in HDL. Right. And then what about non-HDL? So all the particles in non-HDL have an ApoB. So an ApoB has a very high correlation to non-HDL cholesterol. So if someone’s using that non-HDL cholesterol, there’s less discordance with ApoB. And I know there’s a lot of focus on you have to measure ApoB. You’re not necessarily in everybody. I mean, and it turns out a lot of people, you don’t need to measure ApoB with it. Why is that? So let’s break down because I will tell you, ApoB is the most popular. That’s all we hear about. So it’s been popularized by some people. I’ve done a lot of research in this area.

[ 00:46:56 ] And if you take a look, like in UK Biobank, this huge study, the correlation between ApoB and non-HDL cholesterol was 0. 95. 0. 95. 1. 0 is perfect. That means they’re the same. And if our lab runs assays from two different companies, measuring the same thing, if we get a 0. 95 correlation, we’re quite happy. You’re very excited. Yeah. That’s great. So how much extra information do you get from an ApoB versus non-HDL? A little bit. Now, from LDL, you get substantially more. And the problem is, so ApoB, you know, so why? It’s because of this triglyceride issue that you bring up. Why is ApoB important? Is that what you’re saying? ApoB gives us more information about what kind of particles are in those people with high triglycerides.

[ 00:47:51 ] Because some people with high triglycerides have lots of small LDL particles. So someone might say, ‘Oh, wait, isn’t there, there’s another test using NMR that looks at LDL particle concentration.’ And so would this be, this would be the Boston Heart? So Boston Heart does it, but so does, so does LabCorp. And you can get a LDL-P concentration test, and they’ll, and they’ll break it down into small LDL. And they’ll also give you an LP, incident resistance score sometimes with, at least with LabCorp. Now, that technology is actually newer than ApoB. And the confusing part is, unfortunately, the labs use different software and different magnets. And so if you get it with LabCorp or Quest or Boston Heart, they may not be using the same modalities to get the same numbers.

[ 00:48:45 ] So it’s hard unless you’re, if you get the, you got to get the same labs on the same patient. And that’s the, that, that, I think that’s a really good methodology. Unfortunately, because of these competitions and it’s all proprietary software, there’s not a single platform that ApoB is all standardized. So there’s an advantage of the standardization. Now, the thing that you don’t see from the lipid profile is lipoprotein A. So, and just to wrap up ApoB. So ApoB, ApoB100 is a marker is, how would you explain it? It’s a, it’s related to your particle concentration of bad particles. Non HDL cholesterol is related to the cholesterol concentration of the bad particles. And the NMR gives you the actual nanomoles per liter of those particles with it. So it’s another way of looking at it.

[ 00:49:47 ] And it breaks it down into the small particles, it gives you the different particle sizes. So, you know, NMR actually gives a lot of information for patients. If you were to pick one marker, let’s say, you could pick LDL cholesterol, you could pick non-HDL cholesterol, and I know I’m putting you on the spot, ApoB, Lp(a), out of any of the markers that you have access to, and you, obviously, you told me that this is a multifactorial disease. Is there one where you would say, ‘you know what? I need to know what this person’s number is.’ So I still start with a lipid panel. And the reason for that is I like to see what the triglycerides are. And I like to know the HDL cholesterol because it’s still a risk marker.

[ 00:50:31 ] So, you, it sounds like you care more about triglycerides initially than really. Well, I care about LDL, but I also want to know about triglycerides and HDL. Every risk equation always uses HDL cholesterol. And that’s because it’s a more powerful marker. And when HDL cholesterol, the reason it is, this goes back many years ago, some brothers, Patch brothers, Austrian at Bader, they said, listen, you know, it turns out that it’s just like, you know, hemoglobin A1C is a better predictor of cardiac events than fasting glucose. And it’s because during the day, your glucose goes all over the place. And hemoglobin A1C is looking at the area and at the curve of your glucose measurements, looking at, what’s, what’s happened to this person’s glucose over a six-week period.

[ 00:51:21 ] So their hypothesis was that HDL cholesterol is the hemoglobin A1C of lipids, that it tells you. That’s interesting. So it tells you what’s happening with your postprandial lipemia. That’s really interesting. And so that the HDL cholesterol is actually telling you what is happening postprandial. So it’s telling you, it’s like, it’s integrating what’s happening in the postprandial period. That’s fascinating. Okay. And now, with all this recent data on triglycerides and triglycerides, lipoproteins, it makes a lot of sense that it turns out if you measure triglycerides, they bounce all over the place. Just like glucose. I have a, I have a question for you. We typically do labs that are fasting, right? Is there some merit to doing, for example, you’ll do a glucose challenge test, nor a glucose tolerance test.

[ 00:52:11 ] Is there some merit to doing a standardized lipid challenge test? Or carbohydrate challenge test where you’re looking at triglycerides? So, you know, we’ve, we’ve done these types of studies and you can see there’s a marked variation in terms of the postprandial triglyceride excursion. Uh, we also looked at this in the ERIC study and it looks like there wasn’t that much more predictive value than. So it wasn’t really valuable. It didn’t add that much. You know, it’s, it’s a little bit like the fact is, in terms of predicting cardiovascular risk, the hemoglobin A1C is just a, you know, about the same thing as doing a glucose tolerance test. Now that might give you not exactly the same as when did they get diabetes, but for cardiovascular risk, hemoglobin A1C is easy to get and it gives you a lot of information.

[ 00:52:58 ] So that’s why if you take a look at it, everyone gets a new hemoglobin A1C now. It used to be everyone got a two hour glucose tolerance test. What a pain. Well, it was good. It’s also cumbersome, you know, and, and doing, doing that, doing a two hour, it’s the worst. The, the post-prandial lipemia test is six hours. The post-prandial lipemia test. Okay. Yes. That sounds terrible too. When we do the studies, we go at least four hours out because the peak, the peak is at four to six hours. And how much did you dose them? What was the, the dosing? So we’ve done, trying to, we had, we did one with, so this is standardized test meals. And also gross. You have to drink that, right?

[ 00:53:32 ] Well, you can, or else you can give test meals. So, we like; we did it once with McDonald’s, you know, for people. And we did something else in another trial with it to try to, and, and you can see even four days of that diet. So, and it turns out we were doing something; we’re going a high saturated fat, but also having fair number of carbs in there. So that’s quite different. You know, if you throw in a high saturated fat with carbs, you get an adverse response. When it comes to health, what works for someone else may not work for you because we are unique. We have unique genetics, habits, and health goals. That’s why I’m so excited to tell you about InsideTracker. You’ve heard me talk about it before.

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[ 00:57:55 ] Do you think that you would see abnormal an abnormal lipid profile if someone is calorie-controlled with high saturated fat? Saturated fat diet and protein. So I think there’s going to be variable responses, and some people might have a bump up. Many people, most people will not. So I think there is, and I don’t know what the genetics are because some of these people, because most people, when they go keto, they do not have a big spike in their cholesterol. So, I don’t know why some people do. And the genetics of that, you know, I’m talking to Ernie Shaffer, who’s head of Boston Heart Labs, trying to understand why do some people have such a dramatic response? There’s some mystery in this, but most people do not. And let’s say they had a dramatic response.

[ 00:58:43 ] Wouldn’t the body somehow regulate four to six weeks later in terms of? I have one patient. It’s just a complete mystery. It’s like he doesn’t regulate. It just stays way up there and he’s very healthy. So, I don’t understand why that is. So, but I do think that for, you know, that’s always, there can always be a few people who are outside the norm. But for the majority, would you say 90% of the population? So, I think for most people, you can end up doing these things. The bigger culprit in our diet tends to be carbohydrates now. And I think it’s, you know, the food advertisers, when they said no cholesterol, low cholesterol diet, what’d they do on the potato chips? No cholesterol. Well, there was never cholesterol on a potato chip.

[ 00:59:24 ] So then they said low fat and they sold snack wells, right? Full of sugar. Simple sugars too. So people have used, you know, the low cholesterol, low fat advertising to sell unhealthy foods, which were very high in carbs. And that spikes your glucose. And in fact, what we’ve seen, as you pointed out, if you have this, now, if someone’s triglycerides are 2000, you’ve got to cut the fat out. Yeah. But if you see someone running into 250, 300, it’s usually their carbohydrates. 250, 300. Yeah. I mean, that’s, and that’s pretty bad, but you know, that’s not a normal triglyceride, but that’s usually going to be the carbohydrates driving that. They’re overproducing and they have insulin resistance. How fast would you see a course correction within two weeks?

[ 01:00:10 ] I mean, we, we saw it within two weeks. I don’t know if you see it differently. If you see it in two weeks, you can see big changes very rapidly. And for someone who’s really high triglyceride in the thousands, you can see it two days, through a few days, if they just, you know, change what they’re eating and start exercising. So going back to your hierarchy of what is most important for how you start to risk stratify patients. So we get the lipid profile and then all the other risk factors. And then the first extra test I like to get is a lipoprotein A over ApoB, over ApoB, lipoprotein A. I can have, I have a pretty good idea of looking at those numbers, what’s going on.

[ 01:00:50 ] Now, some cases I’ll get either, I can get an NMR profile or an ApoB because I’m worried about the risk. I’m worried about discordance with it, particularly when the triglycerides are up a little bit. So if the, if the triglycerides are 50, you don’t really need that. You’re not worried about it. Yeah, I’m not worried about it. If they’re higher than I worry about it more, but I worry more about a lipoprotein A, because if the lipoprotein A is normal, great. If they’ve got lipoprotein A of 350 nanomoles per liter in a family instrument, oh boy, you inherited this. So, you know, I got a whole different perspective on that patient. If there’s an apoB, it’s a few points higher. Where do you like to see apoB?

[ 01:01:30 ] Well, I mean, you know, your optimal apoB, it’s like, where’s the optimal LDL? We used to say under 100, and then we said under 70, and now we’re saying under 55. Depends upon the individual. Could it ever go too low? Would you have issues with, I think there’s probably some genetic disorders where they, they don’t make enough cholesterol and then they’re not absorbing these, these fat-soluble vitamins. So, so there are, there are, you can have a mutation in apoB or MTP, and you don’t, you have super low levels. Now, some of the people get fat malabsorption and they get fatty liver. But it’s, I don’t think the low level of LDL is the problem. The problem is the fatty liver, in that case, because you basically, you’re not secreting the particles.

[ 01:02:10 ] They get, it just builds up in your liver. At least in the trials, when we use PCSK9s, the, the LDLs were going down to on average 30 milligrams per deciliter, really low. And they didn’t, they didn’t see any side effects from that. So, and there was also a big cognitive study in one of them. No, no, no problems with cognition. So you would say that the guidelines, you would follow what typically they’re recommending, apoB less than, I don’t know, 89, something like that. Oh, 89 is high. Okay. So that, that, so that, that, that, so we, there’s another one that came up from the National Lipid Association. Which by the way, you’re the president of. Yeah. So things like 60 is a, you know, the number they had in there.

[ 01:02:52 ] I mean, I think they had something ridiculous in the ACC guidelines. It was like, I don’t know, apoB was like 120 or something. They didn’t say it was a risk-enhancing factor. Well, 120 is out the roof. So for a risk-enhancing factor, you’d have to go lower than that. What, where is your, in an ideal world of a healthy person, where do you want to see their apoB? Well, I mean, I think you’d like to be, you know, ideally, ideal with anything. You’d like to have your LDL probably in the sixties, ApoB around 60 or 60. I don’t think my LDLs are in the sixties. What’s that? I don’t think my LDLs are in the sixties. Yeah, but you’re, that’s, you know, you probably don’t need it.

[ 01:03:27 ] You probably, everything else is, you know, where it’s supposed to be. Yeah. And that’s the whole thing is, it’s all depending upon. It’s complicated. It’s complicated. You don’t, you don’t need to use a bunch of drugs in someone who has no atherosclerosis. If you have more problems, you’ve got to figure out where it’s coming from and then try to treat that. So if there is a lipid problem, we know it can benefit that person. But a non-lipid problem, an ApoB of 70, you’d love that? That’d be fine. 80? Probably fine also. I mean, it just depends upon the individual. Okay. Tell me about LpA. What is it? Why are we testing it? Most people don’t. Correct. Tell, tell me all about it.

[ 01:04:08 ] And this is actually where you’ve done a lot of your work, both basic science, translational science and clinical. So, so lipoprotein A, it’s, you know, we’re talking about these particles and we have carrying cholesterol. It is another one and it’s distinct from LDL and VLDL. It’s, it does have an ApoB molecule, but hooked to the ApoB molecule is something called ApoA. I don’t know how they call these numbers. It could have done like a better job naming all this stuff. And it’s Apo, it’s Apo little a, because if, if somebody orders Apo capital A, that’s something different. That’s ApoA1. That’s an HDL. So there’s this specific particle. So it’s an, it’s an interesting, cause it, it has this shape of a, a Kringle, which is like a Danish, the Danish.

[ 01:04:58 ] I don’t know what those are. We don’t need those in our house. Yeah. Yeah. So it’s, so, and they, and it’s this molecule that’s attached. It’s mostly genetic, much more so than the other factors that we talked about. So many people have an extremely low level and that level will always be very low. When you say low, so yeah, that’d be seven milligrams or, you know, 25 nanomoles or something like that. So it’s really low. They measured two different units. Other people have extremely high levels. Can you, can you give us some numbers? So, so, so we have a recent statement, update to the National Lipid Association scientific statement. But basically if you’re looking at milligrams, less than 30 milligrams is desirable. Over 50 is high. Okay.

[ 01:05:47 ] Now that’s, there’s notice there’s something in between there. And that’s, we’re talking about, there’s not a single cut point. So your lab slip would stay elevated if someone has a 40 milligram per deciliter. So it’s important that physicians and patients know when they, it was on the same page, the lab company is telling you that’s elevated. It is elevated. It’s not desirable, but it’s not in what we’d call a really high risk zone. Okay. The numbers for nanomoles are 75, less than that is desirable. Over 125 is high. So that’s for nanomoles. And then you have this kind of gray zone in there or intermediate risk. Now, intermediate risk, we say it should be measured at least once in a lifetime. So if you’re low, like if you’re at regular level, you’re going to stay low.

[ 01:06:36 ] Even if you go through menopause and some of these other things. So now that’s where we have this intermediate risk group, because it takes, it turns out that you can change. And if someone goes through menopause and they were running, let’s say they were a hundred nanomoles, they may end up being 150. I mean, some people have big changes. That’s a really large change. If someone is normal, let’s say they’re desirable-Lp little a of 35. In general, in general, if they have an LPA that’s very low, you know, 35, 30, now 30 is milligrams. Do you have 35 nanomoles? Which one are you talking about? You pick. Okay. If it’s 35 nanomoles, 35 nanomoles, you’re going to probably stay low. I have a question.

[ 01:07:16 ] When you are looking at these labs, and it’s not, I have to go back and think about it. Are they reporting it in various? It depends on the lab. Sometimes it’s milligrams. So this gets confusing to patients. So if you, you may say, Oh my look, I used to be, so, you know, I said, Oh, I was, you know, 40 milligrams. And now all of a sudden I’m a hundred nanomoles. And you’re like, okay, that’s the same number. And you recommend going and utilizing the same lab with the same person. Yeah. So it’s easier to understand. And we prefer to get nanomoles now. Okay. Nanomoles. So what is the LP little a) ideal range for nanomoles? So, that would be less than 75. Okay. Less than 75. And over 125 is high.

[ 01:08:01 ] You’re in trouble. It is no longer the silent killer; we are. So it’s, you’re worried about it. So it turns out if you were a woman, you might jump up from a hundred to 150. So we looked at this in the, in the, the Eric study. And we saw that first of all, women tend to have higher levels of LPA than men. So it’s, I don’t know. Women are different than men. Smarter, better. I don’t know what it is. I’m just kidding. I’m, I’m kidding. But so it, it there’s, but it ends up is that they tended to increase more. The other one that comes up is if you’re black, you have higher levels, substantially higher levels and then kidney disease. Are the risks the same? So is.

[ 01:08:41 ] So for the fourth, depending on the level. So the risk does go up if you have a higher level and then. No matter what, even if genetically a subset of people have higher levels of LPA. Correct. Okay. And then, renal disease, particularly if you’re spilling protein and we know that’s very important with diabetes, but then, the risk, the levels of LPA go up. Hmm. And then, so, what is the function of LPA in the body? That’s a good question. We don’t know. What does the healthy function? We don’t know, but we know it’s; it ends up increasing the risk for coronary atherosclerosis, aortic valve stenosis, calcific or the valve stenosis is increased. And there’s also some increase in peripheral arterial disease and even some increase in heart failure.

[ 01:09:27 ] So, it’s; it’s adverse for cardiovascular. Do you think, you know, it’s interesting when I, when I hear stuff like that, I always think, okay, well, do you think that it plays a role in the body doing something else outside of cardiovascular disease? Is there, do you, uh, you know, so it’s, it’s, it’s, so this is one of the things is it’s gotta have some kind of function, right? Right. So I, I don’t know. I, you know, it’s one of the things that most animals don’t have LPA and the people with extremely low levels seem to do just fine. Animals don’t have LPA. No, it’s, it’s just, it’s just, it’s all evolutionarily. No, it’s, it’s only in primates and humans. And then the hedgehog has a different, uh, genetic architecture. Matt, you’re related.

[ 01:10:10 ] I knew it. Um, that’s fascinating. So we don’t, just to be clear, we don’t know of any positive influence LPA would have, or any relevance except for something that’s damaging. Yeah. Um, do we know how it works in the body? So it affects the, so it’s thought to be basically it’s something that it, it, it carries oxidized fossil lipids. It’s felt to be pro-inflammatory, pro-arthrogenic in the head. It’s felt to have an effect in regards to increasing calcium deposition and, uh, fibrosis in the aortic valve. Would you expect someone, for example, a woman who is, has an LPA of um, nanomoles? So let’s say it’s 200, which is okay. Okay. So, 200, would you expect her in her postmenopausal, uh, phase of life to have a higher calcium score?

[ 01:11:07 ] I would be worried. I don’t want to check it. So what we, so this is the same thing. You know, we mentioned one risk factor, like an LDL, not everybody with LDL gets in trouble. Uh, some people smoke, they never get problems. So it’s, it’s, but it increases your risk. So we would like to then do risk stratification. What’s your blood pressure? What’s everything else? Calculators. You guys have calculators that you use. Yeah, you can use, there’s an account there online. The European Atherosclerosis Society published their update. And if you look online in that manuscript, there’s a calculator you can find where you can basically plug in the LPA value with the other variables. And it shows the change in risk.

[ 01:11:52 ] You can also, if you want to do it in a simpler way, think of it as a risk enhancer. So if someone’s LPA was 200, then you might say, okay, if I use the risk calculator by the AHA, and it was 12 at 55, 50%, so it’s 18, you know, how, uh, you had mentioned it. I mean, I think it’s very fascinating that, uh, an individual should get their LPA tested once. Right. But I think at least one time, okay. At least once, uh, number one, is there an age at which we should start? So for example, I have a three and five year old. I, they have not had their LPA, uh, taken. We, um, I on my side have no cardiovascular history. Would you say by the time they’re 15, we should see?

[ 01:12:42 ] So, so yeah, I think you can get that. So in general, the, the levels don’t hit steady state until like after puberty. But you mentioned 15. Why is that? Once again, I don’t know. We know there’s sex hormones make some difference in terms of the levels with it. So, and we know that it’s same thing with cholesterol and other liposomal lipoproteins. They, they, they vary somewhat. You can look at the trajectory. So, and the LPA level, but you know, you don’t know what the final level is going to be, but you can see by age-adjusted norms if they’re different. But we don’t usually recommend it until uh unless there’s a very strong family history. We’ll check that, but that’s a reasonable age to check, yeah.

[ 01:13:20 ] Um, you mentioned sex hormones change it and women so actually, if we did see that HRT replacement lowered LPA, HRT meaning just testosterone or HRT for women, yeah, for women getting estrogen. So that was done in some older studies where they were testing you know back in the day when they were testing estrogen and progestin to see if it would reduce heart disease, but it did reduce LPA. That would make me think that um potentially it would reduce heart disease. So you know unfortunately the Women’s Health Initiative uh study failed, but and so everyone says well I mean you’re being very kind about it, failed miserably, so it well it failed. But you know

[ 01:14:05 ] then I was at a we were in a conference and an endocrinologist saying he says now let’s take a look at the endocrine system, you know think of the way how firewood how confident it is and think of the estrous cycle and can you imagine any medical treatment where that has to do with the endocrine system first of all look at the choice of hormone so where where did the estrogen come from you mean like the that they use oh from horse urine yeah so thinking about so you’re you get you get everybody the same dose of estrogen from horse urine and then and then you add the same dose of progestin irregardless of their metabolism

[ 01:14:47 ] and remember that the ovaries don’t secrete into the portal circulate i mean they go to systemic circulation not the portal circulate so you take this medicine you go straight to your liver right and because that increased you know thrombosis and maybe you gave it the wrong medicine the wrong way i mean i mean you only tested one thing and and so and i thought wait a second you know most things that we give we don’t give you know let’s protect like hormones you don’t give everybody the same it makes no sense it makes no sense right it’s not very physiological it just it makes no it makes absolute no sense so i don’t know that for sure we can say that if you did hormone replacement in a different manner at the present time could you

[ 01:15:35 ] see different results particularly if you started earlier uh because even in women’s health initiative looks like the women who are younger didn’t seem to have as much you know harm from it as when you give that to older women who had been menopausal for a number of years so i don’t know i think there’s a lot of questions out uh and it’s it’s the same thing you know we look at you know sex hormones are very complicated uh with it it’s the same you know the testing even for men’s you know recently showed that giving testosterone if someone had a low testosterone was not harmful you mean in the traverse trial yeah were you involved in that no yeah that would have been amazing um from a cardio you know it’s interesting i i’ve now since uh prepping uh for this podcast my team prepping for this podcast i always thought about cardiovascular disease um but it it’s almost like cardio metabolic

[ 01:16:31 ] disease is first and then everything else filters down to that then that is probably one component that drives cardiovascular disease it’s really that metabolic component and we see a lot of changes as individuals age through their body composition with uh perimenopause menopause uh andropause i know it’s not a real thing friends um but you see changes in lipid profiles right with these decreasing sex hormones do we have a lot of changes in lipid profiles right with these decreasing sex hormones do we have a understanding as to why and my Follow-up question: Is it not there’s nowhere in the guidelines that I’ve seen, that part of the treatment of treating lipids or abnormal lipids or um cardiovascular disease includes hormone replacement. That is that true, yeah?

[ 01:17:18 ] And I think that’s because of the we used to in the past you can basically androgenic progestins lower triglycerides; androgenic progestins, progestin so we used to do things sometimes with hormones and then you know that there was a thought that HRT was protective, so we would sometimes you know, but with a failed study uh, so difficult that went that went out the window, so you know I don’t I Don’t know, uh, of any there’s so there’s right now, there’s that’s not done um, I think it’s important to take a look at for example cutaneous preparations have less adverse effects and we know that you look at if you look at the doses in oral contraceptives they have different effects on raising cholesterol.

[ 01:18:02 ] So can you talk to me about that? Well, I i think it’s important to take a look at you know what’s what what is someone taking, is it oral or cutaneous so if some people have a big increase they can’t have an increase in cholesterol on they can have an increase in cholesterol so so then we might say and is there a different? Preparation, uh, and the other one ends up being is you know if like if their triglycerides went up, could you put an androgynous component in there sometimes there’s so there can be some back and forth between I think someone’s you’re doing the lipids or internal medicine or family practice and then their, uh, ob-gyn in terms of selection of optimal uh, yeah.

[ 01:18:41 ] I remember I had one patient and she was going through menopause and her LP little ‘a’ was normal and this was, you know, this was many years ago and this is really before um it was favorable people to say okay well you don’t want to use estrogen in someone who’s menstruating. right and so she was still menstruating it was normal and her lp little a skyrocketed and i kept thinking well if we had put her on or if we put her on an estrogen patch like let’s say we don’t use oral estradiol or oral or anything and we put her on um an estrogen patch would that have lowered because it’s not in the guidelines to treat lp little a with um hormones but that’s when we see the changes so a lot of things are you know the guidelines move take a lot of trials

[ 01:19:31 ] large numbers and so the center of the earth is going to cool faster yeah so i it turns out sometimes the uh expert pathways are at least a little faster but then you Have areas where we just don’t have enough data, so someone needs to do trials. Like you said, have you thought about that? You know, because you are an expert in LP Little A, arguably one of the world leading experts in LP Little A, how are we? Have you thought about the hormone influence on LP Little A and if it, you know, if that’s a tool in the toolbox. You know, we do have some therapies that lower LPA 95 that we’re testing, so he’s laughing. Is that I think I think I think if those work, they’ll get precedent and so, and they’re tested in randomized control trials.

[ 01:20:15 ] But I think if you were to think about like you’re saying, could you design? A trial which might, in a more selective and thoughtful way, take women and then treat them with it other forms of HRT, like you know giving something cutaneously. Have you seen it? Have you? I have not seen a study like that but have you seen in clinical practice no because you use other agents right so you know. But I think the issue of you know the whole thing of cutaneous administration makes a lot of sense uh with it and and I I don’t know unfortunately, you know. It’s interesting like for example we used to have no trials with diabetes and cardiovascular outcomes because they’d done a very big negative study university drug.

[ 01:20:59 ] Project and it failed, and looked like all the careers went downhill. What happened? It was because they increased events, so they saw Bonnie Urias, and it increased events, and so that there were no studies on outcomes for years and years because they were afraid of doing harm to people, well not just because everyone was afraid to do the trunk that it failed. So now we have positive trials, and the next thing you know, there’s so many studies going on about obesity agents and everything else because, like, GLP-1s, which we’re definitely going to move into yeah, so so I think it’s the issue is unfortunately, you said Women’s Health Initiative. Failed, it was a spectacular failure. A lot of money, probably the biggest failure, a lot, a lot of a lot of money spent.

[ 01:21:40 ] And so, as a result, years went by; it really has been a barrier towards doing good, powered studies with you know things like you’re talking. It’s challenging and I would say as physicians, it’s challenging because we-gosh, you know? I can speculate and I’m not a cardiologist, I’m not a lipid expert and I always would refer to you or you know I’m not a cardiologist, I’m not a lipid expert and I’m not a um, you know. We have cardiologists that we refer out to. It’s it’s challenging because as family practice and as a geriatrician. I’d love to be able to say, ‘Okay, well could this be used off-label?’ And someone said to me, ‘Well, you can’t. There are other ways.’ I mean, you could, but there are other ways that we would impact LP little a.

[ 01:22:23 ] Yeah, and we just… we don’t know. Are there um LP little a is genetic, you said that there is one case in which we see it change and that’s through its about 90% but there are there are things that can the other things like protein urea and Aphrodite syndrome. Uh, there are some medications that might alter it uh, that people take sometimes. But any lifestyle factors, a lifestyle is and this is one, it turns out in terms of lifestyle is. That actually is that here’s one where the high-saturated-fat diet has a lot of protein in it, and it’s a lot of protein in it, and it’s a lot of protein in it. Has the more favorable effects than the high-carbohydrate diet. Do people ask you these kinds of things all the time about diet?

[ 01:23:04 ] Because, you know, lipidology, I don’t know how involved in nutritional sciences you guys get. So, unfortunately, there used to be much more support in terms of the ability to afford nutritional counseling. And then also, we had a lot more nutritionists, and they could specialize in certain areas. And it’s, you know, it’s one of the problems with medicine right now is that the focus on prevention; there’s way more money that goes into interventions and end-of-life care than it does for prevention, and particularly things like lifestyle. So, nutrition, exercise, physiology, you know, it’s unfortunate. You see, you know, we were working with our hospital towards taking over cardiac rehab, and they said, oh, we decided just to close this one and just have it one location somewhere else. And you’re like, okay.

[ 01:23:55 ] I can’t get my patients there, right? Yeah. LP little a, tell me about diet impact. So, you said that there’s really kind of two divergent pathways. So, you don’t change LP much with diet. However, this is one where you don’t change LP much with diet. However, this is one where it looks like. Uh-oh. I’m not trying to be biased here. This is one where it does look like that the diet that is typically not recommended should be a, you know, a higher fat diet. It has a more favorable effect on LPA than the typical low-fat, higher carbohydrate diet. Can you expand on that study, and maybe we can link it or whatever it is? You know, I wouldn’t know that.

[ 01:24:38 ] I don’t know that we have really good studies on that, but that’s just, if you look at the reviews of it, that’s where it stands. Nothing makes a big impact, but if anything, it’s kind of favoring, you know, not the traditional approach. It’s fascinating because it’s probably. I, from what I would think in nutritional science, that it’s actually just the lowering of the carbohydrate, potentially. I mean. It might be. I don’t know. You’re the lipid expert. What can someone do to treat LP little a? And we should also, and I think we should start on the actual treatments for LP little a. What is available? Who is a candidate? And then kind of circle back to what you think about treatment of the other. So, you want to think about LPA.

[ 01:25:23 ] The same way we think about other risk factors, you have to see it in the perspective of the entire patient and it will say, ‘Well, why would I? I don’t have a drug to treat LPA. Why do I need to know it? Calcium scores are very popular. Uh, and you have patients getting calcium scores all the time, right? Hard inside. We usually use something called the clearly scan. So, clearly scan is CTA also, but if you just get a calcium score and even the same thing with Clearly, they say they have got lots of calcified plaque. Do you ever send them to Kiva? No, you don’t treat the calcium. You treat the risk for having an event.

[ 01:25:59 ] So, if someone has an LPA, I may not be able to treat the LPA, but I do know that first of all, we’ve talked a lot about nutrition and exercise, blood pressures and more, you know, I, I can make sure they’re not at their blood pressures treated. I can, I can use a statin if they have a high cholesterol, uh, you know, cigarette cessation, vaping. I mean, there’s a lot of things that are increasing cardiovascular risk. We know how to do that. So, yeah, it’s, if you know, if someone knows that they’re having a greater risk, let’s just use the things that we know that work, uh, for it. So, I do, I disagree with people saying, ‘Well, I, I’m not going to do anything with, but it’s, why should I measure it?’ You measure it just the same way you measure a calcium score.

[ 01:26:45 ] I don’t get rid of the calcium, but I treat the risk factors. When you are thinking about physical exam. Yeah. Are you. Are you looking at obviously blood pressure and how would you stratify, uh, most important to least important? That’s probably an irrelevant question because they’re all important. Blood pressure, waist circumference. What are, what are targets that you can say? Okay. I want your blood pressure to be, um, I don’t know, 120 over 80. So, so ideal blood pressure is 120 or 80 or under. It’s not 140, so that’s. What about in an older population for cerebral perfusion? So in. In older individuals, you can still be getting down. I don’t know if you’re going to jump from 160 to 120.

[ 01:27:28 ] You’d have to be moderating going down, but what we can certainly see is that middle age, middle optimal blood pressure is going to be probably 115, uh, with it. And I think in general, even older individuals, you want to keep yourself under 130. Uh, if people get, do you have to give some warnings? People get orthostatic even without any hypertensive medications as they get older. Or changes in postural position, your autonomic nervous system is a little slower. Uh, so they have to be warned at, okay. You know, you, if you get those symptoms, sit down; but in general, I think it’s lower is better. You can’t get too low and you’ll get symptomatic. So you just, but it’s, it’s manageable for it.

[ 01:28:12 ] So, I mean, and so, you know, and I will see the kids, something that we forget about is, um, I think it’s like, you know, it, it’s like you were saying, if you had a. If you’re, let’s say when they’re 15 or 16, or maybe they’re maybe a little older, seven or 18, they get an LP that’s out the roof. Sometimes I have them come in and we’ll talk about lifestyle, diet, exercise, and also some things like. Cigarettes, vaping, cigarettes, or vasoconstrictors vaping is the same as intravenous injection. So the vaping is that nicotine or what? So when people are vaping there and they have all these chemicals in the, you know, they, all these flavors and stuff. So when you breathe. Breathe these in, it’s just like, you know, we used to do cardiac arrest.

[ 01:28:55 ] If you couldn’t give epinephrine, uh, injection, put it down at the ET tube because the lungs is immediate absorption. So it’s, it’s like snorting cocaine. It goes straight into your system. So, and that’s another one that comes up is, you know, young people go to parties. Someone is doing cocaine. They may do cocaine. Cocaine was used by surgeons to, it’s a vasoconstrictors. They wouldn’t bleed on, you know, ear, nose and throat guys. So you might be the. The young person who has the heart attack because you had some plaque in there, a soft plaque. And so I think that knowledge is something that’s get something that would make it. You know, I got this genetic disorder might not be very smart for me to smoke or to vape or, you know, when my friends are doing cocaine, it’s not a good idea.

[ 01:29:40 ] It’s never a friend. Well, it’s not a good idea anyway, but it’s just, you know, young people do, they go to parties and they, you know, they do things. And so alcohol, people always ask about alcohol. So, alcohol. It’s not going to be that same kind of vasoconstrictor or something else. It has lots of other health, you know, harms to it for itself. But so I think just the lifestyle part, then the issue of, you know, you mentioned it in terms of the exam. Yeah. Waste is important. Weight waste combined with weight BMI alone. Not so great. But if you put the waste in there and also be looking at it, someone’s South Asian and, you know, maybe their waste isn’t that impressive. But it gets to the point.

[ 01:30:21 ] BMI is 26, 27, skinny arms, skinny legs. The abdomen is clearly, you know, waist is increased for that body habitus. And then you see insulin resistance. Well, that person actually has lots of visceral fat. So those, the exam is useful. And probably low skeletal muscle. Yeah. And you can look at things like acanthosis nigricans and other things which are showing, you know, insulin resistance for it. And usually they are, you know, the skinny arms and legs, not enough skeletal muscle. Body distribution, fat distribution. It’s going to be wonderful when it becomes routine to test skeletal muscle mass. We don’t have access. No one really does to be able to do that in a meaningful way yet. But that’s going to be tremendous. You know, there’s a lot of discussion. You mentioned.

[ 01:31:06 ] So you’re doing impotence. How are you measuring it in your clinic? So we do. Well, there’s a few ways. We do an in-body scan, which is not amazing, but it’s what we have. The gold scanner. Right. Yeah. Impedance. So the. Yeah. We would, you know, we can do MRI. Most people aren’t doing. Right. It’s expensive. And doing MRI. But we would love to do that. But then the question is how often, for example, if someone is doing an MRI, then how are we following those trends? We’re not doing an MRI every. Yeah, it’s expensive. Yeah. And it’s time consuming. But an in body is adequate. And then also. Yeah, there’s not a great truly. There’s not a great way. I mean, you know, the ultrasound is dependent on the.

[ 01:31:49 ] But, you know, once you’ve done that simple things, every time you see them, weight, blood pressure, see the lipids, usually all three go out of whack at the same time. Yeah. And we want people to be getting stronger. Yes. I think that strength is really important. You know, there’s a lot of discussion around GLP ones and various generations of those on cardiovascular health. What are your thoughts? And are you guys using that? Well, I got to say, you know, obesity in terms of pharmacotherapy has been very, very difficult until recently. Most of drugs like Fin have adverse cardiovascular effects and GLP ones, and then GLP-1, G-I-P. And there’s a whole host of things in the pipeline. I mean, they’re really exciting. I mean, they have traumatic effects in terms of weight loss.

[ 01:32:37 ] We see a select wrong cardiovascular event reduction. They’re very expensive. So, in terms of a societal answer, you know, there’s no way that society can be putting everybody on these drugs. And the other one that comes up is people do need to understand that when you’re losing weight, you’re also losing muscle. So I think that one of my concerns is, is older individuals wanting to do these for cosmetic reasons, who might be trying to get themselves down into lower BMI’s that are reading. It’s BMI’s a funny thing. But if we take a look, it’s in the shape of a U, right? So and that’s because of frailty. Yeah. So if people are in their 70s and they get a BMI of 20 and they’re not exercising a lot, that’s a set up for osteo osteoporosis, falls, fractures, and actually increased mortality.

[ 01:33:36 ] Even have path for some reasons, increase would you? How can someone who’s thin get into that? But it’s happening. So I don’t know. There’s a thought. This whole issue of sarcopenia. And then, you know, even some people are overweight, but I think we have to be a little cautious that the injections be still accompanied by trying to get healthy eating habits and very important to get some exercise. For this in particular, if there’s any hope of reducing the drugs, we do know that the one thing that seems to really make a big impact for sustaining weight loss is exercise. And they’re one study from Copenhagen that looks like they could at least reduce the dose, which is the home of Novo Nordisk. Oh, yeah.

[ 01:34:25 ] At least they were able and a number of people to reduce the dose and some of them stopped when they got in some pretty successful lifestyle changes. But I am a little concerned about potential. The drugs look great, but this is four or five years that you know, in the study with it. But some, some people may be trying to go a little bit too much for the cosmetic rather than the medical, and that could actually hurt their health. Are there benefits to various supplements on cardiovascular health? I mean, there’s, you know, there’s been a whole slew of okay, use niacin to lower HDL. Okay, that’s kind of gone away. We used to use a lot of high-dose niacin. Right. And then, you know, I think that there’s been red yeast rice.

[ 01:35:11 ] There’s just various supplements. Red yeast rice in the United States lacks the active agent. So in Canada, it basically turns out that the lovastatin, which these statins were discovered as fungal metabolites. So basically, red yeast rice-red yeast rice actually has a fungal metabolite like a statin. And what happened is that the FDA made them take it out because they said, ‘Well, if people are taking statins, they’re taking this.’ They make it into, you know, higher dose side effects, but it also doesn’t work without it. So in Canada, it works. Here, it doesn’t work much. What about omega-3 fatty acids? And I know that you’ve done some various trials on omega-3s. So omega-3 fatty acids, so if you look at the typical, when you see fish oil, first thing is what’s in it?

[ 01:36:00 ] Because it usually says that 1,000 milligram capsule, but it usually, you look in the back at how much EPA, DHA, it’s usually 300 milligrams. Now, they lower triglycerides. How, at what dose? So if you’re using, for example, 4-glycerin. 4 grams a day of EPA, DHA, omega-3 fatty acids. Now, that’s a lot if you’re getting supplements because if they’re only having 300 milligrams, you can just, you do some math there. You’re taking, what is that, 14 of those capsules and they’re big capsules. The prescription generic is a gram, two, basically, you take two grams twice a day. And that can be EPA or DHA or the combination. They work fine for lowering triglycerides. In terms of cardiovascular event reduction, the only one that’s showing benefit is EPA.

[ 01:36:50 ] And it looks like the benefit in that study was probably not, there may have been a little bit from triglyceride, but it’s probably other aspects of EPA. EPA is involved with resolution of inflammation, resolvents. There’s a lot of biochemical derivatives that have biological functions. So I don’t know the exact mechanism. And it looks like it’s not explained mostly by the lipid changes. It’s explained by other vascular protective effects. So if you’re wanting to, for cardiovascular risk reduction, if you’re going to use omega-3 fatty acids, it was EPA and it was 4 grams a day. If it’s lowering triglycerides, you can use the combination there fine. Are there any other supplements that you guys talk about, are you interested in? No. I’m interested in nitric oxide or any of those kind of compounds.

[ 01:37:47 ] You know, nitric oxide is very important biologically. John Cook’s a friend of mine. He started a company up about trying to give a nitric oxide supplement. It didn’t seem to work all that well. But anyway, so I’m just dubious as to, you know, did they work? There was a recent study that was done and it compared, you know, garlic and a bunch of other things to statins. Yeah. And they really were all pretty ineffective other than the statin, low dose of statin. And do statins affect men and women differently? I know that there’s fat-soluble and water-soluble statins. Is there a difference? So, yeah, there’s an issue that women have more statin and tarts than men. And is that defined by the outcomes of myalgia or inability to tolerate? Okay. Even any dose.

[ 01:38:37 ] But it’s also interesting, you know, if we look at in glycerin, which was an injection. Yeah. What’s that? Is that still used? No. Glycerin is an injection of SNS-RNA. Okay. It’s a new therapy, PCSK9. But it turns out women had more injection site reactions than men. So, you know, so there’s two ways of looking at this. Some people say, which I wonder what it is, are women simply more perceptive? Some people say, well, they’re, you know, you might see. I think. So this would be one of us that, you know. Like maybe do they notice it more or something? Well, yeah. I mean, you know, women may be more. People say women are more in touch with their feelings. Well, that actually may be true.

[ 01:39:19 ] Maybe women actually, even in terms of what’s happening with their body and sensations or something like that, I don’t quite feel right or something like that. I don’t know. I think you were saying that, you know, then you said your husband’s a Navy SEAL. He didn’t get to be a Navy SEAL by, you know, oh, my toe hurts. You know what I mean? No. So men get, we get taught at an early age. Maybe he did. Maybe they’re giving out Navy SEALs. Maybe they’re giving out Navy SEAL cards, but. No, but I mean, you’ll get taught at an early age to push things aside. Don’t worry about it. So, you know, I don’t think, could that be? I mean, it’s a little bit. It’s just maybe there’s something that the perception of medications is.

[ 01:39:57 ] But we don’t know any other outcomes that statins seem to. They work equally well in women. But it was, you know, when I saw this thing within Clistrin, I thought, well, that’s really strange because it’s, that’s an injection. And yet there’s the same thing in terms of these. The side effect profile: women were more; had more complaints about it than the men. And you see this, and I wonder if there’s actually a biological basis to it or a neurological basis. I don’t, I don’t know. You know, women clearly have more autoimmune disease. Yeah. So I don’t know what it is, but when I saw it happening with something else, it made me think that there is this issue of perception of side effects. And maybe, you know, who knows?

[ 01:40:42 ] But it’s, it’s, it is a fact. What does that mean? That, yeah, you try the multiple statins, but it means you don’t give up. Okay. We have other; we have things like pimboic acid. We have ezetimibe. If they can’t take a statin, the last thing you can do is tell someone it was just in your head. Everything’s in our head, right? All of our feelings and perceptions are in our head. So I do think that. If you say that, you’ll be on a, if you were to say that to your wife, you’d probably be on a milk carton side. I would be. So you got to be thinking is that this person came to see me. They need help. They’ve tried it. It didn’t work. I need to listen to them.

[ 01:41:18 ] I know you can, you can try a lower dose. You can try every other day. There’s lots of things you can try, but you can also consider other treatments for it. It’s, you know, my, I see that, you know, my job is I function as a guide. Someone comes to see me. It’s their heart. It’s their cardiovascular system. I try to help them avoid a major problem. But, you know, they’re driving the car. Yeah. So, but there are other choices that one can make so that if we do everything we can to get them on some dose of a statin, but we have other agents in it and you certainly cannot challenge that because there are clearly some people that do have serious problems with statins. It happens.

[ 01:42:01 ] And you know, you just accept it. Is there a choice whether it’s a fat-soluble? Do you prefer a fat-soluble versus a water-soluble statin over one or the other? Having something that’s, you know, water soluble, it might be useful. I mean, a lot of times we use, I use, sometimes I’ll use half of a rosubacin, so 2. 5 milligrams Monday, Wednesday, Friday. Very low dose. Very, very low dose. Can they tolerate that? If they can, let’s add a zetamine. And surprisingly, that combination can give you some very big reductions in LDL. Interesting. Would you ever just use a zetamine alone first? And I sometimes use it. If someone’s tried all the statins with all the complaints, they’ll say, look, I don’t want to take a statin.

[ 01:42:37 ] Fine. Let’s try a zetamine. We can even try a zetamine half a pill Monday, Wednesday, Friday. There’s this issue of just getting someone to tolerate something, you slowly build up. But I do think it’s important is that since, you know, it was interesting, there was a study done with benpidoic acid. And for the first time in a trial, you actually had equal numbers of men and women because it was a trial of statin intolerant high risk patients. Because there are more women who complain of statin intolerance. And so, rather than telling you know, I think we just, okay, that’s a fact. We just deal with it. And then we do the best we can to make sure that they get treated adequately. Women tend to be undertreated for risk factors, for cholesterol, for a lot of things.

[ 01:43:20 ] Why do you think that is? You know, I think there’s the perception they don’t get heart disease, but I do think for whatever reason, what we see is there’s a lot of undertreatment of women and then also written off for chest pain sometimes. Yeah. We were reading that women take seven minutes longer to diagnose a heart attack when they go into the ER than their male counterparts. Sometimes symptoms are slightly atypical and then people say, well, look, you know, it’s a woman, she looks younger and younger women are having events and getting blown off. So I do think it’s important that we treat cholesterol aggressively. And if you end up having to take a little different approach, you can make progress.

[ 01:44:03 ] And it may end up being, well, maybe I can’t get the LDL lower, but maybe we can work on the blood pressure. Working on, just try to improve the entire risk profile. And how important would, say, a VO2 max or stress test be for your, say, a young, healthy person? So I still like stress testing because it gives me a baseline of their, you know, performance. And I can see what happens with blood pressure. Some people, blood pressure really goes high. And then I say, okay, you’ve got a hypertensive response to exercise. That’s good for me to know because I might, I’m going to really watch your blood pressure. Do we need to monitor at home some? Are you going to be someone who needs blood pressure medications? And what’s their fitness level?

[ 01:44:41 ] I mean, poor fitness levels, poor prognosis. I think it would be nice to get VO2 maxes just, you know. Yeah. It’s difficult, you know, for a patient. That’s a problem. I mean, it’s just not. I know. I mean, we were doing that when I was at WashU and it’s just, patients don’t want to do, it’s a lot to ask of a patient. It’s a lot. So we don’t routinely, we don’t routinely get it. Would it be nice? Yeah, it’d be nice. But we know that the more fit you are, the longer you’re going to live. The more muscle mass you have, the longer your, and better your trajectory and survivability will be. What are you most excited about that’s coming out in cardiology or lipidology coming up?

[ 01:45:19 ] I mean, there’s, we’ve got all kinds of new therapies coming up in terms of, I think that the thing that to me is the most exciting is how much we can do. We, it’s still the biggest challenge is adherence to get a good lifestyle and exercise program, but the blood pressure medications are so much better. The lipid medications with many more in the pipeline. Diabetes medications, my gosh, how much better they are. And now we have obesity therapies. So, I mean, it’s, it’s really pretty remarkable what we can do. So to me, it’s a, and then, you know, the things in genetics and imaging, I mean, it’s phenomenal how the science has evolved. Unfortunately, the lifestyle style has gotten worse.

[ 01:46:08 ] It’s, you know, you’re listing off all of these things, these medications, and I can’t help but think here we are spending all this time and all this money looking for external solutions to things that are right in front of our face. So, yeah, so I, and this is where it’s all very exciting, but, and this is the, the issue is, as a society and in general, children, starting at young ages, you know, teenagers, young adults, we’ve got to do a better job with nutrition and exercise. We have to. Because, you know, we’re not trying to raise children. We’re trying to build stronger humans, you know. Dr. Christy Ballantyne, thank you so much for spending time with me. And really, the listeners are going to love this episode.

[ 01:46:55 ] And you’ve cleared up so many myths and brought up things that I think people are going to love. And I think people would benefit so greatly for, from. So, thank you so much. Thank you. The Dr. Gabrielle Lyon Podcast and YouTube are for general information purposes only and do not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice. And no patient-doctor relationship is formed. The use of information on this podcast, YouTube, and other materials linked from the podcast or YouTube is at the user’s own risk. The content of this podcast is not intended to substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have, and should seek the assistance of their healthcare professional for any such conditions. This is purely for entertainment and educational purposes only.