82. Preventing Cardiovascular Disease, Cholesterol & Lipids, Lifestyle Interventions for a Healthy Heart | Nicole Harkin, MD (Ep 55/56 Rebroadcast)

Hello everyone, I'm Dr. Darsha, and I'm Dr. Altamash Raja, and welcome to Medicine Redefined. A podcast where we will explore the often overlooked but necessary components of health, what we consider to be the fundamentals. We will investigate topics and practices that can give you and your patients the best chance to optimize a healthy lifestyle. It's time to move the needle forward and put the health back in healthcare. Today's episode is going to be a re-broadcast of episodes 55 and 56 where we interviewed Dr. Nicole Harkin, cardiologist. So why the re-broadcast? Because cardiovascular disease is so prevalent across the whole world, and it's actually the number one leading cause of death in all cause mortality. So because of that, whether you're new here or whether you've been with us at Medicine Redefined, we think it's so important to keep cardiology and the technicalities about it so fresh in your mind. It's important to think on a daily basis, on a weekly basis, what are those things that we can do to ensure good heart health? And so in this episode, we delve into cholesterol and lipids, what an APOB might mean, what's an LP little A, there's so much research coming out. So we want you guys to be advocates for yourself when you go into the doctor's office so that you can be confident when you tell your doctor what type of tests you want so that you can really look into certain risk factors. And of course, we delve into those lifestyle interventions to keep us healthy, exercise, diet, stress management. So yes, this is a two hour episode. We are combining our two previous ones, but again, it is technical and I think it serves well to relisten to this if you already have, because if we can do one thing to really become healthy, it is to look at our heart and to reduce that risk. All right, enjoy the episode. Dr. Nicole Harkin, thanks so much for coming on to this podcast. You're so welcome. Thanks for inviting me. I'm excited. Absolutely. So, you know, Ultimation I have had Medicine Redefined now for about a year and for a year now, we've been saying we need to talk about cardiology, right? The number one leading risk factor and death, you know, when we talk about being healthy and lifespan longevity. So finally, you made our way to come true. So again, thanks, but I really want to delve into your journey, right? I think there's a lot of pre-meds and medical students who think about going into cardiology, you know, when they think about medicine. What made you choose cardiology? Take us through kind of, you know, back then, you're a little bit about your journey. Yeah, absolutely. So I started actually thinking I was kind of a late bloomer into cardiology. I feel like a lot of cardiologists who talk to you, they've like known they've wanted to be a cardiologist for a really long time. I sort of came into it later in my medicine training. So early on I was actually, and remained interested in, but very, very interested in global health and international health and did a lot of work abroad. And so at that point, I really thought I was going to be an infectious disease doctor, which is kind of as a natural compliment to that experience. And so throughout medical school, that's really what I thought I was going to do. And thought I was going to do a public health sort of degree and things like that. And then eventually started kind of getting interested in cardiology. I think a lot of that started actually when I was in Africa, and obviously a lot of my work there was infectious disease related as well, AIDS and TB and things like that. But started to actually really truly understand the global impact that cardiovascular disease has. So it is the number one killer worldwide in every country. And so just seeing just reproering uncontrolled hypertension, lots of premature heart disease and things like that, and started kind of, and that's kind of, I think, when the first light bulb went off, like, oh yeah, like there's a lot else out there. And then I mean, the heart's cool too. So then I started getting really, you know, I mean, it's the physiology of how the heart works and all the things that happen is really just intellectually very interesting as well. So just really started kind of thinking about that. And then I went to Columbia for intramedicine residency, and it's hard not to like cardiology there. The cardiology department is huge there, very influential, did a whole rotation there and just really kind of fall in love. And so ultimately decided to sort of marry my two interests in kind of preventive health and cardiology and really kind of become a preventive cardiologist. So that's when I, in fellowship at NYU, they have a huge preventive cardiology group there. So work with them a lot, which was a great experience, and I can talk about that more. And then eventually decided to get boarded in clinical lipidology, and that's sort of where all of that experience kind of evolved for me. I love that. The heart is very, very cool. And I always tell my colleagues that in another life, if I didn't go down the sports medicine pathway, which is my calling, I certainly would have done cardiology. And yeah, you've had a long journey, right? I mean, so three years of internal medicine, three years of cardiology. And lipidology is that more fellowship time, or do you just sit for boards on that? How does that work? Yeah. So it's just really independent study and then you sit for additional boards. So the National Lipid Association has kind of some self-study stuff that you can go through and go to some of their conferences. They've got like a crash course for people that are looking to get into lipids, and you can attend the conference, and then take it and was definitely mentored by many at NYU. I actually was the first general cardiology at NYU to take those boards and pass them. So that's kind of exciting. That's awesome. And I agree. Now, as you alluded to, that cardiovascular disease is the number one killer globally, right? Particularly in the developed world, I mean, that's certainly the case. And we've talked about metabolic ill-health several times in this episode, right? And I think this stat that I've thrown out several times, I wonder, 43% of BCD in this country, United States, right? And the expectation is that in another eight years, that's going to be 50%. And I don't... Well, I shouldn't say this, but I think largely lack of education isn't a problem, right? We spend a lot of time talking about fruits and vegetables on this, and we could do all these things. Yet, people continue to get unhealthy and healthier. Recently, a study that I can't remember, but I think it was 2018, it was published that 88% of Americans had at least one marker for metabolic syndrome, right? I think that the most recent data, when you look at weight gain during the COVID-19 pandemic over the last two years in just not only the adult population, but in the pediatric population, I think that was some stat that between the millennials, which I think all of us are millennials, probably, it's like 25 to 40 something pounds. So I say all that to say that it doesn't seem to be getting better, despite all the information that's out there. And one of the things that, you know, taken all those things into account, that's important for us to do, is spend a lot more time talking about risk stratification and diagnostics and things that, how can we identify these things earlier on, which is what you're passionate about, right? Preventive cardiology, rather than later on, sick care, you know? And so what are some ways that you tend to detect disease much earlier on? You know, maybe not in their people in their 50s and 60s when people really start worrying about their heart health, but 20s and 30s. Yeah, so, I mean, we have a pretty robust understanding of the major risk factors for cardiovascular disease, right? And I think in general, we don't do a great job of employing those tools and using them on a regular basis. So I think, I don't know what the stats are for how many millennials have a primary care doctor, or have ever seen a primary care doctor, but I'm sure it's pretty low. So unfortunately, what happens is a lot of people don't get screened early on and have don't identify cholesterol, high blood pressure, all of these things that we should be screening for on a regular basis, right? And so, you know, just kind of even taking some of the traditional risk factors that we know about, high blood pressure, BMI, smoking, you know, all the usual suspects, I think that those don't get identified early enough on. And that's just kind of some of the stuff that we all know, right? That's even before you get to some of the more advanced stuff, which I'm sure we'll talk about in terms of really fine-tuning risk and looking at different advanced cholesterol markers and in early signs of insulin resistance and all of this other stuff that we should arguably be doing as well. Dr. Harkin, at what age would you say you would typically look at risk factors, then? You know, I mean, I would assume when you look at the AACVD, it's like 40 to 79, right? I think for optimal results. But now when we see obesity rates climbing so high, are we looking even younger, less than 20 maybe, to kind of look at these lipid panels, for instance? Yeah, no, for sure. So pediatricians are supposed to draw cholesterol panels in all children at some point. And there, historically, it was because we were screening for genetic dyslipidines, right? So kids as early as eight can go on statins if they have evidence of a very elevated LDL cholesterol, which is diagnostic of familial hyperlipidines. So traditionally, that's what we were screening for. But if you talk to pediatricians now, they're actually screening them early for, you know, and they check blood pressure and things like that, but they are seeing what pressure cholesterol PMI, as you mentioned, in adolescents. And so now we're not only seeing evidence of genetic dyslipidemias and issues of true genetic, but really, truly lifestyle-related elevated risk of cardiovascular disease. And that's truly scary because in the prevention world, we talk a lot about primordial prevention, which is like really starting young. Well, what's primordial prevention anymore? Is it, you know, utero? So I think that the ball feels like it keeps moving in terms of, okay, you know, in the cardiovascular world, we have lots of conversation about this blurred line now between primary and secondary prevention, based on some of diagnostics and things like that we can do now. But I even feel like we're blurring the lines completely and totally. And, you know, and we know from studies decades and decades ago that young men and women who died of other causes, if you look at, so I don't know if you guys are aware of some of these studies, but from decades and decades ago, I think it was even the Vietnam War, they would do autopsy studies and look at men and women who had died in war. And there was already signs of atheroscopies, these young people, and this was then. So, you know, I'm sure that that is even worse today. Absolutely. I mean, I think in all of our pathology classes, we learn that this, you know, the atheroscopic process begins in your teenage years, right? And it's kind of exactly where you're describing here. So let's dive a little bit deeper into, you know, we've talked about the lipid panel. You've alluded to LDL and how that can be diagnostic when it's extremely high in the pediatric population. For those who might not know, what are the different things that would pop up on a lipid panel, like, you know, total cholesterol, and then from your cardiologist I, what stands out to you most? What are you looking for? You know, what do you make of the lipid panel? Yeah. So if you go to your doctor, the traditional lipid panel that you'll get is something that's comprised of the total cholesterol, which is all the cholesterol that we can measure that are contained within the lipro protein particles in our bloodstream. And then that gets broken down into HDL cholesterol, LDL cholesterol, which is calculated and triglycerides. So LDL cholesterol is what I mentioned is it's calculated based on the other parameters. And that is a measurement of the amount of cholesterol contained within your LDL particles. And that's important and does not get discussed enough and we'll get into why that's important. But it is a, a lot of people think that that's kind of the end all BL number. And for, so it's calculated. And second of all, it's the cholesterol contained within in the particles themselves. And so the reason it is important to look at your LDL cholesterol is that is where most of our data is at this point in terms of if we, what does an LDL, elevated LDL cholesterol mean? And we have tons of data, Mendelian randomization, epidemiologic, RCTs, all of this that lines up that shows that elevated LDL, as your LDL cholesterol goes up, your risk of cardiovascular disease and death from cardiovascular disease goes up. And as we lower it, your risk goes down as well. And so that's where a lot of our data is. And it's a very strong correlation and a very robust correlation. And so much of the drugs that we use are kind of the first line of defense against cardiovascular disease is working on lowering that LDL cholesterol. And so that is our primary target. And we're probably remain so for some time in terms of trying to get that to a lower level to prevent cardiovascular disease. Because it is causative. It is it is necessary to develop cardiovascular disease. And maybe it's worth briefly going into the pathophysiology of what is atherosclerosis. I don't know if that's worth it or not. Yes, now. Yes, please. Yeah. So super high level of it is, as I mentioned, these, these lipoproteins, predominantly your LDL particles that contain cholesterol that are thought to be atherogenic. And there's also VLDL and other types of lipoproteins and we can get into those at some point. But those are the primary. In most individuals, the largest population of atherogenic particles are those LDL. And so what happens when those are those, that concentration of apopic containing lipoproteins is elevated, that concentration is higher in the plasma. And then, you know, defuses across the endothelium into the arterial wall. And through complex things that occur, the LDL cholesterol gets oxidized. That's highly proinflammatory. And you get the beginning stages of an aproma. And so, and then as those sort of grow, then you can get either, you can get different complications, either obstructive coronary disease, which is when that plaque becomes large enough that it's obstructing the blood flow to the heart. And that's engine on chest pain. Or you can also get a myocardial infarction, which is when that aproma actually bursts. Actually, one of my mentors always compared it to a pimple popping, which I think is, you know, absolutely disgusting, but very like, you can just visualize exactly what's happening. And then that sets off a cat, the inflammatory cascade and coagulation cascade. And you get a clot that forms kind of on that. And that's a myocardial infarction. And so, so those are kind of what we, and importantly with that, you know, studies have shown, and it's somewhat controversial. But studies have definitely shown that it's not always the biggest, you know, we, you know, when we're looking at cats and things like that, you know, get nervous about the 80 and the 90% lesions. But sometimes it's those 20 and 30% that that can cause the M.I. So, so those are, that's what we're trying to prevent. And endothelial dysfunction is important, and allows those atherogenic particles to get into the endothelialium more easily. So smoking, obesity, you know, all that kind of stuff can hypertension, make our blood vessels more prone to allowing that cholesterol to deposit. But you have to have cholesterol in order to make a plaque, right? And so while it's important, obviously, to control these other risk factors, if we really control and lower that concentration of LDL particles in the bloodstream, we can really prevent the deposition and then, therefore, coronary artery disease. I love that you said that. And it's funny because you started off with this is going to be a high level discussion, which it is. And I think that for you, you understand that. And I think for most people when they look at a lipopanel, they kind of just characterize good versus bad cholesterol, right? Like, oh, HDL high, good LDL high, bad. And it's much more complex than that, as you just briefly touched on. You mentioned LDL particle limber and particle size a couple of times, or you alluded to at least particle size. And I want to go down this rabbit hole a little bit further, because there are some people who will talk about how it's critical for us to evaluate particle number and particle size, because that's really what matters, right? And you kind of mentioned that LDL is calculated, the LDL C that's typically shown on a lipopanel. And so say a little bit more about why it's valuable, if at all, in your experience to check an LDL particle number and size and what that means in terms of small, medium and large LDLs. Yeah, so this is somewhat controversial. And it remains that LDL cholesterol is for many a very good indicator of cardiovascular risk associated with your cholesterol. That said, it misses many people. And in particular, it tends to miss, and I have seen this time and time again, in individuals in whom there is the risk factors of metabolic syndrome, obesity, et cetera. And as you mentioned, now 42 to 43% of our population fits that criteria. At least has obesity and is likely also has a metabolic issues associated with it. And so in that population, the association, the discordance between your LDL cholesterol and the number of particles you have is higher. And so you will underestimate their risk associated with LDL cholesterol if you're just looking at that LDL cholesterol. And so what I mean by that is that in, as I said, for most people, when you measure the cholesterol that's in these lipoproteins, you're getting a good sense of about how many they have. Now in individuals who have very high triglycerides and metabolic syndrome, you tend to get several. So instead of having, say, five large fluffy LDL cholesterol, you'll have 10 small dense LDL particles. And what we shown in those individuals is that those who have this LDL discordance, meaning they'll have higher ECOB or LDL particle, however you kind of want to measure it, then their LDL cholesterol would lead you to believe. So you'll get their LDL cholesterol back, their standard lipid panel back. Oh, your LDL cholesterol is 95 or 100. And that's so bad. But then you draw an ABOB or an LDL particle on them. And their risk associated with that is much higher than you would anticipate based on their LDL cholesterol number. That's discordance. And their risk studies are shown that their risk of cardiovascular disease in those individuals is much more closely tied to that elevated ABOB or LDL particle. And so that's where measuring those kinds of numbers can be really important and dramatically impact that individual's risk modification strategy. Gotcha. Now in a standard lipid panel, we're just getting the concentration number correct. We're not getting the particle number. Yeah. So you're just getting the LDL cholesterol is 100 milligrams per desolate or correct. Okay. So then in order to obtain the particle number, is that you would have to do a separate test for that or? Yeah. So you can order ABOB separately. And many people are doing that. And in fact, if you look at the European guidelines, they really are taking that into account and recommending that you, it's considered a secondary marker. But the European guidelines do kind of mention ABOB as something to follow as well. And kind of do outlines some of what we just discussed. So you can order that separately. If some people also do what's called like an advanced lipid panel and you can get it through quests and lab core and all your usual suspects. And that will give you sort of the LDL particle number and then give you the sizes and things like that. This might not be a great question to ask. But when you're looking at the advanced lipid panel, you're looking at LDL particle number. It shows LDL particle number. It'll show small, medium, large. Am I missing anything? What else will it show? Yeah. And then it does look at like the HDL sizes and things like that. But does when you if you use that to treat, do you ever use the particle number to treat? Yes. Okay. If you're using that, are you more concerned with the small LDL or the number of small LDL or are you looking at the total amount of particle like the particle number? So I think the data is stronger when when looking at counting numbers of atherogenic particles. So whether you're using APOB, which is capturing kind of all of the atherogenic particles or LDL particles, that's kind of looking at numbers. That to me has the better data behind it in terms of more closely estimate and cardiovascular risk. And so I tend to pay attention to those more. Typically though in individuals that you see this discourse phenomenon in which case measuring those kinds of things is more important. The small they will have a predominant small LDL pattern. So you're kind of taking it in, it goes hand in hand if you will. I got you. So you're sort of taking into account anyway. You mentioned at the outset that it remains controversial. And you have eloquently described that in cases of discordance, which tends to be high with again metabolic syndrome. And I think for those who don't know metabolic syndrome. So the five things that you know triglycerides about 150. Oh my god. I'm actually forgetting all someone. You guys help me out. What are the other four? Yeah. I know your waste your comforts. Waster comforts is one. Your blood pressure, right? I'm not sure. Elevated blood pressure. A1c of six. How high is he? What's he? It's just glucose. Just glucose. Yeah. What's the last one? Over 100 and then HDL. Low HDL, right? Low HDL lower than 40. Is that what it is? 40. 50. Me on your mail. 40. Okay. So and we mentioned, again, you know, recent study showing that 88%. We talked about the obesity numbers. Why? Why not use LDL, right? If we know that if we have compelling enough data to support that when you have discordance. And again, we've I think we've all made the argument that metabolic syndrome is on the rise. Why not? Why is it controversial? You know, I'm not part of the guidelines. I think that. So what I would say is that, you know, I think that we do have a robust data set looking at LDL cholesterol. It's what all of our clinical trials for the most part. When you look at, you know, using statins, PCS, can I never just all these drugs, the target, the goals, the numbers are all based on LDL cholesterol. And so some of that, I think, to be fair is because that is sort of what our data is on in terms of of targets and things like that. I think also what's brought up is, you know, cost, all the grocery is not very expensive at all that on. So so that is a little interesting to me. What I also hear is sort of making it more complicated for the average busy clinician to sort of sort through. We're all so, I mean, you see an LDL cholesterol number rate and you kind of intuitively have a sense of, okay, that's high low or not. I don't think average the average clinician, you know, so we'd have to really switch over our thinking, oh, if we were to then focus on particles or able to be or something like that. So, you know, I think that these two things take time to shift over in terms of kind of all of that stuff. I think that the European guidelines, I think are a little bit more reflective of what a lot of us are doing who are really, you know, seeing individuals who, you know, we really want to focus on optimizing heart health and not just like, oh, yeah, oops, you had a heart attack, you know, of optimize it early. Preventing, yeah. That heart attack, right? So, you know, in terms of measuring L.P. Little A, they're very, they recommend checking that once and everyone, which I think is totally appropriate. So, you know, I think things will evolve over time, hopefully. Yeah. Yeah. It takes time. Yeah. Yeah. You know, it takes time. Absolutely. Now, I do like that. And, you know, what's interesting, actually, a recent podcast that Alan Snyderman on Peter T.S. podcast just a couple of weeks ago, we'll link to that and they go into depth. And a lot of things that you just mentioned right there in terms of, you know, at the individual level, why the guidelines are the way they are. Of course, there's a lot of narrative in that rather than evidence. But, you know, if Alan Snyderman is, you know, you probably, you know, he writes a lot about particularly ApoB, you know, and he's not necessarily on the guidelines as well, but he's got a lot of great work on this. So, we'll link to that. But let's let's talk a little bit more about ApoB, right? I think that there is probably more of a consensus. You already mentioned that the European guidelines, I think you're alluding to the ones in 2019. Yeah. It is 2018. Yeah. That are already using that and suggesting that this is maybe a good marker for, you know, cardiovascular health. Some people, again, will argue that, hey, non-HDL cholesterol, which I think a standard lipid panel it tracks it close enough. And I've had a conversation with one or two lipidologists who have made that argument. However, my, just, you know, brief understanding of literature, the issues that you mentioned in terms of discordance for metabolic syndrome tend to be the same when it comes to non-HDL, particularly when triglycerides are high, which we'll talk about in a future episodes, Huck can be easily manipulated with diet. Non-HDL does not track well with ApoB. I'm curious to get your thoughts on that. And, you know, when it would be good to use that versus just get ApoB, you know, that kind of stuff. Yeah. So, I think non-HDL cholesterol is, is, is, so before LDL particle and ApoB became a little bit more mainstream, that was definitely what I was, I was taught to use even more so above and beyond the, the LDL cholesterol. So, I think that a lot of people call it the poor man's ApoB, because it is in that panel already. And I think that it, it can be really useful if you don't readily have, and, and one of those other markers available to you, that said when you look most of the studies have shown that, that ApoB has the strongest association in terms of cardiovascular risk, and it counts for all of those other things, right? So, so sure LDL cholesterol is typically associated, maybe non-HDL is like a little bit better, but really ApoB has kind of takes into account all of these, these things, and is, is probably the, the most accurate thing to measure in terms of assessing cardiovascular risk. Does that make sense? Yeah, absolutely. And, you know, again, just to kind of drive the home that point, I would argue that ApoB, as you mentioned, it's going to be the lipoprotein that's going to be in all of these markers. You talked about IDL, VLDL, and although LDL are primarily the ones, as you highlighted, that are going to be responsible for, you know, pathogenesis, and that process throughout the entire body, there is evidence to support that VLDL does that in preparation for this discussion right here. I was just kind of doing some light reading and cardiology journals. Absolutely reading and lipidology. I don't think there is any such thing. Yeah, if they're, you know, it can be really fun. Like you said, you would really have to have a passion for it. And, you know, I saved this, it didn't really go through this, but this article in 2020 and, and actually in Jack was published, talking about how VLDL cholesterol counts for one half of risk of MI, associated with ApoB, cutting lipoproteins, right. And so my thought would be why not, you know, rather than use the poor medicine, why not just get the marker that's going to be, and you're going to see, you're going to capture what you're going to see an IDL's VLDL, you know, I think in a world where we're getting closer and closer to taking care of our patients at an individual level, like this word precision medicine gets used a lot. And, you know, why not check that. And so I have difficulty from, again, this is a non cardiology bias. This is just a person who wants to optimize health rather than just treat people who are sick. But I'm, you know, from your sense, who has the wisdom who've been in the conversation with lots of cardiologists, you've trained in some prestigious institutions. What's the argument on the other side about not doing it, at least in this country, in our, in our health care system? I think it is continuing, it's an evolving conversation, right? I think that it's taken as with all of scientific endeavors, it takes time before something becomes more mainstream. It just does. And so, you know, I don't, there isn't great arguments against it other than the ones, the ones that I mentioned, right? So people argue against cost, people argue against, you know, really having to re-educate the general busy clinician as to what to look for. And so, you know, do we overly complicate it? That sort of thing. And, and, and, and there are some, some that say that there's not given our robust data with LDL cholesterol. There's not enough evidence yet that, that, that we need to necessarily pay attention to ABOB. I personally find that we have enough. And I, I think that I've seen it, and enough, anecdotally, and enough of my patients. I have seen this, this major discordance, and where I get lots of patients who've just had a basic lipid panel, oh, my docs told me my cholesterol is fine, my cholesterol is fine. And then either they have an event. And so then they come to see me and they're like, what's going on? What happened? Or hopefully not, they didn't have an event, but they eventually found me. And we look at either LDL particle or ABOB. And, and it's definitely much higher than you would predict from their LDL cholesterol. And, and so, you know, I think that given we have so many medications and lifestyle changes at our disposal to really lower risk due to cholesterol, it's just, it's, in my mind, it's a missed opportunity. I love that. And, you know, and I think as much as, as both Darshanire and our passionate about, you know, optimizing health and practicing precision medicine, you know, I'm, I'm, I think, just as passionate about being practicing cost-efficient medicine. I think there's something to be said about that. I think in that episode that I referenced with Alan Snyder, and they actually discussed this issue. I'm not sure if you had a chance to listen to it, but Alan Snyder, I'm in practice in Canada, so they have different obviously. But at least Peter T. Had mentioned that he called the lab. And I think it was $250, $2.50 for APOB, right? Something like that, right? I haven't verified this personally with Quest or LabCore or whatever. But, you know, if it is, that doesn't, that doesn't really, you know, so, so I don't want to call them in every creation in the hospital gets like, you know, the, the regulars that every morning, and you're like, you know, yeah, I think that handled the $250. So coming back to your practice, right? If, if a new patient comes in, maybe in their 20s, some individual, he's active, he's healthy, she, he, whoever, and they want to, you know, optimize your chances of, you know, living a healthy life and a longer life. What are some of the basic things that you're going to look at, you know, of course, I know you've talked about this length family history is, you know, super, super important, you know, back and stuff. But aside from that, when you're looking at objective things, what kind of lab values really stand out in that initial consultation that you'll order? Yeah, so there's definitely not, as you mentioned, I try to practice a, both evident, based and kind of precision type medicines. There's certainly not kind of a one-size-fits-all approach. But certainly we do, I do tend to look at both advanced cholesterol panels, so many of which we've discussed already, the benefits of either an LDL particle number or an ABOB. I also almost always measure an LP little A if someone hasn't had that measured already. And we probably haven't touched on that yet at all, but let's do that. Let's do that now. Yeah, really important marker. So, LP little A, lipoprotein little A, is another, so as we've mentioned, LDL particles are kind of, for the average person, the primary aprogenic lipoprotein that's circulating in our bloodstream. For potentially, as much as one in five of us, lipoprotein little A may also be significantly elevated and a major risk factor, as well. And so, lipoprotein little A, it's basically like an LDL particle, except it has the little A moayati on it, which, incidentally, is very similar to plasma nitrogen. And so that's thought to be part of why it has increased risk of thrombosis. So, what we have found is that individuals who have elevated LP little A certainly have an increased risk of cardiovascular disease. And so, it's LP little A is thought to be aprogenic, just like LDL cholesterol. And it is, unfortunately, genetically mediated in that it's very much, and this is why the European guidelines recommend checking it once and at least once in everybody's lifetime, because it's genetically mediated, so if you have it, you have it. And it doesn't appreciably change that much over someone's lifespan. In women, it does go up a little bit, postmenopause, but that's really about it. It is influenced somewhat by diet, but not nearly as much as, say, LDL cholesterol. And so, in addition to being associated with cardiovascular disease, after school, or specifically, it's actually also, as I mentioned, associated with an increased risk of DBTPE, and then it's also associated with an increased risk of aortic stenosis. And so, those are kind of the things that we need to just be mindful of in individuals who have an elevated LP little A. And I have plenty of patients who have had cardiac events, and that's really their only identifiable risk factor is the cell pill delay. And so, at the moment, we don't have any therapies for it, really. So, as I mentioned, diet does not tend to change it dramatically. Stattons, if anything, might increase it. And so, really, what we're left with is kind of niacin and PCS kind of inhibitor. So, niacin can definitely lower it. It's pretty controversial to use it. I typically don't. But some of my patients have been on it for some time and are pretty pretty, want to stick with it. We don't have any outcomes data. So, while we know that increased LP little A is associated with cardiovascular disease and causative, we actually don't have any data yet that lowering it will definitely reduce risk. It's, so, PCS can and inhibitors are best fed. They can lower LP little A by 20 to 30 percent depending on some, it depends. And there's some signal that when that individuals who had an elevated LP little A when they're on PCS canine inhibitors, they had lower risk of events above and beyond what would be expected just by their LDL lowering. So, when I have patients who meet criteria for PCS canine inhibitors and have elevated LP little A, I definitely encourage them to use them. So, you know, for people who are like kind of anti-medication right and we we hear about this population all the time, they get their LP little A measured right and it's high. Are we measuring it just to see what type of medication and therapy we can use towards it? Because you said it's not going to change much really not much effect from diet. So, there's not much lifestyle medication that can lower the LP little A. So, are we really just drawing it to see what we can give? So, currently how I use it most typically in my practice is really to be able to guide treatment decisions about other risk factors. So, it is and in our guidelines it is recognized as a risk modifying factor. So, so certainly in individuals who have an increased LP little A, my threshold for where I'm okay with their LDL cholesterol, for instance, or credible or epiv is really up, right? So, I push those people down as well as I can. I really make sure that we're optimizing everything else that we possibly can because of what I've seen LP little A do. Yeah, you know, I think it was maybe a different podcast. I actually might have heard you've said that diet or at least maybe it was diet or plant-based diet tends to increase LP little A. It has. There was one small study where it actually increased. It was it's strange. I mean some of it's like I said, but it's it's not I mean it definitely it goes along with the statin data which also increase. So, paradoxically some of the things that we have that we know that can lower LDL cholesterol either don't do anything to LP little A or make it like a little bit worse. So, I don't want to go too far down this pathway in terms of treatment, but if you did get the LP little A and it was elevated and now you're going to be you know taking that information, you'll be a bit more aggressive and everything else that you do in terms of prevention, primary prevention, but also keeping it in the fact in the back of your mind with the statin data. Would you still put somebody on a statin for a protective standpoint because that's strong enough evidence? Yeah, so I definitely definitely and even though I know that it's possible LP little A may increase a little bit with us with statins. If their LDL is not where it needs to be with diet alone, I have a very low threshold to add it. Do you find when you're having this discussion with your colleagues possibly working in academic centers that they are quicker to or they put less of a fight to order this test? Like what's your sense in that? I do think that LP little A is definitely way more recognized at this point. Unfortunately, I still think people are thinking about it too late. So again, but this is true of a lot of medicine and exactly what you guys discuss a lot on this podcast is that I hear my colleagues thinking of ordering it in an individual who's 42 and comes in with their first MI and their LDL cholesterol is not so bad, right? Maybe this is LP little A, which is why I think that you're being guidelines would say we should just all just get it checked at whatever age is a great idea because I'd much rather pick it up before that 42-year-old had the heart attack. And again, we don't yet have rate therapeutics, so I'm not saying we 100% could, but I'd at least like to give it a shot. You know, I find that really interesting because one of the things that we all learn, most of us have to say learn in medical school and during a training is that you don't order a test unless you're going to know what to do with it, right? Unless it serves their purpose, right? We don't want to do unnecessary testing again for the cost of the healthcare system, what not. And kind of what we talked about, you know, niacin is one treatment. I think that's the very, very cheap PCS-K9s can be ridiculously expensive when you're paying out a pocket. And they're not going to be covered in a 20-year-old for primary prevention. There are some things out there. ASO is, I think, is anti-sens illegal nucleotides, right? I mean, but that's like super, super early and for ridiculously high risk patients and you know, somebody who's had already had like a 42-year-old who's had an MI and a couple of stents that you're talking about. But you mentioned that some docs might be quicker to order this test, but at the same time, we don't have much that we can do. Yet people will not order ApoB or LDL Particle when we have therapies that we can, you know, target them and kind of modify them if you will. I find that interesting. I can't say that I am able to explain that phenomenon. Yeah, so do you want to say something about the ASOs just so people have a sense of what that is and what your experiences, you know, in terms of where we are with the current state of the evidence with that? So in terms of there is a one medication that's in kind of late-stage clinical trials that's looking at lowering LP-little-A in individuals who have established cardiovascular disease and are considered high risk. And so I think we're at least a couple years out from that clinical data though was the last time I looked. I think it's like two years away or so. So, but I definitely, you know, am letting my patients who meet that criteria know because I mean, and again to that point of what you've said about feeling like you're drawing something that you can't do much about. I think that's important that in patients who do get this drawn and it is elevated that you are able to educate and counsel them as to what the implications are of this and what they can do about it so that they're not completely totally defeated. So yes, I let them know that there are some medications on the horizon, but I think just being very aware and not just ordering it to order it and then and then not know what to do about it because I definitely have patients come to me and they are very fatalistic and they're like, I'm going to have a heart attack like that's and I can't do anything about it and I can't take a medication about. So you definitely want to make sure that if you are going to order something like this, you do know what to do about it. And right now, the state of affairs is is really helping them get super aggressive about everything else and that gives that does give them a back essence of power, right? Okay, your LDL is currently 130. I wanted this, right? This is what we're going to do to get that down. We might not be able to do something about the LDL delay, but we can absolutely change your trajectory. Yeah, and I think that what you mentioned right there is a really important point that needs to be, I just want to underline a little bit further. I think that, you know, with the cost, the harm of, you know, unnecessary costs aside, the harm that it might increase anxiety in a patient and, you know, Dr. Beth Freides came out a long time when we talked about her initial passion about what stressed us to the cardiovascular system. I think, you know, we don't want to order tests and if you're not going to be able to do something about it and if the patient's not going to receive that well, that hey, you know, I can maybe take care of all these other boxes, that might end up doing more harm than good. So that we got to be cognizant of that fact as well. Absolutely. Yeah, Dr. Harkin, I wanted to take a step back to LP, little A, you know, you talked about how our genes really influence this and some of our audience might be thinking, well, I wonder if I have the genetics for that, right? Can you tell us which populations typically might have high LP little A, worser cholesterol panels, etc? That's a great question. I actually don't know the exact distribution in terms of which, you know, ethnicities are more likely to have it or anything like that. I think there are, it is known some populations, but as far as I'm aware, I don't think that it would be able to, you'd be able to reliably say, oh, well, you're ex-wise, so it's super likely, don't worry about it. You know, I think that, as I said, with the European guidelines, they do think that it's, you know, quite reasonable to screen one time and everyone. And again, keeping in mind some of the considerations that we've mentioned, it's very reasonable to check at some point as long as whoever is going to be checking it has a game plan forward about what to do about it. Gotcha. And I just want to clarify, this test is separate from the APOB correct in the advanced lipid panel for listeners. Okay. So, West, there is an advanced lipid panel, so Quest has several advanced lipid panels. They do have one advanced lipid panel that also has LP little A in it, lab for it's a separate test, in Quest there's one bundle that does include it and then there's another one that doesn't. So it's highly confusing. So for your average person who's rightly drained order these, so yeah, but it's something that if you wanted to get drawn and you felt comfortable understanding what the implications are going to be, you could certainly talk to your primary care doctor and say, hey, I'm concerned about this, I'd like to get it drawn. I mean, I definitely think that the people who should consider getting it is definitely anyone who has premature coronary artery disease. I think that's a given. And then certainly in anyone, any of my patients who have a family history of premature coronary artery disease, that's definitely something that I think should be checked because it's a common cause of of familial premature CADs. So those are, I think, you know, your average person, do they need to get it drawn? I don't know that we're definitely there yet. Certainly our guidelines don't support that, but I think in people who have some of these family histories or that they themselves do, I think it certainly warranted. Awesome. So we spent a lot of time kind of defining and talking about blood markers that might give us some insight into cardiovascular health, right? What are other tests, some objective measures, you know, such as imaging and that kind of stuff that you might pull out of your toolbox to give us some insight on how somebody's heart is functioning. Yeah. Or their risk. Right. So I think probably one of the best tools that we have right now that I think bears at least a couple minutes of conversation on is the CACS score, the coronary artery calcification score. So for any listeners who don't know what that is, it's basically a specialized CAT scan that takes pictures specifically of and focuses on the heart, specifically the coronary arteries, measures and quantifies the amount of calcium contained within the coronary arteries. And so, you know, many of us kind of refer to it as the colonoscopy of the heart in that it's seen very much as a preventive tool. It is not to be used necessarily when people are having a chest pain. It's more to look at disease with a preventive lens. It's sort of widely thought to be picking up quote unquote early stages of heart disease. That's a little bit of a misnomer because calcified plaque is by definition old plaque. It is not new plaque. And so really you're picking up old disease. But regardless, it is a great, great tool that we have at our disposal now. And so essentially how many of us use it is when you're trying to sort of further fine tune and assess someone's risk. And it can give you a really good view into what's happening with someone's coronary arteries. So, you know, some of the examples that and in our guidelines, it's very much acknowledged as a great tool that we can use to try to help reset, stratify people, particularly in those individuals who fall at like say a borderline risk like that five to seven and a half percent, 10-year cardiovascular risk. Do we start stands? Do we not start stands? Or if a patient is sort of on the fence, if they want to start them, it can be really helpful to sort of see where they're at. So there's a lot of great robust data that we have at this point that it can really be value added in terms of stratification. Specifically, if a coronary artery score is zero, in the right patient that can be helpful to help us say, okay, so far, so good. Let's keep watching if someone is truly opposed to satan therapy. Yeah, I think an analogy that really helped me. And I'm still in this one, Peter, I hope I'll paraphrase because I remember him talking about how a CAC will show you something after the damage is already done, right? Like, for instance, if I did my training in Baltimore and if you go to a place and you go to a home and you see jail bars on the windows, then you know you live in a bad neighborhood, right? I mean, that's kind of preventative. But a CAC seeing a fleck of calcium or a CAC score in a young person, it's like somebody's already broken and there's a glass shattered in the back door. The damage is already done, right? And it's not, so in a 30-year-old, if you have some calcium there, then at that point, like the red flag, the alarm bells are ringing, like, you know, something is going on, right? That's an indicative of advanced cardiovascular disease at that point. Is that fair to say? Yeah, so and that's what I meant in terms of a CAC score of zero in the right patient, right? So it certainly is, so not only does the CAC score give you an absolute number, so it gives you, you know, you're a zero or you're a 10 or you're a 400 or then, which means, and that's what I was talking about earlier with the lines, blending between primary versus secondary prevention, because of that point, your secondary prevention. So it gives you that exact number, that absolute number, but that also gives you a percentile. And it sort of tells you kind of relative to other people, your same age group and gender, this is kind of where you fall. And so, you know, the CAC score is great, but it has to be used in the right context. And that's why I think it's one really important to distinguish that, that this is not, you know, the very earliest stages of coronary artery disease to your point. This is healed up old plaque that has been there for some time. If you're seeing that in a 30 year old, that's like really, you know, we need to get on this now. That is very highly concerning to me. And also in by that nature, you have to be careful in interpreting a coronary or calcium score of zero in a 30 year old, because it should be 30, it better be 30, right? And so, so just because it's 30, doesn't, or just because it's zero in a 30 year old, sure, I'm like, okay, this is good. You don't have any CAC right now, but it doesn't roll at soft plaque, right? Which is what I would expect that we would have another year old. And so, where the coronary artery to calcium is CAC score is typically most useful, is traditionally we use kind of 40 and above, and in super specific scenarios where you're trying to kind of figure out adding therapy or not. So, I wanted to switch to, because we're talking about satins quite a bit, and I think that we have tremendous data to support their role, you know, in all kinds of prevention, and you've touched on on those quite a bit, or at least you mentioned it quite a bit, but I'm wondering before we do that, isn't worth talking about high sensitivity with CRP, because I've heard you talk about that quite a few times, and I don't know, use it in your practice. I do. Yeah, I think we can definitely, that's definitely something I also tend to look at, and I think is, again, something that is recognized within the guidelines as a risk-modifying, sort of thing that you can kind of take a peak at and help you kind of make decisions. And so, certainly we know, as we mentioned, you know, cholesterol and elevated lipoproteins are a necessary in order to create atherosclerosis, but inflammation is also critically important as well, because that damage is the endothelium, and makes it more likely that we'll see that happen. And so, we see certainly in, so obesity is an inflammatory disorder. So, we see that in that population. We also definitely see it in kind of the autoimmune population. So, we now know that individuals with lupus and psoriasis and rheumatoid arthritis are at much higher risk of cardiovascular disease, likely because of this underlying low-grade inflammation. We also see it in HIV and AIDS. So, now individuals who are surviving and living long, long lives because of the amazing medications that we have, they tend to have very premature and really just definitely a lot of atherosclerosis, likely because of that inflammation. And so, those are kind of examples of people that we that have known inflammatory disorders that we definitely see that association with, but it becomes just just kind of important in sort of the average person who has the maybe metabolic syndrome or kind of earliest stages of that or really early insulin resistance or something like that. So, HCRP can be something that we can measure to get a sense of what is that that in inflammatory state, it's associated with an increased, you know, an elevated HCRP of 2 is associated with an increased risk of cardiovascular disease and, you know, we have radiators done those studies of, you know, that residual risk, right? So, even when we treat people with statins, we still see this inflammatory residual risk. Even those statins do, you know, help have in terms of leotropic effects, they do reduce inflammation. You know, I think, you know, that's that next big area of research is how can we we modify inflammation in a way that we reduce risk of cardiovascular disease, but also don't impair our ability to fight off infection. And so, so we're still obviously that that's still kind of in process, but it's certainly something that we can we can look at and in terms of what to do about it, definitely we do have some some data to show that eating whole food plant-based diets can help lower inflammatory markers, along with lots of other helpful lifestyle changes, which I think we'll get into. I assume we'll come to the next on the next episode, but so that's one of the things I do I do look at because that's something that we we can definitely work on. Well, I don't think this podcast episode can be complete unless we talk about statins, right? I mean, I think it is one of the most ubiquitous drugs we see, especially ultimation eye in the rehab world, right? I can't name one patient that comes through our rehab doors that hasn't been put on a statin. And I'm sure our audience have heard of statins, probably have, you know, if they're younger, have parents or grandparents who might have been on it, but just from like a basic standpoint, what are statins? What do they do? Why do we use them? Okay, that's a big task. That might be a three-hour topic, so. Okay, so give me a wee little bit, a couple more minutes. So, statins are past medications. Okay, so they super high-level, they essentially block and enzyme within the liver that is necessary to synthesize cholesterol. And so actually the mechanism by which they lower our blood levels of cholesterol is actually because what that does is it makes the liver upregulate the LDL receptors on its surface. So then it pulls more LDL cholesterol from our bloodstream. So that's kind of super basic how how statins work. And as you said, they are kind of the bedrock of preventive cardiology practices all over the globe. They are a class of medications that have been around for quite some time. They were absolute game changers in terms of our ability to lower cardiovascular risk. We now have decades and decades and decades of really sound robust data demonstrating that that in particularly in secondary prevention, we reduce the risk of cardiovascular events. And by as we said, mostly by that LDL lowering effect. And but also well-recognized for these pleiotropic effects, which are poorly understood, but definitely we see some anti-inflammatory effects and things like that. Because certainly we see that that you know in trials that where we look at initiating statins the day someone has an MI when you know they get wild in the cath lab, they get their aspirin and they get their stent and they get their statin and they get their high dose statin. And so we know and we know that even within those first 30 days post-MI, people that get that high dose statin early on do better. So there's clearly some other effects other than just that that lowering of LDL cholesterol. So they are widely used, widely studied, definitely safe lives. I'd be remiss if I did not mention that they do have some side effects certainly and in some real ones. And so probably you know the most commonly complained about side effects are the myologias, the muscle aches, things like that. Some of those are dose response. Some of those are sort of the effects and there actually was a really interesting recent study which I'm sure you guys saw where they looked at that really they took. So the sort of the nocy, nocy, I can never say that word. Nocybo. Thank you. I say cocebo just fine. I don't know why it's it's it's it's it does not go together for me. The nocybo effect. There I said it. So so it's so so there there's definitely been some studies the where they have have looked at you know giving patients placebo's and and you know it turns out that that that we all just have muscle aches right particularly as we get older and we've you guys know that there is everyone who has aches and pains. So ways that clinicians can side sort of so anytime before I start to stand I definitely start at a lower dose possible and work my way up. If and then I also actually have patients do a like muscle aches and pains notation. So I tell them to like pay it like right now pay attention to your body with the next stair to what are the aches and pains you get right them down because this is not the statin. And then when we start the statin next week if you still have those aches and pains that's not the statin right. And so actually having people kind of take a catalog of those those muscle pains can be really helpful and I found that I get a lot less people complaining about those side effects. That said I have had patients who have had you know true debilitating myologist because of statins and so that can be a really limiting kind of side effects. The other one that I do monitor and probably concerns me the most is just the diabetes risk and it's there and so we do have to just kind of be cautious and careful and monitor closely for worsening insulin resistance and diabetes. I'm really glad that you brought that up. I think the study that you're talking about was published in BMJ 2020. I came across this one as well but I think this is worth briefly mentioning. Basically they took statin intolerant patients right and they put them into you know they either gave them a placebo or a statin and they repeated that three times or actually yeah they repeated that three times and there were six periods overall in random order and the patients either got a statin or placebo and afterwards they were queried and the patients weren't able to tell like when they were getting a statin versus a placebo right so they were able to show that hey it's not necessarily a statins. That being said though there are physicians who will argue that you know these adverse events or effects I should say are much lower in randomized control trials than they are in clinical practice right because again the population for RCTs is much smaller than the amount of people in clinical practice that are seen that are taken stands and you know prior to just over the last couple years as I've looked at some of the literature you know again clinically or anecdotally I should say I do have a lot of patients in sports medicine and rehab who tend to be maybe a little bit more active who will say hey listen like you know I I don't like it I don't like how it makes a feel. Again we can argue it might be no SIBO but at the same time you know there are some statins that are more likely to cause that I mean so maybe a case study here would be good right so let's say you get a young individual who's highly active maybe borderline athlete who comes to you and and you want to start this because it seems to be appropriate is there one that you might reach for initially considering that that my algeas might be something or you know that kind of stuff. No so I typically use my if I'm using a statin because I want a desired effect I I typically reach for I mean and I see a very specific patient population that typically needs a lot of LDL lowering so I'm not I'm typically starting with kind of the big guns if you will so I usually am using a resumed statin low dose but that's typically what I'm doing I I think it's easier to because you never know who will have a problem and who won't so I think personally I start with what I would prefer to use and then if that doesn't work you change your game plan so so as I said others and then there's other strategies you know you can go to every other day dosing you can move to a different statin so I'm proud of Patava if you need to kind of go a different statin you can do that that's that's lower potency or you know instead of uptry trading you like say you know Resuba 5 was fine but 10 it's not go back down to 5 and Adzadia or go to every other day dosing and then try to work your way up so there's different ways that you can kind of modify your dosing schedule as you need to if someone has side effects but I'd prefer to to start with what I want to use first absolutely well Dr. Harkin I want to be respectful of your time I know a lot of the topics we just talked about today will probably come up again in part two and I'm excited for part two because we're going to be talking more about lifestyle modification the way you practice kind of your day-to-day and what you do with patients so definitely excited for that but before we let you go tell our listeners where they can find you yeah so I am typically most active on Instagram so Nicole Harkin MD and then I also have a website wholeheart cardiology allonword.com and they can sign up for my newsletter I if patients if people are interested in becoming a patient I see I'm licensed in New York California and Florida so I see patients via telemedicine in those three states I think those the main the main ways to get a hold of me and see me yeah gotcha well awesome thanks so much excited for part two thanks no Harkin sounds great thanks so much all right hello everyone welcome back to another episode of medicine redefined this one is a part two with doctor Nicole Harkin so I'ma say this right off the bat if you haven't listened to part one highly recommend listening to that verse getting the fundamentals down in regards to cardiovascular disease lipidology and then this episode we're going to be touching on kind of high-level interventions right especially from lifestyle focus nutrition sleep etc so welcome back Dr. Harkin thank you guys so much for having me on again I'm excited to be here for part two yeah absolutely as as as we are so let's get right into it you know we want to focus this talk mainly on your approach to patients and kind of you know when a new patient comes in when you're looking at it not only from a pharmacological perspective but also an intervention perspective that you know we obviously know exercise sleep all these things matter take us through I guess just general overview for now when a new patient comes into your office what's your approach yeah so it really depends on the patient I have a very tailored and personalized approach depending on who the patient is is this primary prevention is it secondary prevention what are their risk factors what testing they already had done what further information do we need to really determine sort of their overall cardiovascular risk and then figure out how to optimize it are they eating a standard American diet right now are they whole food plant-based no salt no oil no sugar you know where are they on that spectrum and so so every patient obviously is different and I think that's really important and where it sets preventive cardiology clinic approach apart from sort of other kind of standard visits which just aren't as well equipped to really go in depth and analyze these approaches and so we know from data that the average patient seeing the average cardiologist gets no more than three minutes of lifestyle modification advice and typically that ends up being eat healthier right and we know that doesn't work and so so really looking at a patient from an individual as an individual figure out what are their goals what are their barriers to change and where do we need to go from there so in terms of a high level approach I typically have my patients fill out a pretty in depth intake form prior to seeing me I also like them to upload any prior testing both diagnostic as well as laboratory in advance the appointment so that we can really hit the ground running and I also include on that form you know what are your goals like what do you identify as as your major risk factors and what are you hoping to achieve and then just as you know typically going through a typical visit in terms of their personal history their family history their medications their supplements you know all the things that were used just sort of really getting into but then I also do a pretty in depth lifestyle intake so I do ask them a lot about nutrition not only what's a standard sort of breakfast lunch dinner snack situation for them but also how often are they consuming red meat unprocessed red meat packaged foods things like that to get a really good understanding of sort of where they're at I also ask about sleep with quantity and quality I ask about stress levels sort of rating them on a scale and and and all of and the exercise obviously as well what they're currently doing and then we go through together the current tests that they have done and then decides of what other further testing might help us fine tune what their risk is and I think we talked about this in in part one some of the typical tests that I typically look for in order again depending on the patient and where that's appropriate and then we circle back and we look at everything together and then really figure out where what is their biggest risk factor that we need to really work on and modify and how what's our approach going to be as in line with our guidelines more often than not it is a lifestyle first approach so how can we make changes make tweaks to your diet your exercise program what have you to achieve our goals and then we reevaluate and then if pharmacologic therapy proves itself to be necessary then then we talk about that at that point yeah I mean the word that comes to mind is comprehensive right I mean you talked about just even prior to seeing the patient and how much data that you're looking at and and we spend a lot of time as you mentioned talking about diagnostics particularly lab markers but I really love the fact that you talked about hey what are your goals what are you hoping to get out of this I think that's so important to to highlight right at the beginning and then I think that that this concept of therapeutic alliance that Dan Pope came on long time ago talked about although he was referring to it from you know musculoskeletal rehab standpoint but I think that applies here as well I think that if you can identify the patient's goals you're much more likely to to have that relationship with their pedicillin and so I really you know appreciate that thank you I think that you know when we're focusing on lifestyle medicine right some of the things that we've talked about offline is when we look at it depending on who you're talking to the pillars or you know sleep exercise distress challenge or stress tolerance you're looking at nutrition right am I missing anything else or is there any other bucket that you look at it from that perspective one's lifestyle medicine also specifically delineate substances such as alcohol and tobacco separately as well and then community support love that sort of thing as well would be kind of the last pillar so I have a framework in my mind of how like I like to approach it when I'm looking at it from cardiovascular health but wherever you want to start which one do you think out of those is kind of the bedrock if there is even one or wherever you'd like to start we can we can go down that pathway first the bedrock I like that I would have to say that in terms of you know levers that we can pull that truly impact in oftentimes dramatic ways nutrition is is really king I think in terms of how can we make major changes that can either lower blood pressure or lower cholesterol or all of the above awesome so let's start there and it's a pretty big that one I mean right off the bat we're going to pick the most polarizing topic I love it all right this is going to be the biggest one to tackle but but I appreciate that I think that you know again I get it the sense every single time we we have the conversation that again it's talking to the patient and really assessing where they are what kind of diet you just mentioned right are you taking a lot of meat you know what what's your current diet like and then we can help you get to your goal so this is a highly contested highly debated topic right different you know is red meat as you mentioned is that bad for you red meat and cancer you hear about that and then you know every single study comes out whether or not it's a good study is a different discussion but it's all over the media and people in different camps low carb high carb low fat high fat keto fasting all the kind stuff they'll take that study and they'll say well this is what's really good for you the way that I always think about it is well it depends which lens you're looking at it from right for instance let's just take the discussion of okay well can you can you so in my world of fitness and sports medicine and where I'm treating a lot of athletes right let's if you're taking a physique competitor and they need to hit a goal of protein intake right so can you be an all plant or a vegan diet and and be at high level physique better sure you can but we have to appreciate that it's going to have some challenges right can you should you right and so for our lens from a cardiovascular perspective what is your overall philosophy when you're looking at nutrition when you haven't that conversation I know it varies individual to individual but do you have one? yeah I think that from an abundance of data both randomized controlled trials epidemiologic data short contained feeding trials and as is reflective of the ACCAHA guidelines we know that ideally our diet should be composed of as much vegetables, fruits, whole grains, legumes, nuts and seeds as possible and how in what context and with what other things those are sort of the margins at which we debate about those things but I think that and it's interesting you mentioned from the offset that this is the the area where we see the most is the most highly contentious and it's interesting because it isn't it isn't right like if you listen to the media and these different fringe camps about diet I think it does end up getting really confusing really quick for the average person but I think if you bring together sort of nutritional experts across the globe there's actually a lot more commonality when it comes to these diets than you would otherwise think so sure maybe they argue over you know the relative component of starchy virtues non-starchy vegetables but I don't think anyone is saying that vegetables in general are bad I think most nutritional camps would agree that that processed and packaged foods and sugar is is is not good for you so I think there actually is if you actually line up sort of a helpful plant-based diet a helpful Mediterranean diet a helpful low carb diet you actually see a lot of commonalities and then sure we can definitely talk about sort the differences afterwards but when you look at from a helpful cardiovascular perspective I think the ACCHA guidelines did a pretty good job of sort of delineating what is known what is not known and what should we we really emphasize and again then it gets back to sort of what are the patient's goals where they at right now and where they want to go but in general moving patients towards eating more whole unprocessed foods is is definitely supported by the data so Dr. Harcett one of the touted diets out there that has been at least shown I put quotes on this to reverse heart disease is the Dean Ornish diet right which I believe he created in the 70s and I think I'm getting this right the Dean Ornish diet is at least it's low fat I think is like the main thing and then it's whole food plant-based but to me I find it interesting at least that creating the 70s that surround the time where we thought that was terrible for you and you know we've since changed our mind since then but one what are your thoughts on that diet right I think that word reverse there is it's pretty key you know we talk about reversing we're stabilizing heart disease so what if patients come up to you and they ask you about this diet or they've tried this before what what's what's your take at least on the Ornish diet yeah so the Ornish diet is as you said it's it's actually a vegetarian diet so it does not allow low fat dairy in it and it was created by Dean Ornish as you said and it was also importantly part of a comprehensive lifestyle program so in his studies it did incorporate moderate exercise stress management social support and all of these other things and you know importantly they were pretty small trials but they were randomized and they did show improvements in as I recall exercise tolerance and reduction in angina reduction in needs of medications and things like that so I think as with any sort of smaller trials they're very provocative and hypothesis generating but I think in terms of diseased reversal we have to be very cautious with how we say that and and I think when patients ask me about that my response is you know most modern cardiology trials what we're looking at is not most of them are not repeating angiograms and looking at black burden right that is not a typical endpoint for a cardiology trial most cardiology trials we're looking at mace right so we want hurt outcomes you know revascularization heart attack cardiac death you know big heart outcomes and ultimately that's what matters to patients right they don't care if their plaque went from 30% to 20% now if their angina went away that's really important right if they don't have a heart attack that's really important so I think that we have to be careful in terms of does plaque go away maybe but in general that's not likely the largest maybe partially that's happening and take statins for instance statins do likely reduce plaque in in studies we now know that there's definitely plaque burden that gets reduced but that's very unlikely to be the major mechanism at least at first by which they're reducing cardiovascular endpoints right we know that statins early on as soon as someone has an MI you give that and they have better outcomes in 30 days that's not plaque regression right that's in the field of dysfunction changing that's inflammation that's all the other things that happen so I think it's a really interesting conversation but I think that ultimately it's it's not really what matters and so I think I I prefer with patients to really focus more on how can we make you feel better and a little longer if your plaque goes down by 10% great I like it yeah that's good one awesome so you know you mentioned that there aren't there isn't anybody who would say the plants are bad for you I would argue there are some some very there's the chemical crowd that's true right right right and so so and and they would argue that some of them how the toxicity and plants and whatnot and I don't think that we're going to visit that aspect of this conversation but if I'm not mistaken you are are you plant predominant or are you vegetarian only at this point or for your personal time I'm playing based so I I was vegetarian I became vegetarian a little redecated ago now and then plant based within the last couple of years gotcha so for those who don't know the differences what does plant based versus vegetarian mean yeah so plant based has variable definitions but for the most part it's defined as either plant exclusive or plant predominant and specifically distinguishing from say vegan or vegetarian diets is defined not only by limiting or completely eliminating animal products but specifically focuses on consuming whole food products so as much as possible whole foods in their whole form without being as processed and so so the foods can be you know minimally processed bread for instance or even you know something like tofu but ideally not not processed so this distinguishing it from say a vegan diet which can and often may include highly processed foods like french fries and Oreos that would not be inclusive of a whole food plant based diet awesome so and to your earlier point I would point the listeners to John Brody's podcast I think we're one of the very first series that came out that thing was called diet debates very interesting where it's a three-part series and they're looking at and you know to your point his podcast is all about finding the common ground between different points of view and it's actually quite interesting that when you when you really sift out the the people who have the loudest that platform but just the the message on either ends of the spectrum most people kind of fall in that camp and so I think that was pretty interesting but you you talked about a little bit about the mechanism stats right or you touched on briefly and I think no discussion can be complete science based discussion without talking about mechanisms so I think the American diet which is heavy on meat consumption and processed foods and whatnot and very little on plants and most folks agree who are in that middle ground that we need to increase our plant intake as you've already said mechanistically what's so good that is beneficial for our heart health yeah so plants are and when we say plants again we're talking about vegetables, fruits, whole grains, legumes, nuts, seeds, essentially plant oils as well so so in general we know that they that plants are high in things like fiber things like potassium and magnesium polyphenols typically in the heart healthy fats such as poly and mono unsaturated fat and they tend to be very low in cholesterol and saturated fat and sodium and things like that and so we can go down we can go through sort of different mechanisms by which all of these things are are helpful to our bodies but essentially we know from sort of long term epidemiologic with perspective and retrospective studies looking at large populations and whether you're taking omnivorous populations and looking at say and hein's data or if you look at specifically sort of plant-based communities like the Adventist Oxford things like that regardless of sort of where you fall on the spectrum in general we see that in the more plants you consume the lower the risk of heart disease now obviously there's lots of limitations to epidemiologic data but you know it's patterns that we're looking for right and when you see it time and time again you see it in people who eat exclusively plants or who eat some plants I think that it becomes it becomes very helpful and and it definitely can can inform us so so that's sort of a lot of the the big data that we have in terms of of heart health outcomes and then we can also break it down into sort of the risk factors right and that's where we get more of the the randomized control trials and the feeding trials and things like that and so we know that eating plant-based diets like for instance say the portfolio diet that's a specific plant-based diet that's very helpful and we do have randomized control data that shows that it can lower LDL cholesterol significantly and so we can look at at different plant-based diets in terms of how they can lower cholesterol blood pressure body weight inflammation and all these other risk factors and so taken together that's sort of how we understand how the impact that plant-based diets can have on our heart health yeah I find the the various mechanisms to be quite interesting and it obviously would be several hours here if we try to explore every single one of them but as a study that I read actually recently or just kind of screened the abstract when I was you know thinking about our discussion later today was the at least the the lens of looking at the gut microbiome and we had Dr. Will Bolsheviz come on and we had a two-part series with him talking about all the different aspects of how the short-term fatty acids and feeding or gut microbiota can really help augment cardiovascular disease and a bunch of these markers that we've touched on in the first episode so I think that's also something that's cool still relatively new I think mainstream I think that the gastroenterologists will tell you that they've been having these conversations for a long time darsha is fascinating with GI systems so he I'm sure that he's well familiar with this now the other thing I'm talking about the sad diet right most of us are practicing in America as we're recording this in March and and here you know on or at least when the patients come to you right and they'll say well you know what Dr. Harkin that all sounds dandy but for the July comes around and I need my hot dog and I like the hamburger and I like all that kind of stuff and just like plants can be challenging I mean meat it's delicious and they're not ready to give that up obviously you strike me as a person who doesn't get the patient to you know just completely switch and you're you're working with the patient as you mentioned several times how do you work with them with that right where we're not going to completely abandon meat because it's not and all be all but let's make it safer let's make it better yeah absolutely so exactly as you said I think it's it's all about really meeting the patient where they're at and figuring out where what's the low hanging fruit and where can we make important but but impactful changes that feel doable to the patient right and it has to be sustainable so if a patient comes to you and says I cherish my hamburger once a week and there's no way I'm giving that up then they're they're in that pre contemplative stage right they're not they're not making that change and so let's let's talk about other things or how can we mix it up maybe and and see if they're open to that so I think it's all about creating those those and I think we talked about the smart goals last time but really you know specific measurable achievable and and time these changes that are specific to the patient and what they want to do and so I think all number one is creating those goals together because as if they have sort of input into what changes they're making first they are more likely to adhere to those and then and then figuring out where to go from there so oftentimes I try to focus on what can we add into the diet first and foremost so if they're not eating purely any fruits and vegetables we go through okay how can we get some more in right so maybe it's the snack or maybe it's the lunch or what how can we tweak things so that we can get them in and what are the barriers currently is that you don't like them or you think you don't like them let's explore which ones you do like or maybe they just aren't used to cooking them and so maybe they want to subscribe to some any of these millions of of services now that you know you can get food healthy food delivered to you so so brainstorming ways where they can kind of figure out how how to make some of these easier changes can can be really helpful yeah the you know subtraction by addition method is something that I've come to be a fan of particularly you know big shout out to EC Sinkowski previous guest and she talks about the heart 800 gram challenge right when you're eating 800 grams of plants and vegetables and fruits and whatnot just because of the volume you don't have room left for a lot of the other quote-unquote crap and so I'm a fan of that now especially you know no conversation and nutrition is complete without talking about supplementation of course right I mean that's that's where people want to start with unfortunately and it's not that base of the pyramid and and I hear about this on a daily basis I think darshtas as well and I'm sure you do so in that realm again I want to highlight supplements are supplemental hence the name but understanding that are there some that have merit when it comes to cardiovascular health and from your perspective so at this point there's not that many supplements that really do have much benefit unfortunately and from a cardiovascular perspective most of the supplements that we have been enthusiastic about in the cardiovascular community have not typically panned out when they've been studied in randomized control trials and so you know antioxidants have been studied vitamin C vitamin E I mean you name it it hasn't particularly panned out so there are not that many supplements that I routinely recommend for my patients I do tend to discuss in exclusive plant eaters vitamin B12 is important to supplement and so I do have my patients supplement with that um the omegas are going to be a somewhat controversial topic as well and the entire bug gets on itself but the you know a meta analysis that Cochrane did and others have done you know really isn't showing a major benefit of omega-3 supplementation for the average individual for cardiovascular risk reduction obviously the the population that has shown benefit is high dose for grams of EPA and individuals with cardiovascular disease who have triglycerides above 115 milligrams and so that's sort of the one population which we have seen benefit in an RCT and so that's sort of the the one population I do think there is some debate within the plant based community whether or not individual source exclusive plant based may benefit from supplementation with omegas threes simply because they aren't consuming fish we just don't have a trial that supports that really um so that's an area a big gray area um so I think it's not wrong to do to supplement in that case as well um sometimes you know we'll look and because you don't because you can't get so you can in plants um quickly you can get um omegas threes but they're the short chain um and so um so algae oil actually is a way that you can supplement um and get the long chain and so um so many are doing that as well um but again I it's definitely a gray area there um vitamin D is another one that both omnivores and um in plant based individuals are often deficient in um and as I'm sure most of you listeners know that's a a sun exposure um when when we get through sun exposure and and most of us are wearing scents sunscreener inside so many of us are deficient so that is another one thousand iu a day that that I have most of my patients take um but in terms of taking something to actually lower cardiovascular risk we we really you know there isn't a lot out there um that is helpful I think that um fiber is one where um I do look at that closely with my patients particular for trying to lower um cholesterol if they're not able to hit sort of their soluble fiber targets we will add sometimes uh like a uh silly moose for something like that to help um get that uh lower um simply for LDL cholesterol lowering effects um and plant general steriles are another supplement that I will sometimes use with my patients again for for LDL lowering effects i love it dr. harga i think you have a crystal ball in front of you because you're you're answering everything we're we're like about to ask if we're like oh there it is there it is she's got it so awesome no that that was a perfect review i was i was gonna say um as far as omega-3 is yeah that's what I do I do an algae oil um because like you said i do the chia seeds i do the flax seeds but with that alay conversion you know and i actually tested my omega-3 like doing a quant test last year and i was actually on the lower end so i actually got to retest it's been a year now um but quickly do you ever test omega-3 or like omega-6s with your patient population or do you not really think that ratio matters too much when trying to make change great question and i think this is another area where there is some controversy um certainly i think the i think as with many things in nutrition it's much more complicated than anyone understands right now is the answer um and i don't think anyone truly knows i do uh check i think the omega-check is interesting um again i don't think that it is the end all be all um but i will take a peek at omega-3 levels as you said and and and that's one of the areas understanding that there's total gray area um where if it's a low i will potentially you know discuss that with omega-3 supplementation with my patients um and then the six to yeah the omega-6 to three ratio um was very popular for a while um you know we have too much omega-6 in our diet from all our processed and packaged foods it's pro and flammatory we need to eat more omega-3s you know i think it's it's a balance right just like anything we we do need both omega-6s and omega-3s and i think omega-6s has definitely gotten unfairly villainized over um over the last decade or so um again i i don't know that we know definitively the answer to that um but undoubtedly um it is important to lower our consumption of processed and packaged foods um as much as possible um i don't think anyone knows the exact perfect ratio the most people say around 10 to 1 um is less than 10 to 1 is ideal um i don't know that we know that exact answer okay i want to ask you real quick before we jump into like another pillar here um is another supplement that a lot of people like to take with the dinner time around the world which is red wine right which has been known with reserve resveratrol um touted as an anti-aging supplement and i know you recently wrote a blog post or an article on this uh so if you can just tell us what what's the scoop with red wine is it healthy is it not yeah so red wine um as much as i as much as everyone would love that it was super healthy um it's um it's definitely again a good an interesting area of of controversies so um there was a period of time um where a red wine um became very popular from a cardiovascular risk production standpoint um when something called the French paradox was recognized which was that the French seemed to have lower rates of cardiovascular disease than would be expected given their high intake of saturated fat from from butter and such um and so it was postulated that potentially their consumption of red wine um may be uh contributing to that um and one of the active compounds as you mentioned respiratory um was thought to be potentially responsible for that we've since studied it more um and realized that the amount of respiratory that we consume when we're having a glass of red wine is very unlikely to be an active enough amount um to really be having the effect and there was also certainly some some data gathering issues with the French paradox observation in terms of of an inaccurate representation of the amount of cardiovascular events that were occurring in the population so um so so what we do see from uh large epidemiologic data is that there does appear to be um sort of a j-shaped relationship with alcohol and in the sense that obviously those who consume large quantities of alcohol have a higher risk of mortality um but it seems that the lowest point of mortality vis-a-vis alcohol consumption is um is sort of at that moderate level um which is defined in the literature as one glass of alcohol uh a night for women and two for men um in terms of other um it's definitely um there's confounding variables there certainly um and so we have to be very cautious how we interpret that data um and so in general most of us don't recommend that people consume alcohol for its cardiovascular benefits um but that if they do consume alcohol they consume it in sort of that moderate a fashion as I described um definitely what we know is very clear from the data that binge drinking um which is you know having more than that um particularly kind of on the weekends how many of us consume it is detrimental to our health um and and can leave it definitely is associated with the worst endpoints with cardiovascular a-fib um am i's things like that um but also other things like liver disease and such awesome so we're taking a top-down approach here and we've addressed nutrition well we haven't completely addressed it but that's the best we're gonna do today and I'm gonna give you the choice I'd like to either go towards sleep in cardiovascular health or exercise which one would you like dealer's choice? dealer's choice all right let's go with uh let's go to sleep why not? awesome all right so sleep it we all love it we get none of it um everybody the three of us and and of course medical training you've got a couple of children I've got one and feels like a couple because of the first time heard um but uh you know we were talking about this offline and um and I think now the conversation on sleep and the loss of sleep has you know being an epidemic um is the volume on its higher and higher you know we've talked about this with a few different guests and um when you're looking at it particularly from cardiovascular disease um you know both of us read this book who I wasly by Matthew Walker very very good book but you know there were some stats in there that were talked about you know now reported to be controversial but the role of coronary R disease the role of heart attacks um I remember him talking about um daylight savings time and how when we spring forward the incidence of heart attacks increases like it's in the neighborhood of 25% and whether or not that's attributed to the hour of sleep loss I mean that's a for debate um but also when you're falling back the incidence of heart attacks on that Tuesday following the Sunday is down 21% and that really got me thinking about this okay well what is the effect and you know I'm curious to to get your take it from cardiology perspective and your studying of the literature is with the correlation of MI's and sleep loss or sleep deprivation where do you stand on that yeah so I you know I think the literature is fairly clear that insufficient sleep duration which is typically defined as less than seven hours um a night um and then also conversely um too much sleep long sleep duration which is usually defined as overnight hours um is associated with increased mortality specifically cardiovascular mortality um and you know we've again um similar to most of our lifestyle pillars um a lot of what we have is epidemiologic data like that and then biomarkers and so the different biomarkers that um we've looked at um you know we certainly we've seen associations with insufficient sleep duration or poor sleep um with with things like um inflammation higher levels of insulin you know all these different biomarkers I think the one that that's best studied and is most provocative is blood pressure so um so blood pressure has you know variation diner variations and it fluctuates over the day and then it's supposed to dip at night time so we when we're interpreting amuletory blood pressure this is actually I think one of the most useful reasons to do an amuletory blood pressure monitor is because you can actually look and see what someone's blood pressure does at night and it is supposed to dip and if they don't and it's veryably defined but it's usually if someone doesn't if their blood pressure does not go down meaning dip um at least 15 to 20 percent of our night then they're considered a non-dipper and that non-dipping status is associated with increased risk of cardiovascular disease even above and beyond just the diagnosis of daytime chronic hypertension um and so it's and and and that link between of course sleep sleep quality and insufficient sleep duration is most closely associated with this non-dipping status we also see it in individuals with obstructive sleep apnea and other sleep disorders and so I think hypertension is is certainly probably important in terms of it's it's how it increases our risk of cardiovascular disease when we're not sleeping enough or when we're not getting good enough sleep yeah so that indirect mechanism seems to make a lot of sense I'm curious what is your you know explanation if you have one about the prolonged sleep greater than nine hours or greater than 10 hours for increased mortality have you given some thought to that like I mean I think I think it's likely just a marker or something else so you have some sort of chronic disease state something that is isn't usually longer right and I think that again I'm again paraphrasing Dr. Walker when he talked about you know his explanation was that most of those folks maybe are dealing with some type of cancer or some type of chronic disease as you just mentioned and the the fact of the matter is the body or the sleep wasn't able to quote unquote save them and so I think yeah that's as you mentioned a couple of times now with these observational studies in epidemiological data it's very very challenging but sometimes the science isn't perfect and it's the best that we have you know an interesting paper that I read this morning and this was published in plus biology again the senior author is Matthew Walker. Peter T is on a two-dars for you I'll send it to you guys if you're interested and they looked at the one of the proposed mechanism of atlosplerosis was interesting because they took some of the mesa folks and they the objective markers they were looking at was seven days of actigraphy and they were really looking at sleep fragmentation or one night of PSG data and they documented the white blood cell count so particularly neutrophils and monocytes and they correlated that with CACS course what they found both you know well on both instances between actigraphy and PSG data that the neutrophil count after a night of sleep deprivation would increase one night for PSG but also actigraphy, oh my god, actigraphy over seven days I don't understand plaque formation as well as you do and you explain a little bit but is that something that is plausible to you in terms of how that could cause premature heart disease or CAD in particular so maybe just being reflective of overall inflammation perhaps not sure but that's that's definitely interesting yeah is there are there any other proposed mechanisms you talked about hypertension right with the confounding stuff like age sleep apnea that kind of stuff like that but in terms of looking at atlosplerosis what is your understanding of or our understanding of you know how that happens to my knowledge that isn't known I think that as with most of sort of these lifestyle mediated issues it's still not fully understood I think that we have definitely demonstrated that artificially quality and quantity is associated with many of these different biomarkers which then increases risk for cardiovascular disease I think also similarly to something like stress when you're super stressed or super tired you don't make great choices right so then there's the indirect issues that play as well where we don't exercise because we didn't sleep enough or we eat you know comfort foods or what have you so I think there's likely it's likely very multifactorial and there's both direct and indirect consequences apply yeah I'll disclose last night about making poor choices I think it was like 11 o'clock after multiple nights of sleep deprivation I had these peanut butter dark chocolate bars and I had just four of them at 11 o'clock without even thinking about it and this is a point of to be at again in this household the why we shouldn't even have these but let's just exercise my favorite one was that I'm fasting right now you're making me hungry you can't we can't have food talk Marches on 24 hour let's let's switch to exercise now this is definitely my favorite one it's the one that comes easiest to me to do and it's just you know a part of my core identity I think and when I look at it of course to make it simple for folks right we're talking either aerobic or clinical cardiovascular exercise right and most people look at it or a lot of strength training resistance training right and I think those are the big general buckets before I ask you about that I'm curious what does your exercise regimen look like? Hmm good question so I am I typically and so it's it's definitely morphed over the years and I will say that some of that is reflective of kind of having a better understanding of the need to have both quote unquote cardio and resistance training I think I definitely was really into to running and a lot of cardio and pretty much exclusively doing that right now my balance is a little bit better although not as consistent which is interesting so I typically for cardio a couple times a week I am on the peloton and then I actually recently got eternal and so I have been doing more strength training so I'm trying to do at least two two to three of those during the week as well so I have found that to be really helpful for me as someone for someone who earlier in my life did not do much weight training at all it's it's pretty plug and play and makes it pretty easy so why the weight training at least you know for the general public I think many people can understand obviously why we do the running aerobic training at the heart pumping but not many do the weightlifting what's the proposed mechanism behind that being beneficial for heart disease yeah so I think that is also a very good question and not 100 percent fully understood so you know briefly for for your listeners as I'm sure most of them know for cardiovascular disease prevention the ACCHA guidelines really do focus on the aerobic activity we're really trying to get 150 minutes of modern intensity exercise a week or 75 minutes of vigorous aerobic activity and as you said it's kind of easy to easy or to understand kind of the human and the image changes in all these things but like why that that is good for us interestingly the ACCHA doesn't specifically recommend within the guidelines to do strength training I think their language is that it is should be encouraged but unlike a lot of other I mean I think most of the other guidelines I think for diabetes and for sports medicine I think most of the other guidelines do specifically call out kind of resistance training and that's I think reflective of the fact that the level of evidence we have for for strength training in terms of cardiovascular prevention is not as strong that said I think it's it's definitely emerging and it's definitely very provocative and so so I've started to really emphasize that with my patients as well because I think most of them are getting that aerobic activity that they should be getting and not focusing enough on the strength training and so I think the areas in which the data is the strongest is we do have some epi data to show that individuals who do some strength training have a lower risk of heart disease but I think the data is the strongest with specific cardiovascular risk factors so so body composition being one of them so definitely in terms of reducing visceral fat I think the other one where we have a decent amount of data is for hypertension management actually so there's a couple a handful of randomized control trials that show that resistance training definitely can reduce blood pressure above and beyond just that what can be achieved with aerobic training alone and then also in terms of glucose regulation and insulin resistance we also see that that its resistant training is actually better than traditional aerobic activity and actually kind of combine with aerobic activity to get the most reductions and I so I think when it comes to kind of looking at these different these different cardiovascular risk factors those are pretty provocative and really interesting to me yeah I think the insight I'll add out to that in terms of resistance training what I remember learning back in undergative stress sciences well when you increase in the immediate post exercise phase when you're lifting heavy weights and if you're doing valve cell or something like that you're gonna increase blood pressure right and so when you increase that after load your heart has to work much harder right there's this concept of the athlete's heart and we often see right ventricle heart hypertrophy as a response remodeling wise but we also see sometimes left although most of the time that's pathologic where you don't want that is that correct left and the age so we do see both yeah so we see LVH and actually we also see increased systolic like volumes in in resistance training athletes that typically does resolve with de-conditioning although at this point we don't typically recommend de-conditioning so we don't necessarily consider it pathologic right really the main reason we would we would have people de-condition was just to make sure that it wasn't you know that it wasn't pathologic so that it was you know you know hypertrophy recording my apathy or something like that but the increased conductivity that would come with the you know ventricular thickness would that not explain it in terms of in terms of kind of the overall benefit to answer Darsha's question in terms of the mechanisms because if you have ventricular hypertrophy your your contractility would increase right correct typically I mean it depends so so yeah so we didn't but we didn't so so in terms of the athlete's heart we don't consider it necessarily like pathologic in that it's increasing your risk of developing heart disease okay and so from again now quote unquote cardiovascular says or the aerobic training right my understanding is again so you bring more preload right the heart's capacity of how much it can hold before it pumps all that blood out throughout the extremities which will down the road allow it to have a lower heart rate so it has to pump less frequently right and so you can have cardiac output can remain high is that kind of how the conversation you're having with folks when you're explaining why aerobic exercise is beneficial or are there something else like is there something else that that you're talking about oh sorry so going back to aerobic exercise yeah I'm going back to it yeah yeah so I mean we see all kinds of changes in terms of of the the things that occur within the body in response to aerobic training so there's all of these different sort of a human dynamic changes um and then there's also I mean we see you know increased HRV we see you know obviously decreased blood pressure we see you know increase insulin sensitivity I mean there's tons of different changes that occur within the body in response to aerobic training awesome go ahead Dr. Victoria is there a limit that you'll put your patients on in terms of running and how much aerobic exercise I mean I think there's data out there that suggests like a lot of marathon runners actually can develop a fifth later on just by the mechanisms that we're talking about right is there anything like that that yeah so I think we are increasing in realizing there is such thing as too much of a good thing um most of the benefit um so we do so as I said we recommend 150 minutes of modern intensity exercise a week we definitely see continued benefit up until around 300 minutes a week um and then from there definitely likely a plateau as you said there's definitely been some studies with you know really high level athletes having actually a higher levels of coronary calcium um in you know so they've done studies with high level athletes and they have higher rates of CAC and then a fifth as you mentioned there's been some of that as well so I think that there is probably such thing as too much of a good thing and I think that's another way in which I some of my patients who are doing lots and lots of aerobic activity it's a good way to sort of let's diversify your routine a little bit and add in the resistance training um not only because there is potentially that signal of harm at very very high levels but also because of all of these amazing benefits from um from strength training as well I like that yeah and just to mention kind of Peter TS model for exercise with longevity you know he talks about having a solid aerobic anaerobic stability and strength program and we kind of have all those four aligned is where you'll kind of be the most optimized if if I can say awesome so yeah and I'm also just sorry I would just also mention that I think we're talking about sort of the discrete moments of intentional activity that we're doing but I think also what gets missed a lot is sort of all the other movement that we should be doing throughout our day because um you know being sedentary um is really associated with with some of the highest levels on mortality and there's actually some data to show that um even if so if you sit at your desk all day long and you do your 30 or 45 minutes of exercise that may not even discount that sedentary activity and so I think it's also important that that yes we get our 30 to 45 minutes in of whatever our activities that we're choosing to do but then also carving out moments of um other moments in our day where we're not just sitting at the computer all day so if you can take a walking meeting or if you can take the stairs or like all these other ways that we can increase our need I think that's also you know important and bears mentioning because it's not as sexy as the other stuff but it's actually really important that's a very very very important point that you brought up that I don't know how old Josh and I missed were there but no thank you so much for bringing that up um then something I've been doing at least is after a meal trying to just even do like a two to five minute walk right just to get those steps in also kind of help the sugar regulation and everything so very good point all right I want to move on now to stress right something that we could all use a little bit of now um in in a good way but with COVID and with us being in the healthcare I mean stress is always at all time high I feel like for us what is the biggest marker at least in the cardiovascular world that you're seeing with stress is it blood pressure that usually you know you're seeing yeah yeah so definitely stress um you know I think that's another area of within lifestyle medicine that is poorly studied but we we certainly do have data um that indicates that you know chronic uh low grade stress is likely associated with increased risk of cardiovascular disease um previously the data was mostly um looking at kind of acute um periods of high stress like PTSD and stuff like that um but the chronic low grade is is probably not so good for us either um but in terms of pathways and things like that certainly the the blood pressure association is is where um it's best studied um and and interventions like meditation and other stress reduction techniques um while we don't have a lot of data um what we do have shows that we can reduce you know blood pressure with um with specifically transcendental meditations what's been studied best um but but we do have some evidence that it can be helpful so maybe the more important question what's your intervention when it comes to this I think that when we talk to most folks who are maybe in this space right I mean this is maybe the most challenging personally for me it's probably the most challenging we're all in medicine I mean stress is ubiquitous in our daily thing where parents now you talked about getting steps in running out after your children um that's a workout right I'm sure but um you know when your patients are coming to you and you're talking about this distress tolerance um what's your conversation like how are you approaching that yeah so um so I think so first I have them you know talk to me about first I have them rate their stress and I find that a really useful point in terms of figuring out where are they um I do have occasional patients that give me a one and I'm like okay what are your secrets teach me um but most people especially right now are pretty high um you give it you know an eight or nine and so um so that helps me frame the conversation because you only you know I do do our long intakes but again there's a you only have so much time and so I like to know um where how how much stress are they having and is this something that we really should address um and so so I first have them start there and then um if if they are having a lot of stress I talk to them about or I ask them rather um you know where is their stress mostly coming from um and sometimes we're able to do some problem solving in terms of of finding the root cause and working on trying to find ways to reduce that stress if it's one discreet thing um but more often than not it's again this chronic low grade stress from a million different sources um and so so I talked them about um about stress reduction strategies and so um some people um are open to meditation other people aren't um I think that it's it's actually um and quite helpful that there is so many different apps um I think there's like an app for every personality at this point um for medication um and so most people just need um to hear that they should give it a try um and that um and that there are options and you don't have to be good at it and then I feel like I'm quote-unquote not good at it um I don't think many people think they are um and that's not the point the point is sitting and doing it um and so um so yeah I have people try the different apps depending on their personality if they're not at all interested in meditation we discuss other ways for stress reduction it can be as simple as making sure they give their best friend a collar reunite or taking a bath giving themselves permission to take a bath and read a book or whatever so um so oftentimes it's not this like groundbreaking amazing stuff that no one's ever heard of but it's having that conversation and having your doctor tell you this is important and you need to carve this out and let's figure it away and it doesn't have to be long like I meditate 10 minutes before but um you know ideally I have longer but I don't right now and that's okay um and so so it's all about kind of having someone help you figure out a way to put that into your life and try to really make it a priority um and and and also just doing your best and not aiming for perfection I love that I think meditation brings a lot of perspective not only in the moment but also to the rest of those lifestyle pillars right when when you actually get the time to sit down and reflect you start to look at everything else in your daily routine and I think that's where you also get to see the change so not only from the stress perspective but also from okay the diet the exercise how do I kind of get better right by 1% every day I want to touch on another method at least that's kind of in booming now which is in the biohacking world which is the sauna um which I don't even think should be a biohack because I mean there's so many great benefits that we now know and when I listen to other cardiologists on podcasts I've routinely been hearing that this might be of a proposed treatment in the future where we'll actually write on a script saying go to the sauna for 20 minutes what is your take on sonnas based off like the papers you've read and if if people can even tolerate it right I mean I don't think it should be probably for everyone but you probably have to be at a baseline somewhat of a healthy level in order to get into a sauna yeah no I definitely have I can think of one patient who um was not in a a a place in his health where I recommended the sauna because I actually was concerned he was pretty unstable um yeah but but yeah so I think sauna is really interesting I think it um like a lot of things that we're starting to learn um is is is really interesting in terms of the impacts that it potentially could have um simply because of of how it can stress your body um in a good way and get our bodies used to that um and so um so I think it's really interesting I think we're we're definitely not at that place where we're for most of us are quite prescribing it yet um but I think uh the data is certainly interesting and emerging awesome well Dr. Harkin as we come to a close here um I want to of course thank you for two amazing discussions um but I'd be remiss if I didn't ask you about the future of preventative cardiology you know more specifically I think that the first uh discussion that first part of the discussion that we had we spent a lot of time talking about areas where we're trying to understand why um the current standard of you know the standard of care the way we practice it the why are we looking at specific markers like I'll deal a particle number APOB even though the European guidelines suggest that and you know somebody listens to this and and they're convinced that this might be um key or instrument or in their role how can patients have a conversation with their provider for the need of these advanced testing which may you know alter their care or they may be more informed so they can make other decisions so they can you know affect different pillars of lifestyle medicine or whether it's pharmacological treatment whatever that might be um this is a question I wanted to ask you last time but I didn't get a chance to so I'm gonna ask now is how can they have a conversation whether it's cardiologist primary care provider or whoever it might be yeah I think that's a good a really good question because um by and large most people will not um necessarily have a preventative cardiologist as a member of their care team um although hopefully that will change I do think that you know whether it's based on risk factors or just you hit a certain age I really would hope that everyone um would be able to access at least once a preventative cardiologist to really kind of get a lot of their personalized questions answered um but that said I think that um like the American Society of Preventive Cardiology emphasizes that it's not just cardiologist that can be practicing preventive cardiology rate it's and your chronologist it's interest it's it's sports medicine docs it's really anyone who has a an eye towards you know preventing cardiovascular disease which hopefully is all of us physicians and and and other members of the health care team given that it is the number one killer globally and so um so I think that um certainly one hopefully all of us will do a better job of having these types of conversations so that more healthcare professionals are exposed to these different topics um and while it can be difficult to keep up with you know every emerging piece of literature and none of us can um hopefully they're you know at least exposed to some of kind of these topics that are are um increasingly becoming important um but in terms of kind of a patient um specifically being able to access some of these things um you know I think it's it's um discussing with them I think it's really important that um you know it's say you're seeing your primary care physician for your annual physical and um you know he'd talk what do you think is my cardiovascular risk like have you plugs me into the ECCAHA 10-year risk calculator or you know whatever it is maybe not that at that specific exact language um or they could why not have you um after listening to this they will because I think that um you know your average PCP has like eight million things that they need to check and do and so be just kind of bringing that to their forefront of their mind and reminding them that this is something that's super important to them um is um a great way to kind of start the conversation um and maybe the doc will be like oh yeah your risk is pretty low for xyz reason and so maybe you don't need additional testing at that point but potentially they they will be like oh you know I I haven't checked it you know let's check and see what your risk or you know the next question to be hey do you think I would benefit from the coronary artery calcium score or you know whatever it is um and again not everyone needs these types of tests but at least it's you know if you're interested or you think you might benefit having those conversations and if you feel like your provider sort of goals are not in aligned with yours then then finding someone who has you know who is um more in line with with what you're looking for um not everyone's going to be the right fit for everyone it's not a personal thing and that's totally fine um but I think that um you know starting to have those conversations in a really you know just non-judgmental nonaccusatory way but hey I was thinking about this or hey I read this what do you think um and starting that conversation so on the flip side um hey I just checked asbc I actually didn't even know was a thing I'm definitely going to look into becoming a member that's awesome you show it in Louisville Kentucky it looks like in July so that's awesome um you know if I healthcare practitioners or somebody who has an interest right I mean you mentioned last time that cardiology is very very cool I obviously think so as well and and I think you've made a pretty good case that it is cool these last two discussions if if not it is very very important considering the burden of cardiovascular disease and if providers want to learn more about this type of stuff right some of the advanced testing preventative cardiology and specific um what resources could they use or to learn more about this stuff yeah absolutely so I think that um so the ecc has cardio smart which is a lot of patient but also provider resources they have some podcast series at this point lots of handouts that you can use for your patients um they the American Society of Proteology think it's another great organization that has a lot of great content um that um that it's being put out in terms of of guidelines and things like that definitely familiarizing yourself with the ecca guidelines there's the the primary prevention guidelines and then digging deeper right so read if if you're interested you know reading the guidelines and then and then looking at the resources um looking at their sources going into the primary literature if you have time um it's it's really you know illuminating and that's where you can start to kind of better understand where these these these guidelines are coming from you you might have forgotten the most important one I think wholeheart cardiology.com absolutely so my blog my website's wholeheart cardiology um and yeah I have a blog and a newsletter and all that kind of stuff so um it's mostly gear mostly geared towards patients but I actually have a handful of my uh primary care docs that were routinely referred to me that have subscribed and say they they actually really enjoy it. Awesome well Dr. Harkin it's also International Women's Day so happy International Women's Day to you um you know in cardiology women are definitely underrepresented represented and uh you're just proof of that as as to as to why we need more and then the value that you create so thank you very much for coming on here final question for you is uh how do we add the health back and health care? Great question um I think by all of us advocating together um for what we need I think that um both physicians and patients are like are frustrated with where we're at and so I think that the more um of us on both sides of the equation that speak out um the better because they think that um you know patients just come to me time and time again you know uh why is no one talking to me about this for I can't believe I'm hearing this for the first time um and I truly you know it is just um it's frustrating that no one's getting the care that they want we spend so much money as a nation on our health care and yet we are sicker than ever um and so we all deserve better love it yep kind of kind of kind of said it better so thank you so much again thanks so much for having me