518: Cardiology Meets Longevity

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I can't tell you how much it means to me. Is this is this from the twenty twenty six calendar or we still scrape the bottom of the barrel from twenty twenty five? You know it, Paul. Twenty twenty six. Nice. Happy New Year. Actually today. It's today's uh you know, the day we're recording this.

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Welcome back to the Curbsiders. I'm Dr. Matthew Frank Wato here with my great friend and America's primary care physician, Dr. Paul Nelson Williams. Hi, Paul. Hey Matthew. Paul, today we talked to Dr. Greg Katz, a cardiologist, about Cardiology, the meaning of life, the meaning of lipid panels and calcium scores, all sorts of fun stuff. But Paul, before we tell people more about our guests, And introduce our co host.

What is it that we do on Curbsiders and why are we still doing this, Paul? Ten years in? We're doing it because the people need us, Matt. Um and what are we doing? I'll tell you. We are the internal medicine podcast, we use expert interviews to bring in clinical pearls and practice changing knowledge. As you mentioned, we are joined by a third co host, frequent producer, uh Wunderkind, I believe I've called him before and I stand by it. Uh, the great Dr. Paul Wirtz. Doctor Wirtz, how are you?

I'm doing fantastic. I'm just happy to talk about one of my favorite topics tonight. So it'll be a it'll be a great show. Before we get into that, why don't you tell us a little bit more about who we talked to and maybe even sort of the broad strokes about what we talked about? Yeah, today we're joined by Dr. Greg Katz.

Greg is a cardiologist and assistant professor of medicine at the NYU Grossman School of Medicine, where he serves as an associate program director for the Internal Medicine Residency Program. He is board certified in both cardiovascular disease and internal medicine, and he trained entirely at NYU, including his fellowship in cardiology. Greg's clinical work focuses on cardiovascular disease prevention.

managing complex lipid disorders and long-term risk reduction for patients. He's active in the American College of Cardiology at both the state and national level. And he co-hosts the Core IM podcast, specifically their beyond journal club series. in coordination with the NEJM group.

Greg also writes a widely read newsletter on cardiovascular topics. You can find him on Substack at Greg Katz Md, highly recommend, where you'll encounter articles that cut through the noise on cardiovascular risk, exercise, nutrition, and other clinical controversies. Be sure to check it out. So without further ado, let's get to it. A reminder that this and most episodes will be available for CME credit for all health professionals through VCU Health at curbsiders.vcuhealth.org.

Greg, we've been talking for a while. Thank you so much for coming on the show. We have a lot to get to, a very ambitious script as we talked about, but first the audience wants to know what's a hobby or interest that you have outside of medicine?

So I have little kids and that occupies almost all of my existential energy. But the hobby for myself is I love lifting weights and I love the feeling of being in the gym and really like pushing myself to a very uncomfortable place and then The way I feel positive about the world in ways that I didn't feel uh before the workout is uh it's the the best therapy that I've ever felt. Okay.

And what sort of weightlifting? Is this like a group class? Is it like CrossFit? Are you doing are you just lifting by yourself? I've done all of the above, but right now I lift by myself. Um, and I do a full body workout twice a week. My favorite current exercise is the pendulum squat, which if you've never done it, it's worth Googling to see an image of it because it's basically like all of the pain of a squat.

but it doesn't have axial load and so your spine is very happy with you. And you know, like we get older, our joints don't feel as good as they did when we were younger. And so um I could not recommend that exercise highly enough.

Oh I I actually don't know that one. Is it a single leg movement? Or is it double it you can do it single leg, but it's a double leg movement. It's a specialized piece of equipment. The weight is kind of like behind you and it's sort of it's it's a pendulum and so It's your back is against uh a map and it you just need it when once you Google it, it makes total sense what it is.

But until you've seen a picture, it's like uh the picture is a thousand it tells a thousand miles. I actually think I've seen that on like the Jeff Nippard YouTube channel probably. I think that's like one of the one of the pieces of it's a piece of equipment that not every fitness center has. I think that's why Is that is I I think so anyway. Hundred percent. Literally the gym I joined, I joined because they had a pendulum squad. Okay. All right. This makes sense now.

All right, Paul Williams, now that you're let's bring you back into the conversation here. I know this is not your your favorite topic. No, I dissociated for a second there. No, I I every so often I guess I I I don't I I hate um weights and resistance training and all, but I just find it deeply more and I'm not saying you so you're talking about it is fascinating that that is not what I'm implying. I said the me doing the activity itself. I just I cannot

Um, find any joy in it. So it's so nice when I see people to do. I feel like I would look very strange also if I was muscular. So that's another consideration. I think I'm just better, better off scrawny. But um Let me ask this, could you tell us about uh could you share with us some advice or feedback that you've received uh during during your training or that you like to give to trainees that you find especially uh useful or helpful for folks?

So I'll tell you a piece of advice that I heard myself that impacted basically every interaction that I have in the hospital and that I tell to almost every resident or fellow that I work with, which is your job is to not just Know the medicine and take care of patients. It's to elevate the experience for everybody around you. And

That means that you want to bring a positive attitude that makes your team more joyful about medicine. It means you wanna help cheer the patient up. It means you wanna make the experience more academic and look something up that's going to elevate the way that we all think about the case. And it also means that you are kind to all of the people behind you in the pecking order who can't make your job better and d can't open doors for you. So the PCTs, the medical assistants, the

staff that cleans the the hospital, like the way that you treat them and how you make their experience is reflective of how your reputation is gonna look to everybody else. And So your job as a doctor is not just to know the medicine and not just to take care of patients, it's to elevate the experience for those around you. Really fantastic uh advice. Uh listen.

I think uh everybody that's starting in the hospital could definitely um and and actually anybody at any level could I maybe I needed to hear that, Paul Williams. That's a good No, I mean it's I I love it because there are all these sort of agonizing think pieces in in the primary care space. Like how can we attract more trainees to primary care? And I truly think the trick is to actually

have them catch you enjoying it and sort of being joyful in it. I think like that is the that is the thing more than anything else. And I think people who work with me might find that a hilarious thing as someone who tends to spend a fair amount of time stomping around and being unhappy.

But I I do think when you're actually caught having fun and being excited about medicine and sort of and as you say, elevating the experience, I think like that's the ticket to get um to get people interested in the thing that you do. So I just I like that advice very much. And I think we're about to get a lot of people interested in what Greg does because we're gonna give him a case from CashLack and we're gonna talk about some very interesting topics here. So Wertz, do you wanna do the honors?

Absolutely. So we have Arthur. Uh he's our patient. He goes by art e-sclerosis. He is our forty six year old man presenting for a routine visit. He wants to talk about heart attack prevention and longevity. His motivation for this is that his father needed a bypass surgery at age 68. Art remembers how much of an ordeal that whole process was for his family. He himself has no known ASCVD and he has never smoked.

His blood pressure in clinic is one hundred thirty two over eighty four without any medications. His BMI is twenty nine with an elevated waist circumference. He exercises by walking around the block a couple times a week when life allows. He sleeps about six hours per night and uses his CPAP routinely for diagnosed OSA, and he eats a standard American diet.

Annual labs show an LDLC of one hundred twenty three, an HDLC of forty one, triglycerides of one hundred ninety, a non HDLC of one hundred fifty nine, and an A one C of five point seven. The rest of his labs are unremarkable. So, you know, a lot of our guidelines are built around secondary prevention, but this patient is a very common primary care scenario. You know, you have someone with clear risk factors, they're motivated, but they themselves have never had an MI or a stroke.

So when a patient like this shows up to your clinic, what jumps out to you? How do you think about primary versus primordial prevention in real life? And how do you actually help patients understand and act on that risk before something bad happens?

So a patient like this, forty-six years old, very clear evidence of metabolic syndrome, central obesity, sleep apnea, dyslipidemia, uh elevated A1C.

He may be a primary prevention case, but he is a secondary prevention case waiting to happen. And the only difference between him being primary prevention and him being secondary prevention is the time when he's coming to medical attention. And so I look at a patient like this uh and I I I I tell folks like this all the time, you are coming to medical attention at the perfect time because we see a whole bunch of red flags in your history, a whole bunch of red flags.

in your family history and a whole bunch of red flags in all of your objective data. And if we do a good job of taking action, some of that action is going to be things that we give to you in terms of medications. Some of those are going to be things that you do at home for lifestyle adjustments. Some of those things are gonna be ways that we better understand your risk, but

We can help you prevent a heart attack if we understand where you're at right now and we pull the right levers to help sort of optimize the the risk factors that are in our control. I always tell patients. There's some things that are in our control and some things that aren't in our control. Like we can't change who your parents are, but there's a whole bunch of stuff for this patient that we have real opportunity to make his life better.

Yeah, I think Paul Williams, do you think people become desensitized to some labs like this where it's just so common to see this this sort of presentation? Yeah. No, it's it's uh to to Greg's point, like this is someone who's on the cusp of stuff, but is because they've not crossed that threshold, it's kind of easy to not look at it in aggregate and think, uh oh, this this is a potential problem. So I think that's yeah, individually

None of these things are terribly alarming. It's when you sort of add them up that it becomes a little bit more um something to wrap your hands around. Yeah, and I think uh you don't want to be

I I think some patients might be turned off if you if you uh you gotta kinda gauge where they're at with things. I think recently in my practice because of the type of practice I have, people are coming to me wanting to know if they are metabolically healthy'cause I think they're getting this type of like information that like, hey, we need to check to see if

you have metabolic dysfunction. But a lot of uh a a lot of for most of my career it's been people coming to me and like, Oh, my numbers aren't that bad, right? So I I don't need to do anything about it yet, right? And that was kind of That was kind of where things are. But I think now it feels to me at least that like things are swinging and people are more interested in like how can I avoid bad things happening and what should I do about this?

So th there's different perspectives that people have about how to approach stuff like this. And one of the questions that I ask people when they come in like this is how medicalized do you want to be? And like what that means is There's a whole bunch of treatments that we can give you, prescriptions that you can leave the the visit with. There's testing that we can do to better kind of triangulate your individual risk. There's a lot that we have the ability to do.

But understanding like how far down the road of being a person who is part of the medical system is a really important piece of inf like some people want every data point and some people just want to know, Doctor, am I gonna be okay?

And just like some people are willing to take any prescription that you give them or any supplement that you could possibly think of, you know, like the better living through chemistry kind of folks. Yeah. And then other people will not touch a prescription, but they'll only touch a supplement. Some people will not touch a supplement, but they'll only touch a prescription. Some people don't want anything. And so

to understand what are we going to do for a patient like this, we need to under s like you need to take his temperature. You need to understand where he is mentally coming from. And you need to meet that person where they are because otherwise it's just going to be a frustrating interaction for both parties. Yeah, I do what just since we're spending some time on the fluffy stuff and this is my bread and butter, I do

I'm looking at this patient, this is someone who is adherent with their CPAP. They're walking, they are actually coming to their doctor's visit they've had labs done. Like this is someone who who is doing something, so I think it's

The other uh to your point, Matt, I do feel like we sometimes pathologize risk in a way that seems almost sort of accusatory or or like as it we're trying to use it as a scare tactic rather than sort of celebrating the victories and and recognize them as ways that we can still improve and actually prevent suffering. Um

So anyway, sorry, I'm not sure if that point was helpful at all. The the soft stuff, like that's all that patients care about. Patients care that you care about them. And in order to practice the art of medicine, you need to understand the science of medicine, but medicine is an art. And if you don't pay attention to who the humans are, Like a chat GPT will be a hundred percent a better doctor than you. And so I I I just think that it's really, really important to um to not just focus on

like his BMI and the fact that he has uh sleep apnea. But I I will tell you just going to the medicine. I look at this scenario. He's 46 years old and he already has sleep apnea. He already has prediabetes. He has a triglyceride to HDL ratio. That's almost four to one. Uh or it's a little bit over four to one. He's somebody who is not just metabolically unhealthy, he's somebody who already has consequences of that. And um he's somebody who

if you're asking me sort of like how do I approach this from do we do lifestyle? Do we do Uh, do we do medications? Do we do additional testing? I'm an all of the above person. Like all these things are tools and tools are only as good as how you use them. And so for somebody like this, you can like this guy can leave the appointment with four prescriptions and with a blood pressure monitor and with uh statin and with a GLP one and with the the plan to get a calcium score or coronary CTA but

It's I think that the order of operations can end up being really challenging for somebody like this. And so understanding who the human is just matters a ton. This episode is brought to you by Delete Me. Delete Me makes it easy, quick, and safe to remove your personal data online at a time when surveillance and data breaches are common enough to make everyone vulnerable.

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So let's let's talk about you mentioned triglyceride to HDL ratio and we gave you some lipid numbers here. When when I was trained to that was not even something that was on my radar. In fact in pr pro probably before the past year or two that's not something that I had thought about. Triglyceride to H D L ratio.

And so tell us how you look at a lipid the like the standard lipid panel and then we can go into the you know, the APO B, L P little A and some of the other ones that people may be less familiar with. So I actually I I hear that from doctors a lot, that they don't think about the triglyceride to HDL ratio, but I think that you do because you learned about metabolic syndrome and you know about the criteria for that. And you know, you you like

Triglycerides and HDL are part of what goes into a the definition of metabolic syndrome. So I think that all doctors kind of like intuitively know about it. And, you know, it's having a mo metabolic health is having a moment in the longevity space, but It's been part of like classic medical teaching for decades. And, you know, because doctors kind of suck at translating things into normal human language.

It I don't think that the fact that this metabolic syndrome is part of the medical literature and is like Syndrome X was like Gerald Raven in the nineteen eighties. Like we've known about this for how many years at this point? And so it's uh

It's it's a failure of the way that doctors market and we focus on rent seeking that this is not sort of more widely known, that this is something that we should appreciate. But the way I look at a lipid panel is there's two major pathophysiological pieces of information that you're getting from it.

One is related to the LDL or the non HDL, which is your atherogenic particles. It is cholesterol floating through the bloodstream in the form of lipoproteins because cholesterol is not water soluble and blood is mainly water. Um and it's floating through the bloodstream. It can get stuck in the subendothelial space.

That causes inflammation and that's what leads to the process of atherosclerosis. And so the LDL or the non-HDL is telling us about that specific direction, that specific pathogenic process. And then the triglyceride to HDL ratio is helpful for understanding metabolic syndrome, metabolic health, insulin resistance. And so I always describe to patients that metabolic health.

is the spectrum of sort of how your body is processing energy that goes all the way from your health is perfect to you have full blown diabetes. And it's not You're healthy and then all of a sudden you have out of control blood sugar. It's a spectrum and it's a very, very continuous variable. It's not a categorical variable, even though in medicine we like to sort of like lump things in together of you have good metabolic health or you don't have good metabolic health. But

Understanding it as a spectrum, I think is really, really important. So I look at the lipid panel as telling me two different physiologic stories about why somebody might be at risk for cardiovascular disease. Yeah. Uh I I think that's a really good uh a v very smart reframing of the you know, the metabolic syndrome risk factors, which I think what's nice about metabolic syndrome and and thinking about it is just it's it's data points that we have on almost all our patients, right? And I guess

Maybe we don't measure a waist circumference on all patients. That's something that I've started to incorporate in my practice recently, though doing a waist to hip ratio. W waist to height ratio is actually a little bit better than waist. Oh, okay. I didn't know that. Yeah. Yeah. So so that is something that uh

That th but we're getting that on most patients and we know it's associated you this with a lot of the stuff you mentioned, diabetes, sleep apnea, fatty liver is one of the ones, osteoarthritis, C K D. So the list goes on and on with what metabolic syndrome is associated with. So Uh Wertz. Do we have more labs on this guy? Um, yes, so you decide to send an APO B and an LP little A, so we can talk about maybe why we sent those labs and kind of their role in this this slipid discussion.

But we get back an APO B of one hundred and twenty seven milligrams per deciliter and an LP little A of eighty nanomoles per liter. So going off of these numbers, how do we make sense of this? How do we place this into the broader discussion of what we already have?

So yeah, so the decision about what to order, like we should understand what we're looking for when when we order it. And so I look at APOB as helping me understand whether the LDL tells me the story about atherogenic particles. And so You know, the main particle that can get the main cholesterol containing particle that can get stuck in the walls of the endothelium is uh L is L DL. LDL accounts for ninety percent of those atherogenic particles for most people.

But the LDL cholesterol number that you get on a lipid panel doesn't tell you much about the number of particles that are circulating through the bloodstream. And so I think about cholesterol and I think about cardiovascular disease and that relationship as it's almost like a traffic problem. And so if I wanna know what the traffic is like on the street. What LDL is telling me, LDL is telling me the number of people who are traveling up the road.

But what APO B tells me is it tells me the number of vehicles that are going up the road. And so even though directionally knowing the number of people can be informative for understanding what the traffic is like, if I really want to know what the traffic is like, I need to check APO B.

And the reason for that is it m most commonly comes into play in patients like this one who have elevated triglycerides because the triglycerides crowd out the cholesterol on the lipid particles and you need more particles to ferry the same amount of cholesterol around your body.

And, you know, there have been a ton of different discordance analyses. Discordance analyses are basically when you look at two variables that usually travel together but in some cases are a little bit different. And so LDL C compared to APOB. When those two things are discordant, meaning the LDL is either higher or lower than you would expect based on the APO B, APO B better predicts risk. And this has been shown in population after population, in study after study.

It's pretty well replicated to the point that All of the major professional guidelines talk about the appropriate clinical use of APOB and how it can be helpful for better triangulating atherogenic risk for a subset of patients and the folks who have tend to have discordance. are people like this patient with high triglycerides, big waist circumference, insulin resistance. And when I look at a it's really, really tough sometimes to go from like we were all trained thinking LDL.

LDL under seventy for secondary prevention, now maybe under fifty five for secondary prevention. And then I introduced this brand new test that you have to remember to order because it doesn't come with the standard lipid panel. And then We're not fluent in APOB until we've practiced with it for a while. And so a good rule of thumb is that the APOB should be about 15 to 20% lower than the LDL. And red flags to me are when the APOB is actually higher than the LDL. And when that's the case.

APO B is definitely the better metric to track because in study after study. it really clear that APO B better predicts risk of heart disease, risk of MI than LDL does when they're discordant. And so I'll measure them in everybody. And if the APO B is exactly what I expect it to be. somewhere in the fifteen or so percent less than the LDL, then we don't necessarily need to follow APOB. But in this patient, his APO B is 127 milligrams per deciliter and his LDL is 123 milligrams per deciliter.

To me, if you look at his LDL, you're gonna be falsely reassured about his overall cardiovascular risk. Yeah. Wow. Paul Williams, any comments, questions, concerns? I know I know a you've been somewhat of a skeptic about ordering Apo B or just not sure if you needed to order it and it sounds like you don't for every patient, but uh Just just curious. Yeah, I guess my my uh

Functionally, how often does that change actual management? I guess would be sort of my my follow up question. Like I I think if we again looking at this patient who we've we've decided has pretty high cardiometabolic risk, you know, we'll be having a conversation about the stat and if they're open to that, like I guess how?

What how much more does it add, especially if you have like a significant LDL lowering and like how does how does that change management if the APOB doesn't drop as much? Like I guess I'm just not quite sure. Um the impact on management specifically. So if if you plot out kind of like uh the uh on the X axis the L D L and on the Y axis the Apo B, what you see is that across the population it really tracks pretty well.

But there's a fair number of people where there's discordance high or discordance low. And um it ends up being about a third of the population where there's a significant uh discrepancy between what you would think the Apo B would be and You know, in practice it probably has more of a role for secondary prevention than for primary prevention, but APO B is inexpensive. It's readily available.

And like if you want if you're gonna use a biomarker, shouldn't you use the best biomarker? And so for me, if I'm like I don't treat populations, I treat individual human beings. And when I'm deciding about Should we increase the statin dose? Should we add a zetomide? Should we think about a PCS K9 inhibitor? I want to understand with the to the best of my ability, like what if we're if we're gonna track a biomarker, like why not track the best biomarker? Like I fully get.

It's a little bit onerous. It's not part of the standard lipid panel. It doesn't change practice for everybody. And so, um, and there's certain patients where it's totally unnecessary and lots of people will have a drop. that goes down, like their LDL goes down and their APOB goes down by a similar order of magnitude. But I look at it very simply of like, if it's not an expensive test and it's easily accessible and I can get it with a standard bludge, like why not check the best biomarker?

Greg, the most labs that I've ordered from have APO B cut off like less than eighty or less than ninety set off as like sort of the Not ideal, but the normal a normal value or a lower risk. Do you do you have like a target that you if you are treating somebody for secondary prevention, do you have like a target, is it less than sixty or

Down in the thirties or so this I think that this kind of gets to a little bit of where my clinical practice is a slightly different than the guidelines. And so You know, the guidelines and like to a certain extent the way that I take care of patients, I use the Alara perspective when it comes to lipids, like as low as reasonably achievable, just like radiation.

Sure. And so but I think that w the way I try to frame a patient for whose secondary prevention, prior heart attack, prior stroke, is I try to think about what's driving their risk. Was it that they had poorly controlled blood pressure for years and years and years and it's actually hypertension and I need to control that? Was it that they've been they they had an elevated LDL or an elevated APO B for a really long time and that's actually where the problem is?

Do they have a chronic inflammatory disease like lupus? Is that where the problem or is it just their family history? And you know, if somebody starts add an LDL of 170 milligrams per deciliter and an Apo B of 150. And I get them, I get that APOB down to 60. I'm pretty happy with that.

But if it's somebody who is really young or who's had recurrent events, then, you know, a lot of the data from the some of the R C Ts would suggest that your benefit and risk reduction goes down even as you get down to like forty with the Apo B. And so But in real life, what are your limitations? Well, your limitations are how many medications does somebody want to take?

How sort of consistent can somebody be with the lifestyle modifications, more fiber in the diet, maintaining a healthy weight, staying physically active, et cetera. Um and what gets covered by insurance and do people want to do injections? And so In in actual clinical practice, the number of people who get too low is a tiny fraction of the number of people who I'm just struggling to get them to a level that I consider even reasonably acceptable for secondary prevention. Yeah, okay.

I I I think that's great. Um, so that's that's another thing people people can target. And I I've been I've been ordering Apo B for the past year or two and I find You know, it just becomes like it's just like looking at the the lipid panel. It's just it's another number to look at.

another data point that you can get, especially for people that are more on the we had someone you you described it a little differently. We had a past guest d describe s p some patients are maximalists, some patients are minimalists when it comes to to testing. So Uh I've had a lot more people come in a as specifically asking for an Apo B to be checked. But uh I think it i it can be helpful in in in some cases.

Just to just to to tie bow on those, but do we have like are there are there treatment targets specifically in the guidelines yet or is that something that we expect to actually be happening at some point? At some point I'm sure it will be. The you the all the guidelines as as far as I'm familiar with all s have L D L targets. They don't have Apo B targets, but you can reasonably extra I I don't think it's an exane instrapal extrapolation to say that

You know, if your L D L target is fifty five, your Ape O B target should be about forty five to forty eight or something along those lines. Like that that's a pretty reasonable extrapolation to me. But importantly There's never been really any good data that suggests that there's too low of a level. And there's plenty of data that suggests we under treat a fair number of secondary prevention measures.

Yeah, I just remember when the the paradigm shift to the the lipid guideline was it was twenty fifteen where they came out where they just recommended sort of the binary of statin or not statin. And the patients would be like, What should my target be? And you're like, That wasn't one. Like it's twenty thirteen, yeah. It just should be better. So like I just that's that that's the conversation I would sort of hope to avoid by sort of just um

Yeah. So that I I think the lipid guidelines really do a disservice to practicing clinicians and they're overly convoluted. They give these arbitrary thresholds. And very, very importantly, I think the guidelines under treat young people who are at high risk.

And they over treat old people who are at lower risk and Um and so, you know, I I very, very much believe that you need to individualize this stuff and that this It's like turning doctors into algorithms is something that I think is a real disservice to the patient doctor relationship and just like the way that you take care of patients and so Um, you know, the people who work on the guidelines are really smart. They review a ton of data. I don't mean to

Like I I'm not trying to insult them. I have a legitimate disagreement. And I think that reasonable people can look at the same information and can disagree with how the guidelines end up coming out. And so to me, the guidelines are more confusing their than than they are illuminating for a lot of patients.

So Paul Wirts, I I w why don't we talk a little bit I think you had a question about the prevent calculator and that kinda leads into a little bit what we're getting at here with the with this, you know, h how how good are the risk calculators for some especially if it's a young person with like a high cholester high cholesterol. So we're

Yeah. So let's let's say that this patient, like, they want to lower their risk to the maximal extent possible. And you as the primary care provider, what you know how to do is to use this prevent calculator. Uh it used to be the pool cold equation. Uh that used to be the the thing to use and now this is the the thing to use in place of that. So when you plug those numbers in, you let's say you get a ten year risk of about two to three percent.

and a thirty year risk of seventeen percent. What do those numbers actual actually mean and wh why is there a separate calculator for C V D and AS C V D? Like how should clinicians make sense of prevent compared to the the prior risk tools that we used to use? And then how do these estimates influence decisions like let's say you don't know where to go next?

Like how might they influence decisions on getting a CAC score or trying lifestyle or starting the patient on a medication? Um, so at the end of the day, how do you put all that together and decide what to do next?

The the glib answer is I don't use those calculators because I think they misinform as much as they do inform. Um but like the the sort of more thoughtful, really considered answer is that You know, risk estimates are and every kind of risk calculator is based on a retrospective analysis that's usually prospectively validated to estimate risk across a population.

And it's really, really good across a population, but it's not so good for individuals. And I think the people who are really missed in the guidelines are people who have really strong family histories, young people with metabolic syndrome who are at increased risk. Um and because age is such a big factor in what somebody's 10-year risk is or what somebody's 30-year risk is, young people are really who who young people with significant risk are really undertreated by the guidelines.

Again, because age is so important, old people are often over-medicalized who don't necessarily need to be medicalized. And so I think that this is great for a population. And if you take a hundred people who have this exact risk profile, then over the next 10 years. Two to three of them are gonna have a heart attack or a stroke. But that to me, it's I and I also think when we give people granular numbers in risk.

it sometimes misleads us to think that like all risk is created equal. And I uh what I mean by that is

If there there's some the I don't know if you're up you're all familiar with the concept of asymmetric risk, but it's a lot of how I think about cardiovascular disease. It's a lot about how I think about anticoagulation and aphib, which is that If I overtreat you and I put you on medications that you don't tolerate, you know what happens is like if you you go on a statin and you have muscle aches, then I stop the statin and your muscle aches go away.

If I put you on a zetomybe and you have a GI consequence or I put you on a PCS K nine inhibitor and you have an injection site reaction, you know what? Like we stop the medicine and the side effects go away. But Cardiovascular disease is the number one killer. And if I under-treat you because I'm worried about side effects or because

I don't I I think that this two to three percent number is not a high enough number for you to merit treatment for very clearly uncontrolled cardiovascular disease risk factors. And you have a heart attack, like that could ruin your life forever. You know, you have a plaque rupture in the wrong location and you're a little bit farther away from getting medical attention or you don't know exactly what it is, and then you have an ischemic cardiomyopathy and your life is forever different. Or

You have a piece of plaque and a carotid artery break off and go to your brain. You have a stroke and your life is forever changed. And so I don't think that the numbers that we get from a risk calculator capture the fact that risk is asymmetric because Drugs are often going to have side effects like somewhere in the five to ten percent of people who you put on medications will have a side effect of some kind. But

The side effects go away. And I I I think that we we do patients a disservice when we use this risk calculator. It's like it's not written on a stone tablet. It's based on a large data analysis and it's w it works across a population. And so for especially for a 46 year old individual who has a ton of sort of like non-optimized risk factors. I think the risk calculator is going to be more it's it's gonna be more problematic for him than it's gonna be helpful in my eyes.

Right. So w we did it for this guy. It the ten year risk would come out to be two to three percent and the thirty year risk would come out to be around seventeen percent. So um, you know, the that that ten year risk is what a lot of the treatment decisions are based on. So he wouldn't necessarily be treated.

Um, I I do wanna I do wanna swing back uh to his LP little A. We actually forgot to talk about that and then this guy Let's say he heard from a friend that he should get a calcium score and you know, how would you talk to him about those the data points we have already? He had the high APOB.

And he had a L P little A of eighty and he wants to know if he needs a calcium score. Can I say one more thing about the risk calculators before I go into that? So The other thing that to me does not make sense about the risk calculators is that they're used to decide should you lower lipids.

But like no b if you if his blood pressure was one sixty over ninety, there'd be no debate. Oh, his tenure risk is two to three percent. So who cares if we lower his blood pressure? And so There's something very odd to me about treating a very clear causative risk factor like dyslipidemia. a completely different way than we treat a very clear causative risk factor like hypertension. And so You know, you want to talk about his um his LP little A. So L P little A is a fascinating test and

It's something where like you're starting to hear more and more about it. A handful of years ago, one of the personal trainers on the biggest loser, Bob Harper, had w while he was working out, he had a cardiac arrest in the gym. Like by all sort of external uh metrics. He's the picture of health, but it turns out strong family history of cardiovascular and he had a LP little A that was through the roof. And so even for somebody who does quote unquote everything right.

L P little light can still be a real problem. And so Lipoprotein A and the nomenclature is tough because it's lipoprotein lowercase A, not to be confused with apolipoprotein capital A hyphen one, which is the apolipoprotein on HDL. and it's pronounced L P little A, literally little A. And so

It's a the nomenclature, like they needed a marketing person. Yeah, it's a mess. But LP little A is basically an LDL particle that is covalently bound to apolipoprotein lowercase A. And it's problematic for three reasons. One is that it's proathroogenic.

The second that it is prooxidative, pro-inflammatory. And the third is that that apolipoprotein lowercase A has these little things on it called Kringle repeats, which are structurally homologous to plasmin. And so it's prothrombotic as a result. And so some people hypothesize that having high LP little A levels actually was protective teleologically because it protected us from bleeding out.

And so the thrombo the pro thrombotic nature in the modern world, like so many other things, ended up being disadvantageous and Um it's not selected out for because reproduction happens for most people before we develop cardiovascular disease. Um so that's sort of an aside.

The way that I use that um that that test, the L P little A test, is it's a tiebreaker for a million other decisions that I make. And You know, when we have drugs that are available to treat that condition or to treat elevated LP little A levels, which we should have R C T outcomes data later this year, later 2026 or 2027. And so when we have outcomes data, that will

hopefully give us a direct target for treatment. But the way I use it in the real world is I use it in combination with somebody's family history. And so L P little A, most people have normal to mildly elevated levels. And there's two different tests. There's a nanomoles per liter test and there's a milligrams per deciliter test. And You should be familiar with that specific assay that you have and what the percentiles are like for that assay. But in general,

a value of a hundred and fifty or maybe a hundred or over is something where I start to think of that as a real red flag. And especially when it's in the context of somebody in your family, especially a first degree relative with a heart attack or stroke before age sixty. That L P little A being elevated is to me A tiebreaker for all of those 50-50 decisions. Should I treat your blood pressure of 134 over 82 with more medication? Should I add a zetomy to your 20 milligrams of Rosuvastatin?

Sh how much do I need to push the diet and lifestyle component of this? We didn't talk about at all what this person should be doing from uh what should this person be eating? How should this person be exercising? But it that's a real those are really important things. And I talk about sleep and stress management and what someone's diet I I talk about that all day with my patients in clinic.

But high L P little eight is gonna be a tiebreaker for me of do I put this person on a G L P one agonist? And so I use it very much in the context of it's a risk enhancer and the amount that it increases risk is going to be proportional to just how elevated it is. And so It's not something we have direct targets to treat. And a lot of uh a lot of really smart doctors who I respect say, well,

If we're not gonna be able to do anything with that test result, why the hell are we ordering it? And I, you know, like that's a reasonable perspective. But to me, like when I'm thinking about cardiovascular risk. I wanna get the information that I can about things that raise that risk because it's going to understanding the sort of totality and the holistic perspective about how risky somebody is from a cardiovascular perspective.

influences how I manage all of those other things and it influences the tone of my voice with my recommendations. Like maybe that's all nonsense. I'm not sure. I'm like open to being persuaded that I'm wrong. But it's it's definitely like how I how I use that touch. Alright. I I like it. I I I mean I think that's that's what the guy that's on on par with what the guidelines say now too is to use it as a kind it's like one of the things we just

factor in when we're sizing someone up and calculating their risk and it's a it's another data point that might push us towards a decision. So that's why I find it's useful to get for people. This episode is brought to you by Continuing Education Company. Hey curbsiders, have you ever chosen a CME conference because the destination? Only to be disappointed by the education once you got there?

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Paul Wirtz, let's say we proceed to the calcium score. Do we have results of that and then we can talk about it? Yeah, so we have a calcium score of sixty eight in this patient, so If we could maybe talk about why we ordered a calcium score in this patient, like we have this elevated APO B, we have the elevated LP little A, we have all these other

risk enhancing factors, like what may have driven us to order a calcium score. And then now that we have this score of sixty-eight and this forty-six year old, how do you interpret that? What counts as normal borderline or high uh in that age. And then when you're putting that all together

How do you actually sequence treatment? So this patient remembers they're maximally motivated. They want to lower the risk as much as possible. How might you actually talk through a sequence of treatment for them? Yeah. So a cornearity calcium score or a CAC score. is a ver it's a very controversial area in medicine. And I think a lot of cardiologists have been very eager to sort of like jump on the bandwagon of get a lot of imaging.

And there have been a lot of smart people who look at that as the cardiologists are insane because the R C T data just like is not there to support. that as an intervention. And I understand that perspective, but I kind of disagree with that perspective. And so, you know, the a a CAC score, there's two different types of imaging of the coronary arteries that we can do with CT scan. The first and most basic is a coronary calcium score or a CAC score.

That is a low radiation, zero contrast chest CT that basically looks to see is there any calcium buildup in the arteries around the heart. And I always tell patients, you've probably heard the term hardening of the arteries before. Well, a calcium score is looking to see if you have any signs of hardening of the arteries. And That tells you nothing about the degree of stenosis. It tells you nothing about the presence or absence of soft plaque.

It tells you nothing about symptoms that somebody is having. And so a CAC score is a useless test for somebody who's having chest pain or shortness of breath or discomfort of any kind. The other test that can be done as a as a CT scan is a coronary CTA.

Coronary CTA is different than a calcium score because it uses contrast, because it has thinner slices, and because it can see soft plaque in addition to calcified plaque. And so when you get a coronary CTA, You are also getting a coronary calcium score.

but you're also getting a whole bunch of different information. And, you know, I don't think it's worth for the purposes of this case, talking about the sort of more advanced levels of what the coronary coronary CTA can tell you. You can have these add-ons from companies like Heartflow or Clearly where You do either AI or fluid dynamic interpretation of the images to figure out is this a hemodynamically significant stenosis and how high risk are the features of the plaque.

The way that I I I think that those are are sort of solutions in need of problems to to solve right now. But the the way that I use any kind of coronary imaging.

Is it is telling me about the presence or absence of cardiovascular disease. And so for this 46 year old patient. To see a calcium score of over zero to me is a gigantic red flag. I probably wouldn't have ordered a calcium score for a forty-six year old because I would have expected it to be zero and I would have expected that to be falsely reassuring for somebody who's at increased risk. And so if I see a patient who's under fifty or under like fifty-five, if they're a woman.

I think a calcium score has very little clinical utility unless it is unexpectedly positive. This task is Seeing a calcium score that's elevated for this guy. Like what a blessing that this is elevated. He hasn't had a heart attack because It's just adding to this litany of things that we know about this patient that says that he's at much higher risk than he would like to be from a cordi cardiovascular perspective. And importantly. Doctors misuse.

coronary imaging quite frequently. And it's really, really common where I see somebody who gets a calcium score done. Calcium score is over a thousand. that leads to a stress echo and there's something funny on the stress test or they get a nuke and the nuke has a mild inferior reversible perfusion defect. And then all of a sudden this patient is in the cath lab getting a stent that's not gonna make them live longer or feel better. And so

Being aware of what the diagnostic cascade is and how getting this cardiovascular imaging sometimes tempts us into doing unnecessary procedures on patients is it's just a really, really important understanding for us to have of Where are what are we doing with this test? And what what I'm doing with these tests, any kind of coronary imaging, is it's helping me understand. how aggressively I need to medically treat somebody or whether I need to medically treat somebody. And so

For this patient, when I see a calcium score of over zero, I'm like, Holy crap, what a gigantic red flag. Like this guy's at really elevated risk. A forty six year old should have a calcium score of zero. If you're not sure what to make of the numbers, The there's a couple of different ways that you can handle it. One option is the Mesa database has a very good percentile calculator that you can literally type into Google.

Mesa calcium calculator. And the first link will come up. It's a from the it's all built on the Mesa study database, which is the multi-ethnic study of athosclerosis. And you can put in a patient's age, their ethnicity, their calcium score, and it will tell you and their gender and it will give you their calcium percentile based on age and those other demographic characteristics.

But to me, when I see a young person with any calcium, it is a gigantic red flag. For older people over the age of sixty or over the age of fifty five. I'm using the calcium score much more as helping me figure out is this person at higher risk than I would expect based on their age or they are lower risk than I would expect based on their age? That's a great overview. So the the and and the calcium score in my area is usually$300 or less. It's usually an out-of-pocket test.

My understanding is it's lower radiation and the coronary s the C C T A is is a more expensive test, a thousand dollars or more and a higher dose of radiation. Um, but I I do have a lot of people getting calcium scores now, even before they come to me. Some patients are just getting them on their own. Yeah. The uh the calcium score in a young person can be really falsely reassuring. And so

I think it has almost no usefulness in somebody this age. Like in this case it clearly did have usefulness. But that's that's a surprising result. And so I often counsel patients who are young. Like I when I have a forty two year old. Like, I'm not sure the calcium score is gonna be all that helpful. And if a coronary CTA was covered by insurance and it didn't cost them

a thousand or if they're at an academic center, it's probably like twenty five hundred dollars out of pocket. Um It would be a test that I would use for my young folks who I want to better understand their cardiovascular disease, but

In practice, it's a coronary C T A is covered to evaluate symptoms of chest discomfort or persistent symptoms after a stress test has been unrevealing. It's not done as a as a preventive test, I No, I'm not sure that um that's where we'll be in ten years, but that's where we are now. It's kind of

lightly alarming to hear that framework because I would suspect that the CAC score is being ordered for younger patients, right? Like because as you mentioned before, if you're using risk calculators, if you believe there is utility, that's gonna be driven by age. So the person who is older

By just by the calculator they're more likely to actually have a risk score that would actually put them on satin therapy in the first place. So the tiebreaker seems to me to be used more frequently in sort of younger patients and if this is underestimating risk that's a seems like a concern, I guess is all is all I'm saying here. The steel man argument for using a CAC in young patients is that

so much about what we do in medicine is trying to figure out the tiny fraction of people who are really vulnerable and elevated risk from like the huge swath of everyone else who's gonna do fine even if the doctors don't do a great job of taking care of them. And Seeing a calcium score of over zero in a young person is a truly alarming finding. And so maybe it's actually a you like that that's the steel man case, is that it's helpful for identifying the highest risk cohort.

But to me, I I would wanna be treated very differently medically if I had plaque in my arteries versus if I didn't have plaque in my arteries. And You know, whether the plaque is calcified or not calcified is part of what I would want as the under the sort of like comprehensive understanding of disease, but it's not the only data point. So yeah, so I I wanna try to summarize for the audience just to see uh with the CAC score specifically. So

'Cause I'm seeing sometimes people in their I don't I don't think people in their thirties need to get them as un unless maybe they have tremendous risk factors or something and you're expecting it to be positive. But I'm seeing a lot of patients in their forties just proactively getting it now because of the social media environment, the podcast environment, uh, you know, the these sort of like

you know, Rogan Sphere podcasts and things like that. Like people th some of those people are are just telling everyone they need to get a CAC score. So people in their forties, if the CAC score is positive, that's alarming. We should aggressively manage risk factors, medications, whatever. If it's if it's someone we're worried about and it's a zero calcium score, then maybe the plaque is there but it's just not calcified, so we might even consider a C C T A.

for those people. If they're in their mid fifties or above a calcium score is a good starting point. And then if someone's in like their late sixties or seventies, in in my opinion, if they like I'm expecting those people to have calcium, right? So does it become l like as is there like a certain sweet spot age range where you think is it like fifty five to seventy it makes sense and then once they're seventy five or older, I I haven't really

thought to get calcium scores in those folks. So I'll give you a clinical anecdote of how I've used a calcium score in an older patient. And so I I take care I take care of this woman in her seventies. She has had really, really high lipids for decades of her life. Her LDL fluctuates between I think around 160 and around 190 um without treatment. And she has failed every medication that we have. She has had side effects from

four different statins from azetomib, from bempadoic acid, from PCS can I from two PCS can I inhibitors. I don't use enclycerin because there's no outcomes data for it and it's like truly it's uh until there's outcomes data for a drug that doesn't treat an orphan disease, I'm just not ready to prescribe that medication. Um but this patient

failed all of these therapies and her LDL is still really quite elevated. And so what I used the calcium score for her was I wanted to know like, is her cal I think she was around seventy four when we got the calcium score. If her calcium score was a thousand I would have tried to figure out an alternate day statin dosing regimen or something that was really sort of like trying to be creative to get the lipids down. Maybe I would put her on crazy doses of psyllium fiber supplements to try to

bring those numbers really quite a bit lower. Like creative. Yeah. Um nato kinus is really interesting and uh I I don't think we have time to talk about it, but it's totally truly fascinating to me. That'll be a part two. Yeah. So um how I use the calcium score for her. So her calcium score was like two and she's in her seventies. And so

To me, what that does is that lowers the temperature on how we need to worry about her lipids. And so I used it as again, I use it like a little bit of a tiebreaker of do I need to really do something for this patient or can I just leave her alone and tell her like

Like ignore the lipids. Like don't take medicines that make your life totally miserable. And so I used it in the the latter case. But you know, if it had been really high, I'm I would have been uh stuck in a not wonderful position. But that's how I use it for an older person is a de-escalation rather than an escalation.

Yeah. Okay. So the middle in middle age that's that's probably the sweet spot for using it. Yeah. Okay. Greg, so you you mentioned a bunch of meds there in the context of talking about your your older patient who you tried kinda all all the meds.

For someone like Art, who we presented initially here, this is our our forty six year old guy, metabolic syndrome, L D L was one twenty three, his APOB was one twenty seven, LPA, LP little A was eighty nanomoles per liter. So What uh what how might you talk to him and what's your framework for talking to patients about cholesterol lowering medications, cardiac

Risk medications. So honestly, for this patient, you could make an argument that he should go on a GLP one drug before he goes on a lipid drug. That's uh, you know, we don't have data to really understand that, but you could you could certainly make a pretty compelling argument that if you're gonna pharmacologically treat

patient who has metabolic syndrome, sleep apnea, abdominal obesity, that you're better off actually treating something that is gonna probably lower his lipids also. And so it's a reasonable strategy. But in the in the purpose of talking about the lipid conversation. Statins have the most data. They're really well tolerated medications. Like what you hear on the internet about statins is so different than how every doctor who takes care of patients and who makes decisions about

like their own medical health would think about uh statins. And so I look at statins as it is my first line. Eight to ten percent of people have some type of muscle ache. I'm not one of those nocebo guys who thinks it's all nonsense. I take patients at their word when they have side effects from medications and

You know, like these are artificial substances that people are putting into their body. Like people are allowed to have whatever side effect they damn please. And so I never question a patient about whether a side effect is real. And if they have side effects, I just take them off of a drug. And if somebody has side effects on one statin, I usually use Rosuvastatin. I usually start at five milligrams to begin with.

I'll switch to a torvostatin. If somebody has side effect, I'll start at ten milligrams of a torvostatin and sort of like go up as needed.

Um, but if somebody has side effects to that, I will either start them on a Zetamib. Or I will think about using patavastatin. Brand name is Livolo for that. And that what's nice about petavastatin is it comes in a one milligram pill. And so for patients who are medication diverse, one milligram

for whatever reason feels like it's a lot less significant than five milligrams or ten milligrams. And, you know, like I I'm uh my biases go in weird directions too. So I I don't really necessarily disagree with that. But Um patavastatin is the statin that has the lowest incidence of statin-induced myalgias, and so it's a very reasonable option for a lot of folks. Um azetamide, 10 milligrams once a day is a very useful uh adjunctive treatment.

My clinical experience is that the response to that drug is so heterogeneous that I've had some patients who their LDL drops by 50%. I've had other patients where the LDL drops by basically nothing when you put them on azetomybe and probably has to do with the polymorphisms that relate to cholesterol absorption in the intestines and so

With all of these medications, the responses that people have are heterogeneous. And so I put people on medicines, I monitor how they feel on those medications, and then I monitor what their lipids are to decide, is this working? Should we augment it? Somebody not feeling good on it.

Um bempadoic acid is actually my last line drug. It's sometimes nice because it's a pill and it doesn't work in the muscle, it only works in the liver to inhibit cholesterol synthesis through a different enzyme than uh than HMG CoA reductase. The issues with bempadoic acid, one is it's not that potent. Two is that it can raise uric acid levels and it can raise transaminase levels. So you should monitor those things. Um and it's also just a real challenge in the in the in the real world.

to get coverage for it. And so I use PCS K9 inhibitors quite a bit more frequently than I use bempadoic acid. The limitations for PCS K9 inhibitors are are are two real ones. One is it's an injection and some patients don't like needles. Two is that insurance coverage can sometimes be problematic, although that has really changed over the last like three or four years. And it's much easier in practice to get PCSK9 inhibitors approved than it used to be for me.

There's two PCSK9 inhibitors that you can use. There's Evalocomab and there's Alarocomab. Eva Locomab has done such a better the the folks who make that medication have done such a better job of getting it on formularies that it's almost always the preferred medication. You know, it's interesting if you look at the initial data. Sorry, am I talking too much about this? No, this is fantastic. Paul Williams looks like he's uh really Yeah he's thrilled.

Uh RCTs looking at the PCSKI inhibitors because there was Fourier, which studied Evalucomab, and then there's Odyssey outcomes, which studied Alorochomab. So Fourier had this signal for increased mortality in the uh in in the Evalomab group. Like there were more people dead in the Evalomab group than the placebo group at the end of that trial, which was odd because

it certainly lowered major adverse cardiovascular events. And so there was cons I had some real concern after that first generation of studies came out. about whether Evolocomab was actually a worse drug than Alarocomab. And so Alorocomab had a mortality benefit in Odyssey outcomes. And so it seemed to me like when we have a choice between those two, that's the one that we should use.

And then Vesalius came out uh not that long ago, I think uh late last year, which was an interesting study looking at patients who were primary prevention but had clear evidence of Dyslipidemia, metabolic syndrome, and were already treated with statins. Not very many of them were on azetomide.

but a fair number of them had elevated coronarity calcium scores. And that the Vesalia study really sort of laid to rest my concerns about the signal for potential increased mortality with Evaluab. And so that ends up just being what I use mo mo more of the time, mainly because coverage is a lot easier and in the real world those practical things really matter.

Um, PCS can I inhibitors are super well tolerated. I've had one patient with an anaphylactic reaction and a handful who had um who had sort of injection site reactions, but those side effects are very, very rare. And as an aside, if you have somebody who has an anaphylactic reaction to one, Every allergist and pharmacist that I've talked to recommend not putting them on the other PCS can inhibitor.

And I I still get some people worried about their LDL getting too low with that and we need c some cholesterol and Uh we we covered w uh on one of our hot cakes episodes we covered the studies kind of looking at like the you know, cognition and does does this seem to cause any problems and it it doesn't seem to cause any problems as of yet. So v but vascular dementia is a very real cause of dementia.

The vascular hypothesis of Alzheimer's is a competing hypothesis to the amyloid hypothesis of Alzheimer's. And so when patients tell me they're worried about the cognitive side effects, especially patients who I already see evidence of plaque in their blood vessels.

I tell them I'm so much more worried about you developing vascular dementia than I am about you wore developing statin induced dementia or lipid low like low LDL related dementia. And so I the real risk in the real world is very much to me. much more related to vascular events than it is to this theoretical, possible, hypothesized conjecture that has never really sort of been replicated in real world studies.

Can I ask one more question, madam? I am seeing locally a lot of consideration for patients who are pre-diabetic in terms of statin selection, and I'm wondering if that impacts

Um your choice of statin, you know, for someone who's you know, for so Mr. Sclerosis from or his name is his A one C is five point seven, you mentioned you tend to lead with the high potency statins, which I think are more likely to kind of advance um A one C. Is that a consideration or how do you think about that when you're prescribing? Just

One of the one of the um folks who trained me, he s he we would say, If you get diabetes from a statin, you are a Snickers bar away from getting diabetes anyway. And so you know, like statins will raise your A one C by point one, maybe point two.

I look at that side effect as the same way that I look at the side effect of muscle aches, which is if you get it and it seems to be problematic, then we just switch the medication. And I like I think that we put too much emphasis on like making the decision a very high stakes decision and so Patients have all kinds of different perspectives about statins, like especially the most informed folks will often come in with the strongest perspectives. And

My goal of that first conversation, I just like want to lower the temperature of how big a deal this is and how important or a life changing of a decision going on a statin is. And so like, yes, your A1C may go up, but like overall your risk is gonna go down. You don't get extra points at the Pearlie Gates for having a A one C at zero point one uh percentage points lower. Oh, don't say that. That's that's what I tell my patients to get them to lower their A one Cs.

Wurtz, let's go to uh let's go to our next case'cause I I think we have uh a contrasting patient here.

Yeah, so this patient from the doorway looks very healthy on paper. So we've got Miss Lola Lipa. She is a thirty-eight year old runner. She does about thirty miles a week. Her BMI is twenty two. She has normal blood pressure. Her A one C is five point two. Her LDL is seventy-seven. Triglycerides are seventy. On paper, she looks incredibly low risk, but you find out that her father died of heart disease when she was young. She had a brother who had an MI at age 41.

So her informed primary care clinician digs a little bit deeper, finds out that her LP little A comes back at two twenty millimoles per liter and an APOB of ninety-five. So she's she's saying, My LDL is great, I'm fitter than almost everyone I know. Why am I high risk? How how do you use a case like this to explain the limits of lifestyle for LP little A specifically? And even with these excellent habits,

Can biology still drive the risk? And how do you think about lowering her risk if she's already doing everything right, so to speak?

This patient, a young person who takes really good care of themselves, is interested in all of the sort of like lifestyle interventions that lead to really good quality of life for a lot of patients.

her family history is insanely alarming. Her father died when she was young. Her brother had a heart attack when he was forty one. This is the exact patient where a risk calculator does them a total disservice. And so You know, an LP little A of 220 nanomals per liter is a really, really high LP little A. And you add in that LP little A.

along with her family history. And this is a patient who is coming to medical she's really lucky that she's coming to medical attention because this is a very, very scary family history and lab data that we have. And so For somebody like this, it's really tricky because we don't have a ton of levers that we can pull to lower risk. Like we can't change her genetics. She doesn't have metabolic syndrome. Her blood pressure is well controlled.

Her LDL is not even that high and her APOB of ninety five is really driven by that L P little A. And so this is a patient who I do two things for. One thing is I really let sort of Have a f the focused conversation about This is what your genetics are. And I think that those genetics are real and they're concerning because of what has happened to these two relatives of yours. And

To me, the right time to act is this second. It's not something where I would even like try to wait for imaging. Sometimes you'll use imaging in a patient like this. to try to persuade them uh about treatment. But to me, this is somebody who we should be treating pretty quickly. And when I have somebody who has a pretty well controlled LDL or pretty well controlled APOB, but has elevated risk related to something that I can't modify. How I approach it is I tell that patient

Look, we don't have a ton that we can do, but I know for sure that your risk will be lower if we get your LDL down to fifty and your Ape O B down to sixty-five. And I don't think I'm gonna get the L the Ape O B down to forty because

It's just driven by the LP little A, but I'm gonna try to lower those numbers to much lower than I would want them for any comparable person because of what this person's family history is like. And this is also the type of patient who I would think about for primary prevention aspirin. High LP litola. Remember, LP litola is prothrombotic. And she has had multiple first degree relatives who have had premature MIs. And so There's no more.

probably something that is pro-thrombotic about the phenotype of their LP little A. We don't have assays to figure out the Kringle repeats and how actually uh thrombotic they are. But to me, this is somebody who I really think about aspirin for primary prevention and your limitations for that.

are gonna be how much does she bleed during her menstrual cycle? Does she have baseline anemia? But this is somebody who I would truly consider as being an important patient to think about aspirin for primary prevention. The other thing that you need for a patient like this.

a young woman who has a cardiovascular disease history is you need an obstetric history because that's an important part of your risk assessment. You need to know Infertility, you need to know pregnancy complications, preeclampsia, gestational diabetes, gestational hypertension.

that she have PCOS and even young, thin people can have all of those conditions and those are important because those are risk enhancing pieces of information. And when you're trying to understand somebody's risk, you should understand their risk as holistically as possible. So is if she said, No, I'm not gonna take any medication unless, you know, I have more evidence, I'm not just gonna go off one piece of data, is she someone you would get a calcium score?

I would order for I would order her for a coronary CTA and I would push her really hard to tell me about some ti everyone's had chest discomfort at one time or another. And so I would ask her to tell me about a time when she had chest discomfort and I would write that she had chest discomfort in her chart and I would order the coronary CTI.

Yeah. Okay. Look, I want to know if she has a soft plaque. And like the I I fully that is not a guideline recommended perspective. And reasonable, smart doctors are going to hear me say that and are gonna think I'm like absolutely not. But for me, if like the if that's something if looking at imaging of her arteries is gonna be something that would persuade her to um to go on medical therapy, to me

I'm doing her a disservice if I don't get all the data that I that I can to convince her that medical therapy is right. Yeah. Okay. Paul, did you think he was gonna say uh uh aspr uh aspirin, Staten and C C T A for this case? Paul Williams? Oh no, I did not. Yeah. Unless she was telling me that she would only go on treatments if there was stuff in her artery. Like I don't come at patients and say, like, you need a C C T A.

I come at patients and I try to understand holistically what their risk is. And yeah, the most important teaching point from this case is like a risk calculator absolutely misses the boat for each patient. Yeah. No, I'm picking up what you're putting down. I mean I'm I'm following. I I think it it it sounds reasonable to me and I think it's

It's like aggressive um primary prevention. You're trying to make sure that this person doesn't have like a life changing cardiac event which happened to her brother just a couple of years older than her. So I I get it. Um Let's go on, um, for interest of time. We have another case here. Paul Wirtz, do you wanna uh get into our our final case and we can use the rest of our time going through that for a few minutes?

Yeah, so let's talk about Gary. We got a forty two year old veteran. He comes in for his routine visit. His BMI is around. Let me pause for one second here. I'm sorry. Paul. We have Paul. We have Art E sclerosis. Yeah. Um, and then we have Lola Lipa. And now we're doing Gary for this case. Where do you think? Gary is like the What happened when you're writing this? Just ran out of steam towards the end, huh, buddy? Sorry, go ahead.

All right. Uh I thought you were gonna say that your cat was going crazy and we needed to pause that'cause Ollie really No no Ollie's really been uh vocal. He uh If for if people are watching the YouTube video, Ollie's been all over the place and has been meowing uh pretty aggressively for the past fifteen minutes. So probably also production. Sure. Sorry to interrupt. So sorry, carry on.

All right, so Gary, he's our forty-two year old veteran. He comes in for a routine visit. His BMI is around twenty-five. He looks fairly muscular. He says he goes to the gym regularly, but he's under a lot of stress and usually sleeps about six and a half hours per night. His blood pressure has been running in the hundred and forties without med.

When you look at his labs you see an A one C of five point five, but his triglycerides are two hundred ten, his HDL is low at thirty eight, and his LDL is high at one hundred eighty seven. Gary is very interested in maximum health and longevity. He wears a continuous glucose monitor from time to time, and he uses a health ring to track his sleep, his heart rate variability, and recovery, among many other variables.

He noticed that oatmeal or fruit will push his glucose up to around 160 postprandular, so he then cut carbs aggressively. Now he eats mostly bacon and steak for breakfast because he likes that his CGM stays flat.

So what what Gary is really asking here are whether markers of insulin resistance like a HOMO IR matter more for long-term health than his lipid profile, and how much weight he should be giving this CGM data compared with his lipid panel. Um so let's say his APO B is one ninety, his LP little A is thirty seven.

Uh so low on the LP little A. He he points to his A one C of five point five and his improved CGM patterns after the aforementioned dietary changes as reassurance that he is very metabolically healthy. But you see that his triglycerides are over two hundred, his HDL is low. So considering that there may be some underlying insulin resistance present even with his quote normal A one C

For a motivated patient like Gary, is there any value to checking like a a fasting insulin or a HOMA IR? Or can you just use the the triglyceride to HDL ratio to spot the danger? This is suck there's so much to unpack in a case like this. There's just so many layers of it. So when somebody gets a lipid panel and the triglycerides are high, the first thing that you need to do is ask the patient whether or not they were fasting because

fasting versus non-fasting is going to impact triglycerides more than any other parameter in the in the lipid panel. But, you know, presuming that that is a fasting lipid panel and the triglycerides are high, the HDL is low. A1C is kind of like creeping up. It's not in the prediabetes range, but it's certainly at the higher end of the quote unquote normal range.

You know, the whether the metabolic syndrome question is an interesting question in a patient like this because to me it's not clear from the data we have.

how worried we should be about metabolic syndrome. I think that I probably am, but I'm not sure how accurate that is. And so, you know, is a fasting insulin an important piece of information? It's not a vital piece of information, but it's a data point because People will get elevated fasting insulin before they develop overt hypogly hyperglycemia.

Uh HOMA IR is it sounds like a really fancy test, but it's basically just an equation where you plug in fasting insulin and fasting glucose. And so whoever came up with that is pretty good at marketing because it sounds like it's such a big deal more than it actually is. Um The triglyceride to HDL ratio is a great tool and it's notable that it's uh over it's like five to one in this patient, but that's not gonna be perfect for everybody, in particular folks who identify as African American.

often have a higher HDL than you would expect and do not manifest with the elevated triglycerides. as often as you would expect it to. And so in a patient who identifies as African American, I often don't treat that, uh, that ratio as being as important as some other patients. But, you know, like there's a ton of

uh inter ethnicity and interracial variation. And so you can't necessarily say that one person fits into the entirety of the cohort. And remember, metabolic syndrome is a spectrum. And so you're trying to figure out where on that spectrum is somebody. And so I think a fasting insulin is a totally reasonable thing to check for a patient like this.

As part of your understanding of does this patient have metabolic syndrome. You also didn't give us the transaminase levels. And so if his ALT was forty-eight to me. Maybe he has metabolic associated fatty liver disease. And we actually do have evidence of elevated vi like sort of manifestations of elevated visceral fat. And we didn't sort of talk about the visceral fat versus subcutaneous fat. um discussion. But a lot of insulin resistance and a lot of metabolic syndrome.

Gen it really comes down to do your genetics mean that you have a higher depot of subcutaneous fat versus are you more likely to store your excess calories as uh as visceral fat? But what's interesting about this guy's diet?

And the way that it's interacting with his CGM is a a little bit of like a Rorschach test about what do you think about saturated fat. And so You know, I think of officially like RFK just ended the war on saturated fat, so we're not at war with saturated fat anymore, which is I think good news for everybody. But uh the saturated fat question is really, really interesting because saturated fat in our diet. is going to impact fluidity of our cell membranes. And that's going to impact

what happens with the residence time of our atherogenic lipoproteins. And so part of the reason that saturated fat got a reputation for being linked to increased cardiovascular risk. People who have a diet that's high higher in saturated fat on average will have a higher total cholesterol and a higher LDL cholesterol. And that's probably linked to the way that the LDL receptor sits on the surface of hepatocytes differently depending on membrane fluidity.

which is influenced by fatty acid composition in our diet. That said. Whether you think saturated fat is uniquely problematic because of its lipid effect. or whether you think that it is more concerning because of the way that saturated fat is more likely than polyunsaturated fat to lead to hepatic steatosis and whether there's untold biological mechanisms that we don't fully understand of why that might be more problematic, I think is still

something that needs to be elucidated. Whenever anybody tells you I understand the mechanism of this and so we should do this thing because mechanistically it makes sense and you start falling in love with the biology. That is a recipe over and over in medicine for just make making a total error in judgment because

Mechanisms are always more complicated than we think that they are. And so I tell my residents all the time, like, don't fall in love with the mechanism. Do not fall in love with the biology. Like pay attention to what the outcomes data look like. And this question of is saturated fat worse for you than polyunsaturated fat? Sort of like bleeds into the seed oil question and like there's a lot of things that are going to be part of this patient's social media diet.

that are gonna influence a lot of your conversation. And so you probably are not confronting every single one of these questions with this individual the first time that you meet them. And I I think that it For somebody like this. He's very plugged in. He's asking these questions that suggest that he's pretty well informed and he's paying attention to this.

For a patient like this, I kind of just order whatever they want me to order. And I trust my ability to interpret what those lab tests are going to tell us about this person's health. And you know, whether the keto diet, which leads to a really high LDL cholesterol, is atherogenic is a question that I think we have pretty good data to understand. I don't know if you all familiar with the keto CTA study.

Yeah, I was fascinated with it. I I think you wrote about it on your sub stack, right? Yeah. So that study was It's basically they took patients who were the the term that they use is lean mass hyperresponders. Right. Which is a marketing term that basically means somebody who eats a low carb diet, does not have diabetes, loses weight, probably feels pretty good, but their LDL goes up really high.

And the question that they asked was if we do a coronary CTA at these pati uh on these patients at time zero and then we repeat the coronary CTA a year later, what do we see in terms of progression of subclinical cardiovascular disease? And What they found is that the rate of progression of cardiovascular disease in this cohort of patients was basically as fast as any cohort of patients that's ever been studied in terms of progression of subclinical atherosclerosis. And so

Maybe that is mediated by the fact that these diets tend to be high in saturated fat and that tends to raise the LDL. But I don't know that we understand that mechanism with the precision that we need to say definitively that is why. So I look at it as that is an atherogenic diet. And if that is your phenotype, Low carb.

high fat and you have a really high LDL response uh as a consequence of that, that's probably putting you at elevated risk for cardiovascular disease. And the question of whether you can just treat somebody's lipids and keep them on the diet that

makes them feel good, I think is a question that we don't really know the answer to. But in general, patients are gonna eat what they want to eat. And, you know, the amount of um the amount of influence that a doctor has over this decision that somebody makes. Two to three times a day, every day of their life.

I'm under no illusion that the things that I say are gonna drastically cause changes. And I also feel like a lot of patients who are marinating in this uh this ecosystem of wellness and longevity. are distrustful of doctors and my experience with it is that a lot of the time they think I just want to like throw them on a statin and I want to ruin their metabolic health. And so

I I I come at all of my decisions of like the patient needs to understand that I have the same goal that they have, which is I don't want them to have a heart attack, I don't want them to have a stroke. And I read everything. I'm constantly learning about this stuff and I communicate to patients. Our goal is the same.

I get paid the exact same amount of money whether I put you on a statin or I don't put you on a statin or I put you on a GLP or I don't put you on a GLP. And my salary is not influenced at all by any of the prescriptions that I give to you. And I'm gonna give you my gener my my true medical perspective based on my read of the data. I'm not going to

synthesize something that ChatGPT told me. I'm not gonna copy something from social media. I'm gonna look at your data and I'm gonna read the literature and I'm gonna come to a conclusion about what I think is the recommendation that I have for you. And so and I think if you and again, like coming back to like that soft side of medicine.

If you don't talk to patients like they're adults and that you are on the same team and you try to pretend that you know better and they're misinformed. Like that to me is just like one, I'm wrong about things all the time and I don't presume that I have all the answers. Um, but I do think that patients respond well to the idea, like we are on the same side. We both want the same thing, which is for you to feel good and for nothing bad to happen. And so for somebody like this.

I think that you can interrogate whether he has metabolic syndrome. You can check his transaminases. You can get a fasting insulin level. you can look for a hepatic ultrasound or a fiber scan to see if there's any evidence of uh of fatty liver. Um but high triglyceride to HDL ratio, low HDL. You know, uh he has high blood pressure.

He probably has metabolic syndrome to some extent. How much is that dictated by the fact that he's under a ton of stress? He doesn't sleep very well. How much of that is that he probably lifts a lot of weights and doesn't do much cardio? And would he benefit from more aerobic act? Like there's a lot that you can do. from a lifestyle perspective that doesn't involve any medication and

Like are we sure uh his BMI is twenty five? Are we sure he doesn't have sleep apnea? Does he wake up feeling rested? Like does he need a sleep study? Like people who work out a lot sometimes have thick necks, sometimes have sleep apnea that's undiagnosed. And so

I think you can do a lot of different things for this patient. If you're asking me like, what would I do for somebody like this who was basically like, doctor, I will do whatever you want, what I'd probably do is I'd put him on a lipid lowering medication. I would treat his high pr his high blood pressure.

Yeah. We're gonna need to start wrapping up here, but for for the audience, uh there's this group of people that are eating the carnivore diet, if you're not familiar with it, where they're they're mostly just eating meat.

So it's a very high saturated fat diet. And the there's a number of these people and I've come across some of them in practice. That's when I first learned about the carnivore diet is somebody who had a normal total cholesterol, his total cholesterol went up to like five hundred and his LDL went from like one thirty up to like three hundred on on this um ketogenic kind of high fat, high meat diet and

this was a guy in his thirties and he was saying, Oh, it doesn't matter. I have a zero calcium score but as you told us already, is it we expect a zero calcium score for someone in their thirties and if if the longer that you're exposed to the higher

uh cholesterol, like the more we think that that you would be at risk for atherosclerosis. So that's why that study was done, right? So they're saying, okay, for these people that do have that that response does it matter and it right now th the only study we have seems to suggest yes there is some increase atherosclerosis, increase pace of it. Even if it's subclinical. Is that a fair summary of it. It suggests that.

This is a very atherogenic phenotype. And so yeah, I was really surprised by what that data looked like. Yeah. So we can link to your sub stack on that one. And I I I understand.

why a lot of people like that like that diet or like those very restrictive diets because maybe there is something that they were eating, maybe they have some s some food allergy or intolerance and when they go on that very restrictive diet, they're no longer exposed to whatever was bothering them, so they feel better and

Of course if they're wearing a C G M it's th you know, they're gonna get beautiful readings on there'cause they're not really causing glucose to spike and uh so anyway, I I think that's That's an interesting thing that um, you know, you could we could do a full episode on just that topic alone. But uh uh Paul Wirtz, uh Paul Williams, before we uh go for take home points, do you guys have any other questions about this um this specific case?

No, I think we I think we covered everything. I think an and a very interesting point is that with that CTA study, they measured one year, which I feel like is not very much time, right? Like this is Potentially decades. Crazy short crazy short time. Crazy short time. So I feel like that just further emphasizes that point. Yeah. We did a uh a lifestyle medicine episode where we talked to a doctor at Duke who treats people with ketogenic diet and

we talked about the lean mass hyper responder and how we d uh at this time we don't really know. But um I I believe the conclusion from that, or at least my conclusion from that and how I practice is if someone's on a ketogenic diet and their lipids look okay.

you know, it's it's not as concerning, but if their if their lipids spike up like that, I'm looking for it and and we're we're gonna change course. So um I as as far as as far as we have the evidence right now, I think that's that's where it's at. But concur.

Greg, uh we talked about so much here and we'll we'll have to have another conversation'cause I know the well of knowledge for you in this area is like really deep and we could keep You know, we'll we'll keep monitoring the substack for more uh more interesting things to talk to you about. But uh what what do you want people to remember from this conversation? Like two or three take home points.

Cardiovascular disease is largely preventable. Risk calculators miss young patients who are at elevated risk. And you need to meet patients where they are and understand who the human is, not just what the risk calculator tells you. Uh anything you want to plug, we'll give you a chance to plug, maybe a podcast that you appear on. That's very good. I would say great. Oh, thanks. Uh I do uh the Beyond Journal Club podcast with Core IM and the NA JM group and uh subscribe to my Substack.

Yeah, strong recommend. This has been another episode of the Curbsiders bringing you a little knowledge food for your brain hole. Holes. I was I was praying that Wurtz would jump in with a yummy, but no. I had to settle for what I was saying holes. Still hungry for more general patron. Sorry. Could we do that? I said it. Keep all of this. Alright, still hungry for more? Join our Patreon and get all of our episodes at free, plus twice monthly bonus episodes at patreon.comslash curbsiders.

You can find our show notes at the curbsiders.com and sign up for our mailing list to get our weekly show notes in your inbox. This includes our Curbsiders Digest, which recaps the latest practice-changing articles, guidelines, and news in internal medicine. And we're committed to high-value practice-changing knowledge, and we want your feedback. So please email us atskurbsiders at gm.

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And to our whole Curbsiders team, our technical production is done by the team at Pod Pace. Elizabeth Proto does our social media. Jen Watto runs our Patreon. Krista Chumanchu moderates our Discord. Stuart Brigham composed our theme music. And with all that, until next time, I've been Dr. Matthew Frank Watto. I've been Dr. Paul Wirtz. And as always, I've been Dr. Paul Nelson Williams. Thank you, and goodbye. Nu kan du tanka Night Prime Redefined HVO100 på utvalda stationer.

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