Cardiologist Warns 50% Of Heart Attacks Give Zero Warning

When I started 20 years ago, all I could say to patients was, "You're screwed." Now, when we combine these therapies, there's a way to reduce the amount of plaque that you had. This is an era like we've never been in before.

There's a big trip that's happening for you. You're going to testify before the FDA.

I'm really excited and honored to be a part of this because it's a unique opportunity to influence what's happening in the industry and to be able to really make a change for the better. The potential here is phenomenal.

I don't know any other cardiologists except for ones in functional medicine space that are doing stool tests to look for heart disease and treat it. That's part of the screening process and the treatment process in my patients. And inflammation we know is one of the keystones of creating not just atherosclerosis but arrhythmias and hypertension. So we've got to take a step back, remove that, and look at the whole picture.

Dr. Abid Hussein, welcome to the pathway to peak performance. So great to have you in, my friend. How are you?

I'm doing great, Jock. Thanks for having me.

Yeah. Thanks for coming all the way out from Boulder, Colorado to be on the show with us today. Super to have you in. We got a lot to cover.

We do. Yeah. Where's it start?

Well, let's talk about your charity first. Um, and you selected Charity Water.

Oh, yeah. Great one.

Yeah. I love the transparency and accountability, and it's so basic that—it's unbelievable that we don't have something as basic as water guaranteed for all of humanity. I mean, this is a foundational project for our health.

Yeah. Scott Harrison, who started that charity, is phenomenal. And basically the work that they've done over the years has been just magnificent. And you think about—you hear—you see these stories when he does that presentation of women walking miles and miles and miles to get water that's just completely contaminated.

That's right. Yeah. It's really—and the lack of safety that they have to when they're going to get the water, too. It's just a whole life change for a whole community.

It's amazing. They put that well in, everything changes.

Yes. Yeah. And it makes us realize—it's something we're going to get to if we have time today. We're going to talk about cardiology today. But maybe when you come back and see us next time, we can talk more about hydration and how important that actually is.

But Charity Water is a great place to start. Um, the show is sponsored by KetoneAid. You're well familiar with ketones and how they actually work, the mechanism of action in the body, what we call the fourth fuel. And nobody better to explain it than you. So, um, what I'd like to do is—would you like to use K2 or K4?

I'm a fan of K4.

Me, too. That's the one I love.

Yeah. So, here you can see it's a closed, brand-new bottle.

Yep.

So, if you will take it, and you, the doctor, will dose us with the appropriate amount. Um, as we're doing that, I'm going to cover some items. Um, you're originally from New Jersey.

That's right.

Um, and you grew up in an area that's not far from where I lived in New Jersey at one point in time in my life. I really—I love it, New Jersey. It was fantastic. But you made your way out to Boulder, and you're at Boulder Longevity Institute, which is like a mecca for um, for what it is that you do. But you're—you're trained as a cardiologist.

That's right. That's right.

Yeah. And when we think about it, um, well, first, cheers.

Cheers. Thank you. Thank you.

You like to chug it? I'm going to sip it. I like the effect. Gets me zoned in.

I love—I love this stuff. I use it every day, three times a day.

Hey, real quick. YouTube tells me that over 95% of the people who actively watch this channel are not subscribed. Do us both a favor. Go ahead and subscribe now so that we can continue to provide you with the high-quality guests and the information that's going to keep you on the pathway to peak performance. We really appreciate it. Thank you.

So when we think about it, what is it? Two out of what? One and two—half of the population—half the population is going to—is going to either suffer from or die from heart disease.

Yeah. It's still the number one killer globally, and half the population that—that has heart disease that's going to die of heart disease never even makes it to the emergency room because they die of sudden cardiac death. That's a huge percentage of the population that never even knew it was coming and couldn't even get any form of care to help prevent it.

Scary thought.

It is. It is tremendously scary. You know, you're looking at, you know, what is it? The numbers are astronomical. I think it's like 300 million people uh that potentially can—that are affected by this, and then half of those are—are never going to make it to the—to the emergency room.

They'll just—all of a sudden, that's it. Um, so with that in mind, on the pathway to peak performance for anyone, I think we've got to really think about uh our cardiac health, our—our cardio, and what we can do in order to make sure that we're living a life that's going to make sure that we don't wind up in that half of the population. And you've got great news for us today about what we can do to make sure that we stay heading in the right direction.

So, first things first, today we're going to talk a lot about cardiology, but before we do that, um, there's a big trip that's happening for you. You're going to testify before the FDA, or you're going to present to the FDA on these peptides that were—are going to be voted on. This is a big deal.

That's right. Right. On July 23rd and 24th, the uh PCAC committee, which is uh going to give their recommendations to—it's the Pharmacy Compounding Advisory Committee—give their recommendations to the FDA on whether they can—we can recategorize a certain set of peptides. And then there's a whole another round later on in the end of the year. And I guess a lot of that will be dictated by what happens here.

That's right. This is—this is a pivotal moment.

It is. It is. And the—the clinical experience that a lot of us practitioners have accumulated over the past 10 years or so is valuable for the—for presentation to this committee. We're going to be testifying or at least presenting our clinical experience about the safety, the efficacy, uh, and then the data that's out there.

Uh, the amazing thing is that this—the committee or the group that's presenting has amassed brand new data about peptides. That's new research that's recently been done as well as old research that's been translated, uh, locked away in different databases that we knew existed but couldn't really get access to. Now we have them and they're translated, and they're being released for everybody to be able to go through.

And when you say translated, that's because they were done in different countries, correct?

Yeah. Yeah.

Yeah. Really interesting. I mean, a fascinating time. The potential here is—is phenomenal.

It is. It is. I'm really excited and honored to be a part of this because it's uh it's really a unique opportunity to influence what's happening in the industry and to be able to really make a change for the better.

I—I really believe that bringing peptides back to the compounding pharmacy creates safety, and it—it really reinforces the patient-doctor relationship. I feel like when the FDA doesn't allow the doctors to be able to make a commitment to patients and—and make that—that agreement that we can provide something for a patient that's looking for answers and—and trust that we're doing it safely as well as with efficacy, I think that uh this helps to bring that—that—that relationship back 100%.

I think nothing more dangerous today than people using um online research chemicals uh that are really—I mean, you have to question number one, what are the materials? How is it manufactured?

That's right.

Um, and a whole litany of other things. Plus, is the COA actually really real? Is it just photoshopped? And then it's a—it's like, you know, there's so much uh crud on the internet uh or on YouTube, however you're finding it, or in large language models uh that's been picked up by inaccurate information.

Yeah.

That's been distributed by those—those um those companies that are just trying to pump, make money. The question I think really becomes, um, you know, are you going to be your own—your own physician? Are you going to be the person that you're just making this decision based on information, what you think is right?

I—I mean, how do you get the dosing right? How do you really know? Um, and I—I'm going to say this, and it may be controversial, but I really do feel this is true. The um sort of the mills, if you will, of hormone replacement therapy as well as uh GLP-1 therapy um doesn't look at the whole patient. It's not like coming to see, you know, where you get a chance to get a sense of, hey, what am I really dealing with as a human being?

We're going to talk about all of it today, but we're going to focus mainly on cardiology today just because I think that's a great place for us to start. And um so, forever cholesterol demonized, um HDL, LDL, and, you know, like that seems to be the only metric that most of the time you—you go in, you talk to your doctor and they're like, "Hey, you've got high cholesterol. You should probably take a statin."

But I think the great news, and what I know about you and listening to you in lectures and hearing you for as long as I have, you've got a lot more to talk about today uh about what people need to know, and then we're going to talk about some things that are really cool that are new that can really help people um to figure it out, and then what are the uh forms of treatment that they can expect thereafter.

So let me start with the big cholesterol debate.

Yeah, it's the one nail that we keep trying to hammer. And I say we as the cardiologists in conventional medicine. It's not the only thing that needs to be addressed when we're looking at atherosclerosis, what we usually call heart disease. It was the only thing that we could—we could effectively change for decades because we had a medication like statins.

But the more we look at this—and part of this is seeing what happened with GLP-1s—it's really expanded our understanding of what therapeutic options we have and what the mechanisms of—of heart disease really are. The mechanisms have been studied for a long time, and we know that it's not just cholesterol.

And—and really, I want to take a step back, too, because the—the dialogue is cholesterol, it's LDLs. What we really need to do is shift it to ApoB. If we're going to talk about a cholesterol-based dialogue, ApoB is—is the marker that we should be looking at. It's got the most data to support it, and it tells us reliably the amount of particles that are in contact with the arterial wall.

That's important because each one of those contacts can be a potential timeframe where atherosclerosis can develop, where that particle can get under the lining of the artery and start becoming atherosclerotic. Now, our body's got the ability to put down particles, cholesterol, and it's got the ability to remove them. That's where the HDL or ApoA1 comes in.

So it's a much more complex process than we have given it credit for, and it is much more layered. GLP-1s come into this process where we're looking at receptors on the—arterial wall, inflammatory issues, nitric oxide dynamics on the arterial wall. So the concept that it's just LDL that we're going to focus on is completely neglecting the whole process of atherosclerosis.

When we look at the whole process, it's so layered that using one—one biomarker just does a disservice to the whole process and really does a disservice to our patients. To give you a perfect example, when we look at just LDLs, when you're looking at LDLs, you're just getting a total mass number or a volume of the amount of cholesterol. It doesn't tell you how that volume is distributed.

When you look at an ApoB, it tells you the number of particles. So that gives you some information. The important information is how are those particles, or how is that volume distributed through the particles?

Now, is this where we get into like particle size?

Exactly. Yeah. So you can have larger particles of ApoB that have cholesterol, and then those particles, those larger ones are less prone to causing plaque. You can have smaller ones that are more dense that can be more likely to get under the arterial lining, and that will cause plaque more frequently. So that's important because we have to look at the dynamics that create that.

It's metabolic dysfunction, high oxidative stress, you know, it's a fatty deposition in the liver, all these metabolic problems that we know are associated with it. We have a clear, clear path to understanding why it happens. The liver becomes inflamed. It generates a different type of cholesterol. It's more dense, and then that creates plaque.

Then we look at the larger inflammatory picture that drives that plaque. Once it gets underneath the artery, it becomes inflamed. It irritates the immune system. The immune system reacts to it and causes it to become calcified and become plaque. That's really—that's it in—in a nutshell, but there's so much more that's involved.

So you can see that just focusing on the one aspect of cholesterol and LDL in the depositing is—is really not doing any value to the patient and the process.

It's interesting if you think about it. Um, this would be just like we would talk about neurocognitive decline, a disease of decades. So, in other words, what we've done, the choices that we've made along the way—and we think what—what impacts the liver—liver, excuse me. So, drinking alcohol, uh when we say fatty deposition, meaning that we're eating lots of like sugar or things that are going to basically cause uh fat to accumulate in the liver.

That's right.

It's important for young people to understand that the cho—the choices that you're making today as a teenager, as a 20-year-old, a 30-year-old, a 40-year-old, where we may—may start to see these things really start to show up uh as problematic, um it's—it's uh you don't maybe have as much uh leeway or runway as you think. It's maybe more important to really start thinking about those things at an early age.

How young do you need to be, or how aware do your parents need to be of these things to make sure that you're on the right path?

When you're looking at it from a longevity standpoint, you really have to start young. The earlier you start, the better. When we're young, we don't necessarily have the wisdom to know that we've got to temper our—our habits and some of our extreme behavior. But you know, when we're young, we want to really experiment, and that's okay because we have the flexibility to do that. We have the hormonal—the hormonal backup. Our system is more resilient. Our cellular function is more resilient and adaptable.

It's when we get older that we lose that resilience, that adaptability, and that flexibility, and then we start to get an accelerated increase in risk. Everybody should be checked early on for genetic problems. Easy to check for Lp(a), ApoE genotype, MTHFR mutations. Those are simple, easy, more easily available tests via serum testing. Everybody should know that because it can impact what they're doing from a dietary standpoint and exercise standpoint early on and give them early risk.

Do you feel like um also, is—is factor V Leiden in that same category that something that you'd want to be testing for, or are you only looking for that if it's in your—in your, uh, you know, family history?

Factor V is—is uh less prominent. Certainly will increase risk, but not nearly as common as these other mutations. So if you do see family risk for it, definitely worth checking; not something we need to screen everybody for. Uh, as well, the—the added risk from the mutation is generally not as high as we might see with Lp(a), ApoE genotypes, and MTHFR. So those—get those checked early, young. Ideally, you could do it at any time—early teens, early 20s.

When you look at uh when you want to start screening for heart disease, heart disease probably needs to start getting screened in your 20s, 30s. And that's controversial because most places don't really—don't really recommend doing it that early, and you might not find plaque. But if you find abnormal lipid dynamics or some of these risks, then you can address them early. The general population, you got to get it done before 40 years old.

Okay, so we've got that out of the way. The things that we should be testing for to understand, okay, what are the risk factors associated with—beyond that, there are the simple things of lifestyle. So we're going to talk about, obviously, you know, hydration, diet, exercise, sleep as sort of like the four pillars I always look at. Is there anything else we should account for in that?

Well, definitely we need to account for social—social support network, stress levels. Those are the—the unseen and unaccounted-for risk factors that are really starting to emerge in the modern era.

You know, it's really interesting because um I just saw you talking about something recently. You were at um the uh Dave Asprey conference, um and that's was sort of what they were focused on in that was that the whole social aspect of—and you know Dr. Richard Louis Miller, a friend of mine. Richard always says, "We're—we're living in an epidemic of loneliness and isolation."

Absolutely.

Certainly started with, you know, the onset of these mobile devices. They're emitting lots of blue light and causing all sorts of problems and sleep disturbances for people, sleep hygiene issues. Uh, but we become sort of disconnected from one another, and we're not seeing some of the same things. Help us understand how you see that.

I see that show up in—if you want to look at biometric numbers, you can see it show up in heart rate variability, cortisol numbers, activation of the sympathetic nervous system in whatever biomarker you want to see, and—and total autonomic dysregulation. Uh, it's—we're in a society that's completely disconnected from our support structures that we've been designed from an evolutionary standpoint to rely on.

Yeah. The tribe.

That's right. Yeah. And we've also not been designed to be on all the time. We are in a information constant stream that is high-intensity, sort of high-alert, stress-provoking information, and we're not designed to—to be receiving that all the time, whether it's from our senses, whether it's reading mentally.

And then when you look at the devices, and from a physical standpoint, we're spending too much time seated. We're spending too much time at the computer and staring down at these things. So all of this combines to really put our nervous system in a situation where it's being activated. It's being triggered and stimulated, but we're also giving it a confused signal like, okay, we're seated and we're sort of in this crouched, uh, you know, uh, um huddled position. When from an evolutionary standpoint, we were designed to move. When we see—when we see a threat, we run from it or engage it, and then we recover.

Yeah. I think about like my life and sort of running multiple companies, and the fact that I just kind of go from one thing to the next. The only time I can get the gym time in during the week is early in the morning, because by the time I'm into my day, you know, I'm talking to people way earlier in the morning than I even get to the gym.

And then by the time I get to the office, I mean, it's just an onslaught. At the end of the day, sometimes I just go home, and I'm so kind of wiped out. Um, you know, I'm going to try to get my postprandial walk in to make sure that I kind of keep my insulin sensitivity up.

But I also find myself at times playing chess. Uh, you know, I'm a chess player, and I always have loved the game. But I noticed recently that the higher the stakes are with regards to the chess match, um, the more stressed out I'm getting. And it's actually not relaxing to me in any way, shape, or form, uh, and I—I'm starting to think I need to actually kind of chill out on the chess. Maybe limit myself to one game that satisfies that kind of urge to do that, but not play it incessantly like I—I was for a period of time. I go home and I just play game after game, match after match.

You know, you think about it, American culture—uh, we'll just focus on America and make it easy. We have this entire structure that socially revolves around things like drinking alcohol um and uh eating food that may or may not be good for us, uh and this entire sports culture that kind of exists around all of that. Um, when we take a look at that from a social standpoint, certainly that idea of going to a game with somebody and doing those types of things, going out to uh social settings where people gather, but there are all this—these things that are sort of permeate that uh that aren't really great for us.

Mhm.

So when you think about that, how are—how do you see the world sort of turning? How is it changing now that people are becoming more aware of it? I mean, the—the information that you've brought to the world about um this—this um sort of new way of thinking about cardiology um is so profound. How do you see like people changing their lifestyle? You see it probably every day in clinic, right? There are people that have decided that they want to go a different direction.

What do you—what do you see as the future of in this kind of world as it's—as it's hurtling? It's kind of a complex question. I'm not even sure how you would answer that.

What—the way I see it, it's that if you look back at how we've treated patients in the past, what the methodology has been for treating large-scale medical problems, it's been specialization. It's reductionist thinking. So we've created specialists. We've—and—and then subspecialists—people that are the—the electrical specialists of the heart, and they only do that, or—or the hepatologists that only look at the liver and not the rest of the—the gastrointestinal system. That's create—that's created many discoveries and advantages.

Yes.

But it's also created the very problem that we're facing right now, which is the reductionist thinking that one thing is going to fix a larger-scale problem. So if we want to take this back to the cholesterol discussion, this is a perfect example: that we keep thinking that cholesterol is going to fix all of the heart health problems.

You know, we look at the marker—the—the panel that the labs create. It's called a heart health panel. What it starts out with is your cholesterol. It doesn't talk about anything else. If we're lucky, it talks about a C-reactive protein or some inflammatory markers if that's a progressive-thinking panel. So you're dealing with reductionist thinking that looks at a specific marker when it really shouldn't be.

What we have to do is take a step back and go to a more global thinking. We've got to treat the whole person. We've got to look at all of their risk factors. We've got to look at not only the—the cholesterol—how is it being—how is it being created? Look at not the cholesterol, but the ApoB, right? See, I'm even being caught saying that, too. But look at the ApoB. Look at the inflammation. Look at the metabolic profile. Look at what other vascular issues they might have, genetic issues. Then you got to look at the psychosocial problems. It—it's a larger—larger assessment of overall patient health.

When I—when I look at patients that are coming in right now, they still ask me, "Okay, what do I do with my cholesterol?" And I'm—that's—and that's the last thing I'm looking at. I start with the panel just to make them happy and address their initial concerns. But—but invariably, it goes into: what do your hormones look like? How are you moving? How are you moving? What are you eating? How are you sleeping? Those are—are fundamental questions. What's your gut health?

I don't know any other cardiologists except for ones in functional medicine space that are doing stool tests to look for heart disease and treat it. That's part of the—the—the screening process and the treatment process in my patients. And invariably, I find people, even if they think their diet is pretty good, there's going to be some inflammatory issues that we can work on.

And inflammation, we know, is one of the—the keystones of creating not just atherosclerosis, but arrhythmias and hypertension. So we think that there's a singular thing that's going to fix our problems, and then we add up these singular things in a list of supplements and—and uh and pills. We've got to take a step back, remove that, and look at the whole picture.

Yeah. I think that's the—the beauty of what it is that you do, is getting that—pulling back from the myopic view of this one thing, and getting a complete view of: what are we dealing with? How do we address this patient from that—that place that allows us to have the—the—the complete picture and—and identify how do we start to work a plan to get heading in the right direction?

All right. So, you know, you said something that's kind of interesting that made me think about, um, well, is there one diet that is the right diet? Because we have all these different diets. We have carnivore come up, which to me seems maybe not such a great idea. Um, there's been keto, where it's like, hey, just live on fat. Uh, there's the Mediterranean diet, there's this diet, that diet—all these different diets.

Um, there's been one doctor—I'm not going to mention his name, uh, but he's been sort of all over the map and has had a lot of press, and been, you know, um an advocate of one thing one point, another thing another point, to this next thing. When you take a look at diet in the microbiome and the gut, what's the one thing you would say around diet that we should be focused on?

The diet that works best for you to keep you from overeating is a diet that is the one you should be following. Usually, that ends up being something like a higher-protein, Mediterranean-style diet. And I defer to that because it provides the right fats, it's got complex grains, and it has—has protein. But it also still honors the needs for vegetables, polyphenols, carotenoids—all of the things that we need to get from vegetables and fruit. It also honors the non-digestible fibers, which are vital for our gut health.

With all the stool testing we do, one of the things that I see most commonly is reduction in the amount of butyrate that our gut makes. Butyrate is vital not just for gut health, for colonic health, but for brain health. And there's even data to suggest it might help vascular health. So it's—it's the compound that our gut microbiome makes in response to fermenting non-digestible fibers. So that's a—a foundational thing that we need as humans, as omnivores.

If you're going to consume a carnivore diet that doesn't have any fiber, you're lacking some very important foundational things in—in our diet. And this is—you know, we got to look at this from an evolutionary standpoint. I—I whenever I have a question about whether what mechanism or what kind of behavioral changes I want to advise my patients to do, I look back to what we would be doing 100,000 years ago, because we're still in that same physiology. So we were a feast and famine creature. We would have the opportunity to make a kill, eat it, feast, store it, and then we would starve. And so we're not meant to have food availability all the time.

Or if we were lucky and we had food availability back then, it was a variety of foods that changed with the seasons, and even then, protein wasn't always available. So in that—we're keeping that in mind, our bodies adapted to that. It created a microbiome that responds to the foods that come from our vegetables, from our fruits, from those polyphenols. So we need those. We need to introduce those.

I'm not against keto diets if they're done in the right way, and if they're cyclical, if they're phased. Carnivore diet, you got to be careful with, because if you do have apolipoprotein(a) or ApoE4 genotype, then you probably aren't going to tolerate the high saturated fat very well. For the most part, saturated fat is okay. It's not the villain. Uh, but in certain populations, you got to be careful. So that's where the—the testing comes in again early on in life.

But when we're looking at diet, most people can tolerate it in good amounts. When you're talking about a carnivore diet, you're talking about your whole diet of saturated fat, and that's not a good idea, either. So I—I generally recommend a higher-protein, uh, low-carb diet, or higher-protein, uh, Mediterranean diet.

And then it also depends on the person. If you're an athlete, if you're a professional athlete, then you're going to need a lot more fats. You're going to need a lot more proteins. If you're obese and you're trying to lose weight, then it's going to be a calorically restricted diet, and that's where I might do keto and low-carb for a period of time. So it depends on what the goal is and what works for you.

You know, as I look at my macros and then micros, um, there's always this focus on macros, but there's not always a focus on the micros. And in—I think in the gym world, um, and I think, you know, I know how many grams of protein I want to get per day, the quality of that protein, you know, what's the carb amount, what kind of carbs those are going to be, and then certainly the fat—what—what kind of fat is that? Obviously, that's going to come a lot of times from the protein, but, you know, olive oil, things of that nature, are really high quality.

I really try to pay close attention to my diet now. I actually find it difficult to eat out a lot of times now. Um, so it's really kind of tough these days. The more I've learned about what's in the food, you know, uh, this hyper-palatable stuff with tons of seed oils and uh ultra-processed stuff that we're just not meant to really eat, um has found its way in, and it's got to be having a significant impact on people's cardiac health.

Sure. Yeah. And—and to your point, the more you engage in eating a healthy diet, the less you will be able to tolerate eating out. You're going to start feeling bloating, gas, and abdominal discomfort when you didn't before.

When I was young, I used to love going out to eat late. When I was in college, we used to go out to the grease trucks and eat after going out all night. And it would be either nachos, or pizza, or some other god-awful thing. I do that now, and I'm regretting it for a day, for two days, three days. And forget about uh drinking as much as I used to. I can't tolerate any alcohol now because the more I refrain from drinking, the more sensitive I am, and the more I realize how much it was affecting my mental clarity, my performance, my functionality, and just my mood.

So, you know, these things—the—the diet that we engage in has a—a profound effect on our mood. You know, it changes how we metabolize tryptophan and tyrosine and our neurotransmitters. So if you haven't done it, give it a shot, and you'll see that it will change your relationship with food and improve your quality of life.

Yeah, 100%. I mean, we should really talk about alcohol, because I think what people really don't—I mean, it's like if somebody said, "Hey, um, doctor was saying, I'd like you to drink this rat poison." You know, you'd say you're crazy.

Yeah. No social circle is going to have, you know, people gather around and let's drink some rat poison.

Yeah. But, you know, at the end of the day, alcohol really is a poison. Uh, and there isn't, you know, there isn't much benefit to it other than the—the way that it makes you feel in the moment. The consequences thereafter are probably really significant. And as we get older, they get worse and worse and worse.

Just how bad is alcohol? Because it does affect our sleep patterns, for sure, which—if I—if I'm not getting the right amount of sleep, that's when I'm getting grumpy. Yeah. So how—how bad is alcohol? And how much is that going to have an impact on our cardiac health?

I don't know that we can quantify it, but I can really—I can tell you that it's—it's one of the worst things we can do for ourselves, up there with smoking. Arguably, you know, smoking we know and it's documented, has horrible effects on your body. It's not the nicotine per se; it's the combustibles that we smoke when we light up a cigarette or a cigar or what have you.

The problem is uh nicotine's been lumped into that, and then um and—and but at high amounts that also causes a problem. With alcohol, there's really no positive agent in there that helps us. There is not—there isn't that nicotine component that might be helpful at low doses. The old studies that looked at whether alcohol was cardioprotective were flawed, and then they looked at spec—they didn't really tease apart whether what type of alcohol, how much, and—and what the effects really were.

Um, when we look at what it does metabolically, there are the—the effects that happen immediately. We get the—the um the intoxication that happens immediately, and we think that once that wears off and it's the next day, it's out of our system. But that is not true. There's metabolites that stick around for up to 36, 48 hours. And so those metabolites also have an effect on our metabolism and continue to decrease our cognition and—and poison us, and those are much more subtle.

So when we look at it from a cardiovascular standpoint, alcohol will reduce your sleep, increase your caloric intake because it will uh create insulin dysregulation and make you crave high, you know, high-potency carbohydrates that are highly processed, and those are so easy to get a hold of. Um, and then if you're, you know, if you're hungover, you're going to have a greasy meal, right? Someone's going to say, "All right, I'm feeling a little off. I'm going to go eat something to settle me down," and it ends up being something high-calorie and greasy.

So our food choices become completely messed up. Our sleep gets dysregulated. That messes up our—our cortisol, uh and—and it take—it'll take days for that to recover. So there's a lot of—a lot of downstream cardiovascular effects.

Now, our cardiovascular system is very resilient. If you take a hit like that once in a while, once a month, you're probably going to survive that, and it may not have a lasting effect. But if this is a regular part of your life and you're drinking on a regular basis, you're constantly changing your decisions. You're constantly changing your ability to make healthy decisions, and then you constantly are challenging your—the resilience of your system.

And um that shows up in higher—higher uh epinephrine, higher stress hormones, and those tighten down the vascular system, increase the adhesion molecules on your vascular system. It will create inflammatory burden, oxidative stress, and all of that drives plaque that may have been benign and inert. It now becomes active and becomes something that could be more prone to rupturing after you do that for a prolonged period of time.

Yeah. So either way you look at it, just not good.

Yeah, that's right. There's just—all the data is there to support that now, that it's like not a good—not a good idea.

Yeah. I mean, taking it back to the liver health, you know, looking at fatty liver disease, that's one of the reasons, mechanisms, we get deposition—another form of inflammatory burden that uh drives multiple forms of heart disease.

Yeah. The insulin piece is—the insulin sensitivity piece is really interesting. You said the GLP-1s, and then, you know, how that's impacting what's going on with uh uh cardiovascular health. We know that insulin sensitivity is like—like a big thing to look at these days.

Definitely. Yeah. And keeping it in the right ranges.

It's interesting, you know, I would imagine for you to come to the place where you are today with your specific knowledge on the system of the body. That's like so like—I mean, if your heart doesn't pump, everything's done, right? So, um, but now you look at the entire individual and what we just talked about—uh, alcohol. There were some studies that came out that clearly indicated alcohol was correlated with um cancer. Um, it's just like smoking.

So I think the reality is that we're in this point in time where people are starting to wake up. What's it like for you on a daily basis in your clinic? How many new patients are coming to you all the time wanting to learn more about how they can live a healthy lifestyle?

Patients are coming into the office on a regular basis looking for options on how to improve their—their lifestyle and reduce their risk. Cardiovascular risk is still probably—it's still the number one reason I see patients. They come to me because even—even if they want to optimize their health, there's always the caveat that, "Oh, I want to—I want to—I want to reduce my risk for dying of a heart attack and—and improve my heart health." After that, it's dementia, and it's—it's brain health for sure.

But there are patients that are coming in on a daily basis looking for this kind of help. We spend about an hour, an hour and a half with our patients on—with each of our appointments. Oftentimes, the evaluations are—are an hour and a half to two hours. And so it's a—it's a long discussion. We go through all of their aspects of their life, their goals, and then—and then, yeah, it's a—there's a high demand for this right now. People are hungry for this type of medicine. It's really just starting to take off.

And one of the things I think is really cool about your practice is you practice with Dr. Elizabeth Yurth. It was—I mean, you guys are leaders um in the—in the space. And what's really phenomenal—I mean, I—I'm just such a fan of her, so—

She's amazing.

Um, she is—I mean, you kind of get to like, you know, chills when you kind of think about some of the things I've heard her say. Wow. Um, the reality is, you guys are in a point in time where you have information that is so powerful, it can impact people in a way that um it really can change lives.

You know, I was on the phone this morning with Dr. Suzanne Ferree, and she said to say hello to you, by the way.

Yeah, she's fantastic.

Yeah, great. Um, and we're talking about, you know, the um dysregulation of the autonomic nervous system. Uh, this, you know, sympathetic situation that we find ourselves in non-stop all day long, and how do we get back to a paras—parasympathetic uh kind of reset? Um, you know, there's just comes up all the time every time I talk to her.

Yeah, she's a big supporter of all that—all that therapy, and—and for rightfully so.

Yeah, I think it's like—you think about it, um, in some ways we should talk—probably talk about that the next time we see each other. But the reality is like, you can do all the things in the world uh the right way, and if that's—if that's out of whack, um you're only going to get maybe halfway there. I don't know what the actual numbers are. It's probably N of 1 to everyone. But the reality is that you're not going to get the full impact of anything until you get that under control, uh which goes back to what you're talking about, the social side of things.

Yeah.

All right. I want to cover something that's really cool. You talked about it on Cell to Systems uh when you were on that show with us: the Cleerly test.

Yes.

This is huge. I didn't know anything about it until you told me about it, uh which I think is just amazing. The notion of being able to get a scan—well, here, listen. I don't want to do a disservice, so let's hear direct from you. Okay. What is it? How does it work? Maybe we can help the general population who's, you know, focused on peak performance understand: how does a Cleerly test, and why, impact them, and why should they—they should go get one right now?

Yeah, the Cleerly test is an add-on test for a CT coronary angiogram. So it's kind of what we lump together when we talk about a CT coronary angiogram with AI processing. So let's take a step back and talk about all of the testing that we use for imaging.

Right now, what a lot of people get is called a calcium score. And a calcium score is a CAT scan that just looks at the heart, and it just detects the calcium that's deposited in the arteries. Now, as part of our discussion, we've talked about how plaque forms. All right? Plaque will create and turn into the calcium. That's part of the plaque. The other part of plaque is the cholesterol. There's two forms of the cholesterol in that plaque: there's inert, usually benign or inactive cholesterol, and then there's highly inflammatory cholesterol.

When you get a calcium score, all you get is the calcium, and no assessment of that cholesterol. It still gives us a risk, but you could have somebody that doesn't have a lot of calcium, but a lot of cholesterol, and that's the person that dies of sudden cardiac death because they have a highly active amount of inflamed cholesterol. It gets missed. There is a population that oftentimes has developed a lot of calcium, and that will be detected. And so it detects that high-risk population, uh but it—it misses that—that middle—that middle ground.

And that's where that 50% of people oftentimes never make it to the emergency room. They may get detected with the calcium score, but sometimes not. A CT coronary angiogram is a CAT scan with contrast. A calcium score takes 10 minutes, no contrast, in and out of the machine. A CT coronary angiogram is done with contrast. It means you start an IV. Got to control the heart rate a little bit, and it takes a little bit longer. But it takes a look at the whole artery, the area inside the artery, and then it gives us pictures of the arterial wall.

That's important because it gives us all the information that I—that this—the calcium score misses. It gives us information about the arterial wall and how much cholesterol is in it. Now, you can take a—you can tease apart how—what the cholesterol composition is like, whether it's inflamed or not. They didn't do it in the past. And when I was training 5 years ago even, and certainly not 10 years ago, did they have the technology to be able to really tease that apart.

7 years ago, Cleerly started coming out. Cleerly takes the data from the CT coronary angiogram, puts it through a cloud-based AI system, and looks at each pixel and tells us what the density of that pixel is, and can then predict what type of structure is in those images. Is it inflamed cholesterol? Is it regular, non-inflamed cholesterol? Or is it calcium? And then it can tell us what's the degree of blockage in the artery.

So it is giving us far more robust information than we ever had. Even when we compare it to cardiac catheterization, which was when we would go into the lab and then put a catheter into the arm or the hip and take those pictures directly of the heart, because those pictures looked at narrowing of the artery, but could never tell us what was going on in the wall. So the Cleerly is that AI, cloud-based post-processing—the processing of the CT coronary angiogram that's an add-on that we can do now.

And the better the CT coronary angiogram, the higher quality, the better—better the Cleerly will be. So what this has done is allowed us to visualize the artery in extremely high detail and screen those people that are high risk for sudden cardiac death before they—before they have the event, before they potentially don't even make it to the emergency room.

It's expensive. It's starting to get covered by insurance, but it's certainly worth it to get looked at. Um, in my mind, everybody that can afford it, I think, should do it before the age of 40 so you can know what's showing up in your arteries. We can do all the biomarker testing we want, but there's still a gap in our ability to predict who's showing up with disease, and that's why these images are important.

You just made a clear distinction: the quality of that scan, of the imagery. So what's the difference? How do we get a different level of quality?

This is the machinery that we're using. It's both the machinery and also the way the machinery has been programmed. So the modern CAT scans that are best for—for imaging the heart are called—or they have what's called 256 slices. And so it's the—the slices are—that's the amount of slices that they—they image the heart in. Think of it like a loaf of bread, and the thinner the slices, the more quality—the better quality of images. So you get more data, and less gets missed.

128 is the next step down. Those are probably acceptable, and you can use those to still process data to get Cleerly. 256 slices is what we would prefer. So you could ask the center if they have that capability. Usually, they do, because if—if they're using it for coronary imaging, they have to have a certain quality of machine just to do that.

The reason why it's taken so long is because the heart—to get these images, like I said, only 5 to 7 years ago did it really start becoming clinically usable. The reason is because the heart moves all the time. It's because it's constantly moving. It—it—it doesn't sit still for X-ray or CAT scan or MRI images.

So, you know, when you—if you've ever gotten a chest X-ray, they tell you, "Okay, put your hands up," or what, "Stay still." You know, your heart doesn't do that. No. Only—only in between beats. So, which is why you got to take something to slow it down, too.

Sort of take some sort of like beta blocker or—

Exactly.

Okay. So long story short, you slow it down, and then they're looking so in between the beats. So it's taking the images of the slices, so it's at when it's at or contracted or expanded. So, okay, I get it. Um, so everyone should do this. It costs money. So I think you can get it covered by uh Medicare, right?

But at that point in time, I mean, shoot, if you're getting it covered by Medicare, your Medicare age is probably late. And then Medicare asks that the patients that are getting it have a reason: chest pain or shortness of breath. So that if it's reached that point, then it's pro—it's too late, you know? Or, you know, there's a young population that has those symptoms, and we need to determine if it is really heart disease. So those are the ones that can actually get it covered and—and use the indication.

Okay. So let's use me as an example. Yeah, go to the gym, train regularly, living, I think, a pretty clean lifestyle. Not perfect, but you know, I get better and better. I'm getting better and better. Uh, the more I hang around people like you, the more I learn, uh, the more I see, the more I go, "Oh, man. I got—" It's like—it's like this slow, iterative process that it's like—like little—just—just keep chipping away at it, and you keep going higher and higher and higher on what's acceptable for your lifestyle.

And I think what you said before is absolutely true: you get to a certain point where you look at like, hey, I can't eat that food, I can't drink that, I can't do this, I—because I felt so good. I don't want to go back there and check that out. So getting this Cleerly scan is an investment that's—I mean, in—in my eyes, uh, from where—where I'm sitting, that you—you just can't afford not to do.

Yeah, I agree. You—it is really important to get that risk assessment done. Now, it's not perfect, okay? This is the fir—there are all the other scans that can give us similar data. There's HeartFlow, and there's also another one called Caristo, which is coming to the United States. Cleerly is—is widely available and, I think, more applicable to the—the outpatient population that's looking for prevention. And it's still in the first generation, you know?

It's—this is not perfect. There are issues with the AI processing. There—there's what's called AI drift, which a lot of folks have—have complained about with—with Cleerly. If you run the same scan twice, it will tend to drift to show a little bit more plaque, which is a little disconcerting. But you got to give it that margin of error, all right?

And at the same time, if it shows up with a lot of plaque, it doesn't matter if there's a small drift. You've got a problem.

You're already there.

You're already there. You got to address it.

Yeah.

And so, you know, this is—we're doing a lot of screening now, right? We're—and you have to take the same mentality when it comes to, say, full-body MRIs. You know, you—we see something. Is it something that needs to be acted on? Is it something that is—that that is an emergency or—or—or a serious problem? That requires judgment. It requires a little bit of guidance from a clinician. And it requires that the patient don't be as anxious about every single disorder, every single thing that's detected, because humans are not perfect, you know? And there's going to be some irregularities in each human.

Yeah. You got to—you got to stay calm.

That's right. Through the whole thing, which is sometimes hard to do, especially people who are prone towards being anxious. And we know that there's, you know, a huge, massive population of people who are on SSRIs and um anti-anxiety medication. It's prevalent.

Yeah. There's another thing I wanted to bring up that you—you were kind of alluding to. Um, it's—it's timing. We got—we also have to remember that if you're getting the test after decades of—of not checking yourself, not living with a little bit of intention and—and—and care, you can't expect to reverse those changes in a short period of time. This is a—we're working on a long game here.

And unless there's high-risk plaque, high-risk disease, which requires aggressive therapy on multiple levels, even that takes years to reverse. But what you have to remember is, it's time under therapy, time under the right lifestyle. We can't expect to change everything quick. So it takes some patience and—and retesting.

So it—it goes back to the theory of a little bit back to the theory of ApoB, cholesterol. It is a true risk, but it's more about lifetime risk. What is your trajectory over your lifetime? And if you do make a trajectory change, everything that you built up before, is it going to reverse quickly?

You know, it's funny, you said "time under therapy" is almost like time under tension from a gym standpoint, right? We know we're not going to build muscle, especially, you know, as we get older, when we're fighting, you know, sarcopenia and—or anabolic resistance, is I would say. We're in this position where it's like the same thing: the older you are, the harder it's going to be, and you've got to be sort of patient and willing to actually go through that.

All right. So let's take it to the—you catch them early.

Yeah.

And then you're going to keep them on a regimen that's going to keep them in line. And you're going to be able to then look at—I mean, is Cleerly something that I'm going to do once? Am I going to do it twice? Am I going to do it three times? If I'm—if I'm early, like let's say I'm—I'm starting in my 30s, I'm going to Cleerly. Is that a stupid question?

Not at all. No, it depends on what we find.

Okay.

If, say, I find you in your 30s and you wanted to get screened, we do a Cleerly scan and it shows minimal disease. I don't need to do one for five years at—at least, assuming that we've managed your lifestyle risk and we've got baseline markers that I can track. If there's no major issues, five years.

And then we can—and there are ways to check in intermediate five years. You can do what's called a carotid intima-media thickness check, the carotid arteries. That's—that's cheap, and you can do that at the same time as getting a Cleerly scan, and then correlate—take the two. They—the studies show that the carotid should give us a good correlation with—with what's going on in your coronaries.

It's not directly correlating, meaning I do see patients that have discrepancies, so that's why I like to get both. But when you get both, I can correlate what's going on in both those arteries. This is easy to screen; it's an ultrasound, it's cheap, and we can do it annually if you wanted to. We can track that over time and then delay having to do a CT coronary angiogram.

So the—in somebody that's healthy, it's probably a one-and-done test for a long time—minimum of 5 years. If you're—if we do see some plaque and we're making some changes, we reduce that to maybe three years, and we can still use this—the carotid intima-media thickness testing. If it's stable, maybe we push that out to five years, too. If you have aggressive disease and/or if there's high-risk disease, then we're looking at a lot of changes and something we want to track regularly. A lot of medications as well—two years, maybe even a year if it's high risk. So it—it really depends on what we find.

Let's imagine you get me.

Okay.

So I'm—I've never tested any of the stuff that you've talked about.

Yeah.

So I've never tested those things. I've never had a Cleerly—Jock, sir, I know it's terrible. And—and I—the last time I saw you, uh I was like, "Oh, man. Uh I gotta do this." And so I started to investigate it immediately. But the reality is, I'm probably going to have to come see you, because that's just the way it's going to happen to me.

One of the things I wanted to ask you is, let's imagine—uh, I'm not going to freak out, by the way. Uh, let's imagine it's bad. It's bad.

Yeah.

And you're like, "Dude, you're the guy that's going to be—never going to make it to the emergency room. You're going to be training in the gym one day, and you're going to keel over and die."

Yeah.

That AED on the wall over there, uh, is that what it is? A—that's not going to do anything. That's not going to save you, right? So bad. What do we do then? What do—what's—what's when it's really bad? Yeah, how do you handle that?

Well, I try and calm the patient down first. I try and calm you down. There's a lot of treatments that we would have to start, you know, where we're looking at different ways to mitigate the inflammation. All right, we're looking at ways of lowering the ApoB. So it's going to be multi—multiple therapies for that to help reduce the risk, help your vascular system start to uh to be able to remodel itself, reduce the inflammation, and change how your metabolism is depositing and progressing, advancing that plaque.

What you do is, you give them the—the precautions. You let them know—I'd let you know that if you're having chest discomfort, if you're feeling short of breath, if these are the things that are even close to suggestive, then go get help. We also need to do physiologic testing.

There—there's a—a difficult in-between space when you have plaque that's not exactly enough to decrease the blood flow, but it may be highly inflamed and reactive. That's the really high-risk patient because they feel great. They're exercising. They don't have any limitation, but they've got that thing that's—that's a ticking time bomb.

Yeah. It breaks loose, and boom, you're done.

Yeah. And so that's what we want to check with the Cleerly, because there are things that can be done, and it's a multi—multiple amounts of medications and supplements. Uh, and—and then there's frequent follow-up to see what the biomarkers look like. There's something that we can track. If you have that much risk, it'll show up on your biomarkers, and we can track how that's reversing.

Yeah. That—the reason that I asked you this question um is—it sounds self-serving uh for me, and in some ways, you know me, I always call it like it is.

Yeah.

I definitely wanted to hear from you uh that piece.

Yeah.

But the real question is for the listeners. We have a wide range of—of uh listeners and viewers on this podcast. We reach a lot of people. There are a lot of, you know, we're in the—in the tech community, so there are a lot of, um, you know, people in the tech business, uh, and AI is booming, and we develop AI technology, and so I know about drift and hallucinations and all that kind of stuff, right?

Um, so we have this younger group that I'm trying to hope that they will take action. I have the money, so let's take action. Let's get after it. And then there are the older uh folks that have been around that are tech veterans. And what I'm hoping they'll—they'll hear from this is: do it now. Find out what you're really dealing with. Don't put your head in the sand and hope that it's okay, um because there actually is something that can be done.

I think we all wondered, right? Holy smokes, what can I possibly do? And is it too late for me?

Yeah.

What I think I'm hearing from you is, it may be really bad, but it's probably not too late.

That's right. And even if it is bad, you can get a stent. You can get something done that's relatively non-invasive or—not—it's an interventional procedure, sure, but it's not open-heart surgery, and it's not the end of the world. And it can—it can definitely save you from having—from having symptoms.

But unless you have symptoms and that blockage is significant—meaning greater than 70%—because that's—that's the—the cutoff usually, when we look at hemodynamics in the blood vessels here, it's got to be more than 70% blocked for it to really impact blood flow, even at exercise. So you could have from 70 down to, you know, 40, and that range is where we start to see that risk happen.

Yeah. So—so you can get a stent to put in, and that's not the end of the world.

But the amazing thing, and what really excites me about cardiology right now, is that we are in an age like we've never been before. We're talking about like space-age types of treatment that we feel like we have at our disposal right now. There are so many medical tools that we never had before.

And I'm talking about when I started 20 years ago, the only thing we had was aspirin and a statin. And that was all we could do. I mean, and all I could say to patients was, "You're screwed." All right? And there was no other way to really treat them except say, "Okay, exercise. We'll watch you. If this plaque gets worse, we'll have to put in a stent."

Now, when we combine these therapies, the experimental data shows that we can potentially reverse plaque. I've seen this happen clinically with our patients when we aggressively lower ApoB in the right situation. It doesn't have to stay low for that long, but there's a way to now reduce the amount of plaque that you had, and we can document it with the pictures. So this is an era like we've never been in before that really makes it exciting to practice in cardiology and help people work their way through this.

That's an amazing and uh uplifting thing to hear, that notion that we're making progress—what everybody wants. Um, and the—the fact that you can actually really target it, address it. How does that happen? How—how—I mean, through the combination of all of these medications and modifications of lifestyle, etc.

When we have plaque in an artery, let me say we're at 70%. Where does it go? How do you take that—that inflammation down, reduce that? I mean, my understanding is that it gets underneath and it starts to bubble out. How do you actually reduce it from that? How—where does it go? How do you get it out?

That's where the reverse cholesterol transport happens. So that's when our HDLs are important. So HDLs will be able to go to those areas, and the—that—that lipoprotein A1 particle as well as the enzymes that are associated with HDLs can help to calm down and then pull those—that—that cholesterol that's deposited out. They can remove it and then take it back to the liver.

So that's—that's probably where the most amount of research and advancement has to happen right now—that reverse cholesterol transport—because we've really figured out the process of development. We've got to really tease apart and then figure out how to—to—to tweak, improve this process of removal. And I think that's where the next phase of cardiovascular development has to go.

It's an exciting time, right? It's sort of—we're into this point in time where we're constructing things that are like—require serious engineering.

It does, because we can't target a specific lesion. We can hope that the body will be able to impact change in a specific lesion, and if—and oftentimes, we can see some regression, and it happens globally. And it'll go to the area that—that has—or will pull from the area that has the most to pull from, usually. Um, but it can't be guaranteed, and so results do vary.

Um, we can't, you know, we can't guarantee that a—a high-risk plaque is going to reverse, but we can stabilize it. We can reverse the inflammation in that, um, because that's where the body is going to take where the—these compounds we give it, and where it's going to affect the improvement.

It seems almost like spot reduction of fat, right? So we have, you know, visceral body fat, and then subQ body fat—subcutaneous body fat. And it almost seems like the same principle: the notion of, hey, we can start to reduce fat overall, get our body fat percentage down. It sounds like almost the same—same thing. And so you can't say, "Well, I just want to target my android, the area around my belt." I—I've got to reduce everything in order for that to happen. I got to do certain things in order to—to make that happen of diet, lifting, cardio, etc. Um, but that's really exciting. That's so cool.

All right, time to check in on the ketones. You're a frequent flyer on those. Um, how do you use them, by the way? I'm just curious really quickly before we go too much further. Do you use those pre-workout? Do you use those—

Uh, there's just—it's multi-use. I—I have a steady supply of ketones at home. I—I will use them for a lot of different processes. So, yes, in the morning when I get up, I have my coffee. I love my coffee; it's my ritual. Uh, I love the taste of it. But I will also have a—a jug of water, and in that has ketones.

Mhm.

Uh, and that's my pre-workout. It gets me awake, gets my brain going. Uh, and one of the things that I do in the morning is uh I do something that's non-medically related, something creative—work on an instrument or do something like that, do some reading. It perks me right up so that I'm dialed into that, and I get the most out of that. And then I hit my workout. If it's a heavy workout, then I'm going to do it again afterwards.

Good.

Um, and then throughout the day, depends on how my energy goes. If it's been a crazy day at the office and—and my brain is feeling taxed, one of the best things for me to get back into alertness, back into focus, is another dose of ketones. I can do that, maybe mix a little creatine with it, and bam, I am ready to get back into it. Um, because mental processing is very different than physical processing, and ketones help both.

Really true. So I—I have a protocol that's personal to me that is very similar to yours. Um, so I get up in the morning, I'm taking water uh and then EAAs. Uh, I like the Perfect Amino, and so I take those with ketones pre-workout. Um, and then I get a little caffeine in, which—I tried doing it without caffeine. I tend to just like—the caffeine with the ketones works better for me.

Yeah.

Um, and then, uh, mid-afternoon, going to use those uh again. Uh, just kind of like keep me going. Um, and then at night, I like to take them before I go to bed.

That's right.

Which is really interesting. They're—they're, you know, anti-catabolic, obviously. Um, but they also have an effect on uh GABA, right?

That's right, yeah. Improving deep-wave sleep.

Right. Right. Yeah, so I—since I've started doing that, I found that uh things are just much better for me in my sleep. And—but you got to take a really small amount, right?

Yeah, you can't take like the regular dose, because otherwise you're going to be kind of like energized, right?

That's right, yeah.

So, you know, Dr. Hussein, it's been a pleasure, and it's always—and every time I see you, I'm just like—I—you're just uh a pleasure to be around. The one thing I would—yeah. Uh, thank you for coming. Uh, one thing I would ask you: you have so much more to share uh than just the cardiology portion. Your practice is way beyond. I know your panel is really full. It's hard for anyone to get in to see you.

So there's some other things I'd like to talk to you about in the future. I'm wondering, you know, tall order asked you to come back, but would you come back and visit with us and—and—and have another session so that we could talk more about these things?

Sure, Jock. I'd love to. It's been a pleasure to be here, and thanks for those kind words. I'd love to come back and have a discussion about everything else we do at the office there.

Yeah. Well, you're truly an inspirational guy. Uh, I always love to listen to your lectures, and uh you're—you're just a—a phenomenal person. So thank you so much.

Thank you.