Understanding Human Health Systems for Healthy Living

This session was on Understanding Human Health Systems for Healthy Living. Josh Wageman is a Clinical Lipid Specialist who practiced clinically in Endocrinology. His PhD work focused on cholesterol disturbances in Alzheimer's Disease. Although he has a Doctorate in Physical Therapy, he is best known for his role in teaching lipid physiology. He serves as an adjunct professor at several medical programs and is the author of the book, "The Home Security System and the Lipid Neighborhood," which aims to bring "clarity and hilarity" to a historically contentious, confusing, and controversial topic. His goal is to prevent heart attacks, strokes, and dementia by explaining complicated biochemical concepts in a relatable way! 

Transcript

SPEAKER_01 0:00

All right, good morning. Good afternoon. Good evening. I'm excited to be here today on this episode of solution in the minute of the podcast. I'm excited to yeah, we might guess we're gonna be talking about understanding how the liberty very unable to clinical physical geology. There it is. Yeah the whole security system and liquidity never hood. This is the book we're gonna be talking about. Right. And if you're here, I suggest please put in the comments that you're here, where you're joining us from. We want to hear from you. We want to hear your questions, we want to hear your comments and your contributions. Please also welcome Josh, the lipid guy. I see that you changed that.

SPEAKER_00 2:02

Yeah, thank you. Thank you so much. Thank you for those kind words. And and basically all of that is can be summarized to say I have very few useful skills except going to school and taking tests. But then after I go to school and take tests, hopefully I can then disseminate what I have had the privilege of learning in a relatable and even fun way. And people read my book, The Home Security System in the Lipid Neighborhood, on cholesterol, and they're like, wow, I never imagined I would laugh so much reading a book about lipids. And I say, Well, yeah, you know, that's the best medicine still sometimes. And so anyway, it's I've been very, very blessed to have many adventures. And the best part of all my adventures is the amazing people I get to meet along the way. So I'm really happy to be here.

SPEAKER_01 2:50

Good, good. Thank you so much for being here. Of course, the book was very exciting. Uh, we're going to be discussing that today. I mean, so you know a lot about lipid, and uh, we can basically call you a clinical lipid specialist. So, my first question is who is a clinical lipid specialist?

SPEAKER_00 3:08

Yeah, so with clinical lipid specialists is interesting because when you're a physician, you can actually take the board exam to be a clinical lipidologist. But there's a very, very similar, nearly identical board exam that you can take if you're a PA, if you're an NP, if you're just somebody who decides to become a lipid geek, and you you maybe you read this book and you get the itch and you just want to join the crowd to be a lipid specialist, and you can sit for that board exam. You generally have to have some clinical experience in some capacity, but there are people who are registered dietitians who are clinical lipid specialists who have taken that board exam. And so I think it's fun. I mean, I think tests are fun though, because I'm kind of a weird guy, but I take I I have actually helped many physicians study for their lipid board exams. I've helped many other advanced practice providers study for their lipid board exams. I like these things and I write books about it. So that is official by board certification, one of the many things behind my name, because it it's this obnoxiously viscous alphabet soup of letters. You're like, what does this mean? And I fancy myself as some sort of academic platypus. But ultimately, it's what I'm best known for these days because as Toled mentioned, my first doctorate was actually in physical therapy. And so, anyway, that was an interesting segue into being the lipid guy I am now. But, you know, movement is medicine, motion is lotion. And, you know, if whatever the question is, if exercise is the answer, I feel pretty good about that. However, there are many, many amazing, fascinating things that go into the biochemistry of cholesterol homeostasis in our body. And for me, orthopedics is amazing, but they're not discovering new bones in your lower leg, you know, on a on a regular basis. Whereas with lipids, I have been very blessed to learn a bunch of stuff about lipids and I learn new things every day. And I think it's amazing and an amazing privilege to be able to continue learning something every day. And if you can immerse yourself in a topic that you know that you're never gonna learn at all for sure, then it's a it's a pretty cool thing.

SPEAKER_01 5:22

Wow, interesting. Thank you for sharing that. Josh the lipid guy. So that means that you know a lot about home security systems and lipid neighborhood. Uh liquid neighborhood. And that's part of what you had in your book. Yeah. As a way of introducing the topic today, what what do you what how would you describe the home security system under the umbrella of the lipid neighborhood?

SPEAKER_00 5:49

Yeah, yeah, yeah. So so really there's a lot that goes on when it comes to not having heart attack, strokes, and dementia. And whoever you are, for the you know, 14 people worldwide who are live right now and listening to this or or whoever, you know, I know that you and I both don't want to have heart attack, strokes, and dementia. So, how can we simplify these things? And so what I say is if you are that person who wants to optimize the years that you have been given, I want you to have a great home security system and I want you to live in a safe lipid neighborhood. Your home security system has four basic pillars: normal blood sugar, normal blood pressure, keep inflammation low, and don't smoke or do drugs, because those are bad. But then your lipid neighborhood, that's your cholesterol panel. Because every APOB containing particle, the vast majority of those being LDL particles, are potentially criminals that can infiltrate your arterial abode. And then the LP little a particles, those are potentially the felons because per particle, if you picked the wrong parents with that genetic lipoprotein, those are about six and a half times as likely to cause mischief in your arterial wall if they get in there, then you're run of the mill LDL particle. And so, back to our home security system. No matter what, across your lifespan, nobody's New Year's resolution is to be more insulin resistant. Nope, that's an axiom. Nobody ever says, boy, I wish my blood pressure was more out of control. Also, no, life is not better systemically inflamed versus non-inflamed, and then drugs are still bad despite what the kids are doing these days. And so those are your axioms. No matter what, you can take those things to the bank. And there are very few things in biology that are binary. We want them to be good or bad, but rarely is that the case. Most of the time it depends. However, those four pillars of the home security system, you can be pretty confident that you want those in working order, no matter what your lipid neighborhood looks like. But let's look at your lipid neighborhood. We don't want to ignore that either. Because every one of these particles, these LDL particles, these APOB containing particles, is potentially a criminal. Not necessarily a criminal, but potentially. Okay, well, what kind of neighborhood are you living in? And so on paper, it can look like you're living in a rough inner city neighborhood, but people don't live on paper, do they? And so, do we have better ways that can inform our decision-making process about potentially moving to a safer lipid neighborhood? We do. And so one of my catchphrases, because I have lots of catchphrases, is got plaque, get a CAC. What's a CAC? Coronary artery calcium score. I call it the colonoscopy of the heart without the nasty pregame show. Because you lay down, and a low-dose CT scan shows if you have calcified plaque in your coronary arteries, which means there's been a break-in. And that's a late finding in the atherosclerotic disease process. And so if you've been broken into, well, hmm, do you want to keep living in the same rough lipid neighborhood that got you broken into, or do you want to maybe consider moving to a nice, safe, gated community with fewer lipid criminals? That seems reasonable, right? And so that's just the kind of the basic framework for the home security system and the lipid neighborhood. And then I all throughout the book I elaborate on the individual pillars of the home security system and then all of the things that go into making your lipid neighborhood a nice place where we can live happily ever after.

SPEAKER_01 9:03

Wow. Thank you so much for explaining that. It's more like the body we have is like a house, and when it gets broken into the problem that needs to be fixed. Thank you for explaining that. So I mean we can quickly hide the fact that all this can lead to medical emergency. So basically experience with clients, with research and things like that. Are there specific situations where by these breaking into houses that led to medical emergencies? That you that you remember somebody in a very serious situation or that it's almost like they're not gonna make it, and things like that. Any particular one that you remember?

SPEAKER_00 9:51

Yeah, so what's what's funny about this is usually when people get into lipids or they get into preventive cardiology, it was because of some personal experience, you know. And I I wish there was some more humanitarian reason that I got into lipids, but really I was sitting there on a dark January day many years ago, and I had one of my patients cancel, and I'm always reading stuff. And I pull up this article, and it was the title was just something obnoxiously condescending, like basics of lipids and lipoproteins. And I'm like, okay, I'm you know, I'm pretty good, pretty good at biochemistry. How hard can this stuff be? And so I read this article, which was supposed to be a rudimentary review of cholesterol homeostasis, and I barely understood any of it, and it made me mad. And so I'm like, well, that's unacceptable since this is pretty important, you know, and a lack of cholesterol is incompatible with life, but a cholesterol-laden perpetrator in the wrong place at the wrong time is going to lead to the cascade that results in a maladaptive immune response that can subsequently result in clinical events like heart attacks. And so I was like, okay, well, this is probably worth learning, and I'm going to try to learn everything there is about lipids. And what's amazing is you will inevitably fail when you try to learn everything about any topic. But in the process of failing, man, you can learn a lot of stuff, and then hopefully you can help some people along the way with all the stuff you've learned. So that's how I got into lipids, but there have been so many, so many amazing things that have happened because I immersed myself into lipids because I was rankled about not understanding an article. And so one of the stories, and this is a story I tell in chapter six of my book, which is about LP little A, which is the felon of the lipid neighborhood. And really the reason why LP little A is, well, there are many reasons it's so nefarious, and we're still elucidating the specific pathophysiology of it, but it's an independent risk factor for cardiovascular disease, meaning you can have what looks like a fine lipid neighborhood. Even your LDL cholesterol and your APOB can be, quote, normal. But if you have elevated LP little A, you are still at heightened risk of having cardiovascular disease. And so one of my good friends, and so we were, we actually met and we were running together. I was helping him train for the Boston Marathon actually and qualify for that. And we were out on a run at 5 30 in the morning, and I was talking about lipids, of course, because what else would you talk about at 5 30 in the morning on a run? And and and he starts telling me about his family history. And his family history was really pretty bad as far as people having cardiovascular disease. And I was like, huh. And I was like, Well, have you gotten your LP little A checked? And have you gotten a CAC? You know, that coronary artery calcium score. And the common question, and he's he's a medical professional himself, and he worked in dermatology. And so he's like, Well, what's that? And that's what I hear a lot of times is what is that? What is a CAC? What is LP little A? Because these aren't, to this point, these haven't been traditionally taught in in medical programs. And so I think the the landscape is shifting there, though, thankfully. And so anyway, so we start talking about the LPLA, the fellow into the lipid neighborhood, and CACs. And so he ended up going and getting this LP little A checked. Well, his LPLA was 128 milligrams per deciliter. And there are various ways to test for LPLA. The preferred way is nanomoles per liter, which gives you a particle count, and then milligrams per deciliter is mass. But regardless, 128 milligrams per deciliter is really high. And then he gets his CAC. And a CAC of zero means that, hey, there hasn't any evidence of break-in as far as calcified plaque goes. And then conversely, a score of 300, you have equivalent risk of having a heart attack as people who have had prior heart attacks. And so his CAC was 2,814. 2,814. And he actually ended up having to have a five-vessel coronary artery bypass graft because he had such extensive atherosclerosis. Now that's an amazing story, but here's the deal: he had no other risk factors. He actually had no insulin resistance, even by my advanced standards, okay? Because most people are insulin resistant, which is not picked up on just your basic fasting glucose, A1C. And so he wasn't even insulin resistant by my standards. He didn't have hypertension. He had no systemic inflammation. So we had checked his HSCRP, which is a common marker of systemic inflammation. It was 0.4. So he was totally fine on that. And he had decided not to do drugs, which is good. And so this guy had a perfect home security system, and his LDL cholesterol was not remarkable at all. But he had this felon of the lipid neighborhood and it had caused lots of problems and had committed serial crimes over the past decades, apparently. And so that is a good example of, hey, just knowing a couple of things. LPL delay and CAC can help you identify somebody who would go undetected by our standard risk calculators. Because a lot of times clinicians are taught to use a 10-year risk calculator. And now there's this new prevent risk calculator, which is a 30-year risk calculator, which is, you know, trying to it does some good things as far as identifying a few more things than the standard 10-year risk calculator does. But those risk calculators miss a lot of people, unfortunately. His 10-year risk calculator was 2.3%. 2.3%, which is the low risk category. And you're told, hey, keep on doing what you're doing. You're good. Keep keep crushing it. But no, I mean, he probably wouldn't be alive if we hadn't gotten these, his LPAA checked and that CAC. And so I'm a big fan of being preventive and shifting the paradigm from reactionary to preventive when it comes to cardiovascular disease. And so that's a pretty remarkable story of just a couple different things that you can easily add in, whether you're a primary care clinician, whether you're a cardiologist, whether you're an endocrinologist, whoever you are, whether you're a patient who goes into your doctor and teaches your doctor about these things, which does happen if they're willing to listen. And then, hey, that's good because we can identify things before they become problematic. And I'm really grateful that we were able to identify that. And what's really cool about this guy is it was last year, it was, it was actually, no, it was 2024, that he had his bypass graft. And then last year he was able to train and complete this half Iron Man triathlon and not only complete it, but he did so well that he actually qualified for the world championships for his age group in France. He didn't end up going and doing it because of other life obligations. But I mean, that's that's pretty awesome. So when those stories are continuing to be lived out, that's a it's a neat thing, and hopefully it inspires people to get the itch and to catch the bug when it comes to prevention as well.

SPEAKER_01 16:43

Good, good. Thank you. Thank you for explaining that in detail. So you mentioned something now the absence of incompatible. I was tiny, a lot tinier than these, and my dad would say, Well, this guy needs to eat eggs one egg per day. And I didn't know why that could be the solution. When you say, Well, cholesterol very important to life and absence of each is incompatible to life. That kind of made me remember that experience when I was growing up. So thank you for the same thing. Yeah.

SPEAKER_00 17:30

And honestly, that's there's a couple things to that. So what we see on a blood panel, you know, when you get your cholesterol panel, that's only about 10% of your total body cholesterol. Because every nucleated cell in your body synthesizes its own cholesterol. Cholesterol is a critical part of cell membranes. It's a precursor for steroidogenic hormones, it's a precursor for bile acid synthesis, uh, 20 to 25% of total body cholesterol is in the brain. So it's very, very important. And so that's why every cell in your body that has a nucleus will synthesize its own. But really, what we see on a blood panel is just the cholesterol in lipoproteins. And lipoproteins are basically mailmen. You know, the APOB lipoproteins aren't inherently bad, but their job is to be mailmen. And what do the mailmen deliver? Well, triglycerides primarily to the adipocyte and the myocyte, and a few phospholipids, a few fat-soluble vitamins. And then what are they supposed to do? Deliver the mail and then go home to the liver at the end of the day. However, if the mailmen, instead of delivering their triglyceride packages, start delivering plaquages to your arterial wall, and the mailmen are bad drivers and they get in the wreck, then, well, some well-intended inflammatory civilians rush to the scene, but in the effort of trying to clean it up, a lot of times they make it worse. And it's that maladaptive immune response that ensues in the arterial wall at the scene of the crime, so to speak, that results in plaque formation and that can subsequently result in clinical events down the line. And so really these things aren't necessarily good or bad. It's a matter of if everybody's doing their job and the malemen are doing their job and they have a good GPS system and they find their way back to the liver at the end of the day, then we're all good. However, there are a lot of factors, especially the home security system elements, that result in these mailmen unfortunately getting lost along the way. And specifically, too, if they get caught in a sugar storm, uh as in people who have diabetes have enhanced risk of cardiovascular disease, even when their LDL cholesterol levels appear, quote, normal. Well, the problem with that is their mailboxes are full because of insulin resistance, and the mailmen are driving around and they get caught in a sugar storm. Anybody who's ever gotten caught in a storm knows how difficult it is when you're in a whiteout and you can't see anything, it's terrifying. And I even live the song Jesus Take the Wheel at one point because I got caught in a blizzard and my car rolled off into the side of a snowbank. That was terrible. And so, anyway, so these things are difficult, and it's no wonder that people with diabetes actually have enhanced risk of cardiovascular disease. If you're caught in sugar storms, then the mailmen probably aren't going to get to their destination. And so, anyway, so there's all these factors that result in a traffic jam or a traffic wreck, and we don't want that. And so that's why we need to look at all the things. We don't need to just look at your lipid neighborhood, but we also need to look at those pillars of the home security system. And it's more than just putting in some numbers into a risk calculator, it's about understanding the individual utility of each biomarker and what to do about it for that person. And so that's what I encourage my students and anybody else who I'm talking to to evaluate is understanding each biomarker and what it means and what to potentially do about it. And then with your with your egg thing, I mean, in general, the cholesterol in food has pretty minimal effect on your blood cholesterol. It'll it'll go a little, maybe, but then there's always exceptions because there are people who are hyperabsorbers who they start eating eggs and then their blood cholesterol jumps up a whole bunch. But most people, it doesn't have much of an effect on that. And there are specific reasons for that. And I I discuss that in my book, and I'm always happy to discuss what happens when you do eat an egg, if people are interested in that.

SPEAKER_01 21:11

Yeah, wow, thank you. Thank you for I like the way you're explaining things, the analogies and things like that. Because when I teach in a class, that's what I try to do uh with my students. At least those that really want to pass the class, they will pass the class because the way I explain things, uh the the analogies, the examples, the mailmatch, and things like that. I really appreciate that. If you hear uh please put your name in the chat when you do the question for the liquid guy, liquid questions and non-liquid questions, and we have to take any of those questions in the chat. Um I believe one of the biggest reasons like we can what does that mean? And do you are you do you think the situation has changed or is it becoming better?

SPEAKER_00 22:27

Yeah, so I've been on and I I tell this story in my book. I've been on this quest against mediocrity since I was in first grade. And it's kind of a funny story because I was, you know, I was in first grade and I had this blonde bowl cut actually. And so I was I was really, really rocking it at the time. And what's also funny is I couldn't see. So I have really bad vision. And so this was back in the day of chalkboards because I'm old. And so I would just go up to the chalkboard, I would memorize everything on the board, then I would go sit down because I couldn't see across the room. I just figured everybody did that because I was in my little world of blindness. But anyway, so maybe that helped me, but just because I remember everything now and I was forced to because I couldn't see anything. But anyway, so in first grade, I was you know crushing it on all my spelling tests and getting all my assignments done and all the things. And so they had this thing called breakfast of champions. And if you were apparently a good student, then you got to wake up even earlier than normal and have a cinnamon roll and some chocolate milk and your picture taken with the principal. And this was, I thought, the pinnacle. This this meant that yes, I am doing what I'm supposed to do in first grade here at Meridian Elementary. And so the first month of school goes by, and I get this Breakfast of Champions award, and there's this little certificate, and it goes up on the fridge at home, and I'm like, yep, I've I have truly arrived at the at the pinnacle of elementary academia here. So, you know, I'm feeling pretty good about that. And then, you know, the next month goes by, and there's a couple other kids in my class, and you know, they they get the Breakfast of Champions Award. I'm like, okay, that that makes sense. They're at least literate and not completely disruptive. So that kind of made sense. And then then this the school year goes by, and everyone is getting a Breakfast of Champions Award. And then the final straw was this kid who was just a disaster. He was always in the principal's office. The only thing I ever saw him do is just eat his own boogers. He was just his weird kid. And he he was not a good student or a good example. And he got the Breakfast of Champions Award, and I was like, that's it. So I went home, I ripped off the Breakfast Champions Award from the fridge, threw it in the trash, and said, okay, this means nothing. And so that was actually in first grade. I recognized, you know, a lot of these awards are just silly. And even nowadays, I mean, people will go and whoever gets any award, and even in academic circles, I mean, they just it's usually a quid pro quo. You know, you got it last year, I'll give it to you this year. We published on a paper together, you know, and and it's it's more comfortable just to rub shoulders with people who always agree with you and drink your Kool-Aid, probably for disingenuous reasons. And so I observe all these things, I think it's obnoxious. And so I think that it fosters a culture of group think and a culture of mediocrity. That said, I would hope that the landscape is shifting because of genuine people, because of people who truly care about shifting the paradigm from reactionary to preventive, for us to understand a little bit more about the home security system and the Lip and Neighborhood. And I and I'm encouraged. And even if it's not changing on a broad level, I know it can change at the individual level. And no matter if you're in a system that's mediocre, if you're in a healthcare system that's oppressive, if you're in any whatever system, you can be a transcendent paragon of excellence no matter where you're at. And that that's on you. You know, you don't have to just continue just checking off boxes and doing the bare minimum. It's awesome to actually see how well you can understand this and how you can have expertise in the subject and do the best you can because people's lives are at stake. And if you're in a clinician, if you're a clinician and if you're in the position to help somebody with their lives, there's some things I think you should know. And that's why I write books about this stuff. And, you know, I can't work with somebody who doesn't care. And I can't work with people who won't listen. But if you're willing to listen and you care, hey, let's go have some fun together. And I can learn from you, you can learn from me, and then people's lives are going to be better because of it. And so one of the things that is is difficult is there's a lot to lipids. And what we're taught in medical programs, even fantastic medical programs, is LDL bad, HDL good, everybody take a statin. And there's a lot more to it than that. And so I think that hopefully with books that I write and other people who are really good lipid educators, that we can actually help flesh out some of the didactic programs for medical students, for PAs, for MPs, for anybody who is in this and in the position to help people with their cardiovascular health. And then we can hopefully elevate the level of the education being purveyed because that's going to help a ton as we go forward.

SPEAKER_01 27:16

Good, good. Thank you. Thank you for explaining that. Again, if you're here, please put your name in the chat. Questions for your journalists. If you have a comment or you have a contribution, it doesn't have to be a question. Um for people who have autos.

unknown 28:03

Yeah. Yeah.

SPEAKER_00 28:03

So there are lots of factors with this. And one of my mantras, because I have many of them, is control your insulin, control your life. And I have I have a t-shirt that says control your insulin, control your life, and I'll wander around and people will wonder why I'm wearing a shirt that says this. And then we get to talk about metabolic health and the importance of not being insulin resistant. So, anyway, so to put it, there are many avenues we could go on, and this is chapter one of my book, but really the most simplistic and straightforward as it relates to the lipid neighborhood is insulin is a storage hormone. And so when you eat, insulin should rise because its job is to put the clothes in the suitcases, so to speak, or put the mail in the mailboxes, if you want to use the mail metaphor. And as long as your mailbox isn't full, as long as your suitcases aren't full, then you're able to put the mail or the clothes in, and then you can go on your merry way. And so really you're storing it for later in the adipocyte, or you're using it as fuel in oxidative tissues. And that's how it's supposed to be. However, if you are in a chronic state of overnutrition, well, and you continue to eat, well, what happens? Well, the mailmen are trying to deliver the mail and the mailboxes are full.

SPEAKER_02 29:17

Hmm.

SPEAKER_00 29:18

Well, those mailmen remember they are on lipoproteins and they're driving their trucks around and they aren't delivering the mail. Well, what do they have to do? Well, they're more likely to get in a traffic jam and potentially get into a wreck in your arterial wall. And that's no good. That's a bad mailman, and potentially we need to even address the corrupt workforce at that point. Additionally, when you are, you know, you basically insulin's still gonna rise, you know, even if your mailboxes are full, even if your suitcases are full, well, insulin's gonna try to recruit stronger insulin friends to jam the mail in the mailbox or jam the clothes in the suitcase. But when insulin continues to rise, rise, rise, rise, rise, eventually, you know, you're you're just asking for burnout. And then the amount of insulin that is required to normalize your blood sugars eventually at some point fails as well. And hyperinsulinemia itself, if you're if your insulin is high, and even if your blood sugar is normal, that's associated with a 50% increase in all cause mortality. But then when your blood sugars and insulin are high at the same time, 232% increase in all cause mortality. And so you're you're just asking for trouble at that point. And most people, most of the people that I saw with type 2 diabetes, they still were making insulin. And even there, when you would check a C peptide on them, and you should check a fasting insulin in anybody who's not on insulin as well, then you know it's it's a lot of times it's really high. And so I encourage people to check a fasting insulin in addition to their basic metabolic panel, because you can have people with a hemoglobin A1C of 4.8, which is the average blood sugar for the last three months. You can have people with a fasting glucose of 78, but their fasting insulin is like 30. Oh, wow, that person's making way, way, way too much insulin in order to keep their blood sugars normal. And so that is a surefire sign of early insulin resistance. And so at some point it's gonna fail, blood sugars are going to trend up, and then we're in all sorts of trouble. And so, just like we're trying to prevent cardiovascular disease with things like the coronary artery calcium score, by checking things in addition to our basic lipid panel, like LPLA, like APOB, because APOB is a particle metric and particles dictate risk. It's not the mass of cholesterol that matters, it's the amount of particles, potential perpetrators in your lipid neighborhood that really, really dictates your lipid-mediated risk. And so by identifying some of these things for from the lipid neighborhood standpoint, preventatively, we also want to take the same approach to metabolic health. And a fasting insulin is a really good way to identify insulin levels trending upward before blood sugars start to become abnormal. And that's that's a huge thing because if you are not insulin resistant, well, things, things tend to go right. The mailmen tend to deliver the mail how they're supposed to. And so it's a it's a very, very important thing. Obviously, there are other factors that are important as well in this whole framework, but if I could pick one thing not to be, it would not be insulin resistant. So I've chosen not to be. And so that's that's a wonderful thing. And it's it's a very modifiable thing from a lifestyle perspective. And in general, sometimes people before they hear me actually discuss all these things, they they ask me, so so how do I not be insulin resistant? And I'm like, well, here you go. It's it's sleep, move, don't eat crap, and then you know, do that every day the rest of your life. And like, dang it, that's not the answer I wanted. And so, but that's that's really and now now, of course, that's you know, easy for me to say since I've been doing this every day of my life since I was, you know, had a blonde cut in first grade. But the thing is, are there tools that can help people catalyze that shift, you know, to a lifestyle that is sleeping, moving, and not eating junk? Yes. And so do we have tools? We have we have some amazing even medical catalysts these days that can help shift that for people. Because, you know, the person who is 120 pounds overweight and has raging type 2 diabetes, they come to me and I say, hey, you know, just just you know, just move more, you know, just you know, just eat eat better food. I mean, that's not helpful, is it? And so, however, if I come alongside them and I say, hey, here's where we're at, you know, we're or maybe we're in a little bit of a rough spot, but I got your back here, and I have some tools that I know can reduce your risk of cardiovascular events, but can also help catalyze a shift to a sustainable lifestyle for you so that you can get your life back and you can add some life to your years. And that then I'm gonna use those tools to help you. And it's really, really cool when you have somebody who comes to you. And I remember one patient who was on 320 units of insulin, he was a type 2 diabetic on 320 units of insulin a day, and his hemoglobin A1C was still like 9.8 or something like that. So it was not working anyway, and he still made insulin. And I checked a C peptide on him, he still made a lot of insulin. And so giving more insulin to an already insulin resistant person who still makes it is silly, right? And so I was like, hey man, let's let's do this thing. And so I gave him a specific dietary approach. I gave him a medical catalyst that helped him, and then he was able to get off all his insulin. He was able to lose 70 pounds. He was getting back to riding his bike with his wife, and you know, he felt like he was a better husband, a better father, a better friend, and all the things. And so that's wonderful. And so, you know, that those are the sort of things that we are able to do, and the things that we can do as clinicians, and it's really rewarding, you know, just to be able to help people with their with their lives. And so, anyway, I I just think that, you know, control your insulin, control your life is obviously going to be one of my mantras for everybody. And the closer you can have the mitochondria of a pro athlete, the better across the lifespan when it comes to cardiovascular health, when it comes to mitigating neurodegenerative disease, and hopefully for as long as you're around, you can just be having some fun and and go crush it at life. All right.

SPEAKER_01 35:12

Thank you. Thank you for sharing that. Thank you. The liquid guy. I'm learning a lot of liquid from the liquid guy. If you're here today, please let us like a name. So if you're talking about cholesterol levels, we also know that you can be connected to RGMOD. So how is RGMOD connected to cholesterol? Cholesterol levels.

SPEAKER_00 35:54

Yeah, so this is a really, really fascinating topic. And if you think lipids below the brain are complicated, get up, get up into the central nervous system. That's that's a real trip. And so in general, what's good for the heart is good for the brain. Okay, so exercise is associated with a 45% decrease in Alzheimer's disease. Like I say, if exercise was a drug, it'd be a miracle pill. And so that's that's wonderful. And then people with the highest cardiorespiratory fitness have the lowest incidence of dementia at a population level. Okay, well, that that makes sense. And then if we look on the other side of the equation, if people have established cardiovascular disease in midlife, that's associated with a 29% increased risk in Alzheimer's disease from the UK Biobank. And then also there is a signal for increased Alzheimer's disease if people have elevated APOB in midlife. And APOB is a measure of potentially atherogenic particles. And it's a much better measure of the risk in your lipid neighborhood versus just an LDL cholesterol. When people have normal, normal LDL cholesterol, but elevated APOV, that person still has increased risk of cardiovascular disease. And those people do have an increased risk of Alzheimer's disease from the UK Biobank as well. Additionally, midlife obesity, you have nearly a fourfold risk of Alzheimer's disease. And, you know, I mean, and obesity is more than BMI, it's more body composition because you know, every NFL player is obese. And yeah, I'm not worried about that guy, am I? So so anyway, sorry, but really, you know, obesity in midlife, you know, you're probably retired at that point, and you know, that's that's probably not great. And, you know, and and so anyway, so fourfold risk of Alzheimer's disease and diabetes, 56% increased risk of Alzheimer's disease. And then people with the highest CAC scores in in the Mesa consortium have the highest incidence of dementia as well, and then control your insulin, control your life. People with hyperinsulinemia have an over two-fold risk of dementia as well. So all of these things make sense, right? And most of these things are related to more the home security system element. But if there's been a break-in, we see increased signal for Alzheimer's disease or other types of dementia as well. That said, the lipid neighborhood is a lot more complicated when it comes to the brain, because what's in general, the what's going on with cholesterol transport below the brain is kept separate from what's going on in the brain. Now, 20 to 25% of total body cholesterol is in the brain, but the half-life of cholesterol in the brain is six months to five years. Whoa, that's a long time. And so conversely, below the brain, the half-life of cholesterol is a few days, you know, and the plasma residence time, even on an HDL particle, if they linger a while, maybe five days, you know. So it really is recycled very at a at a with a greater frequency than it is in the brain. However, in the brain, instead of the Apo B lipoproteins being the primary mailman, it's actually ApoE HDL-like particles that are the primary mailman in the brain. And how it's supposed to work is the astrocyte, which is a star-shaped glial cell, and glial is like a support cell for the neuron. Those are the guys that actually synthesize cholesterol. And then that cholesterol is transported via these ApoE particles to the neuron. So the neuron can use the cholesterol for its whole host of synaptic transmission and all the other things that the neuron uses cholesterol for. And the reason why this is important is because cholesterol is very, very energetically expensive to make. It requires 36 ATP in order to synthesize molecule cholesterol. That's a lot. And the neuron's got all sorts of other stuff to do, right? The neurons run in the show, the neurons run in the body, and he's kind of like the CEO of the body. And so the last thing the neuron needs to do is okay, hold on, guys, let me let me synthesize all this cholesterol. No, that's that's grunt work, that's what the astrocyte's there for. And so ideally, the astrocyte makes the cholesterol and gives it to the ApoE particle. And the ApoE HDL-like, and it's called HDL-like because it's in the same density range, but it's not really an HDL. All these things have similar names, but their functions are different in the brain, and that's why it's like, oh my word, I don't even know if I want to be friends with this guy anymore when you start talking about topics that are this complicated. But anyway, so but really the astrocyte synthesized cholesterol and passes it off to the ApoE HDL-like particle. And ideally, the ApoE particle transports it to the neuron, and the neuron uses it, and then we're all good. The problem is people with something called ApoE4, and so I say ApoE Thor sometimes because Chris Hemsworth, who plays Thor in the Marvel movies, has two copies of this APOE4, which is the number one that we currently have identified genetic risk factor for late-onset Alzheimer's disease. And so people that have one copy of APOE4 tend to have a two to three fold risk, and people who have two copies of ApoE4, maybe eight to twelve fold risk of Alzheimer's disease. But it's not deterministic. Just because you have one of these doesn't mean that you're going to get Alzheimer's. It just means you might have less margin for error. So, anyway, so basically though, these ApoE4, if you have ApoE4, then they're like easily distractable members of the office. And so when you get the cholesterol memo from the astrocyte, instead of actually delivering it to the neuron, the ApoE4 particles are easily distracted. And it's like, oh, what's that? And then they leave messes in places in your brain. And then when cholesterol accumulates in places it doesn't belong, it's very, very pro-inflammatory. And what happens is the microglia, which are the immune cells in your brain, get annoyed with the ApoE4 distractible members of the office. And they're like, ah, this is the worst. And so they try to clean up the mess and mount an inflammatory response in the brain. And that's not very good. And what happens too is the neuron will start synthesizing its own ApoE and its own cholesterol. But when the CEO is doing things that the support staff should be doing, you're asking for burnout. And so that's why in the Alzheimer's disease brain, we really do see consistently three cholesterol disturbances. We see defective cholesterol transport, and that's the easily distractable APOE4 guys. We see impaired cholesterol elimination. And so basically messes are accumulating and then they're not getting taken care of. And there is a way to eliminate excess cholesterol from the neuron. It's called 24S hydroxycholesterol, which is a separate topic. But if we are unable to eradicate the cholesterol that's accumulating there, then we're asking for problems. And then the third hallmark we see is decreased cholesterol synthesis because it actually negatively feeds back on overall cholesterol synthesis in the brain. And so once again, we see defective cholesterol transport, impaired cholesterol elimination, and then decreased cholesterol synthesis consistently in people with Alzheimer's disease. And so, really, when you're a hammer, everything looks like a nail, but I think Alzheimer's disease is a lipid disorder. And I think that really the problems we see with amyloid beta accumulation and hyperphosphorylated tau and the neurofibrillary tangles and subsequent neurodegeneration that we see in Alzheimer's disease, I honestly think is a consequence of impaired substrate utilization, specifically impaired glucose utilization across the lifespan, which leads to the lipid disturbances that we see in Alzheimer's disease. And then we get caught in this nasty cascade where we have these abnormal protein signatures accumulating as well that further perpetuate that disease process. And so, anyway, there's all this to say. But I do believe that there's hope on the horizon. I believe that as research is improving, and especially as biomarkers are improving, because people aren't just signing up to get brain biopsies or get cerebrospinal fluid taps, which is, you know, how crazy is that? And so it's it's hard sometimes to know what's going on in the brain when it comes to metabolism and when it comes to cholesterol homeostasis. However, we're getting better at having these blood based biomarkers like P tau 217, like amyloid beta 4240 subfractionations, and then also. Having a better understanding of some of the specific things that we can understand about cholesterol regulation, such as desmosterol levels, and potentially if we're able to have a better understanding of things like PCSK9 in the brain. And so I actually am very optimistic that we're going to have an individualized regimen for people who we have identified in the early stages of Alzheimer's disease or subclinical Alzheimer's disease or myocognitive impairment so that we can actually act in a specific, nuanced way to help them not go down that terrible, terrible road of neurodegeneration. Because there's a big difference between living and existing. And I often say that one of the best prescriptions I can give, possibly the best prescription I can give for anybody, is hope. And I 100% am hopeful and optimistic that we will be able to intervene appropriately, like we can from a preventive cardiology standpoint, but also for preventive neurodegenerative disease. And that gets me really excited. It keeps me going. And I hope that if there's somebody listening to that, that that kind of gets you excited as well.

SPEAKER_01 45:18

Oh wow, thank you. That's very detailed. I guess we we have more time to go. So in your book you mentioned unicid, it's very important to do it has to know the levels of uric acid because that's kind of what is going on in the body. So how would you recommend to do that test? Is there a home-based test for people to do it?

SPEAKER_00 46:10

Yeah, so and and this is in the the part where I talk about hypertension as well, because nobody ever said, you know, it it would be ideal if I tried to get my systolic blood pressure over 200 today. No, and that's that's not a good life goal, you know. So anyway, but your uric acid is an interesting one. And this would be in my second tier of test. Do I think that everyone who's on this call or listening to this should go and get their uric acid tested? Well, it's probably not necessary, but uric acid itself is interesting. And uric acid can actually itself inhibit nitric oxide synthase. And so that's your vasodilator and kind of the guardian of your endothelium. And if uric acid levels are high, that's commonly known to be associated with gout. And so that's the extracellular manifestation of elevated uric acid, is it can crystallize and especially in in joint spaces and cause your big toe to be all swollen and hurt you and all that stuff. But really, what happens with uric acid is it also has deleterious effects on that nitric oxide synthase, and then it has deleterious effects on your metabolic processes in general. And so this gets into the biochemical weeds, but uric acid actually inhibits something called enyl cohydrates, which is the second step of fatty acid oxidation. And so we want to be using fat as fuel. One of the big problems with our standard American society is we rely too much on glucose dollar bills and don't access our savings account, which are fatty acids. And so uric acid itself inhibits your body's ability to properly utilize fatty acids. Well, that's not helpful. And then additionally, it inhibits a mitochondrial citric acid cycle or Kreb cycle enzyme aconitase. And so if the Krebs cycle starts, stops spinning, that is also not good for energy production. And so uric acid also inhibits that aconitase enzyme. So in two different metabolic processes, it impairs your ability to properly utilize substrate and it impairs your body's ability to vasodilate. And so that's problematic. And so uric acid itself, and a lot of uric acid levels are elevated because people are drinking too much alcohol, or they're drinking fructose, or or they're just having kind of a trash diet in general. And so, you know, those things are generally pretty amenable to lifestyle changes. But then there are some people who have some defects and various organic anion transporters who have hereditary hyperuricemia, and we have some potential options therapeutically for that as well. But you know, uric acid is interesting, and then it's also it's it's associated with progression of CAC, so coronary artery calcium. So it's actually associated with increased progression of plaque also in your coronaries. And so it can be a bad guy on many fronts. And so I do think that uric acid is something to consider, is a kind of a second-tier test for a clinician, especially somebody who's really wanting to look at all of the factors that could potentially contribute to cardiovascular disease. And uh there's some there's some interesting stuff about uric acid that makes it kind of a kind of a bad guy, potentially, when it comes to endosterial function.

SPEAKER_01 49:17

Wow, wow. Thank you. Thank you for sharing that. Uh so uh we're still talking about heart attacks, strokes, and dementia. Uh but then uh in your book realistically, well, sleep apnea is one of those factors that can lead to that. So can you make the connection for us as to why it's important for people to get from sleep?

SPEAKER_00 49:39

Yeah, so fascinating. So the quickest way to completely wreck your metabolism is not sleep. And so one of my favorite studies is they took these young kids at the height of their mitochondrial powers, and they'd even done oral glucose tolerance tests on them, college kids, and like they were 20 years old, and they had no insulin resistance even on oral glucose tolerance tests. And so then they took half the group and they sleep-deprived them less than four hours a night, and they took the other group and said, Hey, sleep as much as you want. After five days, half of the sleep-deprived group had levels consistent with pre-diabetes on their oral glucose tolerance test. Five days. And so, I mean, it takes a long time of doing absolutely nothing and eating total trash to get to pre-diabetes, but it takes five days in order if you're if you're not sleeping. So that's phenomenal, right? And if you're stressed when you should be at rest, you're never gonna get anywhere. And I think it's actually a beautiful parallel of metabolic health to spiritual wellness. And I talk about this, this specific case in the last chapter of my book. I had a patient and her hemoglobin A1C was 12.6 when she came to me. And that's, you know, her average blood sugar is like well over 300. I mean, not good, really on the struggle bus. And so I'm like, okay, well, you know, I've seen this a million times. She still made insulin, you know, and so her C peptide was high, high normal. And so I'm like, all right, well, this is cool. We can we can do this, we can reverse your diabetes. And so I've seen this a lot of times, and it's it's cool to do that. So I, you know, I put her on some really good medications, the magic sauce, and I put her on a specific dietary regimen that pretty much works every time if you do it. And she came back after a couple months, and usually people have dramatic success. And her hemoglobin AMC went from 12.6 to 9.8. So 6.5 is type 2 diabetes, by the way. So 9.8 is still not good at all. I mean, it's better than 12.6, but we went from absolutely terrible to still terrible, you know. I'm like, hmm, okay. Well, this is interesting. And she had a continuous glucose monitor, and her morning blood sugars were like sky high, like the highest of the whole day. I'm like, huh, yeah, okay, that's interesting. And so I talked, we talked about have you been doing the dietary thing, all this, this, this, yep, yep. And so she, and and she seemed pretty straight up. And so I was like, okay, and and so we said I said, okay, well, let's keep on with this and let's check back, you know, in another another another month or so. Comes back, no progress whatsoever. And she was really frustrated. And also, I'd seen her at the gym, she had even started exercising. I mean, most people, you know, it's like pulling teeth to try to get them to exercise here, but she'd even she was even exercising, and I had seen her at the YMCA, so I knew she wasn't lying. And she had been meticulously keeping her food logs, and I'm like, yeah, this is looking good. And she was really frustrated because we're not getting anywhere, you know. And so I'm like, hmm, well, and I'm, you know, I'm I'm the zebra hunter, so I start thinking of these weird, you know, monogenic diabetes of the young. I'm thinking about HNF4 alpha mutations and glucokinase mutations and and you know, thinking about getting her GAT-65 antibodies and all these protein tyrophosphatase antibodies and things like that. And then I'm like, hold on, that's probably not necessary. And I asked her, Do you have sleep apnea? And she's like, I don't think so. And she didn't fit the bill. You know, most people with sleep apnea, they've got a neck that's like bigger than my waist and stuff, and it's like, well, you know, that's it's pretty obvious person probably does. And so, but this gal didn't really fit the usual bill as far as the phenotype. And so I was like, I think you might have sleep apnea. Let's get you a sleep study. And she had severe sleep apnea, severe sleep apnea. And so then she gets a CPAP, and then after out of three-month follow-up, after using the CPAP, her A1C was down to 5.8. Wow. And so, but that's a huge example of you can be doing the right things, you can even be on some awesome medications, which I had I had on some awesome medications, and you can be doing the right diet, you can even be exercising. And if you're not sleeping, if your body's stressed when it should be at rest, you're never going to get anywhere when it comes to metabolism. And I feel like that's a a parallel to spiritual wellness as well, because you can do all the right things, you can try to be a good person, you can do all these altruistic things and you know, meditate on something and try to think positive thoughts and fill your mind with chicken soup for the soul, books, and whatnot. But I believe that if first your trust is not in the one who lived the sinless life you and I never could, died the criminal's death that you and I deserve, and then defeated the power of sin and death by rising on the cross, you're never going to get anywhere. Your rest must first be in uh what Christ did on your behalf. And so that's that's what I believe. And I believe that that's no coincidence. And that's how I end my book. And, you know, I think it's poetic, and I think it's beautiful, and it's beautiful to uh be able to rest in those promises and also just to get that beautiful rest that we all need in order to optimize our metabolic health. And when people meet me, you know, they're like, wow, that guy's crazy and he's got crazy hair and all those things. And they wonder, they they all often ask me, do you ever sleep? Because I'm, you know, once I'm when I'm awake, I'm pretty energetic. Oh, I sleep like a champ. You know, when when it's time to hit the hit the pillow, I'm I'm out, you know. And so uh no, it's it's all good. And so, and then you know, when you're able to get that adequate sleep, you wake up and every day is a delicious opportunity to go and hopefully have some fun and help some people while you're at it.

SPEAKER_01 55:13

Good, good. Wow, thank you. Thank you for sharing that. Thank you for sharing that. Uh we're still going. Uh, let me know when to start, and I'm gonna start. Give me a signal when you have to go. So if you're here, please let me know that you're here. Put your name in the chat, put your comments in the chat so that we can know that you're here. If you have a question for uh You also said something in the book about taking people who tend to have to take or not to have a bigger brain. Was that a joke or is it?

SPEAKER_00 55:57

Um that was a that was a cherry-picked study to justify when I take a nap because I like naps. And so I'm one of those guys who if there's like nothing going on, I'll be like, okay, well, I'll just go nap for 20 minutes and then pop up and and be fine. So that was that was when I want to go take a nap. That's the cherry-picked study I use to justify my naps. Now, there are also studies that show something else as far as napping. Basically, what's funny is in the same way, people love to hear good news about their bad habits. And then if you have a certain particular thing that I would say napping, probably the effect size of naps is so minimal and probably doesn't matter. But if you're napping because you have sleep apnea or you have underlying metabolic disease or cardiovascular disease, and that's what's leading to you dragging, then yeah, that's that's gonna be a confounder uh as far as oh, that's you know, napping's not good in that context. I don't really think it probably matters. If you like to nap and you're able to take a nap and wake up and be better off than you were before, fine. If you every time you take a nap, you feel like death when you wake up and you're useless stress today, then you probably shouldn't do that. Um, regardless, you got to sleep, you know. And I think that you know, getting that the adequate sleep is super important. There might be some sleep expert out there who has some other things to weigh in on there, but that was mainly a joke just because I like to take naps. And and so and I think it's when whenever like me know my wife's around, I'm like, hey, I think I'm I'm gonna go take a nap. You know, I gotta keep that big brain going. You know, I'll say something stupid like that. So that that was mainly that. Uh I don't I honestly don't really think there's much much signal at all in the thank you.

SPEAKER_01 57:45

Thank you for sharing that because I was like, I've never heard of that before. If you're here, please put us on that just yeah. So there's one subject that I also want to touch quickly: the fluctuations in the blood sugar level going up and down. So, how does that affect the organs of the body? Uh, especially the kidney, I think you highlighted that.

SPEAKER_00 58:10

Yeah, yeah. So, I mean, in a normal insulin-sensitive person, you're not gonna have much glycemic variation. However, what there's a critical threshold, and it's about 180 as far as glucose goes. And that's a kind of a toxic threshold for three specific organs in your body. And it would be your kidneys, your retina, and also your nerves. And this is why we see the microvascular complications of diabetes as far as the retinopathy, neuropathy, and nephropathy. And so, what happens is your body's really good at damage control to a point, and it tries to actually pick the least acute problem to deal with. And so, what happens is when your blood sugar goes over 180, that is a toxic threshold and there's too much sugar around. And so, what happens is the aldose reductase pathway kicks in and it turns the excess glucose into sorbitol. And so now the problem with sorbitol is sorbitol is toxic to your body. And so it's like, ooh, oh, that was a bad idea. Now, most of your body has the enzyme called sorbitol dehydrogenase, which actually turns that excess sorbitol now to fructose. Now, fructose, long term, is not great as far as you know, tendency towards fatty liver and and some other metabolic problems, but acutely it's not as problematic, right? And so it's like, okay, well, we can deal with this and then you know live the fight another day. So the sorbitol is turned to fructose in most of your body's tissues. However, there are three tissues that lack adequate amounts of that enzyme sorbitol dehydrogenase, and it would be the kidneys, it would be the nerves, and it would be the retina. And so that's why we see when people have persistently elevated blood sugars, we see the damage to those tissues, particularly in people with with diabetes. And so, you know, I think it's it's pretty cool how all these things, it's not cool when you have those things, but yeah, it's actually very interesting how you know it's not just some, oh, I don't know why this happens. No, this is exactly why it happens. And so, you know, it all is is nice. If you follow the biochemistry, it it doesn't really steer you wrong. So, but that's the deal. I've got a couple more minutes here. I gotta I I coach cross-country and track, and so we've got we've got practice here in a few minutes, but but yeah, I just wanted to give you the heads up there.

SPEAKER_01 1:00:17

So a few minutes we're we're gonna be good. So thank you, Sina. So uh you also mentioned yeah in the book driving through fast on Route 55. Drive through fast on Route 55. That's an acronym actually using it. Yeah, yeah, yeah.

SPEAKER_00 1:00:39

And and so, you know, and this is this actually kind of parallels the latest guidelines. And so the the Lipid Guidelines actually just came out last week. And so I actually, except for the prevent risk calculator, which I have my own opinions on. I I'm not a big risk calculator uh fan in general, but I have this acronym as far as hey, your uh your guidelines-based approach to cardiovascular disease. And so it's drive fast on Route 55. And the 55 is the LDL cholesterol or APOB level that you want to get under if there's been significant break-ins to your lipid neighborhood. Okay. And we see reduced cardiovascular events when we get people who have these risk factors and who have uh experienced uh serial break-ins to their lipid neighborhood when we when we get to those those levels. And so the acronym I have drive fast is F is find disease. You know, don't rely on risk calculators, actually, use things like the CAC and our other diagnostic imaging tools to find disease. And then A is for atherosclerosis. Oh, you found the atherosclerosis. Okay, there's been break-ins. What do we do about it? Well, we have tools in our lipid lowering toolbox. And and the whole, the backbone of lipid loring therapy from a medication standpoint is is statins, right? But statins are not a panacea. Statins do a lot of good things, but they aren't a panacea. And the most bang for you buck you get with the statin is with your initial dose. Every subsequent doubling of the statin dose, you get maybe 6% additional LDL cholesterol lowering and you increase side effects quite a bit. And so I'm a big fan, outside of acute coronary syndromes, to use combination therapy, knowing that you're going to not get as much out of the higher intensity doses of statins except for side effects. And then T is toolbox. And you know, if the year were 2004, we would say, hey, maximize your statin and pray. I think we should always pray, but we've got tools beyond the statins that have shown in large cardiovascular outcome trials to reduce clinical events. And so we've got azetomide, we've got ampidoic acid, we've got PCS canine inhibitor monoclonal antibodies. So it's a good time to be in the preventive cardiology space because we have lots of tools in our therapeutic toolbox. It's just a matter of knowing when and how to use them and identifying our patients appropriately and finding the atherosclerosis before it comes becomes problematic.

SPEAKER_01 1:02:58

Wow, wow. Thank you. Thank you for sharing us. So how much minutes do you have more?

SPEAKER_00 1:03:02

Five, um, I've I I've got a head out here and you kind of kind of lay on the plane here over the next minute or two. But this is super fun, man. We might have to we might have to do it again sometime. So last question.

SPEAKER_01 1:03:15

Last question. The hot topic is weight loss. Weight loss. How what's your understanding on these and what's your recommendation about how to ensure people lose weight? Uh I think you mentioned ozombi can be.

SPEAKER_00 1:03:33

Yeah, yeah. And and so, you know, um, you know, there there are many factors that go into this. And so right now, and and I'll I'll touch on this this point because there's a lot of uh hullabaloo around some of these medications. And there's there's interesting, there's there's polarized opinions here. There's like, oh, that person lost this weight, but they used Ozempic, or but they use this. And it's like, well, let's look at it from a health lens. You know, was first off, was there a good reason for this person to use this? And I would say that, you know, if you want to lose five pounds for your upcoming cruise or something, that's not a good reason to be on an ecreton-based therapy. But let's say that this person has cardiovascular risk factors or who has cardiovascular disease and who needs to restore insulin sensitivity and lose weight. Well, yeah, it's a good reason to use these things because they reduce cardiovascular events and they do it by helping you control your insulin, control your life. Well, that's always a win for me. And you know, sometimes people need them long term, sometimes people can use them as a catalyst. And hey, regardless, if you are healthier and you are minimizing your risk of cardiovascular disease, then that's a good thing. The problem that happens sometimes is you might skip lunch when you're on one of these medications, but there's no free lunch when it comes to maintaining muscle mass. Now, that said, if you, you know, heavy weights aren't going to pick themselves up, but if you pull the resistance exercise lever, then you can attenuate the loss in lean mass that will otherwise occur when you're on something like trzepatite or somagite or any of these things. And so you just got to do some work yourself. Additionally, a lot of times people are just not hungry on these medications. And so when they do eat, they just grab a couple goldfish crackers and move on. You really do have to prioritize protein. And my basic mantra for diet is prioritize protein, eat real food. And so, but you really have to get enough dietary leucine in order to continual continually stimulate mTOR, which is your main growth signal in skeletal muscle that you want on, because nobody ever said, I wish I was weaker. Nobody ever said I wish I had less muscle. And you don't want to be trading one problem, which could be obesity for sarcopenia down the line. So that's what I'll say on that. And um, regardless, you know, whatever we can do to mitigate cardiovascular risk is gonna be a good thing.

SPEAKER_01 1:05:44

Yeah, thank you. That's all. Any last thing you want to share with our audience before I'm close?

SPEAKER_00 1:05:49

Hey, um uh whoever you are, uh feel free to reach out to me. Um, home security system in the Lippin neighborhood might set you back like eight bucks or so, but hopefully it leaves you better than it found you. And uh yeah, keep on keep on crushing it. And you can find me at lifelovelipids.com.

SPEAKER_01 1:06:08

Good, good. Thank you. Thank you so much, Josh, the lipid guy. I really appreciate your knowledge, the humor, the laughter, and also a lot of learning opportunities. Thank you so much. Really appreciate it. Take care. Take care.