Cholesterol: Friend or Foe?

In this episode, Dr. Mary Louder teaches about cholesterol: about its function in the body, both helpful and not, and how it plays a role in cardiovascular disease if it gets out of balance. She also discusses the many other factors that can play into cardiovascular disease, and how a holisitic, lifestyle medicine focus can help reduce this major cause of mortality in our society.

Also, Dr. Louder introduces her new community, which you can join for free here to learn more about various topics in health and wellness. Joining is free, though there are also paid levels that include courses and/or health coaching.

Last but not least, if this episode has made you curious about your own cholesterol and how it might impact your health, you can learn more about and sign up for the Boston Health/Cairn Wellness Cholesterol Panel here.

Intro for "Since you put it that way" podcast.

Outro for "Since you put it that way" podcast

Transcript

Mary Louder: 0:25

Good morning, good afternoon and good evening to all you folks listening to the podcast Since You Put It That Way. I'm your host, Dr. Mary Louder. And we're starting a four-ish part series on cardiovascular health. I thought it would be easy to do four, but as I'm looking at the literature, at the data, the things that I've got to say, it's going to be most likely more than that. So and we're going to bring in our guest host down the road too, Carol Ritberger. So we're going to put in the Cosmic Health and Wellness aspect to this cardiovascular discussion, and that's really going to put it out of this world, and it's going to be a lot of fun. So I thank you for joining us. We're going to start today, however, in the Since You Put It That Way podcast, talking about cholesterol: is cholesterol a friend or a foe? And I had come up with some alternative titles

to today's podcast, Cholesterol: 1:27

Friend or Foe, and they went something like this, Cholesterol: The Good, the Bad, and The Ugly. Now when you say that you would expect to hear a whistle, and then Clint Eastwood to show up, right? Well, that's possibly going to happen. So the other the other title I came up

with was Statin Drugs: 1:50

To Be or Not To Be? That Is The Question. And that's very Shakespearean and somewhat poetic. And then finally, kind of a little twist of the Motown is What's Cholesterol Got To Do With It? Moving out the word love, what's love got to do with it? What does cholesterol got to do with it? So as we start on this four party series--four part series, it's all about the heart, cardiovascular disease, lifestyle medicine approach, using genomics, cholesterol, discussing different medications and treatments. And then, as I said, the super fun part with our co-host, Carol Ritberger, coming in with the Cosmic Health and Wellness, and looking at cardiovascular disease and whole-hearted living. So we're going to bring in concepts regarding emotions, trauma, connection, how we're wired for connection, and we'll look at the energetics of all that in some, you know, going off into the quantum field, it'll be pretty fun. But as I lay this out, now, I'm not so sure, as I said, that I can keep it to four podcasts. We'll see, but I think it's going to be more. And so here's the cheesy part, you know, I guess the song we'd have to pick for that, is My Heart Must Go On, you know, the theme song from Titanic. But anyway, moving right along enough, enough with that stuff. But all I can say is I've been digging into the research, and there's a lot of cool new information and all things cardiovascular. And it actually gave me hope and inspiration as a physician, because I've been practicing now for 30 years, give--in the first part of May, actually, of this year, graduated in May 1993. And I got hope, I got full of hope and inspired, and I was grateful for my three decades as a physician with all that I've seen I--tens of thousands or hundreds of thousands of patients, it's hard to know. But to see some of the transformation occur in cardiovascular care, they're beginning to think upstream, they're beginning to look at other options, and really, we've got data now in lifestyle medicine, we've got data on genomics, data on testing, and so using those data points, I think has been very, very helpful. It's also fair to say that there's many physicians and providers who are stuck in a rut. They simply treat guidelines rather than the patient who's sitting in front of them. And however, I feel that the tide is--feels like it's turning and hearts and minds are actually opening up and it's possible. I'm, you know, an eternal optimist. But it's also--what I know for sure is I look for opportunities. And so I see opportunities where the standard medical model can evolve and can change. And I have great hope for that. I don't stand in the standard medical model myself because it's too confining. And I use my intuition, I use integrative holistic approaches, I use all the tools that I've learned, all the skills that I've gathered, all the testing and credentialing and training that I've ever received, comes together to work with the patients and it's--it's quite a bit. So the evaluations are quite involved when folks work with me. And there's a number of articles taking into consideration that I've that I researched and read in preparation even just for this specific episode on genomics, metabolomics, cardiovascular disease as well as looking at inflammation, and something of the metabolism of the cholesterol itself. And what the discussion is having and going in the direction of is that cholesterol is a dynamic molecule. And I don't know that we thought of it that way. We thought of it often in, you know, in my training, it was just what fogs or blocks arteries, we don't really think about it as having a metabolism, and maybe not even having a purpose. Other than, you know, giving, getting, you know, clogging the arteries and giving a cardiologist something to rota-root out, or a cardiovascular surgeon something to bypass, right? But before we get into the specifics of the cholesterol and the dynamics of that compound, I want to do a commercial break. And we do have a sponsor, our sponsor is Cairn Wellness Institute. And this is an institute which is a new platform that I'm releasing here in May, and launching, and it's it's a platform where Wellness Wayfinders come and gather. Well, what does that mean? It means join us if you're curious about your own health and wellness. Join us, and if you join our community for no cost, you sign up--and you can sign up through our web page--and you learn about different health, wellness, lifestyle medicine topics. And I put together a community that's different from social media. So people that log in, we monitor in a way that we keep the conversations completely kind and non-judgmental, and they're driven by good solid evidence and guidance. And in medicine, I've rarely seen an absolute answer being accurate. But there certainly is consensus, and there certainly is things that we know to be true. And so that's how we're building the community. But it's a place where people can come, they can sign up for the Hero's Genome, they can get information on the Anxiety course, Self Care and Connection, we're going to launch some coaching services. So if you're interested in health coaching, actually, you'll start to work with me either once a month, or once a week to work on the dynamics of what you want to alter in your life. And when we look at coaching, it always begins with the genomics because we want it to be patient- or person-specific. So in that community, you're going to join other like-minded people, and you're going to collaborate and learn, sign up for the courses, and it's an evolving and dynamic learning site that as we get some traction and gain some ground, there's going to be many, many more opportunities to learn many things about health and wellness. And we'll have special guests there, too. Well, they'll come on and do a podcast with me or come on and do a webinar with me. And there'll be some live q&a. So I've got a lot of fun things planned for that space to really create a community. What I learned in the pandemic was, we were often isolated. What I learned in the pandemic, that community overcame a lot of cultural conundrums that we face. So if you have your community with you, your tribe as it were, you're able to move that around and take that with you. And so I decided to make a tribe of Wellness Wayfinders that we can all work together to improve our own health and wellness in a space that is dynamic and transformative. So that's what the Cairn Wellness Institute is all about. And I would say it's probably a bandwagon, right? And you know my perspective on bandwagons, if you if you if you see one consider jumping on--or maybe not, but this one in this case, I would say jump on this bandwagon. It's a good place. So and the other thing that we're offering too, in regards to our cardiovascular series, and you can sign up for the website, drmarylouder.com. And that's just my name spelled out: Mary Louder .com. And the doctor is D-R. So drmarylouder.com. And on that website, we also have an offer for a test that was developed for us and is called the Boston Heart-Cairn Wellness Cholesterol Profile. And what that is, is I joined forces with Boston Heart Lab out of Bedford, Massachusetts and that lab has I think the most advanced cholesterol panel testing in the nation. And we were able to use components of all the testings that they do, to put together a very meaningful panel that meets all the criteria for looking through our genomics, looking through family risks, looking at what the genomics influence and looking at not just total numbers of cholesterol, but different aspects of essential fatty acids, if cholesterol is absorbed too much, or you're making too much. And so it's a very powerful panel. What we're offering you is a Boston Heart-Cairn Wellness Cholesterol Panel. And that's in response to or in conjunction with this series of our podcasts regarding cardiovascular health. So right now, we're running a podcast special of 25% off the test, and we're kicking in a consultation, or an education series. So you're going to want to take advantage of that by going to our website and signing up. The kit then will get sent to you, you'll have the blood draw, and then simply, the report comes back and we notify you and you set up an appointment. So it's a really slick idea. And please go to the website to look for more information on that. All right. Now we're back after a word from our sponsor, and you all thought it was Geritol. No, it's actually Cairn Wellness Institute. So looking at cardiovascular disease has multiple components. And we're going to look at a number of them throughout our series. Today, we're going to focus specifically on cholesterol, which is a dynamic molecule that's used in repair of the blood vessels under--that undergo stress, strain and damage. Those vessels are known as arteries. Let's think about that for a moment. Let's think about the difference between the different types of blood vessels we have. We have arteries, arterioles, capillaries, venules, and veins. So, veins don't get clogged with plaque. Only arteries do. Well, let's look a little deeper and see why that is. Some of you may know already. But this will be a good review for you. And for those who don't know, this should be relatively fascinating. So the difference between these two vessels, we're going to discuss that because they're essentially have the same anatomy, mostly. Say each of them have three layers. If you were to dissect them or cut them in half and look at them from a diameter or cross-section. But let's compare an artery versus vein. The veins return blood to the heart. Arteries take blood away from the heart. Veins are a low pressure system, and arteries are a high pressure system and sometimes a higher-pressure system. Think of blood pressure. When we measure blood pressure, we're using it measuring it in the arterial side. There's higher oxygen in the blood in the arteries, and there's lower oxygen in the blood in the veins. Veins are closer to the surface. And if anybody looks at the back of their hand, they can see that, or if they have varicose veins, you can see how superficial or close to the skin those are in the arteries are typically deeper. Well, the arteries are deeper because they're carrying vital blood. And so they tend to run with a deep vein, and a nerve, and sometimes some lymph. So it's always nerve, artery, and vein that run deep with the bones and deep around joints. And so they often and typically often run in cahoots, as I call it. The vein walls are thinner and artery walls are thicker. There's a higher amount of blood that moves through the vein versus the artery so there is a greater volume that moves through the veins than the arteries. Veins have valves, but arteries do not. Each vessel though, either artery or vein, has three different layers. If we were to cut it in half and look at by transecting it. So there's the tunica intima, which is the most inside layer, the tunica media, which is the middle layer that has a bit of a muscular component to it, or it is a muscular component, and then the tunica externa, or adventitia, which is the outermost and that's where connective tissue adjoins to keep those vessels basically located anatomically correct and they don't slide around. Arteries though, have a thicker media layer, that tunica media, that middle layer that's muscular and that handles the higher pressure that goes through when the blood is pumped through that and pumped out from the heart. The veins have a thinner middle layer or the media layer--layer, but it has more give. So in order to counteract that, the veins developed valves. So--and the veins have more blood volume. Well, if we think about it, the veins are working against gravity, right? Because the blood is going, returning back up to the heart. So it's going up the legs, right? Or coming in from the hands, and typically, that's against gravity because it's going to go up the arms. So the valves helped to prevent backwash, as it were. But how does the vein get pushed up if the muscles aren't as strong? How's the blood get pushed up through the veins if the muscles aren't as strong? Our muscles, movement. So, it's really simple. If you sit still with your legs still and your arms down your hands and feet get what? Swollen. So there's fluid, that's not blood, but that is fluid. And that goes to the lymph, but essentially, more blood is pooled. And that's why we say when you travel, please move your legs, please get up and walk around, because we want those muscles pumping around those veins to push the blood back up towards the heart. If blood pools in the veins, you get thrombosis, which is a blood clot. If blood pools in the artery, there's a thrombosis, but it's from a plaque. So we're going to look at the difference between that. And as we go forward. Questions that I still have yet, and I'm seeking, are the difference in the genomics about the arteries and veins and the--they're in the literature. I just haven't looked them up yet. But there are some things we--there are some genomics relative to hypertension, which of course is how the arteries function. And so I'm--I'll be curious to see what some of the cross-sections of those genomics look like between the two types of vessels. So these are the players for where the cholesterol has its heyday. However, it's the arteries, which is where all the action is with--with cholesterol. So, why, do you ask? Well, because of the things we said above, but really, it's So those end to end cells in there, that are squamous all about the pressure. The arteries are under a higher pressure and veins are not. So the veins that the valves have they get leaky and the blood pools, and the veins could swell and get irritated. We call that phlebitis. But they are not laden with plaque. Arteries are firm and muscular and under pressure. And when the arteries stretch and are under pressure simultaneously, they typically develop micro tears in the inner lining. And that inner lining is the intima. But even beyond that, there's even one more slight layer on there. It's kind of like a piece of cellophane on that intimate layer. And those are single cells that are squamous epithelial, like, Why do you say that Dr. Louder? Well, because that's what it is. But they're the type of cell is important. It's a squamous epithelial cell. And they literally line up nose to nose, they don't overlap, there's not layers of them. There's not sections of them, they just nose to nose, end to end they line up. So when an artery gets under pressure, hypertension, think of that, that artery stretches because of the blood that's pushed through there, and blood pressure elevation can be seen in a comparison or an illustration of trying to blow water through a drinking straw, or garden hose. So typically, what happens with blood pressure is that drinking hose turns more into a--or, correction, the garden hose turns more into a drinking straw. And so it requires more muscle to push the same amount of volume through. And so that's how the heart gets thicker, and responds to the stresses placed upon it to pump out against a higher pressure. And there's lots of implications after that, what happens with the heart, but we're looking at these blood vessels right now. epithelium are called endothelium ever more forever going forward, we shall call them the endothelium. Okay? And that's because that's what they are. So looking at this as we've segued into vessel-land, let's go back to the cholesterol. But this divergence is good because we want to know what the cholesterol is affecting. So we needed to know the difference between veins and arteries. So now looking at cholesterol and knowing that that's going to be affecting the arteries, it's time to put down the swords and run into the pain. Cholesterol is our friend, cholesterol is our foe. And ouch, that's very uncomfortable. Why? Because a lot of us have formed strong thoughts and paradigms and opinions about you know, we have to have cholesterol, or we have to have no cholesterol, we have to have low cholesterol. It's just--and there's just a lot of dogmatic thought around this. And so it's an uncomfortable conversation, and I've had this conversation as a patient with a cardiologist, couple cardiologists, actually. And I got varying opinions. And the first cardiologist was exquisitely rigid and just told me to do--take a statin. That's how it goes, end of story, see you in a year. And I was like, okay, but like, what is my cholesterol even doing? What is happening with my inflammation? What is my ultrafast CAT scan or calcium score doing? Well, it didn't matter, because the statin was the answer. I didn't go that direction, as you can imagine, but I was seeking an opinion, and that's exactly what it is: an opinion. So my opinion is different. Does that mean I contradict all the specialists? No, because they have their own opinion, it just means that I see things differently, because I'm looking at things more holistically. I'm bringing in the genome, I'm bringing in inflammation, I'm bringing in metabolic imbalances, I'm bringing all that into the decision making, rather than just saying cholesterol is elevated. And interestingly, my cholesterol wasn't elevated. But there was evidence of some coronary artery changes. And so the response was, you must take a statin to get rid of that or to stabilize that. And I think there's other ways to stabilize that and even reduce that. But that's as we get into other things too. But I just want to let you know that we're really coming from a place of being dogmatic but let's fall--put down our swords, and let's not fall on our swords, let's put down our swords and run into the pain of this being uncomfortable, somewhat, in a discussion. In cholesterol, why is it our friend? Let's go there for a minute because I think this is super important. Cholesterol is in every cell membrane, meaning the walls of every cell in your body are a bilipid layer, and cholesterol is a molecule that makes up the bilipid layer. Got to have it. The cells need it. Cholesterol is our body's main repair substance. So we need it. Bile salts used in digestion of fat, that are come from the liver and are stored in the gallbladder. Primary molecule to make the bile salts, cholesterol. Our immune responses are modulated by cholesterol and molecules made of cholesterol. Lipopolysaccharides is what they are. The mother molecule of all hormones, is cholesterol. So for gentlemen, testosterone starts out as cholesterol goes into pregnenolone. It goes into pre testosterone then into testosterone. In women cholesterol turns into pregnenolone, which turns into testosterone, which turns into estrogen in some women, or cholesterol turns into pregnenolone, which turns into estradiol or progesterone, or DHEA. So we need cholesterol as a molecule in our body. Neurological function, we're definitely fat heads, meaning the primary component of our brain is fat. And that is cholesterol. And then there's the nerves that function because they have a covering on the axon, which is the extension off of the cell that communicates with other nerve cells. And that typically is covered with a coating of cells made with cholesterol. Those are called Schwann cells. And that is like that is an insulation on the nerve to make the conduction go faster. Cholesterol is also used for a healthy balance of inflammation in the body. Part of the repair molecule I'm thinking. And then brain and memory function, and the uptake of serotonin from the gut to the brain, is dependent upon cholesterol molecules. And finally, cholesterol is either a plus or minus an antioxidant. In some cases, it's an oxident. In some cases, it's an antioxidant. So here's where I say too much of any one good thing is probably not a good thing. And this is true of cholesterol. Too much or too many things going on with cholesterol or its environment in the arteries, which influence cholesterol is not so good. Coronary artery or peripheral artery disease, we often lump that together as cardiovascular disease. So coronary arteries are the arteries that go to the heart. They supply blood to the heart for the heart to pump. There's big vessels like left main artery, left anterior descending, right coronary artery, circumflex. And then there are arteries that are smaller that interface or envelop into the heart muscle itself. And those are arteries. So, potentially you could get those clogged with cholesterol, right? So when you bypass and do a bypass surgery, what arteries are you doing? You're doing the big arteries, right? So the ones that sit outside on top of the heart, the coronary arteries left main, right, right main, right coronary, left anterior descending, circumflex. So what about those smaller vessels that have cholesterol in them that are in the heart? How do we get those out? I'll tell you in another episode, because there's really some cool treatments for that. It's kind of neat. So, but anyway, moving back to our cholesterol, with having some things relative to the cardiovascular disease, because it has oxidizing and antioxidizing properties, it's dependent upon our genomics. And

the epigenetics: 26:38

the environment acting upon our genomics and telling the genes what to signal towards or away from, that tend to push towards cardiovascular disease. But those are all modifiable. They're not fixed in stone. Lifestyle, supplementation, medication, diet, stress management, trauma care, all those things can affect how our genes are interacting with our biochemistry, the low density lipoprotein--and we'll define the different types of cholesterol in a few minutes here--but the low density lipoprotein, or cholesterol is now linked as a causal factor, or in a causal manner to coronary artery disease and peripheral artery disease. This is now put to bed. And this debate has been going on for decades. And this was something when I saw this in the literature, it was a study, I think, 2020 study, I was like, Oh my gosh. So what they looked at was, they put meta analysis and meta analysis of the studies. And they ended up with a patient number of in the millions and a patient evaluation length of time over 240 years. So collecting that many data points, it's very difficult to have biases in that and the overwhelm--and then they use somethey look at genomics with that, and they looked at Mendelian randomization which means is that what they're really looking at from a genetic standpoint? Or is that a random gene? Or is that gene really signaling that type of change in the coronary arteries and in the cardiovascular system? And all these things lined up to indicate that the low density, LDL cholesterol is now a causal factor. And so that's a game-changer for me as a physician, because I sat on the fence going well, I'm not sure about that. It's not always about the cholesterol, you gotta look at the vessels, gotta look--so I was, you know, I was dogmatic that way. And now I'm back to All right, I'm going to sit in the middle with the pendulum. And I'm going to evaluate the patient and see what their individual needs are. And I think that's just a better place to be. We also found with cholesterol that the microbiome influences cholesterol, and then it relates to the arteries. So the microbiome is that gut biome of all the bacteria we're--we're carrying around with us, which actually has more cells than we have in our whole body. And that's comprised of bacteria, viruses, probably even a little fungi, as well as you know, the good guys for the bacteria and maybe some ones that aren't so good. But that has its own DNA component, and that DNA interfaces with our DNA, and so then that has an effect upon cardiovascular health. And so then gut health overall, not just the microbiome, but then the gut health, the health of the intestines, the health of your digestion, the health of your liver, fatty liver, or congested liver, or the presence of a lot of environmental toxins. That all goes into gut health and that influences cholesterol and heart disease as well. Infections influence cholesterol and arterial disease things like H. Pylori, Chlamydial pneumonia, mycoplasma pneumonia, hepatitis C, Epstein-Barr. In little kids, we've got varicella, we've got measles, mumps, rubella, that have a correlation into long-term cholesterol changes, long-term artery changes. And there's even one, Kawasaki disease, and that there's an infection that affects the blood vessels and you get an--an acute inflammatory response in the blood vessels. So what's the blood vessel going to do? Repair. What's it going to repair with? Cholesterol. So we're finding that cardiovascular disease begins at a very young age and is a progressive disease over 40, 50, 60 years. It's not just something that hits you in your 30s, 40s, 50s, which is even, you know, a long span. It begins in the pubescent and pre-pubescent age, which was just a bit mind-blowing for me. But it makes sense if cholesterol is our friend as a repair molecule. So then, early childhood diseases then would have an influence, early childhood metabolic problems or challenges would have an influence. If there's obesity, if there is insulin imbalances, if there's essential fatty acid imbalances, if there's the genomic or genetic predisposition towards inflammation, there's going to be more problems coming on, we're going to probably see cardiac disease, cardiovascular disease at a younger age. And we're going to see it more--to be probably more problematic going forward. And then we've got the concept of the Adverse Childhood Experiences. And that's the trauma work. And what we figure is if there's four or more on the ACE scale, and they call it ACE for Adverse Childhood Experiences, that could be where there's a divorce in the home, where there's been multiple job losses or financial instability, food scarcity, housing scarcity, if there's mental illness, incarceration, substance use, alcohol use, so the list is long. But if you stack those up, four or more tends to affect chronic illness, increases cholesterol in response to stress. And arterial disease can be compounded because of that. And then we've got, if we bring in the dental work world, we've got oral infections, dental health and wellness, periodontal disease, that influences cholesterol and arterial disease. So the cholesterol that begins building up in early childhood, 40, 50, 60 years in the making. Looking at the molecule of cholesterol, it's pretty complex. And it's a long molecule, 26-carbon molecule, and oh, correction, a 27-carbon molecule. And it's got some hydrocarbon tails in a sterile nucleus and a hydroxyl group, so it's kind of very complex formula to it and structure, chemical structure to it. Then you take that cholesterol molecule that's pretty complex, and you mix it with proteins, and that's how you get your high density lipoprotein or the HDL cholesterol, and the LDL Cholesterol, the low density lipoprotein. And these lipoprotein molecules are round. So the cholesterol, which could be kind of like a string, as the molecule, joins together with triglycerides, a cholesterol ester, which is fat, phospholipids, which is also some fatty tissue, or fatty molecule, some free cholesterol and apolipoproteins, and those join together to make a round spherical molecule--or actually, not a molecule, it's a compound, pardon me, compound, that's considered a lipoprotein. And these round particles made of the lipids and proteins, those are what travel in our bloodstream throughout our body. And the cholesterol and triglycerides are two parts of this, plus the other proteins that we talked about. So this is where we get into the types of cholesterol. We've got total cholesterol if we do a cholesterol test. What's the--what's the measurement? Total cholesterol. Right there, sum total. Then we break that down into the HDL, LDL, VLDL, IDL, and chylomicrons. And lipoprotein a, so we've got lots of things to break down here. So let's start with the HDL. That's the high density lipoproteins, that's the good cholesterol. Your HDL cholesterol carries the cholesterol that's bad out to our liver to be flushed away. Right, so that it--it matches up and it takes the bad cholesterol to the liver to be flushed away. And the high levels of the HDL cholesterol reduce our risk for cardiovascular disease. Then you've got the next one, which is the low density lipoproteins, which is considered the bad cholesterol. Since we're giving values to these, the good and the bad, right, and the low density lipoprotein, this is the one that increases the risk of the coronary artery disease, the myocardial infarction or heart attack, the end strokes and peripheral vascular disease. low density lipoproteins carry the cholesterol that accumulates as plaque inside of the blood vessels. The plaque buildup can make blood vessels too narrow for blood to flow freely. And we actually follow Poiseuille's Law for that. And then that has to do with fluid dynamics. And really, cardiology is primarily about fluid dynamics. But there's also the immune complex, the immunological response, there's inflammation, and there's a lot of neurology with cardiology, because the heart has its own neurologic center, which we're going to get to in another episode, but it's completely fascinating. But back to the humble cholesterol here. So we've got HDL and LDL. Well, how do you keep them separate? How you remember which one does what? Well , H is for happy is for high density. So you're happy, healthy, high density lipoproteins are the good guys. Low Density is the lousy, so that's the bad guys. So that's how you keep them straight. Then you've got a very low density lipo--lipoprotein. And that's the bad cholesterol that carries triglycerides, and to a lesser degree, some cholesterol into the tissues, so it's just a transporter, then there's an intermediate density lipoprotein. And that's created when the very low density lipoproteins give up their fatty acids. So, so that they go from empty to being very empty, right. And when that happens, they're either removed by the liver or converted back into low density lipoprotein. So these lipoproteins are also going through their own metabolism and changing back and forth, and my hunch is that that's on some genetic and genomic influence, as well as lifestyle. I think we got both things going on there. And then chylomicrons, which are large, large particles, and those also transport or carry around triglycerides, which are a component of cholesterol. Then we also have another measurement within the cholesterol family, the lipoprotein little-a, we call that lipo(a). And that's a type of bad cholesterol because it's genetically set. It's determined. It's--it's a little more set in stone. And the only way we can really treat that, we can bind it to other things like prolene and lysine, but otherwise it floats around and does its job. We can't decrease the numbers of that. And then there's a second pro--protein called apo--apolipoprotein(a), and that loops around. So, remember, we've got this molecule that's--or correction, this compound that's a sphere. And it's got these components of cholesterol and proteins in it. But lipoprotein(a) sticks on the outside of that. And then the apolipoprotein(a) adds to that as a stringy substance, kind of a bit like silly string that attaches around, and what that does is those create increased stickiness of that lipoprotein molecule. So you've got LDL floating around, that's all of a sudden more sticky. So it's going to do what? Adhere more. So sometimes thinking of cholesterol, we can think about it as cars on the highway. If you've got a lot of cars on the highway, and you're going, and I have to say I always think of Denver, because there's this area in Denver called The Mousetrap where two big highways come together, I think it's actually three big highways come together, and it's just the volume of traffic is just amazing. And as long as everything works really well, you can get through there even with high volume. But that's the key, it--things have to work really well. If there's construction, there's the construction cones, there's a barrier, there's workers, or there's an accident, it's just a disaster. So that's kind of true in the blood vessels too, where if there's increased volume of your low density lipoprotein is going in, it's like having a lot more cars on the highway. So there's more apt to be problems that way. If there's less cars, less low density lipoproteins, less lipoprotein(a), you're less likely to have problems, and more likely just to go on through. Now our current guidelines, looking at cholesterol is total cholesterol, if you're 21 years and above, we'd like the range to be between 100 and 199. If you're less than 21 years of age, it's 75 to 169. And then your high density, we like it greater than 45. So remember, high density is for the happy or the healthy density lipoproteins. And then your low density or the lousy ones. We want that to be below 100. And then triglycerides, which are also a component of the cholesterol molecule, cholesterol compound is--you want that below 150. So then what's a plaque? If it's these low density lipoproteins coming together and sticking, is it just those? Or are there other things? Well, there are other things. So what's in a plaque is you've got the fat in the cholesterol, like we talked about previously, but then you get a buildup of calcium. You get waste products from the cells. You get a clotting agent called fibrin. And about 80 to 90% of the weight of that plaque is water. And then 70% dry weight is bacteria, polysaccharides, and glycoproteins. Well, I don't know that we--I didn't--I don't remember learning this part in medical school. So this has evolved since then. Maybe it was there, maybe I didn't remember it because I was focused on treatment. But you know, stopping back now and having perspective, after so many years, it makes sense that we need to look at this cholesterol, this plaque from a multifactorial component. If there's bacteria there, does that mean that there's an infection somewhere? Maybe. If there is a lot of glycoproteins, that causes an--and the polysaccharides, those interact with the immune system, causing an immune--immune response. Well, how do we know if some of the cardiovascular then, is--cardiovascular diagnoses are caused by immune response relative to inflammation? Is it a localized inflammation to the blood vessel that gets inflamed and irritated? Or is it a systemic thing, an inflammation throughout the whole body? The answer to that is yes, it's both. So all of a sudden cholesterol becomes this dynamic compound. It's a complex, rich, layered and textured. And some of the cells within the plaque are also macrophages. And those macrophages, when they gather, they create a foam cell which can make the plaque unstable. If the plaque is unstable, that's what breaks off, floats downstream and clogs the artery creating the thrombus. And that's when you get a lack of blood flow past where that blockage is, which is considered ischemia, which is the cause of heart attacks and/or strokes if they're ischemic in nature. So wouldn't it then stand to reason that our approach to cholesterol management and care is also complex, rich, layered and textured? Yes. And I think the best way to look at cholesterol. Is it our friend or foe? Yes. Can we understand the genomics? Yes. Can we understand our own history relative to cholesterol? So that could mean gosh, what infections did you have as a youngster? What is your ACE score? What your current stress score, what--what traumatic events are we dealing with? What are your hormones, perhaps? What is insulin, what are blood sugar, what are your--what's your estrogen and testosterone and Chole--and cortisol, DHEA, both men and women, because estrogen's seen as a anti-inflammatory. So is testosterone for guys. So we want to look at how much we can balance whatever the cholesterol is, and of course there's thyroid that comes involved with that as well. So the workup becomes more thorough versus just your annual blood draw of a lipid panel with total cholesterol, HDL, LDL and triglycerides and here's a statin. That is so reductive and nearly insulting to your body. It is actually insulting to your body, because the response and what the body is doing is way more complex and nuanced. And so it would make sense to dig deeper and look farther to have a better answer, because not everything requires a statin. And this is the neat thing about using the Boston Heart tests because we can look at your total cholesterol, which is actually a count. And then instead of calculating the low density and high density lipoproteins, we actually count it. And then we can look at if you, how you, the features of your cholesterol if you're absorbing it too much. Or if it's more that you tend to make too much. And so then the treatment modifications, the lifestyle medicine, becomes different answers based upon what we find on that test. And we can also look at the apolipoprotein, lipoprotein little-a, we can look at what your essential fatty acids are, are those imbalanced? We look at inflammatory markers, C-reactive protein, and homocysteine, because that looks at methylation. So those things are super important as we put this together. And all those go into looking at a more holistic view of your cholesterol. Certainly the lifestyle diet, exercise, trauma, stress care management, supplements, there's some--bergamot, liver support, red yeast, rice, absolutely. Then you've got the statin: simvastatin, pravastatin, atorvastatin, restorva--resuvastatin. And you've got Zetia which blocks the uptake of cholesterol cholestyramine that blocks and binds up cholesterol and takes it out through the intestines, and then we've got the new class of medicine that blocks more upstream by a few steps working on the LDL receptors, recycling and decreasing their ability to have the low density lipoproteins circulating in the blood, so less problematic. So,

cholesterol: 47:27

friend or foe? Yes. Is there more to it than what meets kind of some of our standard approach to medicine? Yes. Could we get a much better response and understand by keeping and maintaining cholesterol levels, that it helps us with cognition, it helps us with hormone balance, it helps us with inflammation, it helps memory? Yes. So does everybody need a one size fits all? No. That's not the bandwagon to get on. The bandwagon to get on is, let's look at this holistically. Let's look at all these things, and let's see what is the best choices. Is it medication or not? Lifestyle always is going to be, because it's a chronic issue. And is it going to be multifactorial? Yes, because issues with cholesterol relative to cardiovascular are chronic, therefore, it's multifactorial. So, there's the--the skinny on the fats, as we say, and the ups and downs of the cholesterol. So I hope that this has been informative for you. There's so many more, and so much more information on cholesterol, but I thought this is a great place to start. It's going to lead us into other aspects of the cardiovascular system as we look at the podcast going forward. So make sure you can take advantage of that Boston Heart test, if you can, drmary louder.com, check out through the website, over to the Cairn Wellness Institute to consider joining, becoming a Wellness Wayfinder. And I think that these next podcasts are going to be super informative and important because cardiovascular disease is the number one killer in our country right now, more so than cancer for both men and women. And so we want to really--and we aren't really gaining on it, we aren't. So if we aren't gaining on it, I mean, you know, the definition of insanity is doing the same thing over and over again and expecting a different result. So we need to change what we're doing in order to have a different result. And so that's why I hope that looking at cholesterol differently, putting it this way, seeing things from a new perspective that will gain insight for you and help you on your health and wellness journey going forward. So thank you for listening. I look forward to sharing the next episodes with you. As always, please rate and review our podcasts. It does help us to get more visibility let us know if you have questions or feedback. We're always happy to hear that. You can leave that on the website. And until next time, take good care, be in good health and enjoy every single day that you have. All right. Bye from here.