The Truth about Cholesterol. The surrounding narrative regarding cholesterol and the other blood lipids coming from insurance companies and conventional medicine is full of myths. The conventional medical system looks at cholesterol as a boogeyman, a harbinger of doom. However, cholesterol is essential to life and a vital component of every cell in the body. How can it be the bringer of death and a key to life at the same time? As with everything else, the name of the game is balance. This episode goes deep into the truth about cholesterol and the other blood lipids, how abnormal levels are a symptom and not a disease, and how you can balance your cholesterol and other blood lipids.
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[00:00:30] Welcome to the Strive for Great Health Podcast, I’m your host Dr. Richard Harris, and today we’re going to be talking about cholesterol, AKA the boogeyman that’s in the room. We’ve gotten cholesterol horribly, horribly, horribly wrong, and I’m just being blunt. This is something I get asked on a lot, so we’re going to dive in, we’re going to break down cholesterol, [00:01:00] what it actually is, why it’s not the boogeyman, and why conventional medicine gets this completely wrong.
So let’s start off, what is cholesterol? Well, it’s an word from ancient Greek meaning cholí, which means bile, and sterols, which means solid. And so cholesterol is an essential molecule in everyday life, we absolutely need cholesterol. If you had no cholesterol, you would be dead. Completely, totally dead, there is no [00:01:30] human life without cholesterol, it is so important. So it helps maintain the integrity of our cells, and how it does this is our cells, the walls of the cells are a little bit fluid, meaning if there was no cholesterol that they would react to temperature and the integrity would change with temperature, get a little bit more rigid and cold, a little bit more fluid in hot temperatures, and you don’t want that happening [00:02:00] because that changes the way those cells work. So cholesterol helps ourselves maintain the same integrity, the same consistency, over a range of temperatures. That’s one function of cholesterol.
Another function is it’s a precursor to all of our sex hormones. So we’re talking testosterone, estrogen, cortisol, progesterone, all of these hormones come from cholesterol. And it’s also a vitamin D. Vitamin D is made in our skin when our [00:02:30] skin sees sunlight, and the precursor to vitamin D, which vitamin D is a hormone, we’ve talked about that before, the precursor to vitamin D is actually a form of cholesterol.
So we talked about, just a minute ago, that it’s from the Greek word meaning cholí, which means bile. Well, of course then that would mean cholesterol is in bile, and that’s true, it’s a precursor to bile acids. Bile acids are made from our gallbladder, and bile acids [00:03:00] are what help us digest fats. So if we didn’t have enough cholesterol on board, we wouldn’t be able to digest fats, and there are essential fats, and then we have those fats also to help us bring in vitamins, there are fat soluble vitamins as well.
All cells can make cholesterol, and this is really important because there are very few things that everything in our body can do, making cholesterol is one [00:03:30] of them. Most of it is made in the liver, and this is where we get on the whole dietary intake of cholesterol thesis that was proven to be untrue. We typically make one to two grams of cholesterol per day, and that’s what our bodies make on their own in order to meet our own needs for cholesterol. A high intake of cholesterol in a dietary pattern is on the order of 300 [00:04:00] to 400 milligrams per day. So if you make two grams per day and you’re eating 300, that 300 is a minor, minor impact on your overall cholesterol levels, and what actually happens is if you eat more, your body makes less. If you eat less, your body makes more. Our bodies like to stay in that field of homeostasis, that balance. And there are some things that throw that [00:04:30] balance out of whack, and we’ll talk about those in a minute.
So you can’t talk about cholesterol without talking about lipoproteins. Lipoproteins are exactly what it sounds like, these are proteins that carry fats. Oil and water do not mix, so in order to carry the fats in our blood, we hide them inside proteins called apolipoproteins. So what these proteins do is they have the fats in the middle. The [00:05:00] proteins surround the fats to protect them from the water, and on the inside of these proteins are fat soluble particles so the fats can hang out there and be safe and not have to worry about getting it with that water that they don’t like. So one of the consequences of this whole low fat craze is a deficiency in the fat soluble vitamins, A, D, E, and K, because these vitamins need these apolipoproteins to help [00:05:30] carry them into the cells.
So how do we make apolipoproteins, what determines this? So it’s determined in the intestines by the fat quality and quantity we eat. I’m going to repeat that, because it’s determined by the fat quality and quantity, so both actually matter. And then they’re also made in the liver by numerous factors that determine this, it can be dietary, it could be hormones, as in insulin, [00:06:00] glucagon, which is the hormone that opposes insulin. So if our blood sugars get too low, we release glucagon. Our thyroid hormones, our estrogens, and some of the other sex hormones can determine that. Toxins can determine that. One of the reasons that we’ll talk about cholesterol can be elevated is because of toxin exposure. And of course medications typically work too, on some aspect of this process, to alter it, so to lower the cholesterol levels.
[00:06:30] Okay, so let’s break it down. So what happens? How does the fats we eat end up into these cholesterol molecules, these apolipoproteins? Because usually when people say cholesterol, they mean all of it, they mean cholesterol, their HDL, their LDL, and we’ll talk about that in a minute, but let’s talk about the pathway of getting these in the body. So when we eat fats, they’re broken down into something called triglycerides. [00:07:00] Triglycerides are just a basic element of these fats, and that’s something that you pick up on blood work as well. Your triglyceride levels are one of the things you check in the cholesterol panel.
So they’re made into chylomicron in the intestine, what the triglycerides are made in the chylomicrons, and then they pick up a donation of one of the lipoproteins, the apolipoproteins, and they exchange out triglyceride. So HDL [00:07:30] does this, HDL, one of the “good lipoprotein” that people think of, your good cholesterol is the HDL. And I’m doing air quotes somebody around me to see them. All right, let’s get back on track.
So the chylomicrons pick up apolipoprotein C2 and E from HDL for triglycerides. So after that, an enzyme called lipoprotein lipase [00:08:00] will cleave off fat and a sugar backbone called glycerol, and that can either be taken up by muscles, or fat, and it can be either stored or burned for calories, depending on where you are. So these chylomicron remnants then circulate around to the liver. From there the remnant is turned into VLDL, which is very low density lipoprotein, [00:08:30] and this is something that you’ll see on your cholesterol panel as well. So VLDL particles then circulate around, and they can get a donation from HDL, high density lipoprotein. And again, it’s that apolipoproteins C2 and E again, that HDL donates to it. So that is one that you can create an intermediate density LDL, or IDLs.
[00:09:00] The other way is that lipoprotein lipase again can cleave off more glycerol and fatty acid, which is then taken up by muscle or fat cells to be stored or burned. So those are two different ways that we can create the intermediate density lipoproteins. Then the intermediate density lipoproteins either have the glycerol and the triglycerides removed from them, which turns them into LDL, [00:09:30] or they go back to the liver and they’re turned into LDL, which is low density lipoprotein, or they’re recycled back into those VLDL, the very low density lipoproteins. And then LDLs main function is to carry cholesterol to the tissues. So the molecules before were carrying triglycerides and glycerol to mainly fat and muscle. LDL, its main function is to carry cholesterol [00:10:00] to tissues.
Now HDL is made from the liver, and as we talked about earlier, it donates lipoproteins to these other precursor molecules. In return it picks up cholesterol from the tissues as well, and so it’s part of the cholesterol recycling process, and it’ll either deliver cholesterol to the tissues, or back to the liver for recycling, and when it goes to the liver, then it’s emptied out of the system [00:10:30] via the gallbladder, or it’s recycled back into LDL. So this is typically what the cholesterol system does, in a nutshell.
Let’s talk about HDL more for a minute, because HDL is what people assume and think of as the good cholesterol, it’s the good lipoprotein. HDL is actually a complex that we call a proteasome, these are fancy words that just [00:11:00] basically means a complex, and it’s actually very anti-inflammatory. And so HDL functions more than just as part of the cholesterol recycling, it actually has immune properties to neutralize bacterial toxins, it can prevent the oxidization, the damaging of LDL in such a way, when you oxidize something, it basically means that it’s been damaged, usually through electrons, [00:11:30] and it creates a very inflammatory type of fat. So HDL normally prevents the oxidization of LDL, which is very good. Oxidized LDL is what causes plaque buildup, heart disease, inflammation, that’s a very bad process.
Under conditions of inflammation or stress, however, the content of the HDL molecule changes and it’s unable to function in the immune system, so [00:12:00] it’s unable to neutralize bacterial toxins, and it’s not able to prevent LDL from oxidizing. So LDL will usually oxidize under situations due to high blood sugars, diabetes, that’s why diabetes has a lot of cardiovascular complications, inflammation, and that’s why we see people with high levels of inflammation have a lot of cardiovascular disease, and what happens in that situation is LDL gets trapped [00:12:30] on the arterial walls, oxidizes, and that leads to plaque formation, at least to immune system activation.
Okay, so we’ve talked a little bit about LDL, HDL, all of these things, let’s break it down into what you see on your cholesterol labs, because that matters as well, a lot of people don’t know what they’re looking at with these things. So HDL, or LDL- [00:13:00] C, whenever it says C, that’s a concentration. So a concentration is essentially how much of one thing is in how much of another thing. So we’ll usually see this in medical terms as milligrams per deciliter, or some variation depending on the amount of something like that. So it’s how much of one thing is in another thing. How much [00:13:30] particles are in your liquid blood, that’s a way to think about a concentration, and that’s what you see with the C.
Now we, in functional medicine, in integrative medicine, like to do something where we actually look at particle counts, which is how much of it there actually is, it’s not the concentration, it’s not how much of A is in B, it’s just how many of A are there actually there? And this is the particle count. How many [00:14:00] particle, how many of the HDL or LDL molecules, are there? And so you’ll see that as HDLP, or LDLP.
The next thing you’ll see on the cholesterol panel we run, it’s usually called the NMR panel, is particle size. So instead of just knowing how many of there are, I’d like to know the size of these particles, because large particles, [00:14:30] large HDL, large LDL, these are like buoys, they just float around, they deliver cholesterol and other nutrients to tissues, they’re not inflammatory, and they are not causing plaque, they’re not causing heart disease. In the medical terminology this is atherosclerosis, that’s what the plaque buildup, that’s the medical term, and things that cause atherosclerosis are atherogenic. So the large particles [00:15:00] do not influence the buildup of plaque, they are not atherogenic. You know what it is, is small dense particles.
So small dense LDL is a problem for numerous reasons. Number one, it’s atherogenic. Number two, it oxidizes easily, so it gets trapped in the arterial walls easier. So you don’t want this trapped in the arterial walls, we just talked about when that happens, when you get LDL trapped [00:15:30] in your artery walls, you get inflammation and oxidization of that, which develops plaque, which develops heart disease. Also, small dense LDL has a lower affinity, meaning it doesn’t bond as easily to the receptors for LDL in the liver. Now what does that mean? It means that that LDL is not so easily recycled. So this is why it’s a double whammy problem, because number one, it sticks [00:16:00] to your arterial walls easier, it’s more easily oxidized, which means more inflammation, and then you combine that with the fact that it’s not as easy to get rid of when it’s in your body.
And this is why I talk about statins. There’s lots of people on statins, and if you look at for primary prevention, meaning preventing cardiovascular disease, statins have an absolute risk reduction, meaning if a 100 people get it, what’s the number [00:16:30] of people that actually prevent… or if you’re looking at 100 people, what’s the number that you’re actually going to prevent? Is it three? That would be 3%. Is it 10? That would be 10%. So that’s absolute risk reduction. Statins have an absolute risk reduction of around 3-9%, depending on the trial you look at. So that means 91 to 97% of people who are on statins, primary to prevent the first incidence of a heart attack or stroke, are going to see absolutely [00:17:00] no benefit. And the reason for that is statins do not reduce small dense LDL. So that’s a huge, huge problem with the conventional medicine approach to treating cholesterol, that you’re actually not doing anything for these major source of problems in the cholesterol, the small dense LDL which oxidized as easily.
So one of the things that you’ll also see sometimes [00:17:30] is they’ll actually measure apolipoproteins A and B, there are actually multiple subtypes, A through E are the most well-known. Each has different biological functions, and apo-B is pretty is the major one that we look at. And the reason for that is studies show that elevated apo-B, our risk factor for heart disease, while apo-A has a protective effect. In fact, some studies show that [00:18:00] the apo-B to apo-B ratio is extremely predictive of cardiovascular disease, and the reason for this is apo-A levels usually correlate strongly with HDLC levels, so you usually see them move in the same direction, and apo-A is an approximation of that LDLP, that particle number that we talked about. While apo-B levels correlate with LDLC, they correlate with the LDL concentration, [00:18:30] and they are an approximation of LDLP. So a ratio above 0.9 is associated with an increased risk of developing cardiovascular disease. And I think I said that wrong just a minute ago, the apo-A correlates strongly with HDLC, and is an approximation of HTLP, and the apo-B correlates with LDLC, [00:19:00] and is an approximation of LDLP.
So we’ve broken down a lot about what you’re seeing on your lab test so you have more information, so you know exactly what you’re looking at here. Now let’s talk about what actually causes elevated cholesterol. Number one, dietary cholesterol has very little impact on blood cholesterol for the majority of people. As we talked about, if you eat more, you’ll make less. If you eat less, you’ll make more. [00:19:30] Now there are people who are genetically hyper responders who may see elevations based upon food. However, they usually have elevated particle size, so that means that they may have an elevated cholesterol level, but they’re the particles that aren’t causing problems. And then in addition to an elevated LDL particle [00:20:00] count, they also usually have a higher HDL particle count, which offsets. So you have larger particles, and then you get an offsetting increase in LDL and HDL. So usually these genetic hyper responders, if you’re talking about just that in isolation, don’t have an increased risk of cardiovascular disease.
Multiple studies have shown no link to dietary cholesterol and cardiovascular disease. [00:20:30] You have to look at some of these older studies that first link saturated fat and cholesterol to heart disease, they were bad studies, number one, methodologically flawed. Number two, they didn’t differentiate the sources of these fats. We talk about this all the time, there’s a big difference between eating a grass fed steak and eating processed cured [00:21:00] lunch meat. Big difference in the fat profile, big difference in the inflammation that they cause.
Studies do show that replacing saturated fat with polyunsaturated fat has heart benefit, but then again, this is what we just talked about, these studies don’t look at fat quality. We talked about earlier in the episode that the quality and the amount matters with how much you make these apolipoproteins, So your quality [00:21:30] of your nutrients matters. And this is something we’ve talked about in the Strive for Great Health Podcast so many times before, quality matters. In fact, the current guidelines don’t even advocate for reducing dietary cholesterol intake. Current guidelines say there’s no strong evidence that we should reduce dietary cholesterol intake, and this is for the reasons that we talked about, for most people it doesn’t impact blood cholesterol and it doesn’t actually link with cardiovascular [00:22:00] disease.
So what actually causes elevated cholesterol? The three main things that I see when I work with people, number one, insulin resistance. That is the big one. I would say 90 to 95% of people I see either have insulin resistance or inflammation as the cause of their actual elevated or abnormal cholesterol levels. So how does insulin resistance cause [00:22:30] this? Well number one, it changes cholesterol metabolism. It lowers HDL, raises triglycerides, and then you get a high VLDL, because more VLDL is synthesized, and this is caused by higher free fatty acids in the blood, so elevated blood sugars actually increased cholesterol synthesis. So if you want to lower your cholesterol, lower your blood sugars.
Insulin resistance increases the liver making more fats. [00:23:00] Because insulin resistance, we talked about this and the insulin resistance podcast, the main problem with insulin resistance is you cannot efficiently generate energy from carbs. So the liver starts making more fats in order to generate energy, but you’re already, for most people, in a hyper-caloric, meaning there’s too many calories state, so you end up with more free fatty acids just floating around in the blood, and that’s not good. So usually in insulin resistance, [00:23:30] cholesterol absorption from the diet is very low, because we just talked about that, blood sugars increased cholesterol synthesis if you have elevated blood sugars. So usually in people who have insulin resistance, the amount of cholesterol they’re absorbing is extremely low.
So let’s move on to inflammation. Inflammation is the other big cause. We’ve talked about this in our podcast on [00:24:00] immunity and the immune system, about what causes inflammation. Inflammation decreases HDL, increases VLDL and triglycerides, and this is caused by some of those inflammatory mediators. Inflammatory mediators are things made by cells and immune cells, and we’ll talk about this more in a future podcast about how to boost immunity, but these inflammatory mediators are what [00:24:30] our immune cells use to talk to each other, and what our bodies use to start immune reactions and inflammation. Inflammation increases small dense LDL, that double whammy that we talked about. You also decrease that lipoprotein lipase and you prevent the breakdown of triglycerides in the blood, so those triglycerides aren’t able to be taken up by muscle cells to be burned. [00:25:00] And you decrease that apo-A1, we talked about apo, means apolipoprotein, I can’t remember if I said that earlier, but that’s how we shorthand say apolipoprotein, We say apo. So you decrease apo-A1, which is the major lipoprotein in HDL.
So this main action of doing this acutely with inflammation is to bring nutrients to immune cells, and lipoproteins that bind [00:25:30] and neutralize toxins, viral particles, and parasites. But chronically over time the system gets dysregulated, and that’s usually what happens with the immune system. The immune system, usually at first it tries to do something to acutely fight off an infection, fight off an invader, or run from a tiger, but chronic elevations dysregulate the system and lead to disease. Hormone alterations, alterations [00:26:00] in testosterone, thyroid hormones, low vitamin D, these are all associated with abnormal blood cholesterol levels, abnormal apo levels. Being sedentary is a huge one here in America. Being sedentary, if you’re not getting exercise, first off, and then if you’re not moving throughout the day, you increase insulin resistance, inflammation, you increase triglycerides, [00:26:30] because you decrease the ability for your body to metabolize those triglycerides that we just talked about, and then you directly lower your HDL levels.
Toxins can also influence this, through several different ways. Toxins can sometimes cause insulin resistance, toxins can cause endocrine disruption, disrupt those hormones. Toxins also can cause inflammation, and this is a chicken or egg thing, but [00:27:00] if your body’s under stress, like we talked about, it can increase the cholesterol levels, increase the LDL levels, trying to repair the body, trying to bring nutrients and cholesterol, and then trying to neutralize toxins and viral particles. But the problem is, is with that inflammation they’re more likely to get oxidized. So your body’s trying to help itself, but really it’s hurting itself, [00:27:30] and this is why we put in our five pillars program a section on avoiding toxins, because a major effect of toxins is increasing the bad cholesterol, the bad blood apolipoproteins.
And I say cholesterol, again I mean some of these bad, small dense LDL, that’s what I mean. I typically say cholesterol because we lump everything together, I should be more [00:28:00] proactive at saying exactly what I mean, so I’m going to try and do that for the rest of this episode.
Genetics, we talked about those hyper responders. So these are people who genetically have a predisposition to having abnormal LDL or HDL levels. And then lack of sleep can impact it, through many different ways. One, increasing cortisol, the stress hormone, which has effects on our immune system, which is going to effect our [00:28:30] HDL or LDL, and our cholesterol. The second is improper sleep actually makes you more insulin resistant, and we talked about insulin resistance and how that changes your cholesterol and your HDL and your LDL. And then sleep is when our bodies repair, so if you’re not getting enough sleep, your body’s going to think, hey, I need to repair. And what did we just talk about? When your body’s in a, hey, I need to repair state, you increase [00:29:00] your cholesterol synthesis, decrease your HDL and increase your LDL, so you bring more cholesterol to the tissues, and less cholesterol recycled back in the circulation. But you also generate more of that small dense LDL, the double whammy.
So what are some strategies to normalize your blood lipids? That’s probably what I should’ve said to begin with, because that’s a more accurate term, blood lipids, your blood fats, your blood cholesterol. Obviously if being sedentary [00:29:30] is a cause, exercise. Exercise increases your particle size, it decreases your particle number, it increases your LDL, decreases your small dense LDL, it reverses insulin resistance, exercise also helps us with inflammation. So you can see how all of these things would impact the blood lipid and blood cholesterol levels.
Eat whole foods. Again, the most important decision you make on a daily basis, as far as your health goes, [00:30:00] is what you put into your body. A lot of the things in fruits and vegetables, anthocynins, flavonoids, polyphenols, those all help balance your blood lipids and blood cholesterol. You want to eat quality, saturated fats. Again, quality matters, so grass fed, grass finished. Hyper responders may want to stick to monounsaturated fats, like olive oil, like avocados, those types of things, [00:30:30] especially if you have inflammation. If you don’t have information, then it’s probably going to be okay, like we talked about, but if you have inflammation, definitely stick to those monounsaturated fats. EGCG, the main ingredient in green tea, also is beneficial for balancing our blood lipids and cholesterol. Fiber can help, because it does lower some of the cholesterol absorption. It’s a minor effect, but if you’re not getting enough fiber [00:31:00] that can also influence the levels to a minor degree.
Sleep, of course, get more sleep. You want to regulate your hormones, you want to give your body adequate time to repair, you want to decrease your inflammation, and you want to decrease oxidative stress, so that’s all related to getting enough sleep. Intermittent fasting, one of our favorite tools, it’s in our five pillars system, it’s in our wellness programs. You decrease triglycerides and LDL by fasting, it [00:31:30] doesn’t really affect HDL. You increased lipolysis, which is fat burning, you decrease inflammatory mediators, which is good, because we talked about how inflammatory mediators can disrupt the normal balance of our blood lipids and cholesterol. There is some evidence that shows it may increase apo-A. Hey, that’s good, more HDL, and decrease apo-B. Hey, that’s also good, less LDL particles and less small dense LDL.
You increase [00:32:00] beta oxidation, which is basically the process by how the liver and muscles burn fat as energy, which decreases VLDL, which is also good. And then you may also prevent some of the transfer from HDL to LDL, and so this may stop some of that whole recycling pathway and increase the clearance of cholesterol. And then you decrease [00:32:30] cholesterol, synthesis enzymes as well, through a process called SREBP-2, that’s the gene name for it. We always like to say some science in here, so that might be a term that you hear in the future.
Supplements, that’s always a question. What supplements should I take to help with this? Number one thing we put people on is phytosterols. Phytosterols decrease intestinal absorption of cholesterol, they increase the body’s excretion of cholesterol. Not really sure how this does it, [00:33:00] but it does. It increases clearance of LDL from the blood via the liver, and they’re anti-inflammatory. Fish oil. Fish oil decreases VLDL production, it increases its clearance, so that means less VLDL, less LDL. It reduces inflammation in fat cells, it decreases lipolysis in fat cells, and increases lipolysis outside of fat cells. Well that’s [00:33:30] good. So if you’re increasing the burning of fat outside of the fat cells and decreasing the ability of the fat to accumulate in fat cells, and that should have been it decreases lipogenesis and fat cells, meaning it decreases the ability of fat cells to make fat, and increases lipolysis outside burning fats outside. That’s good. And it increases the beta oxidation, [00:34:00] that burning of fats that we talked about, in the liver and the muscle cells.
Psyllium, it helps to bind bile acids and remove them from the body. And so what happens is then the body has to utilize more of that cholesterol to replace them, so instead of now the cholesterol being elevated and just sitting in the blood, it’s now being shuttled to more to making bile acids. [00:34:30] Berberine, one of our favorite supplements for diabetics, it’s great for blood sugars. Also great for reducing LDL. 20 to 30% reduction in LDL with berberine in some studies. It actually works through a mechanism called PCSK9, which there are drugs now that work through this mechanism. So what happens is we talked about that LDL receptor on liver cells, PCSK9 prevents these receptors from getting removed so you’re able to increase your LDL [00:35:00] clearance. Bergamot is a flavonoid, usually we think of it with citrus fruits. It actually inhibits cholesterol synthesis, and it increases the LDL receptor expression. So you’re making less cholesterol, and you’re clearing more of your LDL.
And niacin, vitamin B3. This is something that people will use to raise HDL. It inhibits [00:35:30] triglyceride synthesis in the liver, it prevents apo-A, the major part of HDL, from being broken down, and it inhibits oxidative stress and inflammatory markers. So lowers those inflammatory markers. But in order to get enough niacin to do this, you pretty much have to supplement it, and the main thing that people worry about in that case is flushing.
So this has been the Strive for Great Health Podcast [00:36:00] with Dr. Richard Harris. I hoped you learned a lot about cholesterol. I know this one was a lot more science-y than the other episodes, but I think it’s very, very important to understand all of this, to get this down, and to have a better understanding of what you’re actually seeing when you look at your cholesterol levels, because most doctors don’t even know this. This is not something that’s taught in medical school, this level of evaluation. I had to go learn this on my own by reading data, by reading studies. And this is [00:36:30] what the functional medicine and integrative medicine classes teach physicians, this is why we always recommend seeing a functional or integrative medicine doc if you want a different approach to a chronic illness.
If you want more information on what we recommend for our lifestyle medicine, you can head to the GHwellness.com, click on programs, our five pillar program, with our building healthy habits course, that is the backbone of how we practice medicine, that is all the lifestyle medicine [00:37:00] techniques to give your health the best shot. We always like to say two things, one, investment in your health pays dividends, and the second, if you do not make time for health, you will be forced to make time for illness, and I’d rather you make time for health, because I’m tired of treating sick people. I’d rather teach a whole bunch of people how to be healthy than treat sick people, and that’s the essence of the five pillar course. I poured my heart [00:37:30] and my soul into that so I can prevent people from getting sick, I’m tired of treating sick people.
So thank you for listening to this episode, and God bless. Thank you for listening to the Strive for Great Health Podcasts with Dr. Richard Harris. If you enjoy the podcast, please leave a five star review on your preferred podcasting platform, and don’t forget to subscribe. If you enjoyed this content, you would love our YouTube channel at Dr. Richard Harris MD, and our Facebook group, Strive for Great Health. [00:38:00] Both of these places contain more health, wellness, and lifestyle information. If you’d like to support the podcast, join our Strive for Great Health insiders group. Insiders get early access to episodes, take home points, links to articles and supplements mentioned, and discounts on our wellness programs. To become an insider, head to our website @GHwellness.com/podcast, and click on the green button to become an insider. [00:38:30] Thank you, and God bless.