Why is cholesterol testing not dead yet?

Why are we still using 1950s technology to predict and manage risk for heart disease in the form of cholesterol testing? Superior methods have been available for >30 years. 

Sadly, the key is money. If superior methods to identify and manage risk for heart disease are essentially without cost, how would the healthcare industry make its money? 

Transcript

Why Cholesterol Testing Should End

William Davis, MD 0:00

Let's talk about why this thing called cholesterol and cholesterol testing should have died decades ago. It's a remnant of 1950s and 1960s technology. Imagine your technology for computing was locked around somewhere in 1960, like an abacus, or maybe a slide rule. Imagine trying to get your job done now using that kind of tool and not taking advantage of modern personal computers, microchips, uh, artificial intelligence. I mean, look how far technology has come. Yet we're still using 1960 technology for gauging risk for heart disease. It's inexcusable. And it did take the willing participation of my colleagues, doctors, who had been brainwashed. They drank the Kool-Aid in believing that cholesterol was the cause for coronary disease. This is absurd. Now, let's think

Why Fats Need Lipoproteins

William Davis, MD 0:52

about why. So cholesterol is a fat. Fats cannot circulate freely in the bloodstream for the simple reason that fats coalesce when they're in an aqueous environment, when they're in a water-soluble environment. You see this when you have salad dressing, right? If you mixed oil and vinegar and you shook the jar, the bottle, you'll see it mixed briefly, right? And then within moments it separates back out into water and oil, because those two things don't mix. But you'll see that the oil layers out, right? It coalesces. And the same thing would happen in the bloodstream. If you had freely circulating fats, they would coalesce. And that would be fatal within moments, within seconds, because if fats coalesced in capillaries and small vessels, it would kill, it would infarct, we say, tissues. Your brain would die, your heart would die, your muscles would die, liver would die within seconds. And so fats cannot float freely in the bloodstream. So that's a basic rule of physiology. So in order for fats to become solubilized, that is to be able to be dissolved in an aqueous or water-based environment, which is that that's what your blood, your blood is. If you remove the red blood cell, it would be clear plasma, an aqueous environment. And fats can't circulate freely in that aqueous environment. So fats must be coupled with something that makes it aqueous soluble, solubilizes the fats. And that's what lipoproteins are, lipid or fat-carrying proteins. And there's a whole range of these things. So it's not that cholesterol circulates freely and gets deposited in arteries. It's a simple idea and it appeals to the simple-minded doctors and public where they think if you eat saturated fat, it goes right to your arteries. This is, of course, complete utter nonsense. There's no such thing. This is not, does not happen in biological systems. Instead, fats, whether it's cholesterol, cholesterol esters, phospholipids, and other things, triglycerides, must be on a protein-solubled vehicle, lipoproteins. And the nature of those lipoproteins, what they contain, their surface characteristics, size, quantity, that's what determines how they may interact with the arterial wall and deposit some of their contents into the arterial wall, that is the process of atherosclerosis. So the process that leads over time to plaque rupture, heart attack, sudden cardiac death, need for procedures like stent implantation or bypass surgery. So it's the nature and quantity of the lipoproteins that determines whether or not those things, those lipoproteins, are going to contribute to the expansion of atherosclerotic plaque. It does not have anything to do with cholesterol. Certainly, cholesterol is not float-free in the bloodstream. It is a component of those lipoproteins. So that does have that role.

The LDL Cholesterol Thought Experiment

William Davis, MD 3:58

Let's play a thought experiment here. If you've been following my conversations, you may have heard me say this before, but I gotta tell you, so many people have so deeply, thoroughly been brainwashed with this idea that cholesterol causes heart disease. That's worth hearing these arguments in a variety of different ways so that it sinks in. You understand that my approach to cholesterol is really simple. Get a big thick black magic marker and cross the values out. Cross out total cholesterol, LDL cholesterol, they're nonsense. But let's just play a thought game. Let's say I told you that your LDL cholesterol was 180 milligrams per deciliter, a level that most doctors would regard as being at high risk for heart disease. What does that tell you about your physiology? Well, you'd know that total cholesterol would be higher because remember, LDL cholesterol and total cholesterol are calculated from each other. So those two, it doesn't offer any additional information because they're pretty much the same kind of value. It does tell you that the protein, apoprotein B, is going to be high. For every LDL particle, there's one apoprotein B. So apoprotein B is a virtual count of LDL particles. So you know with an LDL cholesterol of 180 million milligrams per deciliter, your apoprotein B is likely to be higher also, maybe 160, 180 milligrams per deciliter, something like that. What else can I tell you about your physiology if we know your LDL cholesterol is 180? That's it. That's all we can tell you. What if instead I said to you, we're going to do a lipoprotein

How NMR Particle Testing Works

William Davis, MD 5:32

analysis, right? We're going to look at those actual particles that transact energy, proteins, fats in the bloodstream, the solubilized particles that carry cholesterol, triglycerides, and other things. What if we quantified the low density lipoprotein, LDL particles, not LDL cholesterol, one of the components, but we actually characterize and count the particles themselves. And you can do this. I've been doing it for 35 years. The most popular method nowadays, it's evolved over time, is nuclear magnetic resonance, NMR, lipoprotein analysis. And all that means is we're going to examine your plasma, the clear part of your blood, in magnetic feet, in a magnetic field. And that there's a way to it characterizes and counts the number of particles. There's some other methods like gel electrophoresis and ultra-centrifugation. Those are harder to come by and are kind of falling out of favor over the last 30, 40 years. So for all practical purposes, it's NMR lipoproteins that are the most available, very inexpensive, a little more difficult to interpret. And that's one of the reasons why doctors don't embrace it, because it requires more education, a little more sophistication. And you're going to see that once you understand how lipoproteins work, what they tell you, you're going to find you don't need any pharmaceutical to control, to eradicate risk for coronary disease.

What Small Dense LDL Signals

William Davis, MD 6:55

So if I told you we did an NMR lipoprotein panel, and your total LDL particle number was let's say 2400 nanomoles per liter, particle count per liter. And of that 2400 nanomoles per liter, 1800 or 75% are small and dense. Small dense lipoprotein, LDL particles. So 75%, all the total LDL particles are abnormally small. What does that tell me about you? Well, it tells me a whole bunch of things about you. It tells me that you're going to have a higher triglyceride level. High to me is anything above 60 milligrams per deciliter, so maybe it's 240 milligrams per deciliter. It tells us that you have a lot of VLDL particles, very low density lipoprotein particles that are densely packed with triglycerides, fats. It tells us that your liver is very busy converting carbohydrates and sugars into triglycerides. That process is called de novolipogenesis, making new fats. So taking carbs and sugars, making fats, triglycerides. Some of those triglycerides will stay in the liver and contribute to the fatty liver. So your AST and ALT liver markers will be higher, reflecting liver damage. It means your triglycerides will be higher. It means your VLDL will be higher. It means that you likely have an excess of abdominal visceral fat that is fat encircling the organs of the abdomen, because that fat drains to the portal vein to the liver. And that serves to amplify that process of denoval lipogenesis. Knowing your small LDL particle number tells us you have insulin resistance. Your body is not responding to insulin, liver, muscle, brain not properly responding. Your pancreas compensates by wildly overproducing insulin that further amplifies liver denoval lipogenesis that makes those VLDL particles. We also know that you likely have colonic dysbiosis or even more likely SIBO, small intestinal bacterial overgrowth. Remember that? The invasion of the small intestine, 24 feet of small intestine by fecal microbes. We say gram-negative proteobacteria, because those microbes, when they die, they shed some of their toxic components, but especially lipopolysaccharide endotoxin, into the portal vein that drains the entire gastrointestinal tract straight to the liver. So that's the portal vein system. So the portal vein conveys this toxic endotoxin molecules to the liver, and that further amplifies liver deanova lipogenesis. You can see that your liver's been revved up, being fed with carbs and sugars, being exposed to the contents of visceral fat in the abdomen, insulin resistance, and also inflammation. I should mention that the visceral fat is also very inflammatory. So some of those inflammatory mediators likewise go to the portal vein, then to the liver. So the liver is provoked to produce huge amounts of triglycerides from carbs and sugars and package them into VLDL. We also know that the VLDL is a direct cause for coronary disease. Those particles, VLDL particles themselves, are a cause for coronary atheroscopic plaque. And VLDL particles interact with LDL particles, contributing triglycerides to the LDL particle. There's a series of enzymatic remodeling steps that makes that LDL particle now small. So we know that to get small LDL, there's lots of VLDL preceding it from carbs and sugars. We know that those LDL particles are more prone to glycation, glucose modification of the apoprotein B, and oxidation that makes it much more aggressive in causing carnary atherosclerosis. Because that small LDL particle, now, because it's small, it's better able to penetrate the walls of arteries, it's more likely to enter the wall of arteries and stimulate inflammation, the entry of white blood cells, inflammatory cells. It's much more adherent to structural tissues in the walls of arteries. We know that the small LDL is a persistent particle that lasts five to seven days in the bloodstream. Unlike the large LDL particles, that persist only about 24 hours. So anything that provoked formation of small LDL gives you an increase in cardiovascular risk that lasts five to seven days. And that's why I encourage people to stop this idea of having bad days where one day you have a bunch of pizza or birthday cake or whatever, because that risk is persistent for an extended period. We know that you're likely to be hypertensive because that reflects the can abnormal constrictive behavior of your arteries, both coronary arteries and other arteries of the body that raises blood pressure. We know that if we measured inflammatory markers like C reactive protein, interleukin 6, interleukin 1 beta, tumor necrosis factor alpha, or even something as crude as a white blood cell count, they'll all be higher. If all we knew was your small LDL is high, we know that you have an increase in inflammatory markers. We know that you have that endothelial dysfunction, and thereby you damage your glycocalyx lining arteries. And all that means is there's a very delicate hair-like collection of projections on your arteries that control arterial tone. They're pressure sensors. And by the way, the glycocalyx is largely made up of hyaluronic acid. Isn't that interesting? But anyway, if you have carnival, if if you have an excess of small LDL and thereby endotoxemia, endotoxem is extremely toxic to that glycocalyx. So we know that when you have small LDL, we know you have SIBO endotoxemia, we know that you've disrupted your glycocalyx, we know that you have endothelial dysfunction. Are you getting the picture? There's more, but are you getting the picture? This idea that LDL cholesterol is the cause of, I call it the kindergarten version, right? We're going to advance the gradual level of understanding of caronary disease. You can see that carony disease, it takes a whole constellation of abnormal phenomena for you to have a heart attack. It takes decades of these processes all working together. Insulin resistance, inflammation, portal venous, endotoxemia, endothelial dysfunction, all this stuff combined, that's how you get coronary disease. And just taking a drug to reduce cholesterol, this crude marker, it's shocking to me that this is still the prevailing wisdom in preventing heart

The Lab Panel That Matters

William Davis, MD 13:34

disease. Now, the good news here is when you start to look at these kinds of measures, let's say you did some blood work to show what your risk is. And by the way, the the panel I use to give you a starting place to get a really good handle on your risk for carony disease would be an NMR lipoprotein panel. And it gives you all the numbers we talked about, small LDL, total LDL particle number, and some other things. Make sure the first time you do it to include a lipoprotein A. You only need it once because it's genetically determined, and we do not try to reduce lipoprotein A. That's that's a whole nother conversation for another day. How we manage people with lipoprotein A. Very interesting stuff, by the way. So NMR lipoproteins with a lipoprotein A. It helps know your blood glucose and insulin status. So we get a fasting glucose, fasting insulin, hemoglobin A1C. That gives you a pretty good starting place. We need to know your vitamin D status, so we get a 25 hydroxyvitamin D. And because thyroid disease is rampant and can act as a caronic risk factor, we get a full thyroid panel, a TSH, free T3, free T4, reverse T3, and thyroid antibodies. That simple panel tells you about 98% all you need to know about your cardiovascular risk. And you're going to see right away as you get into this that you do not need any pharmaceutical to make those numbers look beautiful. There's a rare, rare exception. Once in a while we'll see, I've seen this maybe three times in my entire 35 years, where there's somebody who has such bad genetics that there is some benefit to medications. But the vast majority of people do not need nor benefit from medications, whether it's a statin drug or PCSK9 inhibitor or whatever, or fibrate or whatever.

Food Nutrients And Microbiome Fixes

William Davis, MD 15:24

You can get this done wonderfully, completely, in the vast majority of people with nutritional strategies. And by nutritional strategies, I mean a shift in diet, weak grain sugar elimination, restoration of common nutrients that are deficient in modern people, magnesium, omega-3 fatty acids, iodine, and vitamin D. There are other nutrients you can play with, but those four are the most important because they're deficient in the vast majority of people. And when restored, they synergize to minimize insulin resistance and inflammation. And then we address the microbiome, the gastrointestinal microbiome. And we do so using microbes, microbes that colonize the small intestine and are known to produce bacteria since. So if you know what I'm talking about, see my recipe for what I call SIBO yogurt. It's just a collection of three microbes that we cultivate using extended fermentation. Very easy. And it makes a delicious yogurt-like. It's not yogurt, of course, but it's yogurt-like fermentation using human-sourced microbes. And that makes a yogurt-like food that you can enjoy with blueberries. But the microbes are chosen specifically to colonize a small intestine, produce bactericins, natural antibiotics effective in killing those fecal microbes, and that's how you reduce portal venous endotoxemia as well as systemic endotoxemia. But you can see it's all a natural approach restoring factors that we've all lost, and it has nothing to do with pharmaceuticals.