Understand the "Universe" of Small Dense LDL Particles

Why does much of the world cling to the outdated notion that cholesterol is the cause of heart disease and that reducing cholesterol is the solution, even after decades of evidence have more than amply demonstrated that this approach is woefully inadequate? Sadly, it's about money. 

But you do not have to be hogtied by financial concerns. You can take a path that actually works. You can start by measuring small dense LDL particles that gives you a mountain, an entire "universe," of insight into risk for coronary disease and what to do about it. 

Transcript

The Small Dense LDL Universe

William Davis, MD 0:00

Let's talk about this thing I'm calling the universe of small dense LDL particles, the real cause of coronary disease. That is the process that leads to heart attack, angina, need for stent implantation, bypass surgery, and a cause of sudden cardiac death. So serious stuff, right? Well, what I'm going to explain is that small LDL does not occur in isolation. It occurs along with a cluster, a whole universe of abnormal phenomena that in total lead to coronary disease. So compare that to the conventional measure, which is LDL cholesterol. So if I told you someone's LDL cholesterol was high, 180 milligrams per deciliter, what can you tell me about that person? Can you tell me their race, their age, their eating habits? You almost can't tell anything. You might say, if you subscribe to conventional wisdom, that that person might eat too much saturated fat, like bacon or pork or fatty meats. But we know that following that line of thinking led down a disastrous path, right? Of cutting fat, cutting saturated fat, eating more healthy whole grains, and overloading your diet with carbohydrates. That's what people have done in response to the cut your saturated fat and cholesterol message of the last gee, 50, 60 years, something like that. So but you really can't tell about much about a person just by that LDL cholesterol, say of 180 milligrams per deciliter. Maybe a diet speculation, but that's about it. It'll also be accompanied by a higher total cholesterol, but those are pretty much the same kinds of numbers, right? So it's we're not telling you much more. And that's no surprise because LDL cholesterol is a fictitious number. It's not a real number. It came from a very crude and outdated equation called a Friedwald equation or Friedwald calculation, developed by an NIH researcher, Dr. William Friedelwald, in the 1950s, 1960s, when they were using, as you would expect way back then, very crude methods, and they were unable to characterize, quantify the kinds of particles in the bloodstream, the lipoproteins, fat-carrying proteins that cause heart disease. So they used a crude and indirect marker that is an ingredient in these lipoproteins. They couldn't really count them in 1958, 1960. So they used some very interesting ideas. Let's count an ingredient, let's weigh an ingredient, and maybe we can extrapolate what those lipoproteins look like and how many there are. So they chose cholesterol. They could have chosen some other things like apoprotein B or triglycerides or various phospholipids. They chose cholesterol and they used cholesterol as a crude indirect index or gauge of those lipoproteins. Now we can measure those lipoproteins. 40, 50 years ago, it was very expensive to do that. It could cost upwards of$5,000 for a single measurement. Well, over the years that's become streamlined, and now you can get it done for less than$100. There's a number of methods to do that, but the one that's kind of emerged as the gold standard is as nuclear magnetic resonance. And there's some other methods too, but it's nuclear magnetic resonance that's most widely available to most people in conventional laboratories. But so let's say I told you rather than LDL cholesterol of 180 milligrams per deciliter, I told you you had small LDL particles, small dense LDL particles, quantified at 1800, very different numbers, nanomoles per liter. That would be the very rough equivalent of 180 milligrams per deciliter of conventional LDL cholesterol. So let's say we have 1800 nanomoles per liter of small dense LDL particles. Nanomoles per liter is a particle count per volume, in this case a liter. So if your your LDL, small LDL is 1800, what else can I tell you about you? Well, one, you're at very high risk for coronary disease, far higher than the LDL cholesterol would have predicted, because small LDL is a much better, much superior predictor. It tells me that you have insulin resistance, your body's not responding to insulin, and your pancreas is overproducing insulin. That leads to expansion of visceral fat. So I know you have more visceral fat than you should. You may or may not show it on the surface with a pro-tuber and tummy, but we know you have an excess quantity of abdominal visceral fat, at least for your build. So you have excessive abdominal fat. I know that you're likely to have a high measure of inflammation, like C reactive protein and interleukin 6 and tumor necrosis factor alpha. I know that your HDL cholesterol is going to be low, like maybe in the 30s. I know that the HDL particles themselves will be abnormally small because it's large HDL particles that are protective for you for against coronary disease. Small HDL occurs, though, in the company of the small LDL particles. I know that you have high triglycerides. It could be 150, it could be 400, whatever, because triglycerides are the prime ingredient in very low density VLDL particles made by the liver. I know that you overconsume carbohydrates because it takes carbohydrates like sucrose, fructose, glucose, and the amylopectins of wheat and grains, that the liver converts those sugars to triglycerides, a process called denovipogenesis. So I know that not only do you have high triglycerides in your bloodstream, but you also have too much de novolipogenesis from consuming carbohydrates. I know that you're likely hypertensive. I know that your uric acid, another blood measure, is likely to be high. I know that you likely have SIBO, small intestinal bacterial overgrowth, that is an overgrowth of fecal microbes. We say gram-negative proteobacteria, but these are microbes like E. coli and Campylobacter and Salmonella and Pseudomonas. We know that you have an overpopulated those species in your colon that have now ascended into the small intestine. And when that those microbes die, trillions of them in the 24-fifth small intestine. When they die, they release their toxic compounds, but specifically something called lipopolysaccharide endotoxin. And that gets into your bloodstream, but it first goes to the portal venous system. In other words, the gastrointestinal tract is empties or empties its venous drainage into something called the portal vein that goes directly to the liver. So it's your liver that takes the biggest blow from this flood of endotoxin, and that amps up liver de novolipogenesis that converts dietary sugar and carbs into triglycerides and VLDL particles. So we know that you likely have SIBO and endotoxemia. I also know that the insulin resistance is amplifying liver de novolipogenesis and inflammation also. And the inflammation, of course, made worse by the expanding abdominal visceral fat because it's a vicious cycle, right? The more insulin resistance you have, because of endotoxemia, because of uh a bad diet filled with carbohydrates, that drives liver denovile lipogenesis, that causes expansion of abdominal fat, that causes more insulin resistance and inflammation, which in turn makes the liver more active in its liver denoval lipogenesis. You see, so in other words, when you know what your small LDL is and it's high, I would I would call anything above 200 nanomoles per liter high. So anything above, you know you have at least some of those and usually all of those phenomena all working together. This universe of metabolic distortions all leading you down the path of coronary disease. Do you see how silly and simple-minded it is to think that LDL cholesterol, a crude marker for the real life of proteins? So another thing to keep in mind. So LDL particles, not LDL cholesterol, the crude indirect marker for LDL particles, but LDL particles themselves are not one thing. They're a whole family of things. They differ in size, they differ in surface characteristics, conformation, that is the exposure, for instance, of the protein characteristic of LDL particles, apoprotein B. So they differ. LDL particles have different exposure of that apoprotein B. They have different charges, meaning they behave differently. They have different tendency to be ex to be susceptible to such modifying factors as oxidation or glycation, glucose modification of apoprotein B. In other words, if your body is oxidizing and then glycating, we say glycoxidized LDL particles, it makes it much more aggressive in causing coronary disease and getting into the arterial wall and adding to coronary atherosclerosis. And that small LDL, because of its different shape, is not well recognized by the liver. That apoprotein B has to be fully exposed for the liver to recognize it. And if it's concealed as it is in smaller LDL particles, the liver fails to clear it effectively. So a large LDL particle with a fully exposed apoprotein B is cleared within about 24 hours, very rapidly. Small LDL particles, in addition to all those changes, glycoxidation, etc., is also not recognized by the liver, so it persists in the bloodstream for five to seven days, meaning it's given huge, numerous opportunities to circulate all through the body, including through your coronary arteries, your heart's arteries, to get deposited into the wall of arteries or small LDL, much more so than benign large LDL, is more likely to trigger adhesion, inflammation, and uh attracts the entry of white blood cells, inflammatory white blood cells. So can you see that this idea that we're going to use LDL cholesterol and reduce statin drugs to reduce LDL cholesterol is absurd. It's completely inadequate. But if you understand small LDL and all the things that accompany it, you have incredible insight into what to do about them. That's a whole other conversation. But know that it starts at step one, which is feeding your liver carbohydrates and sugars, right? And then all the things that amplify that process, right? Insulin resistance, abdominal visceral fat, portal vein endotoxemia. So see my other videos for conversations about that. See my thousands of blog posts, William DavisMD.com. And of course, if you want support through this process, join my conversations, my live conversations in my inner circle.deardavisinfinfinite health.com. But know that you have astounding control. By the way, why does this not get passed on to people? And why are they still, after years, still focusing on LDL cholesterol? Because it's where the money is. Not for the doctor so much, but for the pharmaceutical industry who entertains and in various ways compensates the doctor for sustaining this outdated, absurd idea of reducing LDL cholesterol statin drugs. The truth is you can gain full control, full control of the entire universe of abdominalities that accompany small LDL by using nutritional methods. You do not need drugs, and it's very effective, and you can prove it to yourself. You can repeat, for instance, your NMR lipoprotein panel, you can look at measures like C reactive protein, other inflammatory measures. You can look at your blood pressure, you can look at your abdominal fat, you can use a bioimpedance scale or other ways to quantify your abdominal visceral fat. You'll see it in the mirror, right? Because you your tummy is flatter. You'll see it measured in other things like your HDL will go up, your triglycerides will come down. So, in other words, all kinds of wonderful things happen when you start to understand that this heart disease risk has nothing to do with LDL cholesterol. It has to do with this constellation or universe of abnormal metabolic distortions that you can use a measurement of small LDL to identify.