Why Are Small Dense LDL Particles Different?

The world has been brainwashed by this absurd notion that cholesterol causes heart disease, thereby wasting your time with talk of statin drugs and saturated fat. 

The tragedy is that the REAL causes of heart disease are identifiable and readily correctable. Small dense LDL particles are the "tip of the iceberg" for an entire constellation of metabolic abnormalities that are the causes underlying heart attack, sudden cardiac death, and the need for heart procedures. 

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Why Small Dense LDL Matters

William Davis, MD 0:00

I'd like to add further to my recent conversations on the importance of small, dense LDL particles as the driver for heart disease risk, coronary disease risk. I do this over and over again and come at it from a variety of different angles because I fear that the world has been so thoroughly brainwashed by this idea of reducing LDL cholesterol with such things as statin, drugs, and others, and reducing saturated fat? This has gone on for about 50 years and it's so deeply ingrained into people's heads, including my colleagues, physicians, that it takes a while to undo all the harm and misinformation that has introduced. That's a whole other conversation, but I want to highlight this issue. What makes that small, dense LDL particle different, unique from, say, a large LDL particle? And by the way, if you had cholesterol testing, you've had no assessment of lipoproteins. Those are cholesterol values that are crude indirect markers. They were designed to be markers for lipoproteins developed at a time, 1950s, 1960s, when it was not possible in local hospitals and clinics to quantify these very tiny lipoprotein particles. So this very crude method of indirect quantification using lipid values was developed. But we've gotten beyond that. You would no more use those numbers than you would say drive a 1958 Studebaker or something like that. Maybe that's not the right year, but you get my point. It's outdated. And we've had access to more up-to-date methods for decades. But it requires a fair amount of education, as these videos are illustrating. That it's not it's not just take this pill and be done with it. It's a whole range of metabolic distortions that uh once you understand it though, it all falls into place, it all makes sense, and you are given extraordinary control over not just risk for heart disease, but risk for other conditions like type 2 diabetes and dementia and hypertension and fatty liver and a whole host of other conditions because they're all related. And small LDL particles, small dense LDL particles are the tip of the iceberg of an entire collection of abnormal distortions, all of which play roles in creating coronary disease and those other conditions.

Why LDL Cholesterol Misses The Point

William Davis, MD 2:30

So let's say you did an NMR, nuclear magnetic resonance, lipoprotein analysis. There are some other methods, but they've kind of fallen by the wayside, and NMR has proven to be the most popular, most successful, and very inexpensive. And you can get it if the doctor says to you, Oh, we don't do that around here. Walk away, find a place that does. Any place can do it. I've been doing it for over 30 years. It's inexpensive. Medicare and most insurance covers the cost. They're gonna say it's experimental. It's not experimental. There have been now 60 human clinical trials, six zero human clinical trials validating the use of this measure. And when you hear what the small LDL number tells you, I think it'll start to click in your mind and it starts to make sense. So let's take a small, dense LDL particle and compare it to a large LDL particle. Large LDL particles are the normal result of consuming fats, fats of any sort, saturated, non-saturated, polyenside, doesn't matter. You're gonna get a large LDL particle. And the liver recognizes that particle when it circulates in the bloodstream and it clears it very quickly within 24 hours. And it's essentially minimally or likely non-athrogenic. It likely does not contribute to coronary atherosclerosis. The small dense LDL particle is very different. Well, how? How and why? Well, the small dense LDL particle is, of course, smaller, is better able to penetrate into the walls of arteries. So just being smaller is an advantage in causing coronary athosclerosis. The small dense LDL particle is much more prone to modifications like oxidation and glycation. And both those things, oxidation and glycation, make it much more aggressive in causing and expanding caronic atherosclerosis. In fact, a lot of people, some of my colleagues, will say it's the glycoxidized, glycated oxidized small LDL particle that is the major driver of the expansion of caronyl atherosclerotic plaque. Because the particle is smaller, the main recognition protein in the LDL particle called apoprotein B, is partially concealed. Its conformation, its surface characteristics, surface conformation is changed, making it less visible to the liver receptor. And so when you have a small dense LDL particle with a partly concealed apoprotein B recognition protein, it's allowed to circulate around and around and around for five to seven days as compared to less than 24 hours of a normal large LDL particle. That means it's given huge opportunity, lots of opportunity to interact with the walls of arteries and thereby gain entry and contribute to coronary atherosclotic plaque. The small LDL particle is also more adherent. Once it gains access to the tissue in the arterial wall, it's more likely to stick and thereby also more likely to trigger an inflammatory response, pulling in white blood cells, inflammatory white blood cells like monocytes. And they are inflammatory, they corrode or damage the walls of arteries, they add to atherosclerotic plaque, which is much more unstable. And when you have an unstable atherosclerotic plaque, it's more likely to rupture. And that's the process that causes heart attack, my cardial infarction, sudden cardiac death, or the appearance of angina that leads you down the path of stent implantation and bypass surgery. If you have small LDL particles, let's say you have an elevated number, by the way, I would regard any number above 200 nanomoles per liter in an NMR panel as being

How Small Dense LDL Causes Plaque

William Davis, MD 6:25

too high and thereby contributing to caronary atherosclerosis. Now, the great thing about this is once you know if you have an excess, let's say you have 1800 or 1450 or 2400, whatever, small LDL particle count, nanomoles per liter, particle count per volume, you also know a ton about your metabolic health. So let's talk about that. So an increased number of small LDL particles. If you're using NMR, nuclear magnetic resonance as your method of measurement, I would regard anything above 200 nanomoles per liter as being too many small LDL particles. But what can we tell you about your health, your metabolic health, if you have an increased number of small dense LDL particles? Well, that one value is the tip of the iceberg, suggesting that there's a whole range of abnormal phenomena beneath it that are all in total adding to your cardiovascular risk. Very different from the almost no information being provided by an LDL cholesterol value. So if you have an increased small dense LDL particle number, you know that you have increased triglycerides in the bloodstream. So on your conventional cholesterol panel, you'll see a higher triglyceride level. Now, I regard anything above 60 milligrams per deciliter as too high. I know the lab will quote 150 milligrams. That's ridiculous. And if you've been watching my videos, you know that any increase in triglycerides above 60 milligrams per deciliter means that not only are triglycerides being produced by your liver, but your liver's causing them to be released into the bloodstream as VLDL particles, very low density lipoprotein particles. And VLDL particles are themselves a contributor to carnary atherosclerosis that actually interact with the arterial wall and contribute to the formation of arterial plaque, atheroscleric plaque. And those VLDL particles that are very rich in triglycerides interact with LDL particles, making them triglyceride rich and therefore making them the target of several enzyme reactions that converts them to the small, dense LDL. So if you have small dense LDL, you know that your triglycerides

The Metabolic Iceberg Behind The Number

William Davis, MD 8:45

are high. You know that you have lots of VLDL particles contributing to coronary disease as well as interacting with LDL particles to make them small and dense. When you have small LDL particles, so you know you have increased VLDL as a major driver of multiple metabolic abnormalities, including the creation of small dense LDL particles. You know that your AST and ALT liver tests will be higher because those triglycerides being made by your liver, while some can get converted to VLDL particles, some also stay in the liver where they accumulate as fat. And that's the origin of fatty liver. If you have an excess of small LDL particles, you know that you have too much abdominal visceral fat because that's one of the drivers of VLDL production. And so even if you have a flat tummy, you can still have an excess of abdominal visceral fat. So it really helps to recognize that. That's a whole nother conversation about how you recognize it, how you measure it, and how you can get rid of it so that it stops contributing to the formation of small dense LDL particles. We know that because you have an excess of abdominal visceral fat as suggested by the increased small LDL particle, we know that you're likely to have what's called ectopic fat. That's fat deposition in other parts of the body that tends to parallel the accumulation of abdominal visceral fat. That fat could be in your knees and hips, and thereby accelerating the deterioration of your joint cartilage and development of arthritis. It could be around your heart, epicardial fat that accelerates the development of atherosclerosis in your caron, in your heart's arteries, and thereby heart attack, sudden cardiac death, etc. It can also suggest accumulation of fat in your pancreas, where it can damage the beta cells that produce insulin, and can actually tip a type 2 diabetic into becoming an irreversible type 1 diabetic. It also accumulates in the kidneys, where it can be have a compressive effect and actually contribute to hypertension and other kidney problems. And it accumulates in muscle, so-called myosteatosis, which accelerates the loss of muscle, loss of strength that occurs with aging, and the accumulation of fat in muscle actually has its own implications for increased mortality and morbidity. That is, an acceleration of loss of independence, frailty, false fractures, and related things. So an excess of small LDL tells you that you have a low HDL on your cholesterol panel, and that if you measure the size of the HDL particles, they're small and thereby ineffective at protecting you. It's the large HDL particles that are the ones that are protective. We know that you have an increase in insulin resistance and that your fasting insulin value, drawn, let's say, after an overnight fast, would be high. Ideal would be zero to four microunits per liter. When you have insulin resistance, your level is much higher. 30, 100, 140 microunits per liter. And that drives a lot of these phenomena. It drives the increase in VLDL production from the liver. It drives accumulation of abdominal visceral fat. It drives inflammation. So it all adds up together. This is how heart disease is caused, not by just one thing. An increase in small dense LDL is accompanied by higher fasting blood glucose. Because of the insulin resistance, because of the bad diet, the consumption of carbohydrates and sugars that gets this process started. We know that your aftermeal blood glucoses are going to be higher and that your hemoglobin A1C will therefore be higher. We know that if we measured measures of inflammation, like C-reactive protein or various interleukins or tumor necrosis factor alpha, they'll be higher when you have small dense LDL particles. We know that your blood pressure is going to be higher. We know that you likely have SIBO and portal vein endotoxemia. That is, if you have clonic or fecal microbes that have overproliferated in the colon, then ascended, which is extremely common, ascended into the 24 feet of small intestine. The small intestine is very permeable because that's where you absorb nutrients like vitamins and minerals and amino acids. But when you have these fecal microbes that have invaded the 24 feet of small intestine, when they die, because they only live for a few hours, they shed their endotoxin from their cell walls, which in turn gains access into your bloodstream. And the gastrointestinal tract is drained by the portal venous system that goes directly to the liver. And the liver receives this pounding from endotoxemia through the portal vein that further amps up liver denova lipogenesis, production of triglycerides, VLDL, and thereby small dense LDL. Do you see what I'm getting at? The presence of an excess of small dense LDL particles is not just one thing. It's the tip of an iceberg of an entire collection of abnormalities, and it's the entire collection that is that operates to cause coronary disease. So there you go. If you know you have an excess of small dense LDL particles, you know that you have a whole constellation of abnormal factors

How To Lower Small Dense LDL

William Davis, MD 14:10

that lead you down the path of heart disease. Now, if you want to know how to deal with this, how to minimize it, and how to accomplish that without resorting to any kind of pharmaceutical, which is very common to do, it's very easy to do, but you have to be given different tools. Has nothing to do with statin cholesterol drugs, has nothing to do with saturated fat. It has to do with turning off this process by the liver of producing VLDL and thereby small dense LDL, and taking steps in your diet and your lifestyle and replacing of certain nutrients lacking in your lifestyle, as well as addressing the gastrointestinal microbiome, all of which adds up to huge across the board correction of all these factors. If you don't know what I'm talking about, see this video that I'm posting here, the link to in YouTube for more uh information.