Making Sense Out of Your Cholesterol Panel

Cholesterol testing is among the most common blood tests run in conventional healthcare, yet it is a perennial source of confusion and, to be honest, abuse by doctors who don’t appreciate the full implications of the values. It may surprise you to know that doctors focus on the least helpful values such as total or LDL cholesterol while often ignoring the two genuinely helpful values, HDL cholesterol and triglycerides. HDL for instance is packed with useful insights into your health, as it is a reliable index of metabolic health. Low HDL, that I would define as less than 60 mg/dl, is a reflection of multiple health distortions such as insulin resistance, inflammation, excessive intra-abdominal fat, small LDL particles and VLDL that cause heart disease. 

You might also be surprised to learn that consuming fats only spikes triglyceride levels for a few hours, whereas the process of your liver converting carbohydrates to triglycerides can cause a much larger increase after six to eight hours or more. Discover the factors that can amplify this process, including insulin resistance, inflammation, excessive intra-abdominal fat, and even dysbiosis and small intestine bacterial overgrowth.

The road to cardiovascular health doesn't have to be paved with cholesterol. We'll reveal how VLDL particles and triglyceride levels are intricately linked, why it's essential to keep your triglycerides below 60 milligrams per deciliter, and how higher triglycerides can result in lower HDL levels. Discover how simple dietary changes can lead to lower triglycerides and higher HDL levels, and why measuring LDL particles using NMR lipoprotein analysis offers a more accurate picture than the commonly used LDL cholesterol. Join us as we dispel the myths around cholesterol and empower you to take control of your cardiovascular health.


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Transcript

William Davis, MD: 0:06

Cholesterol testing is among the most common blood tests run in conventional healthcare, yet it is a perennial source of confusion and, to be honest, abuse by doctors who don't fully appreciate the full implications of values. It may surprise you to know that doctors focus on the least helpful values, such as total or LDL cholesterol, while often ignoring the two genuinely helpful values HDL cholesterol and triglycerides. Hdl, for instance, is packed with useful insights into your health, as it is a reliable index of metabolic health. Low HDL that I would define as less than 60 mg per deciliter is a reflection of multiple health distortions, such as insulin resistance, inflammation, excessive intra-abdominal fat, small LDL particles and VLDL particles that cause heart disease. Likewise, your triglyceride value also indicates similar processes. The higher your triglycerides, the lower HDL tends to be, as triglycerides cause the body to degrade and discard HDL particles. Higher triglycerides that I would also define as any level greater than 60 mg per deciliter also indicates insulin resistance, inflammation, greater intra-abdominal fat and increased small LDL particles and VLDL particles. In other words, while focusing on the least helpful values of total and LDL cholesterol, your doctor nearly always ignores the values with the greatest helpfulness. So in this episode of Defiant Health, let's dive into these values that virtually everybody has had measured to uncover what they mean. Later in the podcast, let's talk about Defiant Health's sponsors that include Paleov alley, who provides fermented grass-fed beef sticks, bone broth, protein rich in collagen, organic supergreens and low carb superfood bars, and now 100% grass-fed and finished pastured meats. And Biotiquest, who provides unique probiotics such as sugar shift to support healthy blood sugars and simple slumber to assist in obtaining healthy sleep, Probiotics crafted with the unique property of combining synergistic microbes. There are four values on every cholesterol or lipid panel there's total cholesterol, there's triglycerides, hdl cholesterol and LDL cholesterol.

William Davis, MD: 2:43

To understand what these values mean, it helps to recall just how this all got started. So a lot of this work was done in the 1950s and 1960s by two scientists at the National Institutes of Health, nih doctors, william Friedewald and William Fredrickson. They were trying to figure out a way to quantify, to count, the number of particles in the bloodstream that cause heart disease. So they would take blood, remove the red blood cells and you'd have a clear plasma remaining that was filled with lipoproteins or fat-carrying proteins. You see, fat can occur freely in the bloodstream because if it did, fat would coalesce and would actually block capillaries and other vessels and you'd have tissue death.

William Davis, MD: 3:30

So fats cast a ride on a protein to make it soluble in an aqueous or water-based environment. Blood is an aqueous or water-based environment, so fats ride on proteins. When they do that, that's called a lipoprotein, refring to the fat on the protein. So when they spun or centrifuged plasma they would see layers "from At the very top. They called that very low density lipoproteins. At the very bottom was the highest density, just like a stone falls to the bottom of a lake Low density lipoproteins at the bottom and low density lipoproteins in the middle. How do you go about counting these particles in the various layers?

William Davis, MD: 4:13

Well, they chose a workaround and that was to choose one component shared by these particles. They could have chosen, for instance, a protein like ApoProtein B, they could have chosen triglycerides, but they chose cholesterol. Cholesterol was a fat fraction in all these layers of lipoproteins and they measured the amount of cholesterol in each fraction. They could measure the cholesterol in the very low density fraction at the top, cholesterol in the high density fraction at the bottom, etc. They used that as a crude and indirect way to quantify how many particles there were in each layer.

William Davis, MD: 4:50

Now they are also mindful that in the 1950s and 1960s, they wanted to make sure this was accessible in community hospitals that often did not have sophisticated laboratory equipment. So they devised another workaround, and that is they would measure the cholesterol in the entire sample that would be total cholesterol. Then they'd measure the cholesterol in the high density lipoprotein fraction at the bottom that would be HDL cholesterol. And rather than measuring the cholesterol in the very low density fraction at the top, they could estimate it by simply measuring triglycerides and dividing by 5, because there's 5 times more triglycerides than cholesterol in the VLDL fraction. So that triglycerides divided by 5 was a quick and easy workaround. Now they also wanted to avoid having to measure that tricky middle level in community hospitals and other poorly equipped labs.

William Davis, MD: 5:40

So they chose to develop an equation that they could calculate the LDL cholesterol from the other measures. So they reasoned that LDL cholesterol could be calculated not measured but calculated by taking the total cholesterol value, subtracting the HDL cholesterol value and then subtracting triglycerides, divided by 5. And that equation is called the Friedewald equation, or Friedewald calculation, to calculate LDL cholesterol. Now this is what's called a regression equation, that is, it falls apart when things change, when circumstances change. So if triglycerides are a little high, let's say 160, it invalidates the measurement. If you change your diet, you invalidate the measurement, the equation. If you cut fat or you cut carbs or make a change in diet, you've invalidated the equation. If you're diabetic, either one or two, type one or type two, you invalidate the equation. In other words, there's lots of assumptions built in. So LDL cholesterol is wildly inaccurate when you compare it to the actual measurement of LDL particles, which you can measure. Now.

William Davis, MD: 6:48

It was believed that LDL particles were the primary contributor to heart disease. In real life it's actually LDL particles, and the LDL particles are the particles that actually contribute to growing or expanding coronary atherosclerotic plaque. That's the stuff that causes heart attack, sudden cardiac death, or gets stented or bypassed with heart procedures. In the ensuing years, since doctors Friedew ald and Fredericksen, early work, became clear that total cholesterol was a virtually worthless measure. It was a very poor predictor of heart disease events like heart attacks. Part of the reason is because, let's say, you had an HDL cholesterol. Remember, hdl cholesterol is a component within total cholesterol, along with LDL cholesterol and triglycerides divided by five, or VLDL cholesterol.

William Davis, MD: 7:36

So what if you did something bad? You gained a bunch of weight and your abdomen, your blood sugar went up, you have inflammation and, let's say, your HDL dropped, say, from 60 to 30. 30 milligrams for an HDL is very bad. It's a high risk marker. So you dropped HDL 30. That means total cholesterol value also drops 30. And many doctors say, oh, this is a good change, not recognizing that it was a drop in HDL that led to a drop in total cholesterol. Conversely, let's say you started with an HDL cholesterol of 30 milligrams and you did good things. Maybe you added exercise program, you lost some abdominal fat and inflammation went down and HDL goes from 30 to 60. Well, your total cholesterol also goes up 30 milligrams and your doctor says, oh no, your cholesterol is higher, we need to treat it with a statin cholesterol drug or other drug.

William Davis, MD: 8:26

In other words, total cholesterol is misleading. It's a composite measure of both good and bad things and so total cholesterol is worthless. I tell people to take a black magic marker and cross it out and pay no attention to total cholesterol. Now, what about this calculated LDL cholesterol, calculated by the Friedewald equation? Well, we know with confidence that LDL cholesterol is not only wildly inaccurate and unreliable when you make those changes like dietary changes, or change triglycerides or blood sugars. We know that LDL cholesterol is a very poor predictor. For instance, the LDL cholesterol of the average person without heart disease is 133 milligrams per deciliter. What's the LDL cholesterol of someone who had sudden cardiac death or needs a bypass operation or had a heart attack? 133 milligrams per deciliter. It is indistinguishable. So LDL cholesterol is an exceptionally poor predictor of heart disease events. So, total cholesterol worthless. Ldl cholesterol very poor predictive power. Yet these are the two values most practicing physicians focus on to assess your risk and then intervene, typically with a statin cholesterol drug or now some other drugs. But the truth of it is there are, even though total cholesterol and LDL cholesterol are nearly useless values, despite all that attention. The other two values, triglycerides and HDL cholesterol, actually do tell you a lot about your risk for heart disease and what your lipoproteins might look like if you were to examine them, not just rely on lipids or cholesterol testing. Let's resume with that topic after I tell you a little about Defiant Health sponsors.

William Davis, MD: 10:10

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William Davis, MD: 11:49

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William Davis, MD: 13:01

All right, let's consider triglycerides. So triglycerides are fats. If you have, for instance, a bottle of extra virgin olive oil, that is a bottle of fat, a bottle of triglycerides. Likewise, butter, fats on meats are all triglycerides. So if you consume a meal that contains fats and oils let's say a piece of a pork chop with fat or butter on your green beans your levels of triglycerides will go up. Now you're actually increasing levels of something called chylomicrons that are triglyceride rich. But that occurs in the first few hours, about the first five to six hours after a fat-containing meal. So there's a modest rise in triglycerides after consuming fats. So at a typical level, let's say you started at 100 milligrams per deciliter of triglycerides and you eat a fatty meal, maybe it goes to 180 or 200, something like that, transiently for a few hours. That's from fat consumption.

William Davis, MD: 13:59

Now there's a delayed process called de novo lipogenesis. All that means is in the liver. The liver has the capacity to convert carbs and sugars to triglycerides. De novo lipogenesis, making new fats. That's all that means. And so you had that meal. You had that initial rise in triglycerides from chylomicrons in the first few hours and then more than six to eight or so or longer hours, there's a secondary rise that's much larger. So triglycerides can go up to 300 or something like that. And that's because it takes. There's a delay in the liver's conversion of those carbohydrates to triglycerides. Now the triglycerides once again cannot occur as triglycerides in the bloodstream. They are packaged into VLDL particles, very low density, lipoprotein particles. So once again, initial rise of triglycerides from fat consumption. Secondary, much larger rise from the liver process of converting carbohydrates into triglycerides.

William Davis, MD: 15:02

The liver has a great capacity for this process of de novo lipogenesis and it can produce huge quantities of triglycerides. That process is amplified in the presence of insulin resistance, inflammation and the presence of excessive intra-abdominal fat, and in the presence of dysbiosis or especially SIBO, small intestine bacterial overgrowth and endotoxin. Let's consider each of those. So when you have insulin resistance, it means your body is unresponsive to insulin. Muscle, brain, liver don't respond properly to insulin and your pancreas compensates by producing huge quantities more insulin 30 times more, 50 times more, 100 times more. A person who's insulin sensitive let's say a slender athletic person may have a fasting insulin level of one or two micro units per liter. A person who, with insulin resistance, may have a level of 50, 90, 130 or more micro units, in other words, many times higher. And that high level of insulin causes abdominal fat to grow, which makes insulin resistance worse, which causes abdominal fat to grow, and so it's a vicious cycle that makes it worse and worse over time.

William Davis, MD: 16:16

But the presence of insulin resistance is a major amplifying effect on liver, de novo lipogenesis, so it causes your liver to churn out more and more triglycerides as VLDO particles Now when you have inflammation from that same abdominal fat. So abdominal fat, that is fat, and certainly the abdominal organs like the intestines and liver and pancreas is itself very inflamed. If you biopsied abdominal visceral fat surrounding organs, you'd see white blood cells infiltrating the fat and flaming it, and that fat produces inflammatory mediators that pour into the bloodstream and that also recall that the gastrointestinal tract is drained by a venous system to the liver it's called the portal venous system. And so the liver takes a beating of inflammation from abdominal visceral fat, which further amplifies the process of liver de novo lipogenesis. It also adds insulin resistance, so it's feeding upon itself. These processes feed upon each other Now that intra-abdominal fat, abdominal visceral fat, is therefore a major amplifier of liver de novo lipogenesis and the production of triglycerides into the bloodstream. So while triglycerides are initially from fat consumption, that secondary, much larger rise is fueled hugely by these processes.

William Davis, MD: 17:39

And then another process fueling de novo lipogenesis is dysbiosis, but especially if it enters the small intestine, that is, small intestinal bacterial overgrowth or SIBO. So what's happened to many people by my estimation at least half the country is that because of our exposure to antibiotics and other factors like glyphosate the herbicide that's also an antibiotic preservatives, emulsifying agents, et cetera, we've lost numerous beneficial species in the colon microbiome. Well, they were suppressing fecal microbes like E coli and salmonella and campylobacter, so we lose healthy microbes. It allows the excessive proliferation of fecal microbial species which in turn can climb up into the small intestine. And the small intestine, you may recall, is by design very permeable. That's where we absorb nutrients like amino acids, fatty acids, vitamins and minerals. Well, when fecal microbes come to occupy the 24 feet of small intestine, they live and die rapidly Trillions of microbes living and dying rapidly. When they die, they release some of their toxins, such as the so-called endotoxin that is able to penetrate the intestinal wall because the small bowel is so permeable, and that's when endotoxin gets in the bloodstream. That's called endotoxemia.

William Davis, MD: 18:55

Endotoxemia in the portal vein system hugely amplifies liver de novo lipogenesis and when it enters the main systemic circulation it makes insulin resistance worse. So you can see that while, yes, fats ingested and diet do raise triglycerides, a much worse situation comes from liver de novo lipogenesis amplified, fueled by these other processes. And that is the problem with triglycerides. Now, recall that when you have your cholesterol panel drawn, it's typically fasting. So if triglycerides are above the ideal of 60 milligrams per deciliter, you know it came from carbohydrates, because if you ate, let's say dinner, at 6pm, you have triglycerides raised but cleared by midnight. Right, that is from the fat, but then it's after midnight where you have that secondary rise from de novo lipogenesis, fueled by those other processes. And when you get to the laboratory, say at 8am, they draw your blood and your triglycerides are 253, that's from carbohydrates right, it's too late to be from fat consumption. It's from carbohydrate consumption further fueled by insulin resistance, inflammation, intra-abdominal fat and metabolic endotoxemia from SIBO or dysbiosis.

William Davis, MD: 20:14

One of the reasons why this is so important to recognize is that when you have excess triglycerides and thereby VLDL particles, very low density lipoproteins rich in triglycerides, when you have an excess VLDL particles, are both a direct cause of coronary atherosclerosis and thereby cardiac events like heart attack. But VLDL particles also interact with LDL particles, not LDL cholesterol, that marker LDL particles and VLDL particles rich in triglycerides transfer triglycerides to LDL particles and these LDL particles go through a series of remodeling reactions by enzymes such as hepatic lipase, which converts them to small LDL particles. Small LDL particles, you may recall, are smaller of course, and thereby more readily able to penetrate into the walls of arteries to initiate the process of forming atherosclerotic plaque. Small LDL particles are also more prone to oxidation, which makes the much more dangerous, also more prone to glycation, and they are much more adherent to the structural tissues in the artery wall and more likely to incite an inflammatory response in the arterial wall. That's the process that leads to atherosclerosis and heart attacks. Not cholesterol, but LDL particles, especially small glycoxidized LDL particles that are adherent and able to initiate an inflammatory response in the arterial wall. So we'd like to minimize this process.

William Davis, MD: 21:46

Because VLDL particles track very well with triglyceride levels, you can still rely, even though lipoproteins are, in general, advanced lipoprotein analysis is a better way to assess cardiovascular risk. You can still rely on the simple triglyceride level of a standard four component lipid or cholesterol panel. Because the triglyceride level does track very well with VLDL particles and I aim to keep triglycerides no higher than 60 milligrams per deciliter. Why? Well, that's the level at which you have almost no VLDL particles to interact with LDL particles to make them small. So when you get your triglycerides to 60 milligrams per deciliter or less, you usually have little to no small LDL particles. Now, there are exceptions. There are some genetic variants. There are some people with SIBO so bad it still drives persistent small LDL, but in general most people can know that they have little to no small LDL particles if triglyceride levels, and thereby VLDL but triglyceride levels are 60 milligrams per deciliter or less.

William Davis, MD: 22:48

Now let's shift over to HDL cholesterol. So HDL particles are protective. They're responsible, or believed to be responsible, for something called reverse cholesterol transport. That's an inaccurate name, but think of HDL particles as a cleanup crew cleaning up arteries. So the higher the HDL, the more protected you are. Now there's a funny interaction between triglyceride particles, vldl and HDL particles, and that is when you have lots and lots of VLDL particles and thereby triglycerides, they cause accelerated degradation of HDL particles and they're cleared from the kidneys. So when you have higher triglycerides meaning anytime above 60, right, you tend to be clearing or metabolizing your HDL particles and HDL levels go down. So it's very common to have an increased triglyceride level of, say, 250 and a low HDL level of, say, 32, 34, 27, something like that. So just as we want triglycerides be no higher than 60 milligrams per deciliter, we want HDL cholesterol to be a minimum of 60 milligrams per deciliter or more.

William Davis, MD: 23:51

Now what you'll find in doing my programs, in which we eliminate wheat, grains and sugars, we address common nutrient deficiencies that plague modern people because of modern lifestyles vitamin D, magnesium, iodine and omega-3 fatty acids. Then we address dysbiosis in the colon, as well as SIBO in the small intestine and the accompanying endotoxemia. We address all those things and it's very common to have a triglyceride level in the 40 range 43, 47 milligrams, something like that. It's very common to have HDL cholesterol levels of 70, 80, 90, or 100, well above 60. And we don't care about total cholesterol, right, or LDL cholesterol, because we made dramatic changes in diet Equation. Free world equation was inaccurate to begin with and unreliable, but we've made changes that invalidate the free to world calculation. So if you want to know what the LDL particles are doing, you can't tell that. You can kind of make indirect judgments right by looking at the triglycerides and HDL, but you're not actually measuring the LDL particle. You can measure it Now. My preferred method is called NMR, nuclear magnetic resonance. There used to be other methods like ultracentrification and gel electrophoresis, but those are kind of hard to get or not unavailable anymore. So we're all using NMR, nuclear magnetic resonance.

William Davis, MD: 25:04

Lipoprotein analysis and many of the big labs like Quest and those big companies will do this for you. You just have to have it specified by your doctor. If your doctor says something like, oh, we don't do that test or oh, there's no proof that works or helps, provides additional information, or it's not covered by insurance. Those are all lies. That's nonsense. I've been doing this for 30 years and almost all insurers, including Medicare, cover NMR lipoprotein analysis. Why would the doctor lie and say such things? I'll translate I can't be bothered going the extra mile of education to understand this more advanced form of testing and I can't be bothered to reading the 55 clinical studies human clinical studies, for instance that validate that small LDL particles are dramatically superior predict of coronary disease. It's not that they're not unavailable or not covered by insurance. That's nonsense. They are covered by insurance, they're readily available and one of the things you'll find when you do an NMR lipoprotein panel.

William Davis, MD: 26:00

The two really necessary numbers to look at are LDL particle number, but especially small LDL particle number. So let's say your LDL particle number total is 2000 and the small LDL particle number is 1000. That means 1000 of those particles in the total particle number of 2000 is small. That tells you this is going to respond dramatically to elimination of the foods that provoke formation of small LDL wheat, grains and sugars, because of the amyl, pectin A, wheat and grains. And then the sugars, the nutrients we address that synergize to minimize or reduce inflammation and insulin resistance. Vitamin D, magnesium, iodine, omega 3 fatty acids and then we address dysbiosis, sibo and endotoxemia and what you get is a dramatic reduction, usually elimination, of small LDL If you start at 1000 or 2000,. Most commonly drops to zero. It's not a percentage better, it's gone, and that's because you're no longer engaging in de novo lipogenesis right from consumption of carbs and sugars. You've reversed insulin resistance, you've minimized inflammation and you've addressed endotoxemia.

William Davis, MD: 27:10

One of the confusing outcomes of all this is that it's not uncommon for LDL cholesterol, and thereby total cholesterol, to go up. But you know the equation is invalid when we've made these changes in our diet and some other of the basic assumptions that are used to justify the free to all calculation. So even if your LDL cholesterol says 236 and your doctor's alarm, think you're going to die of a heart attack. It's not a real number. So what you have to do is get NMR lipoprotein panel to get that small LDL particle number Now one of the things we do not know.

William Davis, MD: 27:43

Let's say you get rid of all the small LDL out of a total LDL particle number of 2000. That means your LDL total LDL particle number typically drops to about 1000, right, because you eliminated all the small LDL particles? At what level of total LDL particle number that are all large and no small. What is allowable before it causes coronary disease or adds to coronary atherosclerotic plaque? Nobody knows. Despite the billions and billions of dollars spent on cholesterol research, no one has settled that basic question. I think, though, that somewhere between 1400 and 1800 nanomoles per liter part of the count per volume of pure large LDL is probably safe, and above that maybe, maybe, adds to risk. But we don't know that for a fact. But know that by addressing the small LDL particle number, which you've done with all the things we've talked about, you've addressed by far the most vicious cause of coronary disease.

William Davis, MD: 28:36

So, in summary, total cholesterol worthless, calculated LDL cholesterol nearly worthless, very limited in its ability to predict heart disease and very misleading information, especially when we change our diets as we do here.

William Davis, MD: 28:50

But there is information in triglycerides and HDL, because they're inverse to each other the higher the triglycerides, the lower the HDL.

William Davis, MD: 28:57

So we're going to turn off your liver's capacity to manufacture triglycerides and VLDL particles by eliminating the foods that initiate liver de novo lipogenesis wheat, grains and sugars, by minimizing insulin resistance and inflammation that would have amplified liver de novo lipogenesis, and we're going to address the unhealthy changes that have occurred in most people's gastrointestinal microbiomes, especially endotoxemia, and we do so by reintroducing keystone microbes like lactobacillus rhodii, lactobacillus gastri and perhaps bacillus coagulants. These are microbes, especially rhodii and gastri, that take up residence in the small intestine where they produce bacteria, that is, natural antibiotics effective against the species of sepo, and this reduces endotoxemia. And there's some additional things you can do to reduce endotoxemia that we can talk about another time. But know that you have magnificent control over cardiovascular risk and it has nothing to do with cholesterol. Now, if you learned something from this episode of the Defiant Health Podcast, I invite you to post a review, share a comment, subscribe to your favorite podcast directory and help us build this movement of self-empowerment in health. Thanks for listening.