Putting The Pieces Together: Cholesterol, Lipoproteins & Triglycerides
Let’s now dig into the point that I’ve raised a few times in this post but haven’t yet addressed: what it is that’s reported on lab reports as cholesterol isn’t in fact cholesterol. What’s being measured and reported on conventional labs reports and referred to as cholesterol by healthcare providers and patients alike is typically:
- HDL—high-density lipoprotein
- LDL—low-density lipoprotein
- VLDL—very low density lipoprotein
These are lipoproteins, not cholesterol. So what’s the difference? You’re about to learn a lot more about the subject than most practitioners have ever been taught, and this is lightyears beyond what I learned in school back in the first half of the 1990’s. My hope is that this knowledge can profoundly open your mind to the devastating (or helpful) effects that your dietary choices have on your health and longevity. It’ll also help you understand how to get your labs to look the way you’d really like for them to look and what to do to make that possible.
Solubility—The First Step In Understanding What Lipoprotein Molecules Are All About
Many things in this world are either oil or water-based, and so it goes within the body. Oil and water don’t mix, and to move oily/fatty things through a water-based fluid and vice versa, there has to exist a specialized means of transport. In keeping with the transportation analogy, shipping material goods from China to Los Angeles is a lot easier when they’re loaded into a vessel that’s designed to carry them to their intended destination. Throwing them in the water somewhere in Asia hoping they’ll end up in Long Beach isn’t likely to yield positive results, but carefully planned transportation probably will.
How does this relate to cholesterol? It’s like this. Blood is a water-based fluid with a lot of things suspended in it. Blood isn’t oil-based. Many things that get transported in the blood, like cholesterol, are oil-based, and therefore have to be attached to specific molecules designed to transport hydrophobic (non water soluble) molecules like cholesterol and triglyceride through the blood vessels to their targets.
This is where LDL, VLDL and HDL come in, and why they’re often mistakenly referred to as cholesterol: LDL, VLDL and HDL are the specialized molecules that transport cholesterol molecules through the bloodstream, and the transport molecules are often mistaken for cholesterol. The various lipoproteins are often referred to (and imagined to be) cholesterol when they’re as different as are the passengers inside a vehicle from the vehicle itself. A cowboy may have a preference for Dodges over Chevrolets, but driving a Dodge doesn’t make him a Dodge. He’s a Dodge-driving cowboy, partner. As we’ll see, there’s an enormous difference between the molecules that carry cholesterol and cholesterol itself. We’ll also see that when we take a bird’s eye view, we can learn an incredible amount about what’s going on with our health when we learn how to interpret the meaning not of cholesterol per se, but of the molecules that exist to move cholesterol (and other non-water-soluble molecules) to and fro within the body.
The above image depicts lipoprotein particles of largest to smallest diameter. It also shows the relative amount of cholesterol and triglyceride content and how it differs from particle to particle. The largest particles, i.e., chylomicrons, VLDL and IDL, contain far more triglyceride (TG) than cholesterol, and the reverse is true for smaller particles. The size difference is even greater than what this chart is able to portray.
Notice that imbedded in the outer circles of the lipoproteins are thick red areas. These are apolipoproteins. The type of apolipoprotein is designated in blue. Chylomicrons, chylomicron remnants, VLDL, IDL and LDL and classified as apoB lipoproteins, and HDL lipoproteins are classified as apoA-I. The classes of apolipoproteins you’ll hear about most are apoA-I and apoB. apoA-I and apoB are named according to how the protein part of the lipoprotein molecules are structured. ApoA-I lipoproteins consist of alpha helices, hence the “A-I” suffix, and apoB lipoproteins are formed largely of proteins known as beta sheets, and therefore referred to apoB. You’ll notice that some of the lipoproteins in the chart, e.g., the chylomicron at the top left, contain E, C2 and B-48 apolipoproteins. Nonetheless, chylomicrons are classified as apoB. The same goes for the HDL particle at the bottom right. The HDL particle in this example contains E, A1 and A2 apolipoproteins, but is referred to as ApoA-I.
To avoid future confusion, there are times when apoA-I (HDL) and apoB lipoproteins (LDL) will be further broken down into pattern A and pattern B. The pattern has to do with sizes and numbers of lipoprotein particles and not with the alpha helix or beta sheet structure of the particles themselves. We’ll explore this in more detail as we go.
Also shown in the above chart is the relative density of the various lipoprotein particles, but it’s not so obvious as it’s implied. Chylomicrons, the largest of the above particles, are the least dense, while HDL particles at the bottom right are the most dense. Density is a function of triglyceride (TG), cholesterol and protein content. Protein? Yes. Keep in mind that particles are called lipoproteins, i.e., they’re a combination of lipids (fats) and proteins. Lipoproteins that contain less TG, e.g., HDL, are more dense than those than contain high amounts of TG, e.g., chylomicrons and VLDL particles. Said differently, fat is less dense than protein; lipoproteins that contain more fat have a higher fat-to-protein ratio and are proportionately less dense. Particles that contain less fat contain more protein and therefore have a higher density. This is part of the nomenclature of HDL (high density lipoprotein) and LDL (low density lipoprotein). Dense stuff, huh?
What The Various Lipoproteins Do
Outside of confusing the heck out of people, what function do all these lipoproteins serve? The short answer is that they primarily transfer TG and cholesterol to and fro. If nature had only created one type of lipoprotein to accomplish all this transport, understanding this complex subject would be a lot easier. But as we’ll see, each lipoprotein serves a different function, hence all the different ones. Once we understand what the various lipoproteins do, we can more accurately extrapolate meaning from our lab reports. And beyond that, we can determine what lifestyle changes to make, e.g., diet, exercise and stress to help nudge our labs in the right direction. With this in mind, let’s have a look at the various lipoproteins and their functions. I’ve laid it out in as straightforwardly as possible (with Cliff Notes in mind), but some of it can be a little technical. That’s just the nature of the beast. If you find yourself rereading some paragraphs, know you’re not alone in doing so. You don’t have to memorize every last detail; get the big idea and all else follows.
Chylomicrons And Chylomicron Remnants
Chylomicrons transport ingested dietary TG from the intestines to the cells of the body. In other words, when you eat fat, these little guys (chylomicrons) (they’re actually large in the world of lipoproteins) get produced and carry said fat from the small intestine to your cells. That’s their primary function: transporting coconut oil to your cells. Chylomicrons contain quite a lot of TG—between 80 and 95% of their cargo is TG. They contain lesser amounts of cholesterol—somewhere in the 2-7% range. In other words, these particles live to transport dietary TG to various destinations, and their secondary (though important) function is to transport cholesterol from the small intestine to the cells.
As chylomicrons deliver their cargo, they become TG depleted and are then described as chylomicron remnants. You can see on the above chart that chylomicron remnants contain far less TG than chylomicrons, and as a result contain a proportionately greater amount of cholesterol. By comparing the chylomicron remnant to the LDL particle in the above chart, you’ll note that an LDL particle continues this trend and contains very little TG and therefore quite a lot of cholesterol. As chylomicron remnants deliver their goods, they’re broken down by the liver. They’re only found in circulation after meals; once they do their job, they’re literally history. A fascinating tidbit about chylomicrons and their remnants is that they last in circulation for about 5 minutes. They’re created, they deliver their goods and they’re destroyed. Nature is cruel, and chylomicrons are shown no mercy.
VLDL, VLDL Remnants And IDL
Whereas chylomicrons traffic dietary fats from the small intestine to the rest of the body, VLDL transports TG produced in the liver to various locations throughout the body. They also traffic cholesterol. VLDL particles contain between 45-65% TG and 26-22% cholesterol. A very, very, very important point is that VLDL transport endogenous TG. This distinction is crucial: chylomicrons traffic exogenous TG—fats from the diet. VLDL transport fats the liver created out of excess dietary carbohydrate and amino acid intake. In other words, when you overfeed on carbs and protein, whatever isn’t needed right now is converted to something else (amino acids are first converted to sugar) and that something else is endogenously-created TG. That’s what VLDL transports. The process of making fat from excess dietary intake is known as de novo lipogenesis, something we’ll discuss in more detail because it’s an important point.
VLDL particles are also flash in the pan lipoproteins: once created, they hang around between 1-3 hours. Think of these particles (and others) like Santa Claus: they suddenly come into existence with a lot of packages to deliver to specific addresses, and the whole process is sardonically steeped in either naughty and nice, i.e., good and bad cholesterol. Saving myself from careening this entire conversation into the depths from which even Freud can’t save me, VLDL deliver their TG goods, and when they do, they’re broken down by the liver, whereas Santa heads north and disappears into a place where no one has ever been save for elves and a lot of mail from children pretending they’ve been good. Pretty much the same fate.
When VLDL deliver their TG to the peripheral tissues of the body, they decrease in TG content and therefore in size as well, but retain their cholesterol. These particles are known as VLDL remnants. In general terms, VLDL remnants become IDL particles—intermediate density lipoproteins. IDL particles are broken down by the liver pretty quickly, but those that aren’t become the ever popular LDL particles. To recap: VLDL become VLDL remnants which become IDL’s which become LDL’s.
LDL, then, are VLDL particles that have given up their TG cargo, shrunk in size and still retain their cholesterol esters. Because they contain very little TG—somewhere around 5%—they contain proportionately high amounts of cholesterol— about 50% of the cargo of an LDL particle is cholesterol. LDL particles are created from VLDL, which transport exogenous, i.e., hepatic (liver) TG to the periphery; therefore, it makes sense that LDL is also transporting something to the periphery. It also makes sense that if the majority of what VLDL is designed to transport has already been transported i.e., TG, then LDL must transport the remaining cargo: cholesterol. See how easy this is? Nothing to it. Notwithstanding the fact that it took me a few years to figure all this out, once it’s laid out clearly and concisely—which isn’t the case in physiology texts and science journals—it really isn’t all that hard to grasp. Grasping it is one thing, remembering it and accurately applying it to a person’s life is the real purpose.
Transporting cholesterol is what LDL does best. One reason why this is so is that LDL particles contain more cholesterol than any other particle; the reasons why this is so are clear by this point. Each LDL particle (LDL-P) contains about 1500 molecules of cholesterol esters. As we discussed quite a while back, the liver altruistically creates and shares cholesterol with the cells. LDL particles, because they contain concentrated amounts of cholesterol, play an integral role in this transport. Every cell in the body requires unesterified cholesterol, and even though all cells can produce their own cholesterol, the liver creates and shares it with cells—and LDL are the transporters of this cholesterol. Unlike chylomicrons and VLDL particles which last a very short time, LDL particles have comparatively long lives of about a day.
LDL is often referred to as apoB. More specifically, chylomicrons, LDL, VLDL and IDL are classified as apoB because each of these particles contains one apoB molecule, i.e., there’s one apoB molecule per LDL, VLDL and IDL. Things get confusing because LDL is often synonymously referred to as apoB; this is because the majority of apoB-containing molecules in existence are LDL: there are a lot more LDL’s in your blood and lymph than VLDL’s and IDL’s. As we discussed a few paragraphs back, LDL’s are further broken down into patterns. There’s pattern A, pattern B, and pattern A/B. Pattern A apoB are larger and more buoyant, while pattern B lipoproteins are smaller and denser. Pattern A/B shows up when there are intermediate-sized LDL particles. There’s quite a range in the size and density of all lipoprotein particles. Some of these variations occur normally in the lifecycle of a lipoprotein particle, and some indicate health issues, e.g., metabolic syndrome. Generally speaking, pattern A LDL is healthier than pattern B or pattern A/B.
LDL plays the villain in the cholesterol story, but this is a half-truth. As this blogpost progresses, we’ll go a lot deeper into the story and go beyond half-truths so we can have a much clearer idea of what it is that’s really going on with LDL. Before we do that, let’s finish up our review of lipoproteins by having a look at HDL.
Here’s a quote from the National Institutes of Health about LDL and risk status:
Historically, cholesterol and, in particular, LDL-cholesterol, has been considered the prototypical risk factor for coronary artery disease. However, lipoproteins alone do not explain all the coronary artery disease risk; one-half of all heart attacks and strokes occur among individuals without hypercholesterolemia, and one-fifth of all cardiovascular events occur in the absence of any of the major risk factors.
High density lipoprotein (HDL) are secreted by the small intestine and the liver. They’re the smallest lipoprotein particles; they’re also the most dense by virtue of having the least amount of triglyceride and the highest amount of protein of the lipoproteins. Small dense particles are generally thought to be associated with poor health, but that’s only when there are high numbers of small dense LDL particles, not HDL. HDL’s live the longest of all lipoprotein particles, having a life expectancy of about five days—the veritable dinosaurs of the lipoprotein kingdom.
Whereas LDL and other apoB molecules transfer triglyceride and cholesterol, HDL’s mainly transfer cholesterol. HDL’s have specific immunological and antiatherogenic properties that can be described as the functionality of HDL particles. In other words, besides transporting cholesterol, they have other functions and benefits besides shuttling cholesterol around (we’ll cover those toward the end of this blogpost). They do transfer cholesterol—about 30% of the cholesterol that gets carried around in your body is transferred via HDL particles. Whereas LDL particles contain apoB, HDL particles contain apoA-I, and are therefore often referred to interchangeably as apoA-I or apoAI.
HDL’s have historically been accorded a protective function because it was thought that they primarily traffic cholesterol back to the liver and away from places like arteries. And while this is be true, there’s a lot more to the story than just transporting cholesterol from one place to another. In overly-simplified terms, apoB particles traffic TG and cholesterol to the periphery of the body, while HDL’s bring it back to the liver and gut whereupon it’s either recycled or eliminated. In less simplistic terms, HDL particles circulate and pick up wayward cholesterol from cells and other lipoprotein molecules, e.g., LDL, and bring it to the small intestine or the liver. This is a process known as reverse cholesterol transport (RCT). It’s described as reverse because rather than transporting cholesterol away from the liver, RCT takes cholesterol to the liver via HDL. At least that’s the story about why HDL has a protective quality. As it happens, it’s not quite so simplistic, and LDL seems to be what returns cholesterol to the liver. Or both. My point isn’t to confuse you, but to show that some of the reasons that HDL has been assumed to be the “good” cholesterol while LDL takes the fall don’t actually play out in the long run. More than anything, I hope this sort of thing is helpful in dislodging from our consciousness the concept that what has been long-believed to be true often times isn’t so. The ramifications are huge, as it means that we’re largely misinterpreting the meaning of a very important aspect of laboratory-based healthcare and arriving at false conclusions.
HDL particles are, again, quite a lot smaller than LDL particles. LDL’s get smaller as they deliver their payload and HDL’s get larger as they gather payload. By the way, HDL and LDL are carrying the same cholesterol, they’re just doing different things with it. There’s a lot more to learn about lipoproteins and we’ll dig a lot more deeply into HDL after we cover the big idea of the blogpost. In a sense, we’ll have a deeper look at HDL to dispel the myths associated with it, but we’ll do so after developing enough context to explain why HDL isn’t the most important lab marker. Let’s first have a look at triglycerides, as they too have a big role in our play.
Triglycerides—Just The Basic (Fat) Facts
In very simplistic terms, triglycerides are a type of fat found commonly in the body. In fact, they’re the most common type of fat in our bodies. Triglycerides are the fats found in things like vegetable oils, olive oil, coconut oil, butter and cream. When you look in the mirror and see fat around your midsection—or anywhere else, for that matter—those are triglycerides.
Sparing you the hardcore technical details, a triglyceride is formed by combining glycerol with three fatty acid molecules. That’s as technical as we’re going to get, and hopefully it’s enough to get the point that they have lots of fat associated with them. Fat fat fat. We’ve all heard about saturated and unsaturated fats, and these are both forms of triglycerides. There’s also varying lengths of triglyceride chains: some are short, some are medium length, and some are long. Coconut oil is a medium chain (saturated) triglyceride (MCT). Things like butter and cream are long-chain triglycerides (LCT’s).
Now that you’re blossoming with triglyceride information, it’ll be easy to understand that just as cholesterol requires a chauffeur to drive it’s hydrophobic self through the bloodstream because blood is water-based, the same applies to triglycerides. That’s why they rely on lipoproteins to get them where they need to be. As we discussed already, chylomicrons shuttle dietary TG from the small intestine to the body, and VLDL’s are the lipoprotein primarily responsible for shuttling TG from the liver to the cells of the body.
The Chemical Structure Of A Triglyceride
The central theme of this post isn’t about triglycerides, but it’s essential to grasp this point: overfeeding on triglycerides (fat) may make you fat and destroy your health. It can whack out your labs and lead to all manner of problems. More specifically, what can prove disastrous to your health is the ratio of macronutrients, i.e., fat, protein and carbohydrates that you ingest. As an aside, a big percentage of my dietary intake is triglyceride, i.e., fat, and my body fat content is very low and my health is excellent. Obviously, then, fats can just as well make you thin and healthy. Triglycerides aren’t dangerous per se, though we still tend to relate to them as though they’re on the FBI’s most wanted list.
Okay, then, how much fat should you eat? There are innumerable factors that determine your triglyceride requirements, and it’s not so straightforward to figure out, as each person’s requirements are different based on a lot of different criteria. A few points of consideration include the energy demands of your cells, mitochondrial efficiency and leptin and insulin sensitivity. Dietary guidelines are only a starting point, and will hinder someone who’s breaking out of the mold that the majority of practitioners adhere to, which aren’t accurate to begin with. Said more accurately: dietary guidelines are what got us into this mess, and they’re therefore unlikely to get us out of it. To once and for all break free of the health issues brought on by an abusive relationship with macronutrients is to take the time to figure out what your needs are based on your personal energy demands. It also requires shifting and changing your consciousness about everything you eat, which isn’t always the easiest thing to do.
Triglycerides And Cholesterol: Which Is Which?
Consider this: the amount of cholesterol found in chicken, beef, bacon and fish is about the same. Really? Really. We can’t hear it too much: cholesterol isn’t the problem. The real point is that chicken, beef, bacon and fish contain very different amounts of triglyceride, and that does make a difference. I reckon you’re getting the point: cholesterol is cool, triglyceride is something you gotta figure out on a personal basis in order to know what amount is right for you. We’ve accepted as fact that fat leads to high cholesterol and poor lab results, and therefore by inference accepted that low fat means healthy labs and longevity, but that’s not the way things play out in the real world. This is misguided guidance at best and dangerous at worst; regardless, it’s simply not the case.
This is a very, very important point. Eating a bunch of triglyceride doesn’t mean your cholesterol and triglyceride labs will be a mess. Just the same, reflexively avoiding fat won’t translate into low triglycerides and perfect cholesterol on your lab reports. If it were only so simple. We tend to take a linear approach to healthcare, imagining that A causes B. Life is a radically non-linear phenomenon; determining cause from effect isn’t always possible when everything happens at the same time and everything influences everything else. All things being equal, go with the simplest explanations. But when things don’t add up, it’s time to go back to the drawing board. And when it comes to understanding how fat and cholesterol relate to labs and health, we’re in the process of rewriting the drawing board. It’s not necessary to go back to the drawing board and do the whole tabula rasa thing, but it is necessary to rethink decades-old positions on what does and what doesn’t contribute to health and disease states.
HDL, LDL, VLDL, TG & Your Lab Reports: What It All Means
Almost everyone these days accepts the idea that HDL (high density lipoprotein) is good—think “H” for happy—and that LDL is bad—think “L” for lousy. Back in the early 90’s I was taught that VLDL is worse than your political opponent—think “VL” for very lousy. And while there’s some truth in these generalizations, there’s just as well a lot about these stereotypes that’s misleading at best and completely untrue at worst.
It’s close to impossible to accurately assess and interpret the meaning of the HDL, LDL, VLDL and triglyceride values on your lab results without taking into consideration more information than we’ve covered so far. As we’ve already mentioned, approximately 50% of the U.S. population demonstrates normal/healthy lab values but experience myocardial infarction, stroke, atherogenesis and other related issues. What’s more, the big idea of these tests is to portend these conditions, meaning that if half the people who develop them are, per their labs, in the clear, then something’s gone seriously amiss with the testing and/or the interpretation of these tests. Said differently, if you get a standard lipid profile and interpret it through a conventional lens, you’re not going to know what’s really going on, and will therefore be making healthcare decisions based on guidelines that don’t work in half the cases.
We’ve all had blood drawn and then reviewed the data on our lab reports, not knowing for sure what it all means. Lab reports contain things such as HDL, LDL, VLDL, TG and may contain some ratios, which we’ll explain. What these lab values actually show is the concentration, i.e., the amount of cholesterol contained in the HDL, LDL and VLDL particles per unit of blood. Another way of saying “amount” is mass. These labs will also show the total amount of TG (triglyceride, i.e., fat) per unit of blood. These lab values, then, can be more accurately designated as HDL-C, LDL-C and VLDL-C, with “C” designating concentration. Again, it’s the concentration, i.e., amount of cholesterol found in the lipoproteins contained in the blood that was drawn from your body that’s being reported on your lab reports. If there were a bazillion LDL particles in the blood you had drawn, for example, and all the cholesterol was removed from those bazillion LDL particles and the amount of that cholesterol was quantified—that’s what’s on your lab report. It says nothing whatsoever about the number of particles, and that’s something we really need to know to accurately assess risk status and health. Cholesterol is one thing. The number of particles needed to transport cholesterol (and TG) is a totally different matter—and as it turns out, it’s the one thing we really need to know.
The Influence Of Leptin And Insulin Sensitivity On Lipoprotein Particles
Without getting into too much detail on this point, it’s incredibly important to consider how full your lipoprotein, i.e., LDL, VLDL and HDL particles are. If the sheer number of particles—especially LDL’s—contributes to atherosclerosis and other cardiovascular issues, then having scores of partially-filled particles will mean—you guessed it—even more particles. There are numerous influences on particle size, how full particles are and the number of particles, and a few important ones include leptin and insulin sensitivity. Leptin is a master hormone in the body which controls energy metabolism, and insulin coerces cells to feast on blood sugar (gross simplification). Due to many factors, a big one being poor dietary choices (don’t discount stress), ever-increasing amounts of leptin and insulin become necessary to accomplish what once took place with lesser amounts.
In other words, poor dietary choices and stress cause chronically high leptin and insulin secretions, and greater circulating concentrations of these hormones means that the cells eventually pay less, not more attention to the hormone signals that are designed to guide them. When it comes to hormones, what you want is for a minuscule amount to have an appreciable effect, not the other way around. When sounds and smells are in your face all the time, you get so used to them that you naturally cease to notice them as much: you become resistant to them.
And when we become resistant to leptin and insulin, one of the many things that happens is that we end up with greater numbers of LDL particles. Not necessarily more cholesterol—although that can and does happen—but greater numbers of LDL particles to transport approximately the same amount of cholesterol and TG molecules, i.e., less cholesterol per LDL particle. When increasing numbers of LDL particles are required to transport cholesterol, one of the undesirable results can be atherosclerosis. What’s that? It’s colloquially known as hardening of the arteries. Atherosclerosis occurs when “plaque” is deposited in the arterial walls, which can interfere with or even entirely shut off blood flow through blood vessel(s), e.g., coronary arteries. And that’s bad. Another way in which this plaque causes problems is when a piece of the plaque breaks free and blocks a blood vessel, potentially cutting off blood flow to areas beyond the blockage.
High particle number is a symptom of other underlying problems, and not the cause of health issues per se; the number of LDL particles, as we’ll see, is the Muhammed Ali of prognostic markers. At any rate, bringing it around full circle, knowing what’s going on with LDL particle number will tell us, among other things, what’s going on with leptin and insulin sensitivity. Everyone is blessed with someone in their life that they find it difficult or even downright impossible to communicate with. At the same time, we all (hopefully) have someone in our lives with whom it’s easy to communicate. If our cells have a rough time communicating, poor health will inevitably result. If our cells can freely and openly talk with one another, good health inevitably follows.
Particle Number, Particle Size, And The Endothelium
Curiously, blood vessels are lined with tissue known as endothelium. What I find curious about the endothelium is that it’s one layer of cells in thickness. In other words, the endothelium is very, very thin. The endothelium could be likened to a coat of paint on the walls of your house. It’s very thin, it’s easily damaged, but nonetheless it serves an important purpose. When the number of LDL particles eclipses a certain threshold, some of them can pass between the cells that make up this very thin endothelial lining and get stuck beneath it. And when this happens—especially when lots and lots of LDL particles pass between the endothelial cells and become lodged between the endothelial layer and the next layer down, i.e., the subendothelial space—atherosclerosis is the (grossly oversimplified) result. This is, again, grossly oversimplified, as a lot more takes place than just innumerable LDL particles passing through the endothelial layer, but it’s enough of an explanation for right now.
As I keep mentioning, LDL particle number (we’ll give HDL particle number its due as well) is the single most important factor in determining your risk/health status. It’s far more predictive of atherosclerosis than elevated LDL-C, VLDL-C and/or low HDL-C. If you remember, we added a “C” to the various lipoproteins to denote the concentration, i.e., amount/mass of cholesterol they contain. We’ll now add a “P” to the lipoproteins to designate when we’re discussing particles, e.g., HDL-P, LDL-P and VLDL-P.
To distinguish a lipoprotein particle from the concentration of cholesterol contained within the particle itself, the following nomenclature is used: an LDL particle = LDL-P, and the concentration of cholesterol within an LDL particle = LDL-C. The same goes for the rest of our lipoprotein friends: HDL-C and HDL-P, VLDL-C and VLDL-P. Easy, right?
- Half the U.S. population has “normal” HDL, LDL VLDL and TG status on their lab reports, yet develop some form of “cholesterol” related issue, e.g., heart disease, atherosclerosis, myocardial infarction, stroke
- Therefore, knowing your HDL, LDL, VLDL and TG status doesn’t give you enough information to go on
- We really need to know the number of LDL, VLDL and HDL particles to assess risk status and health
- The endothelial lining of blood vessels is one layer of cells in thickness, and LDL particles can pass through this layer and become lodged in the subendothelial space, causing atherosclerosis. The more LDL particles there are, the greater the health risk
- Insulin and leptin resistance, stress and metabolic syndrome lead to an increase in the number of lipoprotein particles, e.g., LDL-P
- Chylomicrons transport dietary TG, i.e., exogenous TG, to the cells from the gut
- VLDL transport endogenous TG, i.e., de novo TG away from the liver and to the cells
- Triglycerides aren’t cholesterol and cholesterol isn’t TG
- It’s important to determine the proper ratio and amount of macronutrient intake in order to have healthy lab reports. And enough with the stress already.