By John Meadows CSCS, CISN and Matt Poteet, Pharm.D.
It seems kind of funny to say “made easy” and cholesterol in the same sentence. The truth is that many facets of cholesterol are actually extremely complicated and beyond the scope of our knowledge by a long shot. Cholesterol synthesis is one such facet. There are at least 12 steps to get 2 acety Co-A to its end form of cholesterol, and there are a ton of big words through these steps like, geranyl pyrophosphatase, squalene, and other words that give me a headache. Knowing the terms and complex biochemical reactions are completely unnecessary for the average guy or gal who simply wants to be be healthy, have a great life, and someday bounce their grandchildren on their knee. Seeing the need for both clarity and simplicity in the subject of cholesterol, we decided to write an article where 95% of the technical and medical jargon is thrown out. Only the bare necessities are here in easily digestible, but physiologically sound form. By the time we finish we hope to have presented cholesterol in the clearest and simplest manner possible in a way everyone can both understand and utilize.
We will attempt demystify the things that you usually hear associated with cholesterol though like “good” and “bad” cholesterol. We will talk about the basics, and also talk about what tests are out there in regards to cholesterol and what they really mean. I think you’ll enjoy this part, as it’s fairly easy to understand, and you’ll very quickly realize how the information that is out there, is mostly incorrect. So hang on tight, and get ready for some cholesterol truth!
How many kinds of cholesterol are there?
There are at least 2 right? Good and bad? WRONG. There is only one kind of cholesterol. It is inheritantly good, and it looks like this.
Riveting pic, I know. Exactly what does cholesterol do in the body? Why is it so important?
- It is the beginning structural building block for sex hormones like testosterone
- It is very important for cell membrane integrity and fluidity. No cholesterol would mean your cells would be like mini blobs with no rigidity
- It is a crucial component of Vitamin D synthesis, with a little help from the sun of course.
- It is a primary structural component of your brain and CNS, comprising up to 60% of its overall dry weight. In fact, the highest concentrations of cholesterol in your entire body are in your brain and nervous system.
- It is used to make bile acids which are crucial in digestion and absorption of fatty acids and fat soluble vitamins.
So it goes without saying, we need cholesterol. So far so good, we have established that there is only kind of cholesterol, and it’s very important.
When someone is speaking of their “cholesterol” levels, what they are actually talking about is a group of molecules called lipoproteins. These lipoproteins act as the carriers of cholesterol. They make it possible for very oily components such as triglycerides and cholesterol to travel through the water-based body. Oil and water don’t mix except with the help of lipoproteins! There are many numerous types of lipoproteins known to us today. Medical science are constantly subdividing them based upon various factors such as size, density, and constituency.But there are five main types which we will discuss today. The first three you may not know much about, but hang tight for the cool stuff.
- Chylomicrons – In size, chylomicrons are the largestof the lipoproteins. They are created in the small intestine in response to eating a meal, and their main “job” is to be filled with the dietary fat (triglyceride) and cholesterol after you eat a meal (mostly triglyceride), and then transport these substances to the liver, muscle, and other body components which need them. Once the chylomicron has finished delivering its triglyceride packages to the various body addresses, it is much smaller than when it started. It then travels back to the liver where it is broken down, and possibly reassembled into other lipoproteins like VLDL…
- VLDL (Very Low Density Lipoprotein) – VLDL is the second largest in size of the five lipoprotein classes. It is manufactured in the liver and has a similar role in transporting oily substances through the body. But while the chylomicron’s job is to transport the oily substances that you eat, VLDL’s job is to transport the oily substances which are already in your body from place to place. In comparison to chylomicrons, the triglyceride content is usually a little lower, while the cholesterol content is usually a little higher. As VLDL moves about in the body delivering its packages to the various organ systems, an enzyme called LPL (lipoprotein lipase) removes triglyceride for use by the body. As VLDL gradually loses the triglyceride, it becomes smaller and changes in to….
- IDL (Intermediate Density Lipoprotein) – By the time VLDL changed into IDL it is usually carrying about half cholesterol and half triglyceride. IDLs are further acted upon by enzymes (hepatic lipase), lose more triglyceride and turn into LDL. Ah finally. We made it to something familiar…LDL..the bad stuff!
I know what you are thing, so Matt and John, that’s cool and all, but what does this have to do with anything???
Well remember we said there is only one kind of cholesterol, and you probably thought if there is only one kind, then what exactly are HDL (good), and LDL (bad) cholesterol?
As we said previously, cholesterol does not dissolve in water (thus not blood either). To get from point A to point B it must move through these lipoprotein carriers. I feel that this situation calls for an analogy. Imagine a road with delivery trucks traveling to and fro with passengers. The trucks are the lipoproteins, the people cholesterol, and the packages in the back are triglycerides. The “HDL” trucks are carrying “cholesterol” people on the road to the Liver Station (your liver). Going the opposite direction are “LDL” cars carrying “cholesterol” people from Liver Station to other places such as Heart City. Keep this fresh in your mind because we are going to return to this analogy often in this discussion.
- LDL (Low Density Lipoprotein) – By the time we get to LDL, we only have a few packages left. They are sliding back and forth on the floor. I hope they aren’t fragile! We now have a molecule carrying about 90% cholesterol and 10% triglyceride. When a cell needs some cholesterol, it hangs out a vacancy sign ( in the form of an LDL receptor) The delivery driver is tired of hearing these cranky passengers by now. They have been saying “are we there yet?” for the past 3 hours! So the LDL whips into the LDL recpetor and is transported into the cell. His job is done. Aha, you say. Now it will wreak havok! Well not so fast. More on this later.
- HDL (High Density lipoprotein) – Of course we have to mention these carriers too. They are the taxis of the body, stopping along the way to pick up straggling cholesterols who may have had too long of a night out on the town. They head back to the liver hopefully not running too many red lights. There the excess will be removed by the body as bile or broken down and re-allocated to other places in the body for other tasks.
Now that we have laid some groundwork for what is truly going on with cholesterol in your body, lets address a few of the more common myths in our society about cholesterol.
MYTH #1 – Eating fat will raise LDL levels. BUSTED- As was described above, dietary fat (yes even the saturated kind) is shuttled via chylomicrons from your intestines to the rest of the body. This does nothing to the LDL level in your blood. The amount of dietary fat that reaches the liver also has little to do with the level of total cholesterol production. We know that in general if you eat less fat, your liver makes more cholesterol, you eat more fat, and your liver makes less due to the fact that there are more chylomicrons circulating. Your body is extremely efficient at regulating itself.
So take a step back, where does the LDL come from? It originally comes from the VLDL once it has some fat removed from it. Now remember that VLDL’s job was to transport oily substances which were already in the body, not the dietary fat we have eaten (chylomicrons job). So what raises VLDL? Not dietary fat. Think excess carbohydrates. Excess carbohydrate turns into triglyceride very efficiently in the liver, and since it is already IN the body it is the responsibility of VLDL and ultimately LDL to transport it through the body. It is actually proven that generally a lower carb and higher fat diet LOWERS VLDL level. So eating fat will lower VLDL, and in turn the harmful types of LDL. Oh, there are different types of LDL? Absolutely. We will get to the different types of LDL in just a minute.
We didn’t think of this on our own I am sad to say, the American Journal of Medicine did (Seshadri et all, A randomized study comparing the effects of a low carbohydrate diet and a convention diet on on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Amercian Journal Of medicine 117 (5) 2004 pages 398-405), as they were trying to prove the Atkins diet was bad for you. Oops.
Also, in November 2002 studies were published espousing lower carbohydrates for improvement in cholesterol levels. In one study Duke researchers found that “after six months, participants on the Atkins diet had lost 31 pounds, had an 11 percent increase in HDL (good cholesterol) and a 49 percent drop in their tryglyceride levels. Atkins dieters had a 49% reduction in VLDL levels, versus 17% for those on the low-fat group”.
Ok back to your regularly scheduled programming.
How Big is Your Truck?
Slowly but surely the word is getting out that LDL comes in various sizes. Larger particles are more buoyant and fluffy, and don’t lodge into endothelium as easy as smaller particles do. So if this is true, then the semi trucks, and Escalades on the road carrying it’s passengers (cholesterol) are less likely to crash and do damage. They just sort of bounce off the guardrails and keep moving.
The smaller delivery cars, the freaking Miatas, and especially those dang Dodge Darts have the potential to wreak some havoc. They can get stuck under the guardrails (endothelial cells) when they crash. When they get stuck, tons of emergency vehicles have to come to try and get them out of the mess. (Circulation 2002; 106: 3143-3421). And that is when things get messy and very dangerous through plaque formation and ultimately cardiovascular disease.
How Many Cars Can Be On the Road?
So we know that having smaller cars on the road is bad, but what about having so many cars you have a traffic jam regardless of whether they are big or small? Yes that is also an important factor in this discussion. This is called particle concentration. High LDL particle concentration is also considered a player in increased cardiovascular events. El Harchaoui K et al. Value of Low Density particle Number and Size as Predictors of Coronoary Artery Disease in Apparently Healthy Men and Women. J Am Coll Cardiol 2007;49:547-53.
This area is a little grey, but at some point if you just get overloaded with particles bad things are going to happen.
MYTH BUSTER #2 – The myth is that if you have an in range LDL reading (< 100) you are good to go. This is not always certain. LDL readings in standard blood tests only measure the amount of LDL cholesterol (the number of delivery vehicles)! There is no biological rule that all cars have to be full of people/cholesterol. In some of us, we might have trucks that are only partially full of people, but have a lot more trucks. So think of it this way if this still doesn’t make sense. You can have 10 containers each containing 1 lb of mag 10, or you could have 20 contains that each contain .5 lbs of mag 10. It’s still 10 lbs total, but you have more containers in the second example.
If this sounds far-fetched let me explain. When you eat a lot of sugary food, such as HFCS , your LDL carriers/trucks will fill up with excess triglyceride leaving less room for cholesterol, which requires more delivery trucks to be made and put on the road. The lesson is sugary crap in your diet will give you a higher particle number or concentration that could lead to heart disease and diabetes.
Key points from part 1:
- There is only one kind of cholesterol, and it is inherently good for us
- In order to transport oily substances like cholesterol and triglycerides, there must be carrier molecules called lipoproteins. There are five major types of lipoproteins, with HDL and LDL the most well-known.
- Common LDL lab tests only show the percentage of total cholesterol that is LDL. It does not show how big the LDL is, or how many particles there are.
- Larger, more “fluffy” LDL particles seem less likely to cause CV issues down the road.
- Smaller LDL particles are much more dense and lodge more easily into endothelial tissue, becoming stuck and oxidized, causing an inflammatory response, and leading ultimately to cardiovascular disease.
Stay tuned for Part 2 where we will discuss:
- LDL pattern B. How its really the villain in the story and why we produce it
- How modern commercial food preparation, not dietary fat, is to blame for heart disease
- Dietary strategies to correct a bad cholesterol test like low HDL, high LDL, and high triglyceride.
Great article. For some reason I find myself very intersted in cholesterol and all the myths and mystery that surrounds it. But there is one question I cannot find the answer to.
Should we really care about our cholesterol reading, or does it not have any utility at all?
Great question. The research on cholesterol and heart disease is completely inconclusive. The best we have been able to say that dietary fat and cholesterol do not lead to the increased risk of heart disease that was espoused in the 80’s and 90’s. That is why all of the low fat dietary recommendations stopped about 10 years ago. The other big question is whether the use of “statin” drugs lower the incidence of heart disease. The conclusions that we can draw from the latest research on this is as follows: 1. Females receive no benefit, decreased mortality or increased quality of life, from taking statins at any age. All men over 65 years off age and younger men who have never had heart disease previously also do not benefit from statin therapy. The only group which does show statistical benefit from statin therapy are men under 65 who have already had a heart attack…this is what is called “secondary prevention”. This benefit is probably due not to statins lowering of cholesterol, but to the potent anti-inflammatory effects of the drug itself. This anti-inflammatory effect is due to the suppression of the production of a substance called nuclear factor- kappa B, one of the more potent inflammatory agents in your body. Taken together, the evidence is compelling that cholesterol is and always has been innocent of the negative charges set against it.