You will learn four interesting facts about cholesterol that have two things in common. First, they have been around for ages and don’t want to go away. Second, none of them are true. You’re in for a treat.
- Myth 1: High levels of cholesterol will cause heart attack
- Myth 2: LDL cholesterol is “bad” cholesterol
- Myth 3: Eating a low cholesterol diet will reduce your blood cholesterol
- Myth 4: A diet high in sugar increases your risk of atherosclerosis
Before I started this article I was unsure what would be the best way of debunking the common perception of cholesterol. A myth so persistent and widespread that even a majority of the medical community still believes in it, despite the fact that there has been solid evidence against it for the past 40 years. I’m personally not a conspiracy theorist, chemtrail believer, tinfoil hat wearer, big pharma conspiracy nut, or anything of those sorts, but let’s look at one interesting fact:
A meta-analysis of cholesterol-lowering trials found that trials that were supportive of the lipid hypothesis were cited almost six times as often as those that were not, and although there was a similar number of trials unsupportive of the hypothesis, none of them were cited after 1970; some of the supportive reviews also exclude and ignore certain trials which were less favorable to the hypothesis
The lipid hypothesis is an idea which probably supports your current understanding of cholesterol. It basically states that by decreasing your cholesterol levels, you will have a lesser risk for heart attack. And that’s mostly wrong.
If you dislike long texts, here is a video.
Let’s start with the essentials.
Cholesterol is an essential structural part of cell membranes in all animals, it’s essential for all animal life and almost every cell synthesizes it. It helps with the construction and maintenance of membranes. Moreover, cholesterol is a lipid molecule which enables us to move around and change shape, it changes the fluidity of membranes according to temperature. This happens because, unlike plants, we do not need a cell wall, which would make us immobile.
Furthermore, cholesterol is very important for the synthesis of:
- Steroid hormones (testosterone, estrogen, cortisol)
- Bile acids
- Active form of vitamin Vitamin D
Does that sound like a villain, who makes your arteries clog up and lets you have a heart attack, to you? No, I don’t think that either.
Now, time for some myth debunking.
No, it won’t.
Well isn’t that interesting. If more cholesterol would mean a higher risk for heart disease, we would see a very nice linear trend where more deaths would occur with more cholesterol, right? As it seems, the opposite is true for both sexes.
First, we have to clear up a few things. When we usually talk about “cholesterol”, we’re talking about four main numbers:
- Total cholesterol
- HDL cholesterol
- LDL cholesterol
Even the mainstream medical community today teaches that cholesterol is divided into HDL cholesterol, also dubbed “good” cholesterol, and LDL cholesterol, dubbed “bad” cholesterol. But as we will find out, that’s a “bad” oversimplification as well. The reason why they have been given the nickname “good” and “bad” is because of the jobs they are supposed to have in our body.
The usual heart disease fairy tale tells us that when we have too much LDL cholesterol, our arteries start to clog up and HDL cholesterol comes to the rescue to clean up LDL cholesterol away, therefore making our arteries healthier again. Sadly, that’s another vital oversimplification.
While it is true that LDLs carry cholesterol from your liver to different tissues which need maintenance and repair, and HDLs carry it from these tissues back to your liver, that’s not the story.
Lipoproteins are biochemical compounds that contain protein and lipids. They allow fats and cholesterol to move through our bloodstream.
Firstly, LDL and HDL are not cholesterol per se, they are lipoproteins that carry cholesterol through your body. They have to do this because cholesterol is insoluble in blood and it can only travel through your bloodstream in really tiny concentrations which aren’t relevant. That’s why it gets carried around with the help of lipoproteins, these are bigger particles which have a water-soluble outer part and a lipid-soluble inner part. And the inner part is where cholesterol particles are stored while they are being carried to tissues that need to be repaired.
With that said, HDLs and LDLs are not the only types of lipoproteins, the family involves:
- VLDL: very-low-density lipoproteins
- IDL: intermediate-density lipoproteins
- LDL: low-density lipoproteins
- HDL: high-density lipoproteins
This myth, as the majority of nutritional myths, stems out of false reporting and bad science. In the distant past there have been “observed connections between cholesterol intake and heart attack”. These connections were cherry-picked data. This lead to the common perception of high cholesterol = instant heart attack. But, as I’ve demonstrated, that’s just not true.
Your total cholesterol level is not a particularly informative number by itself. You should be more interested in the ratio of HDLs and LDLs. And that’s also the next myth that will be debunking.
No, it’s not.
Let’s talk about LDL particles a bit more in detail. LDL particles are divided into several classes, based on their size and density. The small, dense LDL particles are much more atherogenic due to two reasons:
- They are more prone to oxidation
- They pass into your bloodstream much more efficiently compared to the large, fluffy LDL particles
People with higher amounts of the smaller LDL particles have up to a three times higher risk for atherosclerosis. 
There are two lipid tests which help you assess the size and density of your LDL particles. One is called the vertical auto profile (VAP), the other is called nuclear magnetic resonance (NMR). With the help of these two tools your lipid blood work becomes much more informative.
Small, dense LDLs are also commonly called LDL pattern B, while large, fluffy LDLs are referred to as LDL pattern A. And people who have the former are much more at risk for heart disease than the latter. I will explain this in a second.
Atherosclerosis, a specific type of arteriosclerosis, is characterized by the thickening of you arteries. This is the result of:
- White blood cells, which get accumulated in your arteries
- Active white blood cells still present in your arteries
- Remnants of dead cells, these include cholesterol and triglycerides
All of these accumulated particles in your arteries make them less elastic and narrow them down. And this is a process which continuously happens for decades with varying intensity, depending on your diet.
Heart disease, with atherosclerosis as one of the most common causes, starts when your arteries become inflamed or damaged. LDL particles start bringing cholesterol to the damaged tissue in your arteries to help the building and repairing process (remember maintenance of cell structures?).
The problem in this process arises when these small LDL particles become oxidized. This happens when the fatty components of LDL particles become exposed to free radicals. As a result, oxidized LDL particles damage the inner lining of your blood vessel. But that’s not the end of the story.
This damage triggers a natural response where another set of cells, called macrophages, come and try to ingest them. They are usually good at this, however, they become trapped between the two inner-most parts of your blood vessels. As another result, these particles start releasing another set of particles called cytokines. These cause oxidative stress. Inflammatory reactions then continue indefinitely if you don’t do anything about it. This continuous stream of chronic inflammation and oxidation of your LDL particles causes more and more particles to clog up your arteries. They become increasingly damaged and decreasingly efficient. If this continues for decades, a heart attack can follow.
Let’s take a breather here. We can see that there is a big amount of particles and molecules involved in this process, all of them doing something. This article doesn’t mention all of them either, I’ve tried to explain this process in the most simple way without sacrificing accuracy of the process. In a nutshell – inflammation is increasingly being recognized as the main and key player in heart disease. 
This has been disproved a long time ago. It won’t, at least not by a significant amount. We also have to ask ourselves whether that really matters considering what we have just learned. Dietary cholesterol from animal products like meat, eggs, dairy, etc. has unimportant effects on blood cholesterol for a majority of people [5, 6 , 7]. There are some who are called “hyper responders” and have an increased bodily response to cholesterol, however, they are a minority.
This is mostly because your body compensates for the production of cholesterol. It wants to maintain balance between endogenous production; the production of cholesterol in your body, and the amount of cholesterol you’re getting through food. When you increase the amount of cholesterol consumed through food, the amount that your body produces will decrease. And vice versa.
- Polyunsaturated fats (walnuts, canola and sunflower oil) decrease both types of lipoproteins (HDL and LDL).
- Monounsaturated fats (olive oil, avocados) lower LDLs and raise HDLs.
- Saturated fats (coconut oil, butter) either raise HDLs or raise both HDLs and LDLs.
- Trans fats raise LDLs and lower HDLs.
No, not really. I’m just joking.
In reality, elevated blood sugar* is a great way for an increased number of glycation reactions to occur. Glycation is an interesting process where a lipid and a protein become joined together with a sugar molecule. And what is the result you may ask? A highly reactive molecule capable of damaging surrounding tissues and just any tissues it comes in contact with.
*We’re in a state of elevated blood sugar levels when we continuously consume a diet high in high GI foods such as white rice, white bread etc.
Moreover, the glycation of LDL particles makes them much more susceptible to oxidation than usual LDL particles. They also become more capable of destroying the functioning of your inner blood vessel lining. [10, 11]
And the last important thing about these glycated LDL particles: They aren’t recognized by the original LDL receptors anymore. They become lonely stragglers flowing through your bloodstream. This makes it easier for them to cause atherosclerotic plaques than normal LDL particles. 
That was it. This article obviously did not cover this topic as a whole, there is much more to read here. That’s why I’m going to throw a few links at you.
A very in-depth read about the biochemistry behind this: Chris Masterjohn’s post about cholesterol. However, it’s possible that you will not be able to understand it completely without a good grasp of chemistry and biology.
What do you think about these myths and findings? Did you believe in them before as well?
Before you go away
If you have enjoyed this article please support my work by sending coffee money my way. While ads are annoying, they pay server costs. In addition, by sending me some coffee money you tell me you really like what I have to write about. I always make sure my articles are well-researched and avoid superficial interpretations of the references. I would like to continue doing so.