Last week I gave the first, of hopefully many, lectures on helping people get in shape. The topic was about burning fat and was called “How to Become a Fat Burning Machine.“ (The video is on my YouTube channel.)
As I was doing research, I came across a lot of great information, much of which I had to cut for time.
I touched a little on some of the misconceptions regarding cholesterol but didn’t go as far in depth as I would have liked.
Since I didn’t cover it as much as I would have liked during the seminar, I decided to expand on it here in this article.
What Is cholesterol?
As far as I can remember I have been taught that cholesterol is bad. It causes heart disease and we should avoid it if we want to be healthy. It wasn’t until last year when I listened to the audio book for Good Calories, Bad Calories by Gary Taubes that I started to question some of these beliefs I had.
Could cholesterol actually be something good? Let’s examine its role in the body and what it actually does.
Cholesterol is produced in the body and is present in the membrane of every cell in the body. Most cells in the body can produce cholesterol but most of it is made in the liver.
It aids in cell repair and also produces hormones like testosterone and estrogen. When you go out in the sun the body can produce vitamin D from cholesterol and vitamin D plays an important role in brain function. So cholesterol is a necessary and vital part of life.
All these all sound like good things, so why is everyone so scared of it?
Dr. Peter Attia explains it best in the video below, but I wrote a simplified explanation with links to some of the studies he talked about as well as a few added points.
Is cholesterol REALLY dangerous?
The reason cholesterol gets it’s bad rap is because of a thing called atherosclerosis. This is where a sterol (such as cholesterol) builds up a plaque in the walls of the arteries. Over time this plaque can harden and narrow the arteries.
Atherosclerosis is not good and can lead to many chronic conditions such as coronary heart disease.
Because cholesterol is what makes up most of the plaque, a hypothesis is that cholesterol is the cause of atherosclerosis. This is known as the lipid hypothesis.
Even though there is little evidence to support this hypothesis, it has become the basis for many of the government food guidelines as well as the low-fat craze from the 80s and 90s.
The lipid hypothesis is based on 2 assumptions. The first is that eating cholesterol and saturated fats will raise the cholesterol levels in your blood. The second is that a lot of cholesterol in your blood increases your risk for heart disease.
Although many people still follow this outdated idea, it has become the subject of a lot of research and debate. Much of the evidence suggests that this theory is incorrect and it is something else that leads atherosclerosis.
HDL vs LDL Cholesterol: Good or Bad?
Most people believe there is “good” cholesterol and “bad” cholesterol. HDL (high-density lipoprotein) cholesterol is supposed to be the “good” one and LDL (low-density lipoprotein) cholesterol is supposed to be the “bad” one.
The truth is that neither of these are actually cholesterol even though they are referred to as HDL and LDL cholesterol. Both are proteins that cholesterol uses to move around the body through the bloodstream. Triglycerides and other lipids are also transported around the body with lipoproteins.
HDL and LDL are the two most referred to, but there are 5 major types of lipoproteins that the body uses to move fats through the blood. The other 3 are VLDL (very low-density lipoprotein, ) IDL (intermediate-density lipoprotein) and chylomicrons.
The reason the cholesterol and other fats need help is that they are fat-soluble and blood is water-soluble. They don’t mix well together. Think of a oil and vinegar salad dressing.
To allow cholesterol to travel through our bloodstream, it needs to attach to these lipoproteins. A popular analogy is to refer to cholesterol as the “cargo” and the lipoproteins as the “boats.”
LDL transports cholesterol from the liver to the tissues of the body. HDL transports cholesterol from the tissues back to the liver where it is recycled.
Both LDL and HDL are important parts of the normal function of the body, so why has LDL been labels as the “bad cholesterol.”
The problems begin when cholesterol penetrates the arterial walls. This is when the plaque starts to build up in the arteries and that is when atherosclerosis can begin.
The only way that cholesterol is able to get to the arteries and penetrate them is if they are carried there by LDL.
Now that you know a little more about “good” and “bad” cholesterol, let’s take another look at what we’ve been told about cholesterol and fats.
Examining the lipid hypothesis
The lipid hypothesis is the basis for most of the food recommendations from the government. It is why we were told to eat a lot of grains and starches. It is why were told to limit our fatty meats and eggs.
There is not a lot of evidence that supports the lipid hypothesis and a lot that disproves it. Before I get into some of the research and why the lipid hypothesis is likely false I need to give you a little more background on cholesterol.
There are 2 forms of cholesterol. “Free” or “unesterified” cholesterol (UC) which is it’s active form and a cholesterol ester (CE) which is it’s stored form.
Only UC can be absorbed by the body but most of the cholesterol from food is esterified (CE.) This means we don’t absorb a lot of the cholesterol from food. Most of it just gets excreted out.
Some of the CE from our foods can be de-esterified but most of the cholesterol in our body is produced from within the body and not from the food we eat.
The exact percentage of cholesterol that the body actually absorbs varies from person to person. The estimates range between 20-60% but that is not a lot of cholesterol compared to what is already in the body.
According to Dr. Attia, of the new cholesterol that is “produced” on a daily basis, is around 300-500mg from food and around 800-1200mg from within the body. These new cholesterol numbers are tiny compared to what is already stored in the body. Most of the cholesterol stored in our body is in our cell membranes and the total stores are around 30-40 grams or 30,000-40,000mg.
So only a portion of the cholesterol from our foods is absorbed and in the grand scheme of things, it’s not a lot compared to what we already have stored. Most people won’t experience a change in their blood cholesterol when they change their dietary cholesterol intake.
One study estimates that 70% of people experience a small or no increase to blood cholesterol when increasing dietary cholesterol. Another study saw an increase in large LDL and a decrease in small LDL when increasing dietary cholesterol. (Small LDL is more of a threat for heart disease and I’ll go into that a little more in a bit.)
So dietary cholesterol does not significantly change blood cholesterol for most people and even when it does the association between dietary cholesterol and coronary heart disease (CHD) is very minor and elevated cholesterol may even be beneficial, but what about saturated fats?
Some short-term studies do show that saturated fats can raise cholesterol levels, but all long-term studies show no relationship between saturated fat intake and blood cholesterol levels (except one but the relationship was weak.)
Another study looked at saturated fat and it’s direct role in heart disease and found no relationship. A Japanese study concluded the same thing and also found that those who had higher saturated fat intake had a reduced risk of stroke.
So the real issue is not the dietary or total blood cholesterol and it’s not even the LDL. The risk is from cholesterol getting into the walls of the arteries. The way to reduce your risk for heart disease is to stop cholesterol from penetrating the arterial walls, but how do we do that?
The REAL risk factor for heart disease
The common thinking to reduce the risk for heart disease is to reduce the total cholesterol. That means there is less of it that can penetrate the arterial walls. This makes sense but cholesterol is vital to the body and is not the real issue.
The other thing were told it that we need to reduce the total amount of LDL (LDL-c) and increase the HDL. This also makes sense. If the cholesterol is not transported to the walls of the arteries it can’t penetrate anything and the more HDL, the more the cholesterol will be taken back to the liver. This also makes sense but doesn’t really tell the whole story.
There are different types of LDL cholesterol. There is the “large LDL” and the “small, dense LDL.” Studies show that the “small, dense LDL” increases the risk for heart disease more than the “large LDL.”
The size of the LDL particles matter, but the more important marker for heart disease risk is the amount of LDL particles (also called LDL-p.) When you factor in the LDL-p the size of the LDL and the LDL-c is less important.
Having a lot of LDL-c can sometimes mean the LDL-p is also high but that is not always the case.
One way to measure the LDL-p is by measuring something called Apolipoprotein B (ApoB.)
ApoB is found in LDL, VLDL, IDL and chylomicrons. Each of these contain one ApoB molecule and about 85-90% of these are found in LDL particles. (HDL uses Apolipoprotein A I.)
Studies have shown that ApoB is a better indicator of heart disease than LDL-c. It has also been shown that ApoB may be elevated even with normal LDL-c levels. The large long-term Farmingham study also indicates that LDL-p is a better indicator of heart disease than LDL-c.
The theory behind why more small LDL particles would increase risk for heart disease is that the more particles you have, the more of a chance that one of them will penetrate the arterial wall.
Reducing your risk for Heart Disease
Let’s take a look at what we went over so far:
*Cholesterol is an important molecule in our body and is essential for life.
*Most of the cholesterol in our body is produced in our body.
*Most of the cholesterol we eat is not absorbed into our body and does not have a big impact on the cholesterol in our body.
*Atherosclerosis increases our risk for heart disease and this occurs when cholesterol penetrates our arterial walls.
*The only way cholesterol can reach our arterial walls is with a ApoB lipoprotein (LDL, VLDL, IDL and chylomicrons.)
*The more LDL particles (LDL-p) you have, the greater your risk for heart disease.
With all of this in mind, the real enemy is the amount of LDL particles in your body, not total cholesterol or total LDL cholesterol. So how can we reduce the amount of LDL-p?
It appears that just like with weight loss, sugar and refined carbohydrates are the guilty parties.
A short-term study showed a dramatic increase in ApoB and triglycerides when increasing fructose and high fructose corn syrup.
A 2006 study saw subjects restricting carbohydrates see a greater reduction in ApoB, weight, body fat and other metabolic markers, than a group following a low-fat diet.
A separate 2006 study also compared low fat and low carb diets. The low carb group lowered their ApoB, triglycerides and other markers with a slight increase in total LDL (LDL-c.)
This evidence may not be definitive but it does suggest that carbohydrate consumption may play a bigger role in heart disease and atherosclerosis than most people think.
Other suspects that may raise LDL-p include inflammation, chronic lack of sleep, lack of exercise, poor gut health, and environmental toxins.
Remember that statin drugs lower cholesterol produced in your liver but do not address LDL-p. (This does not mean they are not useful in certain situations.)
One thing to remember is that studies work at a population level and may or may not be relevant at the individual level. If you are concerned about your blood cholesterol levels get them checked out.
Conventional tests measure total cholesterol, total HDL, total LDL and triglycerides. As we’ve discussed the amount of LDL particles may be a better indicator and ApoB is a good marker of that. There are several tests like the NMR LipoProfile that can measure some of these advanced markers.
I hope this article has prompted you to at least start to re-examine some of the beliefs you have about cholesterol and helped you realize that cholesterol is not the enemy.
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