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| The cover from Time magazine published on March 26th 1984 has painted cholesterol into the major cause for cardiovascular problems in the eyes of general public. Even though it contributed to starting the "health craze", 30 years later, cardiovascular problems are on an all-time high. |
Then I asked them how do they know that eating a lot of fat increases the risk of cardiovascular problems. Again, their answer was unanimous. It's everywhere in the media, everyone is buying low fat food, all the doctors are saying it... OK I thought, that is indeed a strong argument, if everyone is saying it and doing it. But: why are more and more people dying because of cardiovascular problems? Are we really so sure that things are going in the right direction?
First of all, apologies for a long and perhaps complicated post
Not being a medical doctor and not even a certified nutritionist, it certainly is a challenge to write about human metabolism. It is a very complex system which combines the power of several organs, hormones, enzymes and also our nutrition. So I will begin this discussion by summarizing the key points I want to make. Although I wish you would read this entire post, you may as well check out the following key discoveries:
- the idea that eating food rich on cholesterol is a major cause of cardiovascular problems is not supported by scientific observations of human (not animal!) responses to different diets;
- the amount of cholesterol in our blood stream is virtually independent on the amount of cholesterol that we eat;
- cardiovascular problems are caused by lipoproteins, which have a role of a transport system for triglycerides and cholesterol;
- only one type of lipoproteins is dangerous, due to its chemical structure and size;
- if concentration of dangerous lipoprotein is low, there is little risk for cardiovascular disease;
- concentration of dangerous lipoprotein in our blood is nearly independent on the amount of fat and cholesterol we eat, however it depends a lot with the amount of carbohydrates;
- as a consequence of that last point, people on carbohydrate diets are in bigger risks of cardiovascular problems than people on LCHF diet;
What really causes cardiovascular problems?
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| A very bad case of atherosclerosis. The arthery wall is severely damaged by chronic inflammation and is covered with plaque which was created in body's attempt to stop the inflammation. |
The root cause of many cardiovascular problems is atherosclerosis. Atherosclerosis is a process where plaque is built inside arterial walls, along with an ongoing (chronic) inflammation of that area. Because of strong inflammation, muscles around arteries contract, increasing our blood pressure. Furthermore, plaque is an obstacle to normal blood flow, increasing blood pressure even further. Finally, when plaque grows a lot, it can completely jam an artery. Or, a piece of plaque may brake away and start travelling around our body, until it gets stuck in some narrower blood vessel and give us a stroke. So, the most common cardiovascular problems like heart attack, stroke, increased blood pressure are all a consequence of atherosclerosis.
Sure... But atherosclerosis is caused by fat and cholesterol, right?
Surprisingly, no! Atherosclerosis is not caused by fat nor by cholesterol. I know you have been told this thousands of times by all sorts of people, but it just isn't true. The thing is that cholesterol and triglycerides are not swimming around in our blood freely, because they are not soluble in water (nor in blood). In order to transport them around our body, we have a special transport system which consists of lipoproteins.
It is quite possible that you have never heard of a word "lipoprotein" before. But perhaps you have heard of LDL and HDL. Word on the street (and in most medical clinics) is that LDL is "the bad cholesterol" and that HDL is "the good cholesterol". They say that you should have plenty of the good cholesterol and as little as possible of the bad cholesterol, which causes artherosclerosis. That's not very far from the truth, but they haven't told you one important thing: LDL and HDL are not cholesterol, but two kinds of lipoproteins.
Say "hello" to lipoproteins
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| Lipoprotein is a molecular container. It's outer shell consists of lipids (green circles with yellow tails) and proteins (larger circles of different colors). Inside lipoproteins there are molecules of triglycerides and cholesterol. They are completely isolated from the rest of the body. |
Things you should know about lipoproteins
Think of lipoproteins like of boxes or containers. Even better, think of them as boats carrying around cargo. I borrowed this analogy from Dr. Peter Attia, whos excellent lecture of cholesterol is available at Youtube. I included a link at the end of this post, I warmly advise you to take a look at it.
What are lipoproteins carrying?
In short, they carry triglycerides ("fat" molecules) and (real) cholesterol molecules. The reason why it is necessary to transport triglycerides and cholesterol around as cargo is that they are not soluble in water, nor in blood. If there were no lipoproteins, cholesterol and triglycerides couldn't be transported around our body and that would be a very very bad thing. Depending on their structure, there are 5 different kinds of lipoproteins:
- Chylomicrons
- very low density lipoproteins (VLDL)
- intermediate-density lipoproteins (IDL)
- low density lipoproteins (LDL)
- high density lipoproteins (HDL)
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| An illustroations of different kinds of lipoproteins and their sizes. The bigger the size, the higher proportion of triglycerides. |
As you can see, lipoproteins are not just LDL and HDL. If you have been reading this blog thoroughly, you may remember that I have already mentioned chylomicrons in Myth 1. To refresh your memory, chylomicrons transport triglycerides from our gut into our bloodstream and deliver them to our cells. If we have insufficient glucose, then these triglycerides are delivered to cells to be burned as energy, which is obviously a desired thing for overweight people. Otherwise, they are deposited in our "fat" cells as fat, which us the less desirable pattern.
VLDL has exactly the same role as chylomicrons, with and exception that the triglycerides carried by VLDL are coming from our liver, not from our gut. In the liver, our body produces its own cholesterol (which is 75% of all cholesterol we require). Furthermore, when there are abundant glucose molecules floating around, our liver creates triglycerides to be stored as fat. So you can think of VLDL as a transport system for triglycerides and cholesterol which our body produces by itself, while chylomicrons transport what we eat.
Since cholesterol is very important for normal functioning of our body, our liver will always create all the lacking cholesterol. If we eat little fat and cholesterol, than the majority of triglycerides and cholesterol will come from our liver and the concentration of VLDL will go up. Alternatively, eating more cholesterol and triglycerides reduces liver activity and concentration of VLDL, but the number of chylomicrons go up.
Once VLDL and chylomicrons our in our bloodstream, they follow the same metabolic process. Triglyceride and cholesterol cargo is delivered to cells. As they flow around our bloodstream, lipoproteins gradually release their cargo and become small and smaller. To be precise, they also exchange proteins, but that part is quite complicated and not so important for the point I am trying to make. When triglycerides are delivered, VLDL and chylomicrons transform into IDL, and then LDL. IDL doesn't last very long and is not important in cardiovascular issues, but LDL is. You may think of LDL as a grandchild of VLDL. It is a cargo ship at the end of its journey, where most of the cargo has been delivered. Hence, LDL particles are smaller than VLDL.
For know, I won't be mentioning HDL, except that is a different kind of lipoprotein. It is still a carrier of triglycerides and cholesterol, but it is created from a different sort of protein than VLDL, IDL and LDL and acts in quite a different way.
VLDL and LDL are both considered to be "the bad cholesterol". They are prone to oxidation and they are just the right size to penetrate into arterial walls and get stuck there. On the other hand, chylomicrons, IDL and HDL do not cause atherosclerosis. And since we now know that VLDL is coming from our liver, when it creates its own cholesterol and triglycerides, it seems logical to conclude that we should be on a diet that doesn't encourage production of VLDL.
But what about LDL? Did you know that there are two different kinds of LDL? Neither did I...
Introducing LDL-C and LDL-P
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| An illustration of LDL-C (left) and LDL-P (right). For the same amount of total cholesterol, we need a larger number of LDL-P, comparing to LDL-C. |
LDL-C and LDL-P are both subclasses of LDL. Remember, they are both pretty much depleted of triglycerides and are carrying mostly cholesterol. LDL-C contains more cholesterol than LDL-P. Hence, LDL-C is bigger than LDL-P. This means that if we compared two people with the same total amount of cholesterol, but with different LDL particles, person A would have a small number of relatively large LDL-C particles and a person B would have a bigger number of relatively small LDL-P particles. According to Dr. Peter Attia: "there is no dispute that person A is at bigger risk than person B". So apparently, one kind of LDL is more dangerous than the other!
Analysis of 6 years of data of LCL-P and LDL-C along with associating risks has shown that people with low LDL-P and a not low LDL-C (not low means normal or high) were at lowest risk of cardiovascular problems (see blue curve on below chart). On the other hand, people with not low LDL-P and low LDL-C were at the highest risk (red curve). To simplify, cardiovascular risk was increasing with increasing LDL-P, while LDL-C doesn't have a large impact. Another study that spanned over 16 years (!) showed a similar result. If you would like to see further explanation and more data and/or if you are a fan of statistics, I suggest you to read this article.Or, you can just remember that although all LDL particles cause artherosclerosis, LDL-P is much more dangerous than LDL-C.
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| Comparison of risk factors of people with different concentrations of LDL-P and LDL-C. The red curve represents people with the greatest risk, which have low LDL-C and increased LDL-P. It is surprising to see that they are at an even greater risk than people with increased both LDL-P and LDL-C (yellow curve). At the lowest risk are people with low LDL-P and increased LDL-C. |
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| Results of a 16-years long study of cca. 3000 people shows LDL-P has a much greater impact on cardiovascular risks than LDL-C. |
So, to decrease cardiovascular risks, we should focus on decreasing LDL-P?
Correct! Since our body can produce all the cholesterol it requires and since this cholesterol has to be transported around, eating low cholesterol food won't lower your overall LDL. I found several experts hypothesising that the amount of cholesterol and subsequent LDL concentration is mostly defined by genetics and can not be largely regulated. This means, that the sum of all LDL particles may not be regulated much, but it doesn't mean that we can't affect the ratio between LDL-P (the "bad bad cholesterol") and LDL-C (the "good bad cholesterol"). I was very much surprise to discover that this ratio depends a lot on the amount of sugar we eat.
The role of sugar on concentration of LDL-P and LDL-C particles
In 2011, Peter Havel published results of his study on effects of simple carbohydrates on LDL, HDL and triglyceride levels. He divided his subjects in three groups, putting them all on a western diet consisting mostly of carbs, some fat and little proteins. Total calorie intake was low. The difference between groups was the kind of carbs they were given. Group A received 25% of their carbs as glucose, group B as fructose and group C in form of high fructose corn syrup (consisting of 45% glucose and 55% fructose). This was a very typical western diet, especially groups B and C, since we eat plenty of white sugar while high fructose corn syrup is a popular additive in processed foods. Even though it was a short study, results were very interesting, as you can see on below charts.
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| Impact of glucose, fructose and a mixture of fructose and glucose on lipoproteins, particularly LDL. Glucose has a much lower impact as fructose and a mixture of both. |
I hope that so far, you are a little bit more familiar with terms like cholesterol and lipoproteins. Studies presented so far show that against common public opinion, carbohydrate diets are risky because:
- our liver produces more harmful VLDL;
- fructose and a mixture of fructose and glucose increase harmful LDL;
So, if you want to reduce cardiovascular risks, carbohydrates surely are not the way to do it. But, even if carbohydrates increase cardiovascular risks, it doesn't automatically mean that saturated fats advised by LCHF diet doesn't. So let's take a look at another (and the final) study.
The role of saturated fat concentration of LDL-P and LDL-C particles
In 2003, a group of researches published results of a study made with 16 very obese people (body mass index over 39). They were put on ketogenic diet where 50% of calories were coming from saturated fat. After 6 weeks, these were the results:
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| Glucose, insulin, triglyceride and lipoprotein changes after a six week diet rich in saturated fat. As you can see, the most threatening factors for obesity and cardiovascular risks decreased significantly. |
- 5% drop of glucose
- 30% drop of triglycerides
- average size of VLDL particles decreased for 20% (probably because they recieved fat from nutrition, no longer so much from liver)
- slight decrease of total cholesterol
- slight decrease of total HDL
- slight decrease of concentration of LDL particles
- slight increase of average size of LDL particles
- 25% decrease of concentration of medium and small LDL particles (the bad LDL)
In summary, a diet rich in saturated fats significantly improved two major risks for atherosclerosis: triglyceride levels and VLDL levels, while LDL levels didn't change much. In terms of cardiovascular risks, this is a very good sign. The conclusion of this study was that insulin resistance of these people improved dramatically, despite the fact that their calories consisted of 50% saturated fat!
This last study shows that eating a highly saturated fat diet not only isn't dangerous for your cardiovascular system, but is actually very beneficial.
Putting it all together
After an extensive analysis of scientific data, obtained by observing people and not animals, as well as after looking at interpretations of this data by well recognized medical experts, my personal conclusion is that a diet rich in cholesterol and fat (including saturated fat), is not even nearly as dangerous as it is commonly believed. Contraversive, they seem to be quite beneficial. On the other hand, carbohydrates not only cause quicker generation of fat, but also stimulate production of harmful lipoproteins.
While I was writing this post, I was often surprised about how little do we really know about saturated fat and cholesterol, even though all kinds of information are only a couple of clicks away. I am now completely convinced that cardiovascular problems are not caused by saturated fat and cholesterol. The picture of pieces of fat and cholesterol molecules floating freely in our blood and clogging our pipeline, which is so often used to scare us away from butter and bacon, is completely unrealistic. I know now that atherosclerosis is caused by certain LDL particles and that the kind of LDL particles in our blood depends on our metabolic state. And finally, according to all the data as well as to my personal experience so fat, diets which are low on carbohydrates and high on fat (LCHF) are:
- easiest to follow;
- delicious;
- free of starvation and cravings;
- good for your heart and arteries!
Further reading
Since cardiovascular risks is an important topic, I encourage you to gather more information on that subject. In particulat, I can recommend you to follow the works of Dr. Peter Attia, from whom I have borrowed most of the material for this post.
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