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Coronary Artery Disease / Why The Cholesterol-Heart Disease Theory Is Wrong
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Some studies have shown that a high saturated fat intake raises cholesterol levels; others have shown the exact opposite. The longest, most prestigious and widely quoted long-term study on CHD, the Framingham study, clearly shows that those who eat the most saturated fat have the lowest cholesterol levels.
My own belief is that in healthy people, dietary intake, of anything, has no effect on cholesterol levels - beyond a few percentage points of non-significant wobble.
But my belief is not an act of personal faith with no foundation on fact. For the science of fat metabolism confirms that there cannot be any connection whatsoever between saturated fat consumption and cholesterol levels. And I am wondering how best to explain this without getting too technical.
The first point to make is that you do not have a cholesterol level in your blood. Cholesterol is insoluble in blood, and therefore has to be carried around the body inside a small sphere known as a lipoprotein. There are many different types of lipoprotein, ranging from the monster chlyomicron to the teeny, weeny, High Density Lipoprotein (HDL).
Lipoproteins do not just carry cholesterol. They also carry all sorts of other fats, saturated, monounsaturated and polyunsaturated. These fats are all attached to a glycerol molecule, in sets of three, and the resulting substance is therefore called a triglyceride.
Triglyceride = three fats attached to a backbone glycerol molecule. (Just in case you’re wondering, a fat is a fatty acid, and a fatty acid is a fat).
Thus, when you eat cholesterol and saturated fat, they are both absorbed into the intenstinal wall, where the saturated fats are all stuck onto a glycerol molecule, to make triglycerides, the cholesterol remains unchanged. Then, within the intestinal wall both are rammed into a chylomicron before being expelled into the portal circulation system to be moved around the body.
Most chylomicrons go directly to the liver where they are absorbed, broken down, and reconstructed into a smaller type of lipoprotein known as a Very Low Density Lipoprotein VLDL. These VLDLs then go out into the general circulation and gradually lose triglyceride. As they do so, they get smaller, transforming from VLDL to Intermediate Density Lipoproteins (IDLs), then Low Density Lipoproteins (LDLs).
The LDL is either absorbed back into the liver, to be reused to create more VLDLs, or they are absorbed into other tissues where the contents are used by the cell.
So, at what point does saturated fat get turned into cholesterol?
Answer, it doesn’t. You don’t make cholesterol out of saturated fat. Cholesterol, when it is made in the liver, starts out as a substance called Acteyl-co A. This is not a fat; it is nothing like a fat. It has several nitrogen atoms in it, and nitrogen comes from protein.
Point one, therefore, is that saturated fat and cholesterol and completely unrelated chemically, and you don’t make cholesterol from fats. So why would eating saturated fat increase cholesterol production in the liver?….. It can’t and it doesn’t.
But of course, the substance we are interested in nowadays is LDL. Which is not the same thing as cholesterol at all. So why do we called a raised LDL level a raised cholesterol level?
In fact, the nomenclature in this whole area is just designed to make things almost impossible to understand. For example, a raised VLDL level is known as hypertriglycerideamia. Why? Goodness only knows. Perhaps if researchers in this area were to use a clear form of nomenclature, the weakness of the diet/heart hypothesis would be more easily exposed.
Time for a little review
- Cholesterol and saturated fats are unrelated substances and you don’t make cholesterol from saturated fat, or any other type of fat
- A raised cholesterol level is, in reality, a raised LDL level
- A raised VLDL level is called hypertriglyceridaemia
- The only connection between saturated fats and cholesterol is that, because they are insoluble in water, they sit inside lipoproteins in order that they can be carried around the body
- The liver doesn’t make LDL - LDL is the metabolic residue of VLDL.
Suddenly the whole concept of saturated fat intake raising cholesterol levels doesn’t seem so simple anymore, does it? But, if the substance in the blood that causes CHD is actually LDL, maybe we just need to move the goalposts….again, and ask a different question.
Does a high saturated fat intake increase LDL levels?
Just to review some of the facts. The liver doesn’t make LDL, it makes VLDL, and when VLDL loses triglyceride it turns into LDL.
So, if you eat more saturated fat (or any other kind of fat), the liver will churn our more VLDL. NOT because there is more cholesterol around, but because there are more triglycerides around to deal with.
Therefore, presumably, after all the VLDLs have shrunk in size, there will be more LDLs left. Which means that a high fat consumption could lead to a higher level of LDL, via VLDL metabolism - although we have to abandon the whole cholesterol argument at this point, as cholesterol has nothing whatsoever to do with this process, it just gets carried around as an innocent bystander.
But even if you move the discussion onto LDLs rather than cholesterol, there is a further huge and insurmountable problem here. After a meal VLDL levels go up, as you would expect, but the LDL level remains absolutely constant. Absolutely constant….(and there is no delayed response either).
So, the amount of VLDL in the blood is totally unrelated to the level of LDL in the blood. Despite the fact that you ‘make’ one from the other.
What this proves, beyond any doubt, is that the metabolic system tightly controls the level of LDL in the blood. It doesn’t matter how many VLDLs are converted to LDL, the system takes the excess LDL out of play - instantly. It pulls excess LDLs into the liver where it recycles them.
So, although fat intake can increase VLDL production, it has no effect on the level of LDL. Which means that, not only does saturated fat have no effect on cholesterol production in the liver, it also has no effect on LDL levels. In reality, it has no effect at all. And why should it? If you eat too much protein, your blood protein level doesn’t rise. If you eat too much sugar your ‘fasting’ blood sugar level doesn’t rise. Why should fat or cholesterol be any different?
You will not read this type of information anywhere, but here. However, every single fact I have used has been demonstrated many, many times. These are facts beyond dispute. It’s just that no-one chooses to highlight what all of these facts, when brought together, actually mean.
- Fact one: The liver does not use fats, saturated or otherwise to make cholesterol
- Fact two: The liver does not make LDL, it makes VLDL
- Fact three: VLDL is converted into LDL through triglyceride loss
- Fact four: VLDL levels and LDL levels are totally unrelated - totally
Which means that: Saturated fat intake has no impact on LDL levels.
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