Cholesterol levels are usually given as one number, eg 5.3 or 4.6. Occasionally they are broken down into LDL levels and HDL levels. LDL is known as bad cholesterol and HDL as good cholesterol. Now I have known for many years that this whole cholesterol thing is misleading to say the least, and the next blog on cholesterol will be called Does Saturated Fat Cause Heart Attacks? However, whilst writing it, it became apparent that is it very important to understand the cholesterol nomenclature – and I was in for quite a surprise. So let me share my discoveries – and maybe the confusion. The following is based on the above video clip plus the following 3 and also on the book The Great Cholesterol Con by Dr Malcolm Kendrick.
First off the bat HDL and LDL mean high density lipoprotein and low density lipoprotein. A lipoprotein is NOT cholesterol. A lipoprotein (literally fat protein) is actually a transporter molecule. Like a bus, a lorry or a taxi. A lipoprotein carries both fat and cholesterol about the body in the blood. Since neither fat nor cholesterol are water soluble, they have to go inside something for transportation – lipoproteins. There are at least 6 types of lipoproteins and they vary in the relative amounts of fat and cholesterol they are transporting about. So here is the table reproduced from the above video. It only contains 5 of the lipoproteins. I’ll talk about the 6th later.
|
Chylomicron |
VLDL |
IDL |
LDL |
HDL |
|
| Protein |
1% |
10% |
10% |
≈20% |
≈50% |
| Triglycerides |
88% |
56% |
29% |
13% |
13% |
| Cholesterol |
1% |
8% |
9% |
10% |
6% |
| Cholesterol Esters |
3% |
15% |
34% |
48% |
30% |
The table shows what percentage of fat and cholesterol is carried in each lipoprotein. Clearly each type of lipoprotein is doing a different job so here are the definitions. But just before we go there, what does the term triglyceride mean?
This is the primary structure of fats in the body. I don’t know why they are in 3s, but the body puts 3 fats (or fatty acids) together by binding them with glycerol and glycerol is half a sugar molecule. When a triglyceride reaches its destination, the fat is cleaved off the glycerol and the glycerol returns to the liver to be recombined with the other half to make sugar.
The other new word in the table is cholesterol ester. Cholesterol itself is uptaken by the cells in its free form and released by them in the cholesterol ester form which is converted to bile in the liver. More on this when we look at HDL. And the word Cholesterol means chole means bile and sterol is a type of steroid.
Chylomicron. This is the biggest lipoprotein, like a lorry. It is manufactured in the gut and it transports fat from the diet to either the liver or, primarily, to body fat. As can be seen in the table, the centre of the chylomicron carries about 88% fat.When it reaches the body fat cell, it docks onto its receptor site and off loads its payload of fat. When the fat level in the chylomicrom reaches about 20%, it leaves the fat cell and travels to the liver where it again docks, and gives up its remaining fat and cleaved glycerol. The video refers to a genetic defect that makes it not possible for the gut to make chylomicrons and this leads to an excessive build up of fat in the gut, the gut wall and in the faeces.
VLDL – very low density lipoprotein -is produced by the liver to transport fat and cholesterol to tissues of the body. Bit like a bus. The video only discusses the transportation to the body fat, however triglycerides are used elsewhere in the body, eg by the heart when fasting or by the breasts of a lactating mother. VLDLs carry 56% fat, the rest being cholesterol and 10% protein. It travels to the fat cells, docks and off loads the fat. According to the video, when the fat levels drop to 50%, sometimes it leaves the fat cell and returns to the liver for refilling. Sometimes it either remains bound to the fat cell or rebinds to another fat cell and when the fat levels drop to 30% it now becomes called an IDL – and it shrinks in size to more of a minibus.
IDL (intermediate density lipoprotein) The IDL then returns to the liver for recycling as a VLDL. Sometimes IDL stays on the fat cell for even longer until the triglyceride level reaches a lowly 10% approx. At this point the lipoprotein loses its proteins that allow it to dock to the fat cell or to the liver cell and becomes the dreaded LDL.
LDL (low density lipoprotein). This is an emptier minibus containing principally the cholesterol that has been riding about in it all this time. Now the minibus trundles about the blood stream delivering cholesterol to where it is needed. This is one important minibus. To call it bad is quite wrong. As the blog ‘Is there really a link between cholesterol levels and heart disease?’ stated, cholesterol is vital for production of sex and stress hormones, for the fat soluble vitamins, nerve insulation and it forms the synapses in the brain amongst other things. So LDL is taken up by the cells in order to use its payload of cholesterol. When the minibus is empty, it goes back to the liver. However, it has lost its protein that enabled easy docking to the liver, so has to use an alternative one which is not as efficient, so the half life of LDL is much longer in the blood than IDL or VLDL and this, they say, is how LDL is prone to oxidation. How they think LDL causes thickening and hardening of the arteries will be discussed in the next blog.
HDL (high density lipoprotein) – usually seen as the hero, the good cholesterol. HDL is produced by the liver – but according to Dr Kendrick in his book The Great Cholesterol Con this is conjecture – and leaves the liver as a largely empty shell – a taxi if you like. It cruises through the blood stream picking up cholesterol from the tissues. The way it does this means that cholesterol gets turned into a cholesterol ester. This is then taken to the liver where it is turned into bile – and bile is what the body uses to breakdown fat.
There is another form of lipoprotein called Lp(a). Lp(a) is another form of LDL, but carries a pair of proteins on its outside ((some sources say there is only one protein – which goes to show how not enough is known about Lp(a) )). These proteins are attracted to artery damage and stick Lp(a) firmly to those areas forming a very strong, difficult to remove blood clot. Now normally, when a blood clot is formed an enzyme called plasminogen is incorporated which turns into plasmin and acts like a tiny stick of dynamite to break the clot up. This is activated by an enzyme known as plasminogen activator or tPA. When Lp(a) is in the clot, it blocks the action of tPA, making the blood clot difficult to shift. So the form of lipoprotein that we do not want high levels of is not LDL per se, but the subsection Lp(a).
Lp(a) levels seem to be genetic. Statins do not lower its level. People with high levels of Lp(a) are at very great risk of having heart disease. Normal levels appear to be between 14 – 30. The footnoted video is of a sweet man telling us about his triple bypass surgery, despite him having no currently measured risk factors for a heart attack – ie he is slim, exercises, has normal blood pressure etc. He says his Lp(a) level was measured at 259 ((http://youtu.be/4FT5CVDrHtI)) .
So VLDL becomes IDL which becomes LDL. Without VLDL, you cannot have LDL. What raises VLDL? High carbohydrate diet. If going for a ‘cholesterol’ test – which we now know should at the very least be called a lipoprotein test – it would be worth pressing for a Lp(a) test.
Incidentally, heart attacks and heart disease are caused by more factors than just Lp(a). Lp(a) is only one genetic factor. The greatest killer stalks us all in the Western world – and has nothing whatsoever to do with lipoprotein levels. But for now the next blog in the series discusses, ‘Is saturated fat a killer?’