A Scientist's Answer to Good Cholesterol

LIQUID DRANO-LIKE SYNTHETIC "GOOD CHOLESTEROL" PLAQUE BUSTER! IT'S SCIENCE, BUT NOT AS WE KNOW IT

By RFD Columnist Malcolm Kendrick MbChB, MRCGP (email - malcolm@llp.org.uk )

Synthetic 'Good' Cholesterol Helps Clear Arteries

Small Study Indicates the Possibility That Drug Therapy Could Reverse Heart Disease. Rob Stein Nov 5th 2003

A synthetic form of "good" cholesterol has been shown to quickly shrink blockages clogging coronary arteries, offering for the first time the possibility of a drug that could actually rapidly reverse heart disease, researchers reported yesterday….'

I'm writing a book at the moment called Cholesterolmania. That plus a job, plus children and home, an attempt at a social life and columns at redflagsdaily.com. That's a tad busy, and I thought I'd take a short break from column writing, but…I couldn't let the above story from the Washington Post go without comment.

Here is my immediate response. Aaaaaarrrrrrggggghhhhh! Thud.

It's almost impossible to know where to start without ranting. Firstly, just to clear something up, HDL is not cholesterol `good' or otherwise. HDL, stands for High Density Lipoprotein. It is a lipoprotein that is manufactured in the guts and the liver, and it contains a small amount of cholesterol.

HDL appears to have two basic functions in the body. Firstly, it transfers proteins, known as apolipoproteins, to VLDL, allowing the VLDL to be recognised by receptors around the body. Secondly, it removes cholesterol that is floating about and takes it back to the liver.

When cells do break down in body, which is happening all the time, the cholesterol from cell walls is released into the surrounding extra cellular fluid. The HDL lurking in the vicinity `mops up' this excess cholesterol and transfers it back to the liver. This scavanged cholesterol is then used in the manufacture of Very Low Density Lipoproteins VLDLs. VLDLs contain two basic ingredients, fats (in the form of triglyderides) and cholesterol.

VLDLs are then sent back out into the bloodstream. As VLDLs lose triglycerides they shrink in size, becoming Low Density Lipoproteins LDLs (otherwise known as `bad' cholesterol – for some stupid reason). LDLs are then absorbed by cells that need cholesterol, and the cholesterol is unpacked and used to build various structures within the cell, including the cell wall.

Which means that HDLs are part of a re-cycling mechanism for cholesterol. At the risk of repeating myself, the liver manufactures cholesterol and sends it out within VLDLs. As VLDLs lose triglyceride – which provides energy for cells around the body - they shrink into LDLs, and LDLs are then absorbed into cells where the cholesterol is unpacked.

When a cell then dies, it releases cholesterol, which is mopped up by HDL and transferred back to the liver. This is not immensely complex, but for some reason, mainstream researchers have decided that HDL can, in some way, protect against the build up of atherosclerosis.

There are two reasons for this, I think. Firstly, because a low HDL level seems to be an important risk factor for CHD, even more so than a raised LDL level (So surely it must be doing something…Duh!) Secondly, because it has been noted that, as HDL does indeed transfer cholesterol from around cells and back to the liver, it is thought that this reverse cholesterol transport might, in some way, be able to suck cholesterol out of atherosclerotic plaques.

In answer to the first piece of stupidity. If VLDL levels go up HDL automatically goes down, it's all to do with the transfer of apolipoproteins from HDL to VLDL. The raised VLDL itself is caused by underlying insulin resistance – one of the basic causes of heart disease. So a low HDL is merely a `marker' for raised VLDL, which itself is a marker for insulin resistance. A low HDL by itself causes nothing and prevents nothing.

With regard to the reverse cholesterol transport nonsense. HDL cannot, I repeat cannot, remove cholesterol from atherosclerotic plaques. It is impossible for this to happen. The cholesterol in a plaque is not `floating free' in the extra cellular fluid. It is trapped in a solid atherosclerotic lump. HDL is completely and utterly incapable of getting at it, and even if it could, it could not separate it out from the surrounding plaque structure. HDL is a passive inanimate chemical. It cannot carry out complex tasks.

The concept that HDL could remove cholesterol from a plaque is such a stupid idea that I cannot believe it still exists. Once you understand the science, the whole thing is patently ridiculous.

If synthetic HDL can reduce the size of plaques then I will eat my hat. What these researchers are seeing, probably, is what all researchers see. Most plaques, if left alone, do gradually reduce in size – a bit. Alternatively, they have been looking at their findings with eyes of faith. Let's just see if anyone else can verify these results.

P.S. In the Heart Protection Study (HPS), a major study in which the rate of deaths was reduced in patients taking a statin (simvastatin), at post-mortem, the people who had been taking the statin had bigger and more complex plaques than those who had not. In reality, the size of the plaque does not actually have anything to do with how dangerous it is.

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