Читать книгу Panic Nation - Stanley Feldman - Страница 30

The cholesterol hypothesis has always exuded the siren song of simplicity. However, once you start to examine it in any detail, the simplicity rapidly mutates into complexity.

Even at the very start people, should have known that cholesterol in the diet was never capable of appearing, unchanged, in the bloodstream. Cholesterol is not soluble in water (thus blood), which means that, after absorption, cells lining the gut pack cholesterol into a small protein/lipid sphere, known as a lipoprotein, before releasing it into the bloodstream.

Thus, you do not have any cholesterol floating about in the blood: it is all contained within lipoproteins. You do not actually have a cholesterol level. Instead, you have a level of different lipoproteins, with the low-density lipoprotein (LDL), or ‘bad’ cholesterol, being the so-called dangerous one.

Next question: what raises the LDL level? Eating too much fat, or cholesterol? The first problem here is that the cells lining the gut do not make, or release, LDL – they make other forms of lipoprotein. So, no matter what you eat, it can have no direct effect on LDL levels.

So where does LDL come from? LDL is, effectively, the shrunken form of a very low-density lipoprotein (VLDL). VLDLs are made in the liver and used to transport fat, and cholesterol, from the liver to other cells around the body. As VLDLs lose fat they shrink, transforming into LDL.

Therefore, in order to find out what makes LDL levels rise, we must surely find out, first, what makes VLDL levels go up; and what makes VLDL levels go up, primarily, is eating excess carbohydrates. What makes them go down is eating fat!

Recognising this, and a host of other problems, the supporters of the cholesterol hypothesis have twisted and turned. As of today (and this will certainly change), the original – dietary – cholesterol hypothesis has become the following: if you eat too much saturated fat, the body will reduce the number of LDL receptors (things that remove LDL from the bloodstream), forcing the LDL up. A more tenuous, and unproven, link could hardly be imagined, but that is what is left of the originally super-simple cholesterol hypothesis. The diet part, anyway.

But the difficulties of trying to establish a dietary link to heart disease actually pale into insignificance when you start trying to work out how the raised LDL itself level may cause heart disease.

If it were simply a case of excess LDL seeping through the artery wall when the level gets too high, then why doesn’t this happen in all artery walls, everywhere? If I lie too long in the sun I expect to get sunburned on every bit of skin exposed. I do not expect to get discrete patches of sunburn. Yet we do see little ‘patches’ of atherosclerosis. Some people die of heart disease and are found to have perfectly clean arteries, apart from a single killer plaque. So why did the LDL seep through at only one place? What protected the rest of the arterial system?

And why do veins never develop atherosclerotic plaques. They are exposed to exactly the same LDL level as the arteries. They are thinner than arteries, but their general structure is identical. (I should add that if you use a vein as a coronary artery bypass graft (effectively turning it into an artery), it will develop atherosclerosis.)

These questions represent only the tip of a huge iceberg. In an attempt to answer some of them, the cholesterol hypothesis has turned itself into the following, complicated mess. LDL, when it is oxidised, travels through the lining of the artery wall (endothelium) into the middle part of the artery. (How oxidised LDL passes straight through an endothelial cell into the artery wall behind is unexplained.)

In this oxidised state it attracts white blood cells from the bloodstream They, in turn, migrate into the artery wall and start to ‘digest’ the oxidised LDL in order to remove it (This bit is plausible.) However, white blood cells, once they have started to digest oxidised LDL, cannot stop. They get bigger and bigger until they burst. This, in turn, attracts more white blood cells to the area, which then burst. (White blood cells that just burst? This makes absolutely no sense whatsoever. Why on earth would the body develop a scavenger system that automatically self-destructs?)

The burst white blood cells, in turn, release substances that trigger a whole cascade of inflammatory reactions in the arterial wall. After a period of time you have a mass of dead white blood cells, cholesterol, oxidised LDL remnants, and a whole series of other inflammatory agents all focused in one area, trapped in the artery wall. (Well, this is what is found in a plaque, among many other things.)

Anyway, that is allegedly how a plaque starts and grows. I have kept that explanation as simple as humanly possible, but it seems absurdly unlikely. Oxidised LDL – what happened to normal LDL? Well, there’s no way anyone can see of getting that through an arterial wall. Exploding white blood cells – another buttress?

In truth, the current ideas on plaque formation used to keep the cholesterol hypothesis afloat are complex nonsense,. But the entire area is now protected by a ring-fence of scientific jargon that frightens off all but the most dedicated seeker after truth.

To those who have studied the hypothesis with a critical eye, it seems unbelievable that it can possibly still be standing. Dr George Mann pronounced it dead in an editorial in the New England Journal of Medicine in 1977, referring to it as the ‘greatest scam in the history of medicine’. Yet this hypothesis has never had more followers than today. It is time, I think, that it was consigned to the dustbin of history. It is neither simple nor direct – nor understandable. The only certain thing about it is that it is wrong.