Читать книгу A Statin Nation - Dr Malcolm Kendrick - Страница 8
ОглавлениеAtherosclerosis has been described in many ways but, at its simplest, is discrete or patchy thickenings within arterial walls, usually called atherosclerotic plaques. At its most complex, you can read papers discussing seven different types of atherosclerotic plaque, with several subsections in-between. (I remember reading ‘A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis’ – a report from the committee on vascular lesions of the Council on Arteriosclerosis, the American Heart Association – and ending up none the wiser.)
However you choose to define them, plaques start as small areas, usually described as ‘fatty streaks’. Over decades, these streaks grow into bigger and more complex lesions, a lesion being an abnormal/unhealthy thing in the body. At a certain point, they become so big and ugly that they’re termed atherosclerotic plaques. I am not sure when a fatty streak becomes a plaque; it’s a bit like asking when a boat becomes a ship. Nobody knows.
Plaques, in turn, come in many different versions. Some end up hard and calcified (full of calcium). Others have a gooey, fatty centre, known as a lipid core. If the gooey core is covered by a thin, fibrous cap it will usually be called a vulnerable plaque because, if the cap ruptures, the lipid core will be exposed to the bloodstream and triggers an instant, very large blood clot within the artery. More on this later.
DIAGRAM 3
In general, it is thought that calcified plaques represent the end stage of atherosclerosis plaque development and, slightly counter-intuitively, such plaques are probably stronger, better organised and less likely to rupture than earlier stage plaques. It is the transitional phase, the vulnerable plaque with a lipid core, that is the most dangerous and likely to rupture, leading to disaster.
Over the last few years, a test for measuring calcium in the coronary arteries – the coronary artery calcification (CAC) score – has become popular. The higher score, the more calcium in the artery, thus the more atherosclerotic ‘disease’ you have and the greater your risk of a heart attack. This assumes that if you have a lot of calcified plaques you will have a lot of other vulnerable, unseen plaques as well.
Unfortunately, you cannot do a great about the calcified plaques. Once they have formed, they have formed, with some caveats. In essence, what you are measuring with a CAC score is your atherosclerotic history – not necessarily your atherosclerotic future. However, if you have no calcium at all in your arteries, you probably have no earlier-stage atherosclerotic disease either, so whatever you were doing, keep doing it.
Four other facts about calcium in your arteries that I find fascinating:
Statins accelerate calcium build-up in arteries and on heart valves1
You can see considerable calcium deposits in the arteries of mummies from Egypt and other parts of the world
Warfarin (commonly used in treating atrial fibrillation, or AF – an abnormal heart rhythm) accelerates calcium build-up in arteries, due to its action as a vitamin K antagonist2
There is some reasonably strong evidence that vitamin K supplementation may slow, or possibly even reverse, calcium build-up in arteries
At the risk of going too far off-piste here, in vitamin K supplementation, as with many things to do with vitamins, the mainstream researchers have determinedly tested the wrong form. There are three forms of the vitamin (and probably more, but let’s go with three for now): K1, 2 and 3. K1 is often called phylloquinone, which is the one most tested while K3, often called menaquinone, has never been properly tested as a way of preventing or reversing calcification. ‘Overall, the available observational population-based evidence, based on dietary intake measures, suggests menaquinone [K3] intake may be more likely to protect against vascular calcification than phylloquinone intake. Yet currently, the only intervention studies have examined the effect of phylloquinone…’3
So, observational studies show that K3 is almost certainly the only K vitamin that provides protection but, with wearisome inevitability, it has not been studied in any clinical trial. Only K1 has been used. And this, I am afraid, is typical of mainstream medicine’s approach to vitamins. Start by failing to clearly define the ‘normal’ range of a vitamin – see especially vitamins D and B12, then give a very low dose of the wrong form of the vitamin and then claim that vitamins have no benefits whatsoever – on anything. Do I detect the dead hand of the pharmaceutical industry here?
Once you have done this you can move on to claim that vitamins are dangerous and damaging to health and then, to the sound of distant cheers from all pharmaceutical companies everywhere, ban them. Why? ‘Everyone need drugs. Everyone.’
Here is a clue about vitamins. ‘Vit’ is short for vital, as in vital for health. As in, if you don’t get a sufficient amount in your diet, you will die. As in … well, you get the idea. (Processed foods are often stuffed with synthetic vitamins, the natural ones having been destroyed in the manufacturing process. Oh well.) But more on vitamins later. Let’s get back to the main subject: atherosclerosis.
Atherosclerotic plaques are the underlying cause of heart attacks and strokes. They start life as fatty streaks in the middle sections, or media, of the artery walls and grow into plaques. This process starts early. When I say early, I mean early, as it is possible to see thickenings or fatty streaks in the arteries of foetuses within the womb.
The most dangerous phase of plaque development would seem to be the vulnerable plaque which, if it ruptures, can cause a complete blockage in an artery. This can happen in arteries throughout the body but most commonly affects the coronary arteries, which supply blood to the heart, or the carotid arteries, which supply blood to the brain.
