This is from a member of THINCS, The International Network of Cholesterol Skeptics. Extract from book in preparation by Malcolm Kendrick: [email protected] WHY HAS HEART DIESEASE RESEARCH ALL GOT SO COMPLICATED? by Malcolm Kendrick When you have decided that a theory is correct e.g. the world is at the centre of the Universe, and this is essentially an emotional belief, rather than a rational belief, then observations that conflict with the theory have to be refuted, or immunized against. Refutations take one of three forms: *Ignoring the refutation *Denying that the refutation is a refutation *Developing ad hoc hypothesis to support the central hypothesis Ignoring the refutation has a long and inglorious history. The most famous example of this would be the Catholic Church's refusal to look through Galileo's telescope. They knew that could not refute the evidence of their own eyes, so they refused to look. Pretty damned straightforward if tricky to sustain – oh well, there's always the Spanish Inquisition to keep the facts at bay. Ignoring the refutation requires a certain robust, devil may care attitude, but the second type of refutation, denying the refutation, requires even more brass neck. To quote Karl Popper, a much misquoted scientific philosopher: A biologist offers the conjecture that all swans are white. When black swans are discovered in Australia, he says that it is not refuted. He insists that black swans are a new kind of bird since it is part of the defining property of a swan that it is white. In the area of CHD, many examples of this have flourished. ‘A high fat diet causes heart disease.' ‘What about Asian Indians? In America 50% are vegetarians, yet their rate of CHD is three times that of the surrounding Caucasian population.' Ah, you may think it is a low fat diet but they use Ghee for cooking, and that is very atherogenic, so they do have high fat diet (even if it isn't high in fat, and doesn't cause CHD in India).' ‘What about the Massai villagers in Kenya, they eat a very high cholesterol diet, and they don't get any CHD.' ‘Ah, yes, but in their traditional environment they eat an unusual blood and milk diet, which is not really a proper high saturated fat diet, even though it is high in cholesterol and saturated fat, sort of, kind of, ahem, look at the time, must dash.' As we all know, gentle reader, if the diet is high in fat, and doesn't cause CHD, then it cannot really be a high fat diet, because it is a part of the defining property of a high fat diet that it causes a high rate of CHD. One could, of course, just stick one's fingers in one's ears and sing ‘la, la, la, la, la. I'm not listening.' It would be and equally valid scientific method, and have much the same effect. To quote Karl Popper on circularity of logic: Consider the following dialogue: ‘Why is the sea so rough today?' – ‘Because Neptune is very angry' – ‘by what evidence can you support your statement that Neptune is very angry?' – ‘Oh, don't you see how very rough the sea is? And is it not always rough when Neptune is angry?' Anyway, moving on. These first two types of refutation, although pretty effective, and widely used in CHD research, can't keep the evidence at bay forever. There are still those who will question, and push, and do awkward things like present the correct unbiased evidence. When this happens, the ‘defenders,' taking a lesson from the humble squid, release a cloud of black ink that makes it virtually impossible to see anything. Black ink squirting is known as developing ad hoc hypotheses. This works as follows – using three simple examples: Why don't women, with the same risk factors and the same cholesterol level as men (actually it's higher), suffer the same rate of CHD? (keep this one in mind) Why don't the French get heart disease, when they have the same risk factors and saturated fat consumption as the British? Ad hoc hypothesis: because they eat garlic and drink red wine, and lightly cook their vegetables (I kid you not) Why do the Eskimos have such a low rate of CHD when they stuff themselves with saturated fat and blubber? (There's a joke in there somewhere). Ad-hoc hypothesis: because they eat a lot of fish. (Yes it was Eskimos who first created the ‘fish consumption protects against CHD hypothesis') This type of ad-hoc hypothesis development can go on virtually forever, and in the field of CHD it has done. In 1981, a paper was published outlining 246 factors involved in CHD ref some of them caused CHD, others were protective, some of the factors were simultaneously causative and protective. As far as I am aware, this exercise has not been carried out since 1981, but I am certain that a list of over 1,000 factors could now be drawn up – easily. Almost every week a new study proves that, for example, coffee is either good for you, or bad for you. Or is it magnesium, or potassium or folic acid, or vitamin E, or vitamin C, or over-expression of the LOX-1 oxidised LDL receptor. All of this has come about because evidence keeps appearing that contradicts the diet-heart hypothesis, and each bit of evidence has to be wrapped up in an ad-hoc hypothesis to stop it from doing too much damage. In 1978 Hugh Tunstall-Pedoe first noted the French had identical risk factors to the British, yet they suffered about a quarter the rate of CHD. He called this the ‘French Paradox.' I called it the complete demolition of the diet-heart hypothesis. But, despite this finding, the ad-hoc hypothesisers were rapidly in action, papering over the cracks, adding a couple more flying buttresses to the collapsing cathedral. As everyone involved knew that the diet-heart hypothesis was correct, what, they asked themselves, do the French do differently to the British that is providing this protection. What indeed? Well, let us think (dum de dum)…. The French drink a lot of wine…true. They eat lots of garlic….true. They lightly cook their vegetables… compared to the average twenty-four hour super-heated brussel sprout obliteration in the UK, this too is true. As we all know, a lightly cooked vegetable retains is anti-oxidants, and anti-oxidants stop LDL from becoming oxidised and becoming absorbed into the arterial wall. Read Braunwald if it doesn't make your brain hurt too much. It will come as no surprise to find that shortly after the ‘French Paradox' was first expounded, the idea that red wine, garlic and lightly cooked vegetables were protective against CHD suddenly appeared, and even today these are quoted are protective factors - despite a complete lack of supporting evidence – see later Chapters. This constant creation of ad-hoc hypotheses has resulted in a thing called the multifactorial hypothesis. CHD isn't just caused by one thing, it is multifactorial. You can't just look at saturated fat in the diet, or blood cholesterol levels, or smoking, or blood pressure or obesity, or (name another five hundred or so factors). You must consider the risk profile. There are now so many risk factors that it would be impossible to find two communities, anywhere in the world with the same risk factors, so any difference in CHD rates can be explained away in a black cloud of ink. In fact, it would be impossible to find any two people anywhere in the world with identical risk factors, finding one would be like finding an identical DNA sequence, a one in five billion chance – or whatever it is. Over time ad-hoc hypothesisers have created so many add-on factors that the diet-heart hypothesis may well be perfectly protected against any attack. It has become the hydra, chop off one head and it just grows another ten. Oh look, I just found that ear lobe creases are associated with CHD. (Yes, it's true; thank God I don't have ear lobe creases). Jolly good, fling in another risk factor; it should help to make things even more complicated and difficult to understand. What about hair on the palm of your hands – don't look. To quote Sir James MacKenzie, a prominent UK physician on the issue. In a famous speech, he said. ‘I am convinced that the conception of specialisation is a wrong one. Instead of enlightening it tends to darken understanding in a cloud of detail. Specialists have become absorbed in the study of the infinitely varied manifestations of disease, rather than concentrating on the relatively simple forces at work to create disease. What is now called progress is but the recognition of an additional number of these manifestations of diseases, and an ever increasing difficulty in comprehending their significance.' Hear, hear. That, by the way was written in 1919. Forty years ago, we had a nice simple diet-heart hypothesis. Now we have by far the most complicated, multifactorial mess that exists anywhere in medical science. This has all come about because the diet-heart hypothesis was wrong, and still is wrong, and the only way to defend it is to throw so much rubbish into the air that enemy missiles cannot find their target. Perhaps the time has come to dismantle the diet-heart hypothesis brick by brick. Hopkins PN, Williams RR. AA survey of 246 suggested coronary risk factors. Atherosclerosis 1981 Aug-Sep;40(1)1-52)
On Thu, 12 Feb 2004 2:41:12 -0500, Zee wrote (in message <[email protected]>): > This is from a member of THINCS, The International Network of Cholesterol Skeptics. Extract from > book in preparation by Malcolm Kendrick: [email protected] > > > > > WHY HAS HEART DIESEASE RESEARCH ALL GOT SO COMPLICATED? by Malcolm Kendrick <snip> Very interesting. Thanks for posting. -- Steve Weeding the Lord's Vineyards Since 2003
