The Rise and Fall of Modern Medicine (47 page)

The strategy worked brilliantly. The fear of premature death from a coronary was quite sufficient to propel the health-conscious to their doctor's surgery to have their cholesterol level measured; a quarter of whom would subsequently be started on drug therapy. Financially, everyone benefited: the drug companies; those involved in testing for cholesterol; and, in private health-care systems such as that of the United States, the doctors who charged their patients for check-ups on their cholesterol level. The total cost of this drug-company-inspired cholesterol obsession was phenomenal. By the mid-1990s hundreds of thousands of otherwise healthy men and women across the world were taking cholesterol-lowering drugs at a cost in excess of £3 billion a year.
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Together the drug companies and Social Theorists had
triumphed. Snatching victory from the jaws of defeat of the verdict of the trials, dozens of expert committee reports had persuaded most people that ‘Western food is the chief reason for our modern epidemic of heart disease'. This in turn had been the Trojan Horse by which millions had been prescribed cholesterol-lowering drugs. It is interesting to note how the ‘dietary and lifestyle' explanation for heart disease had produced precisely the opposite effects to those anticipated. Its appeal lay in the promise of liberating people from their reliance on doctors, for by simply changing their diet they could reduce the risk of heart disease and thus the need for drugs and surgery. As it turned out the ‘lifestyle' theory massively increased the influence of medicine, as medical experts now dictated what people should and should not eat. Further, it provided a context within which doctors could persuade otherwise healthy people that they needed to take drugs for life. And at the end of it all, Keys's thesis was no ‘truer' than it had been back in 1957, when the first of the American Heart Association committees had observed how it failed to account for the marked increase in heart disease.

The two final events that would undermine the seamless litany of half-truths that sustained Keys's thesis were, first, the ‘rediscovery' that the clot or thrombus in the coronary arteries, not the levels of cholesterol in the blood, is the critical factor in causing a heart attack and, second, the circumstantial evidence for an infective cause for the rise and fall of heart disease over the past sixty years.

The perception of the critical role of the thrombus, it will be recalled, was displaced in the mid-1960s when it emerged that blood-thinning drugs, though effective, had the regrettable consequence of increasing the risk of haemorrhage into the brain. This failure, however, did not mean that the thrombus was
unimportant, just that better ways had to be found to prevent or dissolve it. Ideally, two types of drug are required, a simple compound that will prevent the platelets from sticking together to form a thrombus in the first place, but also a more potent ‘clot-busting' drug that could be administered in the aftermath of a heart attack.

Both types of drug had in fact already been around for a long time, in the case of the former – aspirin – for two hundred years. It is natural to presume that, given aspirin's many therapeutic properties, there must be some common underlying physiological process with which it interferes – and so there is. In 1971 the British biochemist John Vane demonstrated that aspirin blocked the action of a family of closely related chemicals – the prostaglandins – produced fleetingly in minute quantities by many different tissues in response to injury, one of which, thromboxane, encourages platelets to stick together to plug a bleeding artery or vein.
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So here was a very cheap drug that in small doses discouraged platelets from forming a clot thus preventing the two serious circulatory disorders of heart disease and stroke.
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For this most significant discovery John Vane would subsequently be awarded the Nobel Prize.

Aspirin might prevent some, if not all, heart attacks but a complementary approach was needed that would dissolve the clot in the arteries after it has formed, thus restoring the blood flow to the heart muscle. In 1980 Dr Marcus de Wood of the University of Washington demonstrated that the drug streptokinase (originally derived from the streptococcus bacterium fifty years earlier) dissolved the acute blockage of one or other coronary arteries in 110 out of 126 patients.
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When combined together, aspirin and streptokinase, it emerged, have a truly astonishing effect, reducing by over half the numbers succumbing within the first four weeks following a heart attack.
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The much neglected thrombus, marginalised by the baleful influence of the cholesterol obsession, may have turned out to be very important after all, but it still leaves unexplained the epidemic pattern of the rise and fall of heart disease which, as pointed out, is strongly suggestive of an underlying biological cause such as infection.

It is significant here that the narrowing of the arteries by atherosclerosis, when examined under the microscope, is strongly suggestive of an inflammatory process. The specific agent involved would, however, remain elusive until 1992, when Dr Chochuo Kuo of the University of Washington, using a special staining technique, identified the bacterium chlamydia in the walls of the arteries of South African miners who had recently succumbed from a heart attack.
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This prompted a series of studies looking for evidence of chronic infection that would implicate, variously, the ‘atypical' bacterium mycoplasma and several viruses including herpes and cytomegalovirus. Hence it would appear several interacting infectious agents might be involved: it is, observed Dr Stephen Epstein in the journal
Circulation Research
, ‘the aggregate number of pathogens with which an individual is infected that will determine the propensity to develop atherosclerosis and the . . . acute thrombotic arterial occlusion'.
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The scale of the great cholesterol deception as outlined above might seem so extraordinary as to raise doubts about its veracity. But it was the inevitable consequence of the official endorsement of a false theory which, beyond a certain point, admits of no going back without destroying the professional reputations of its protagonists. Further, the chronology of these events cannot be emphasised too strongly. The experimental evidence refuting the diet-heart thesis emerged at precisely the
moment in the early 1980s when the claims of The Social Theory to provide a new paradigm for medicine were in the ascendant. Its proponents therefore had no alternative other than to assert its validity by the means outlined above.

Before examining the other aspects of The Social Theory, readers should now try to imagine themselves back in those times when the link between food and heart disease (and much else besides) was almost universally accepted as being correct, when distinguished professors were regularly appearing on television to assert that ‘the modern British diet is killing thousands from heart attacks'. They must try to imagine how the apparent plausibility of Keys's thesis gave credence to the notion that the causes of all common diseases lay simply in the manner that people lived their lives, where the Western diet was held responsible for virtually all cancers other than those caused by smoking and where the presence of minute concentrations of chemicals in the air and water apparently caused a bewildering variety of illnesses. It is gratifyingly unnecessary to examine each of these other aspects of The Social Theory in the same detail. It is quite sufficient merely to focus on the same cross as that on which Keys's thesis was crucified – the cross of biology. It is a biological fact that it is very difficult to influence the
milieu intérieur
of physiological functions such as cholesterol or blood pressure by simple changes in the
extérieur
, such as small changes in what one eats. It simply cannot be done, and no matter how beautiful and plausible the statistics about heart disease mortality rates in Finland compared to Japan, statistics cannot change the laws of biology. And so now we turn to see how the statistics sustaining the two further instances of The Social Theory are similarly crucified by biology. We start with the ‘causes' of cancer.

Cancer is a grievous illness that causes much misery not just to those who are afflicted but to their friends and relatives as well. It goes without saying that it would be very desirable to be able to identify its causes and thus prevent it but, with a handful of admittedly important exceptions (tobacco and lung cancer, asbestos exposure and mesothelioma), this goal has proved elusive mainly because for most there is no single cause. Rather, cancer is so strongly related to age – the risk increasing by a factor of ten with each passing decade – that it is best seen as intrinsic to the ageing process itself. There are several reasons why this might be so. The replication and repair mechanisms of DNA become impaired with age, increasing the risk that individual cells might turn malignant. Similarly, the immune system loses the ability to identify and destroy potentially cancerous cells, allowing them to ‘escape' and multiply. Whatever the precise mechanism, the relationship between cancer and ageing is so powerful that it is fair to infer that it could only ever be prevented were ageing itself to be preventable – which would seem unlikely.

Confronted by this admittedly harsh reality, the notion that cancer might simply be caused by the sorts of food we eat is strongly suggestive of quackery. Yet from 1980 onwards, for almost two decades, persistently and without equivocation, the Social Theorists have insisted that, excepting those cancers attributable to tobacco, virtually all the rest are caused by the Western diet. Why so?

By 1980 cancer had become vulnerable to the arguments of those, like McKeown, who maintained that social factors were the main cause of disease and hence prevention, by ‘changing lifestyles', was a much better option than being treated, often unsuccessfully, with nasty anti-cancer drugs. Ten years earlier, in 1971, Dr Donald Pinkel of St Jude's Hospital had astonished the world with his news that a gruelling regime of four anti-cancer drugs given for two years combined with radiotherapy to the brain had increased the cure rate of childhood leukaemia from 0.07 per cent to over 50 per cent. But leukaemia and the other treatable cancers of childhood and young adult life represent only a small fraction of the total number of cases and so, fuelled by Richard Nixon's billion-dollar War Against Cancer, specialists took up the challenge of applying the same principles of treatment to the vastly greater numbers of age-related cancers – of the breast, bowel, brain and so on – that occur overwhelmingly in those aged sixty and over.

This approach, as we now know, did not work. With a few exceptions these ‘old-age' cancers failed to respond or became rapidly resistant to the anti-cancer drugs, whose main consequence was to make the last few months of patients' lives even more burdensome with their grievous side-effects. Thus by the end of the 1970s, despite the hundreds of millions of dollars a year being spent on cancer chemotherapy in the United States, the number of children and adults being cured – 5,000 a year – was dwarfed by the 700,000 a year with age-related cancers who were not.
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The futility of such massive and injurious overtreatment is obvious, and provided the right climate for those who argued there ‘must be a better way': ‘80–90 per cent of all cancers in Western nations are caused by environmental factors', observed John Bailar III in the
Journal of the National Cancer Institute
, and
insisted it was time to switch attention to finding out what these might be.
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The same argument would be restated many times over the next few years: the war on cancer had failed, vast funds were being wasted and patients' lives were being made miserable by chemotherapy, to no good purpose. How much better it would be to prevent these cancers in the first place! It sounded plausible enough, but there was only one problem. Besides tobacco, no one knew what these causes of cancer might be – until, in 1980, Sir Richard Doll, Emeritus Professor of Medicine at Oxford University, and now one of the world's most eminent cancer epidemiologists, found the answer. After an exhaustive review of all the relevant evidence, he concluded that, besides the role of tobacco in lung cancer, the Western ‘high-fat' diet was the major cause of cancer which might be avoided were people to switch to a ‘healthier diet'.

It was all very astonishing. For years doctors and scientists had struggled to understand the causes of these diseases and it seemed that all along the explanation was staring them in the face every time they sat down to a meal. Indeed it was only curious how long it had taken Sir Richard himself to make his sensational discovery. Fourteen years earlier, in 1967, he had drawn attention in a prestigious lecture to the well-recognised causes of cancer such as tobacco and high-level exposure to certain chemicals in the workplace, but failed to mention the role of food at all.
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Subsequently, it seemed, he had become persuaded by the evidence from international comparisons, which showed that common cancers in the West like that of the breast and colon were rare in Japan and – vice versa – stomach cancer was common in Japan but relatively rare in the West. It is of course precisely this type of evidence with which Ancel Keys had incriminated the Western diet in heart disease, so it shares its weaknesses. Even if it were true that the pattern of
food consumption was the cause, then presumably switching to a Japanese diet would merely mean switching the risk of dying from the types of cancer common in the West to those common in Japan.
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