Читать книгу Panic Nation - Stanley Feldman - Страница 26

1850s: Rudolf Virchow notes the presence of cholesterol in atherosclerotic plaques. Suggests excess cholesterol in the bloodstream may be the cause.

Early 1900s: Ashoff feeds rabbits fat and cholesterol, notes the development of atheroma.

1912: First heart attack described by Herrick.

1940s: Epidemic of heart disease hits USA, interest in the area explodes. Many researchers blame high fat/cholesterol diet.

1948: The Framingham, study on heart disease starts. Still running today.

1954: Ancel Key’s seminal Seven Countries Study published. Demonstrates clear links between saturated-fat intake and heart disease.

1961: Framingham confirms link between raised cholesterol levels and heart disease.

1960s: First cholesterol-lowering drugs developed.

1970s: Brown and Goldstein find gene leading to extremely high cholesterol levels (familial hypercholesterolaemia) and premature heart disease.

1980s: Statins launched.

1985: Nobel Prize for Brown and Goldstein.

1990s: Statins trials demonstrate that cholesterol lowering protects against heart disease.

Presented in this way, it’s not difficult to see how the cholesterol hypothesis became the dominant hypothesis, effortlessly swatting alternative ideas into touch. Indeed, to question this theory is to risk being placed on the same shelf as flat-earthers and creationists.

However, all is not what it seems. The cholesterol hypothesis can be likened to a cathedral built on a bog. Rather than admit they made a horrible mistake and let it sink, the builders decided to try to keep the cathedral afloat at all costs. Each time a crack appeared, a new buttress was built. Then further buttresses were built to support the original buttresses.

In a similar way, although direct contradictions to the cholesterol hypothesis repeatedly appear, no one dares say, ‘OK, this isn’t working, time to build again from scratch.’ That decision has become just too painful, especially now that massive industries, Nobel prizes and glittering scientific careers have grown on the back of the cholesterol hypothesis. The statin market alone is worth more than £20 billion each year.

In reality, cracks in the hypothesis appeared right from the very start. The first of these was the stark observation that cholesterol in the diet has no effect on cholesterol levels in the bloodstream:

There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.

ANCEL KEYS, PHD, PROFESSOR EMERITUS AT THE UNIVERSITY OF MINNESOTA, 1997

A bit of a blow to a cholesterol hypothesis, you might think, to find that dietary cholesterol has no effect on blood cholesterol levels. However, as everyone was, by then, fully convinced that something rich and ‘fatty’ in the diet was the primary cause of heart disease, no one was willing to let go.

So the hypothesis quietly altered from cholesterol in the diet to saturated fat in the diet – or a bit of both – as if, in some way, cholesterol and saturated fat were similar if not almost exactly the same thing.

In reality, this could hardly be further from the truth. Saturated fat and cholesterol have completely different functions in the body, and they have very different chemical structures.

A saturated-fat molecule (top left) and a cholesterol molecule (right).

As James Black warned over two hundred years ago:

A nice adaptation of conditions will make almost any hypothesis agree with the phenomena. This will please the imagination, but does not advance our knowledge.

JAMES BLACK, LECTURES ON THE ELEMENTS OF CHEMISTRY, 1803

Unfortunately, this adaptation did not work. It’s true that Ancel Keys appeared to have proved the link between saturated-fat consumption and heart disease, but, when it came to the major interventional trials, confirmation proved elusive.

The MR-FIT trial in the USA was the most determined effort to prove the case. This was a massive study in which more than 350,000 men at high risk of heart disease were recruited. In one set of participants they cut cholesterol consumption by 42 per cent, saturated-fat consumption by 28 per cent and total calories by 21 per cent. This should have made a noticeable dent in heart-disease rates.

But nothing happened. The originators of the MR-FIT trials refer to the results as ‘disappointing’ and say in their conclusions, ‘The overall results do not show a beneficial effect on coronary heart disease or total mortality from this multifactor intervention.’

In fact, no clinical trial on reducing saturated fat intake has ever shown a reduction in heart disease. Some have shown the exact opposite:

As multiple intervention against risk factors for coronary heart disease in middle aged men at only moderate risk seem to have failed to reduce both morbidity and mortality such interventions become increasingly difficult to justify. This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration. Not to do so may be ethically unacceptable.

PROFESSOR MICHAEL OLIVER, BRITISH MEDICAL JOURNAL, 1991

This passage followed a disturbing trial on Finnish businessmen. In a ten-year follow-up to the original five-year trial, it was found that those men who continued to follow a low-saturated-fat diet were twice as likely to die of heart disease as those who didn’t.

It’s not as if this were one negative to set against a whole series of positive trials. In 1998, Uffe Ravnskov looked at a broader selection of trials. ‘The crucial test is the controlled, randomised trial,’ he said. ‘Eight such trials using diet as the only treatment have been performed but neither the number of fatal or non-fatal heart attacks was reduced.’

As Ravnskov makes clear, no trial has ever demonstrated benefits from reducing dietary saturated fat. At this point most people might think it was time to pull the plug.

Far from it. In 1988, the Surgeon General’s office in the USA decided to silence the naysayers by putting together the definitive report proving a causal link. Eleven years later the project was abandoned. In a letter circulated, it was stated that the office ‘did not anticipate fully the magnitude of the additional external expertise and staff resources that would be needed’.

Bill Harlan, a member of the oversight committee and associate director of the Office of Disease Prevention at National Institute of Health, says ‘the report was initiated with a preconceived opinion of the conclusions, but the science behind those opinions was not holding up. Clearly the thoughts of yesterday were not going to serve us very well.’

The sound of a sinking cathedral fills the air with a great sucking, slurripy noise. But still no one let go. Instead, more buttresses were desperately thrown at a rapidly disappearing pile of rocks.

Variations on a theme emerged. It is not saturated fat, per se, that causes heart disease. It’s the ratio of polyunsaturated to saturated fat that is critical. Or is it the consumption of monounsaturated fats, or a lack of omega-3 fatty acids, or an excess of omega-6? Take your pick. These and a host of other add-on hypotheses have their proponents.

As of today no one can – or will – tell you which type of fat, in what proportions, added to what type of antioxidant, vegetable, monounsaturated fat or omega-3 is the true culprit. Hugely complicated explanations are formulated, but they all fall apart under scrutiny.

This may all seem incredible, such has been the level of anti-fat propaganda, but it is true. With the exception of Ancel Keys’s flawed Seven Countries Study (he preselected the seven countries for his study in order to prove his hypothesis!), there is not one scrap of direct evidence.

But, of course, there are two parts to the cholesterol hypothesis: diet and raised cholesterol level. Leaving diet behind, surely it has been proved beyond doubt that a raised cholesterol level is the most important cause of heart disease.