Although it became clear that a change in diet had little effect on CHD, that did not end the scientists’ efforts to demonstrate that CHD could be prevented. If diet couldn’t do it, then intervention with drugs would provide the evidence. And since drugs could be controlled much more strictly, and used in conjunction with placebos, the findings would be more demonstrable. But the drugs used to reduce blood cholesterol have all proved to be something of a disaster.

Launched on the public in 1961, Triparanol causes the levels of blood cholesterol to fall by inhibiting the liver’s ability to make cholesterol. Two years later it was with- drawn because of serious side effects. Luckily for triparanol’s manufacturers, a public scandal was avoided as the media’s attentions were focussed on another drug marketed at the same time and by the same company – thalidomide.

More recently, a number of other drugs have been the subject of extensive and expensive trials. First was Cholestyramine (Questran) which reduces cholesterol by interfering with digestion. The gall bladder manufactures bile acid from cholesterol, and the bile acid is used in the intestine to digest fats. But when the drug is present in the gut, it binds with the bile acid, removing it from its normal function. Because the drug is indigestible, it, together with the bile acid, is excreted and the gall bladder has to make more by drawing cholesterol from the bloodstream.

As the trial would be very expensive, the scientists examined 480,000 men over a period of three years to find suitable subjects. They had to be men in the coronary age group and with extremely high blood cholesterol levels. As such men are in the most vulnerable group, their chances of success were greatly increased.

The investigators confidently announced in advance that blood cholesterol levels would be lowered by an average of 28% and, after seven years, coronary heart disease would be reduced by 50% in the treatment group.

At the end of the trial, however, cholesterol levels had fallen by less than a quarter of that called for at the start and heart disease rates were hardly affected. The $142 million trial was a total flop. Even if it had proved a success, however, those participating were so unrepresentative of the population that the question of its efficacy for the typical adult would still have remained. Another flaw that became apparent was an increase in the incidence of oral-gastro-intestinal cancers which could not be dismissed as a random chance. In the Lipid Research Clinics trial there were 21 cases and 8 deaths from gastrointestinal cancer in those taking the drug, compared to 11 cases and just 1 death in the control group.

Other organizations tested other drugs. The World Health Organization sponsored its own trial with Clofibrate (Atromid). This too was targeted against cholesterol and was confidently expected to lower blood cholesterol levels by 30%.

As with cholestyramine, the levels were lowered by much less than the expected amount and at the end of the trial it became clear that there had been many more deaths in the group taking clofibrate than in the control group – notably from gallstones, and cancer of the liver and digestive system. In the WHO clofibrate trial, the drug killed more than it saved.

Among other drugs to be tested were:

a. The female hormone Oestrogen on the theory that if premenopausal women did not get heart disease, perhaps oestrogen would protect men. But the hormone caused heart attacks rather than preventing them.

b. The hormone Dextrothyroxine, which lowers cholesterol levels, abandoned quickly when an increase in mortality was noticed in the treatment group.

c. The vitamin Niacin, which looked promising, but although there appeared to be a reduction in non-fatal heart attacks, there were marked side effects: skin disorders such as darkening, itches and rashes, as well as digestive problems and gout.

d. Gemfibrozil (Lopid) was tested and again an increase in deaths was noticed in the treatment group although this time the numbers did not reach statistical significance.

e. Compactinf. Lastly, despite the previous experiences with triparanol and compactin, yet another inhibitor, Lovastatin, has been approved for lifetime use on the general public after tests of very short duration only. (Derivatives pravastatin and simvastatin are marketed as Lipostat and Zocor.)

A study of all trials into cholesterol lowering by drugs up to 1987 showed an increase in mortality in those treated with drugs of 13.6%.

In 1993 a meta-analysis of all randomized controlled trials of cholesterol-lowering treatments showed that only those with very high risk showed any evidence of benefit. In all others mortality was increased. Its authors conclude that:

“Currently evaluated cholesterol-lowering drugs seem to produce mortality benefits in only a small proportion of patients at very high risk of death from coronary heart disease . . . a cautious approach to the use of cholesterol lowering drugs should be advocated”.

Despite this, nearly eight times as many prescriptions for cholesterol-lowering drugs were being issued just 6 years later!

DR.GREENE’S COMMENTS: As a former pharmacist all I can do is warn you of the dangers of these medications. Let me share this with you: Every medication designed to lower cholesterol has had to be removed from the market because they were causing all kinds of problems… especially with the LIVER.

Just because every knothead physician in this country wants all you guys on these meds doesn’t make these medications any less lethal. BUYER BEWARE!