Last year, for example, researchers at the University of British Columbia concluded that statins may harm as many people as they help. Pooling the data from five separate large-scale trials, the UBC team found that statins indeed reduced heart attacks and strokes - but only by a meagre 1.4 per cent. This means that 71 people with high cholesterol would have to be treated with statins for up to five years to prevent just one heart attack or stroke.

Furthermore, setting this modest gain against a 1.8 per cent increase in the serious side-effects caused by the drugs effectively cancels the benefit, concluded the UBC team leader Dr James Wright, (Therapeutics Initiative, April-June 2003, University of British Columbia).

British researchers arrived at an even starker conclusion - that statins can kill. The University of Sheffield’s Department of Clinical Pharmacology looked at the risk-to-reward ratio of statins, comparing the mortality rates of people taking statins with their underlying risk of death. The figures suggest that statin use 'could be associated with an increase in mortality of 1 per cent in 10 years' (Br J Clin Pharmacol, 2001; 52: 439-46).

Heart failure A small band of doctors are now beginning to ask: could there be a connection between the huge rise in statin use and the current epidemic of CHF?

One of the doctors leading this heresy is Texas cardiologist Dr Peter Langsjoen. 'In my practice of 17 years, I have seen a frightening increase in heart failure secondary to statin usage - I call it ‘statin cardiomyopathy’,' he says. 'Are we causing this epidemic through our zealous use of statins? In large part, yes.'

But how can a drug meant to prevent heart failure possibly cause it? The answer has been unfolding since 1985, when a team led by University of Texas biochemist Dr Karl Folkers found that those suffering from heart failure had a deficiency of the enzyme ubiquinone in their heart tissue - the less ubiquinone, the worse the heart failure (Proc Natl Acad Sci USA, 1985; 82: 901-4).

Ubiquinone got its name because it is found everywhere in the body - it’s ubiquitous. Later recognised as necessary for glucose production, its name was changed to ‘coenzyme Q10’ (CoQ10). It was soon found to be at its greatest concentrations in the heart, where it is now known also to act as a powerful antioxidant.

Folkers immediately set about testing oral supplements of CoQ10 on patients with CHF. His reported results were spectacular. 'These patients, steadily worsening and expected to die within two years under conventional therapy, generally showed an extraordinary clinical improvement,' he wrote (Proc Natl Acad Sci USA, 1985; 82: 4240-4).

These results, together with his earlier discovery, strongly suggested that CoQ10 is an important contributory factor in CHF.

The CoQ10-statins connection During the next five years, Folker teamed up with fellow Texan Langsjoen, the cardiologist who had expressed such concerns about statins causing heart failure. Combining Folker’s biochemical evidence with Langsjoen’s clinical experience, they asked: could statins be depleting CoQ10?

This possibility had never been investigated in any of the official trials of statins, so it was virgin scientific territory.

Folker’s biochemists set about testing their hunch in the laboratory by feeding rats lovastatin, the most widely prescribed statin drug.

What they found was a bombshell: lovastatin depleted as much as 20 per cent of the CoQ10 in the rats’ blood, and about 10 per cent from their heart tissue (Proc Natl Acad Sci USA, 1990; 87: 8928-30). Folker and Langsjoen then went on to test their findings on human volunteers and confirmed the animal findings - lovastatin destroys CoQ10 (Proc Natl Acad Sci USA, 1990; 87: 8931-4).