The Rationale for the Use of Statins is (Again) Destroyed

The diet-heart hypothesis (the basis for the introduction of statin medications) has again been annihilated by two recent studies.

For about the last 60 years we have been told that eating foods containing saturated fat raises cholesterol levels and this increased cholesterol level causes plaques to form in the arteries - referred to as the lipid hypothesis or the diet-heart hypothesis. 

Meta-analysis after meta-analysis has failed to show any link between dietary saturated fat and heart disease. And people who have heart attacks have repeatedly been shown to have normal or average cholesterol levels - not high cholesterol. Now, two more studies have recently been published to yet again destroy the diet-heart hypothesis and the basis for the use of statins - which are estimated to be taken by 100 million people around the world.

The first study, published in the British Medical Journal, examined the validity of the diet-heart hypothesis by recovering and analysing previously unpublished data from randomised control trials. The study found that replacing saturated fat for vegetable oils did lower cholesterol levels, but this did not reduce the amount of heart disease or heart attacks. In fact, for each 30 mg/dL (0.78 mmol/L) reduction in cholesterol there was a 22% greater risk of death.

This fits with all of the other studies done around the world, going back more than 40 years now, showing that low cholesterol correlates with increased deaths from all causes - in particular, deaths from cancer and other diseases related to the immune system.

(The picture above is a screenshot from Statin Nation II, showing average cholesterol levels and rate of heart disease deaths for various countries. We can see for example that Lithuania and Portugal have roughly the same average cholesterol levels, but Lithuania has more than four times the number of heart disease deaths.)

(The picture above is a screenshot from Statin Nation II, showing average cholesterol levels and rate of heart disease deaths for various countries. We can see for example that Lithuania and Portugal have roughly the same average cholesterol levels, but Lithuania has more than four times the number of heart disease deaths.)

The second study was actually notification that a clinical trial had been stopped. This notification was published by the American College of Cardiology. A trial had started on a cholesterol altering drug called evacetrapib, but the results were so poor that the trial was stopped early.

On average, patients taking this drug lowered there LDL level (so called bad cholesterol) by 37% and increased their HDL level (so called good cholesterol) by 130%. If we are to believe what we are told about cholesterol, then this should result in dramatic benefits in terms of heart disease reduction, however, the study actually found that these changes in so called ‘bad’ and ‘good’ cholesterol did not result in any reductions in anything at all to do with heart disease - there was no benefit.

Stephen Nicholls, M.B.B.S, Ph.D., a professor at Australia’s University of Adelaide, cardiologist at Royal Adelaide Hospital and the study’s lead author, said:

“Here we’ve got an agent that more than doubles the levels of good cholesterol and lowers bad cholesterol and yet has no effect on clinical events,” said  “We were disappointed and surprised by the results.”

Actually Professor Nicholls absolutely should not be surprised if he has been taking even the most casual look at the medical literature, because this is just history repeating itself. Back in 2007, another drug with a similar name (torcetrapib) was tested in another clinical trial that had to be stopped early.

Torcetrapib reduced "bad" LDLs by 25% and increased "good" HDLs by 72%, and at the same time increased the number of deaths due to cardiovascular causes by 40% and doubled the number of deaths from all causes!