Just a few short months ago, cholesterol drugs were a dead duck. Studies began appearing showing that even after years of cholesterol drug consumption, patients were no better off in terms of preventing the progression of arterial disease than if the

The growing scepticism was utterly swept aside by the publication of a single trial, the Scandinavian Simvastatin Survival Study. Dubbed the 4S study, it followed 4,444 (“four” obviously was the leitmotif here) patients with a heart condition and high cholesterol level. After five and a half years, the group given cholesterol lowering drugs supposedly had a 42 per cent lower rate of fatal heart attacks and a 34 per cent reduction in heart disease than controls.

Within a week, medical magazines like Monitor Weekly were back on the cholesterol bandwagon. Michael Brown and Joseph Goldstein, the 1985 Nobel prizewinners for their cholesterol work, broke what had been their long silence during the cholesterol controversy to rechristen the 4S trial with alliterative plaudits like “straightforward results” and “spectacular implications”.

As always, there are a few brave souls willing to thrash against the tidal wave of uncritical medical enthusiasm, but they are forced to do so in a tiny vessel a few column inches, say, on the letters page of The Lancet.

In this instance, one Dr. William E Stehbens, of Wellington, New Zealand, quietly savaged the 4S study from end to end (The Lancet, January 28, 1995). For one thing, he wrote, anyone with heart disease, whether or not it was caused by hardened arteries, was allowed into the study. In the treated group, there were 38 extra people who’d already been given bypass surgery or angioplasty and therefore were less likely to die. And 54 extra smokers happened to creep into the control group, which just might have had something to do with their greater mortality rate.

Stehbens also points out (and as a pathologist, he should know) that diagnosing CHD or gauging the severity of atherosclerosis is a highly inexact science until people die. In the 4S study, the actual difference in mortality between the two groups from all causes was only 3.3 per cent.

Finally, Stehbens notes almost in an aside that the control drug took a placebo containing methylcellulose, which when given intravenously to rabbits causes tissue storage in arteries, a condition that sounds suspiciously like atherosclerosis.

What worries me most about this entire cholesterol lowering business is not just the usual bad science and biased reporting, but the blind meddling going on here. Only a very few scientists are investigating why more people die when their cholesterol is lowered. Even fewer have made the connection between an increase in suicide or violent deaths and the use of cholesterol lowering drugs, as well as the new style antidepressants like fluoxetine. These drugs, and the new migraine drug sumatriptan, contribute to a decrease in brain serotonin, which seems to suppress our aggressive behaviour and generally keeps harmful impulses in check.

By some ignorant fiddling about with brain hormones, they could be creating a good deal more havoc individually and collectively than the very worst Western high fat diet.

Until medicine understands more about this hormone, best to let dead ducks rest in peace.

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Written by What Doctors Don't Tell You

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