steak
© Fotolia
For eight years, I faithfully popped atorvastatin pills, without side effects. Then, one day last May, I stopped. It wasn't a snap decision; after looking more closely at the research, I'd concluded statins were not going to save me from a heart attack

When I had a routine health checkup eight years ago, my cholesterol was so high that the laboratory thought there had been a mistake. I had 9.3 millimoles of cholesterol in every litre of blood - almost twice the recommended maximum.

It was quite a shock. The general practitioner instantly prescribed statins, the cholesterol-lowering drugs that are supposed to prevent heart disease and strokes. For eight years, I faithfully popped my 20mg atorvastatin pills, without side effects. Then, one day last May, I stopped. It wasn't a snap decision; after looking more closely at the research, I'd concluded statins were not going to save me from a heart attack and that my cholesterol levels were all but irrelevant.

That uncle or aunt who turns beet red after a few beers or a couple of glasses of wine? Their risk of developing high blood pressure may be far higher than the rest of the population who doesn't drink, or that can drink without flushing crimson, a new study suggests.

While researchers writing this month in the online journal Alcoholism: Clinical & Experimental Research noted that excessive drinking of any type has long been associated with raised risks of hypertension, they were able to conclude after studying data from the medical records of 1,763 men that the higher risk incurred from drinking kicks in much earlier for drinkers who flush red than for those who don't.

When I informed my GP of my decision three months later, I wasn't entirely honest. Rather than say I was skeptical about the drugs, I told my doctor I'd quit the statins because they were causing pain in my arm.

He didn't bat an eyelid. Evidence from the drug industry published this month - evidence I suspect was heavily reliant on data from the drug industry - may suggest that side effects are uncommon, but previous studies have found that one in five people on statins suffers adverse side effects, from muscle pain and diarrhea to memory loss and blurred vision.

The GP simply suggested I try another brand of statin. The sooner the better, he said, given that I'd already been off my prescription for three months. "Hang on," I said. "Could you give me a blood test first?" When the results came back, he was amazed that my total blood cholesterol was lower than when I'd been on statins. After three months without the pills, it was 5.4mmol/L (5.4 millimoles per litre of blood) compared with 5.7 mmol/L a year earlier.

Typically, I was eating red meat three or four times a week and enjoying butter, full-fat milk and plenty of eggs. You would have thought that after three months on a diet so high in saturated fat, my cholesterol would have shot back up to pre-statin levels - but no, it came down and has stayed down seven months on. Not only that, but my levels of LDL (so-called bad cholesterol) were also lower than when I'd been on statins, and my ratio of HDL (so-called good cholesterol) to LDL was under four for the first time, an excellent sign, according to medical wisdom.

Not that I cared about any of this. Yes, it was the statins that originally reduced my cholesterol levels so dramatically. But so what? I believe that high cholesterol has been a scapegoat for too long. Yes, it may, in some circumstances, be an indicator of heart disease, but there is no evidence of a causal link. In my view, high total blood cholesterol or high LDL levels no more cause heart attacks than paramedics cause car crashes, even though they are present at the scene.

Just lowering cholesterol with drugs without sorting out the dietary and lifestyle factors that actually cause heart disease is nonsensical. Besides, there are plenty of other, more reliable indicators of heart-disease risk. What further astonished my GP was that on these indicators I was now apparently better off in other ways than when I'd been on statins. My blood pressure was down. For the first time in years, I was slimmer, especially around the belly. My triglycerides - a type of blood fat with a causal link to heart disease - were lower than at any time in the preceding eight years. My fasting blood glucose was at the optimum level, whereas a year earlier it had been too high. My total white blood count - a marker of inflammation - was lower.

My blood test for a marker called glycated haemoglobin (A1c), high levels of which are associated with heart disease and overall mortality, were bang on normal. Finally, my level of c-reactive protein (CRP) - a protein that rises in response to inflammation - was extremely low. So, biochemically, I was in excellent shape, better than when I'd been on the statins. "Have you taken up running?" asked my bemused GP.

No, I'd always run. For years, I'd exercised three times a week, eaten plenty of fish, refrained from smoking and tried to keep my stress levels low. The only thing I'd changed was my intake of sugar and animal fat.

That checkup was seven months ago and now, at 58, I'm not on a single pill. My GP is happy. I feel better than I have in years and, at the same time, am deeply concerned about proposals advising even wider use of statins.

Until 2005, statins were prescribed only to those with at least a 30% or greater risk of having a heart attack within 10 years. This was then reduced to a 20% risk. Now, draft NHS guidelines would have them dished out to those with just a 10% risk - in other words, most men over the age of 50 and most women over the age of 60.

I am a vascular surgeon. Before founding a private clinic in Dorset 11 years ago, specializing in varicose veins, I worked in the NHS for 13 years. Back then, I didn't question medical guidance on cholesterol, and thought statins were a wonder drug. And so they probably are, for men who have heart disease - not necessarily because they lower cholesterol, but because they may cut other risks such as the inflammation-marker CRP. Exercise, weight loss and omega 3 supplements also lower CRP.

But what about other groups - women, the elderly and people like me who have not been diagnosed with heart disease? The evidence that we will benefit from cholesterol-lowering drugs is ambiguous at best. The 2011 Hunt 2 study, one of the most recent and largest, followed 52,000 men and women in Norway aged 20-74 with no pre-existing heart disease, for 10 years.

The results for women were crystal clear. The lower a woman's total cholesterol, the greater her risk of dying, either of heart disease or anything else, including cancer. This reflects findings in previous studies.

For men, high cholesterol was associated with heart disease and death from other causes. But so, too, was low cholesterol - below 5mmol/l. Again, this is only an association, not a causal link. A range of between 5mmol/l and 7mmol/l was the optimum level. Guess what? This is already the national average. In addition, numerous studies have linked high cholesterol levels with increased longevity in the elderly.

As for me, I have not been diagnosed with heart disease, and nobody in my family has had a heart attack. However, all four of my paternal uncles and my sister have diabetes. Research from Canada, published last year in the BMJ, has shown that statins raise the risk of diabetes, so that gives me little faith. The controversy over these drugs was reignited last week when Sir Rory Collins, professor at Oxford University, warned that doctors' hesitancy about prescribing them to those at risk could cost lives.

GPs are, by definition, generalists. They don't have time to read and analyze data from every paper on every medical condition. Even so, in a recent survey by Pulse magazine, six in 10 GPs opposed the draft proposal to lower the risk level at which patients are prescribed statins. And 55% said they would not take statins themselves or recommend them to a relative, based on the proposed new guidelines.

If that doesn't speak volumes, I don't know what does.