The only major changes I’d made to my lifestyle since coming off statins were eliminating sugar (including alcohol and starchy foods such as bread) and eating more animal fat. Many experts now believe that sugar is emerging as a true villain in the heart-disease story; while after decades of demonisation, saturated fat has been acquitted of causing heart disease by a recent “meta” analysis of 70 studies by Cambridge University.

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 check-up was seven months ago and now, at 58, I’m not on a single tablet. My GP is happy. I feel better than I have in years and, at the same time, deeply concerned about proposals advising even wider use of statins.

Until 2005, statins were prescribed only to those with at least a 30 per cent or greater risk of having a heart attack within 10 years. This was then reduced to a 20 per cent risk. Now, draft NHS guidelines would have them dished out to those with just a 10 per cent 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, specialising 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 Prof Sir Rory Collins from 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 analyse 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 per cent 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.

Original article can be found here: http://www.telegraph.co.uk/health/10717431/Why-Ive-ditched-statins-for-good.html