Statins. Photo: Getty
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Why the stats about statins don't tell the whole story

For those without the relevant risk factors, statins aren't the wonder-pill they've been sold as by the media.

Maggie came hot-foot from a “health check” where she’d had her cholesterol measured. “Six point two!” she told me. “The nurse said that’s high.” She sounded rather spooked. “I’d like you to give me a statin.”

I’ve known Maggie for years. She’s a sensible academic in her early fifties. She’d done enough googling to learn that a “high” cholesterol means you are “at risk” of cardiovascular disease (CVD) – heart attacks and strokes – and that statins lower cholesterol and reduce CVD risk by 25 per cent. Her request for treatment made perfect sense to her . . . except she had fallen for the same myth that leads to several million people in the UK swallowing a statin every day for no good reason at all.

Focus for a moment on that 25 per cent risk reduction. If you’re at high risk of something nasty, then lopping off a quarter of that risk makes sense. The people at greatest risk of heart attacks and strokes are those who have previously suffered one. Giving statins to these patients (secondary prevention) does convey modest benefits. If you take 100 heart attack survivors and get them to take a statin for five years, you’ll save one life, prevent two or three non-fatal heart attacks, and avert one stroke. That is worthwhile, even if the statins will fail to prevent at least 15 other heart attacks/strokes, and will cause two patients to develop diabetes, and provoke muscle weakness in ten others. Notice, though: 95 per cent of these highest-risk patients will derive absolutely no benefit from their five years of statin consumption.

Come back to Maggie. Using a statin on someone without existing CVD is termed primary prevention. Maggie has no other risk factors (high blood pressure, smoking, diabetes, and so on) and so her chance of developing heart disease is very low. In Maggie’s case, because her risk is so small to start with, a 25 per cent reduction is minuscule and meaningless. You’d have to treat hundreds of Maggies for years on end to hope to make a jot of positive difference to one of them, and the side effects from statins (we’re still discovering what these are) will far outweigh any putative benefit.

There are large numbers of people just like Maggie who are taking statins and who should come off the tablets. But what about individuals at greater risk – people with high blood pressure or obesity, or smokers? Is there a level of risk at which primary prevention is worthwhile? For some time the UK’s National Institute for Health and Clinical Excellence (NICE) has suggested a threshold of 20 per cent risk over ten years.

At first glance, the trial data does suggest a marginal impact at this sort of level: roughly two heart attacks/strokes are averted among 100 people treated for five years. But, crucially, death rates are not altered; no lives are saved by using statins. This probably reflects the harm also caused by statins, and how any small reduction in CVD is negated by disability and death from other causes.

Taking up regular exercise, or adopting a Mediterranean diet, reduces CVD risk by degrees comparable with statins – in the case of diet, substantially more so. If someone smokes, quitting is similarly helpful. What’s more, once one has adopted these lifestyle changes, statins become virtually redundant. Lifestyle modification is also cheap; there are very few harms besides. And, unlike with statins, these measures protect against other causes of death and disability, such as cancer and the frailties of advancing age. Oh, and they’re good for mental health, too.

This February, NICE initiated a consultation on halving its primary prevention threshold to 10 per cent risk. If achieved, this would add hugely to the six million people in the UK who take statins on prescription. Rather than exacerbate our statin fetish, NICE could design simple decision aids that would help doctors understand the more effective improvements that lifestyle changes can bring to health and well-being – and which would illustrate these benefits to patients.

Once we’d talked things through, Maggie resolved to start attending the university gym a few times a week. She decided to forget the statin prescription, too. As a nation, we’d do well to try the same. 

This article first appeared in the 26 February 2014 issue of the New Statesman, Scotland: a special issue

Davide Restivo at Wikimedia Commons
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Scientists have finally said it: alcohol causes cancer

Enough of "linked" and "attributable": a new paper concludes that alcohol directly causes seven types of cancer.

I don't blame you if you switch off completely at the words "causes cancer". If you pay attention to certain publications, everything from sunbeds, to fish, to not getting enough sun, can all cause cancer. But this time, it's worth listening.

The journal Addiction has published a paper that makes a simple, yet startling, claim: 

"Evidence can support the judgement that alcohol causes cancer of the oropharynx [part of the throat], larynx, oesophagus, liver, colon, rectum and [female] breast"

So what's especially significant about this? 

First, scientists, unlike journalists, are very wary of the word "causes". It's hard to ever prove that one action directly led to another, rather than that both happened to occur within the same scenario. And yet Jennie Connor, author of the paper and professor in the Preventive and Social Medicine department at the University of Otago, New Zealand, has taken the leap.

Second, alcohol not only causes cancer of one kind – the evidence supports the claim that it causes cancer at seven different sites in our bodies. There was weaker evidence that it may also cause skin, prostate and pancreatic cancer, while the link between mouth cancers and alcohol consumption was the strongest. 

What did we know about alcohol and cancer before?

Many, many studies have "linked" cancer to alcohol, or argued that some cases may be "attributable" to alcohol consumption. 

This paper loooks back over a decade's worth of research into alcohol and cancer, and Connor concludes that all this evidence, taken together, proves that alcohol "increases the incidence of [cancer] in the population".

However, as Connor notes in her paper, "alcohol’s causal role is perceived to be more complex than tobacco's", partly because we still don't know exactly how alcohol causes cancer at these sites. Yet she argues that the evidence alone is enough to prove the cause, even if we don't know exactly how the "biologial mechanisms" work. 

Does this mean that drinking = cancer, then?

No. A causal link doesn't mean one thing always leads to the other. Also, cancer in these seven sites was shown to have what's called a "dose-response" relationship, which means the more you drink, the more you increase your chances of cancer.

On the bright side, scientists have also found that if you stop drinking altogether, you can reduce your chances back down again.

Are moderate drinkers off the hook?

Nope. Rather devastatingly, Connor notes that moderate drinkers bear a "considerable" portion of the cancer risk, and that targeting only heavy drinkers with alcohol risk reduction campaigns would have "limited" impact. 

What does this mean for public health? 

This is the tricky bit. In the paper, Connor points out that, given what we know about lung cancer and tobacco, the general advice is simply not to smoke. Now, a strong link proven over years of research may suggest the same about drinking, an activity society views as a bit risky but generally harmless.

Yet in 2012, it's estimated that alcohol-attributable cancers killed half a million people, which made up 5.8 per cent of cancer deaths worldwide. As we better understand the links between the two, it's possible that this proportion may turn out to be a lot higher. 

As she was doing the research, Connor commented:

"We've grown up with thinking cancer is very mysterious, we don't know what causes it and it's frightening, so to think that something as ordinary as drinking is associated with cancer I think is quite difficult."

What do we do now?

Drink less. The one semi-silver lining in the study is that the quantity of alcohol you consume has a real bearing on your risk of developing these cancers. 

On a wider scale, it looks like we need to recalibrate society's perspective on drinking. Drug campaigners have long pointed out that alcohol, while legal, is one of the most toxic and harmful drugs available  an argument that this study will bolster.

In January, England's chief medical officer Sally Davies introduced some of the strictest guidelines on alcohol consumption in the world, and later shocked a parliamentary hearing by saying that drinking could cause breast cancer.

"I would like people to take their choice knowing the issues," she told the hearing, "And do as I do when I reach for my glass of wine and think... do I want to raise my risk of breast cancer?"

Now, it's beginning to look like she was ahead of the curve. 

Barbara Speed is a technology and digital culture writer at the New Statesman and a staff writer at CityMetric.