The nastiness of NICE: The addled tyranny of the anti-junk food crusade

The idea that thousands of lives could be saved if people stopped eating the ‘wrong’ food is pie in the sky

‘Forty thousand deaths a year due to junk food’, declared the UK Daily Telegraph yesterday, reporting on new policy recommendations produced by the National Institute for Clinical Excellence (NICE). But the evidence on which this claim is made is highly dubious. What the report really represents is the coming together of the same-old NGOs and health policy wonks to tell us - for the umpteenth time - how we must live our lives.

The report puts forward 12 recommendations, including:

* Introducing policies designed to cut our consumption of Bad Stuff (salt, saturated fats and trans-fats);

* restricting marketing of ‘junk’ food to children;

* introducing the ‘traffic light’ labelling of foods - green for good, amber for warning and red for unhealthy;

* assessing all government policy for its impact on cardiovascular disease;

* ensuring that EU farm spending promotes healthy foods;

* encouraging ‘physically active travel’ – for example, by scrapping subsidised car parking;

* providing ‘healthy’ meals in public-sector workplaces, schools, hospitals, etc;

* discouraging, via local authorities, the opening of takeaway food outlets near schools and in other sensitive areas.

This mish-mash of different recommendations simply reflects the wide range of groups that want to get their noses in the health trough or foist their particular hare-brained schemes upon us. The evidence that any of these policies would make any serious difference to our life expectancies - never mind save tens of thousands of lives - is flimsy to say the least.

First of all, we need to examine the claim that such measures could save the 40,000 lives apparently being destroyed by junk food. The report says: ‘Most premature deaths from CVD (cardiovascular disease) – that is, among people aged less than 75 – are preventable. In 2006, CVD accounted for around 30 per cent of premature deaths among men and 21 per cent among women, accounting for just over 40,000 premature deaths in that year.’ So actually, even on this basis, it is only most of the 40,000 premature deaths that could be prevented. But even this seems implausible. Genetics, old age, sheer luck, the quality of healthcare available, and environmental factors that aren’t preventable by lifestyle change - like air pollution - would seem to be at the very least as important as what people eat.

Above all, being a man rather than a woman makes a very substantial difference to life expectancy. The latest figures from the Office for National Statistics suggest life expectancy in the UK at birth is now 77.5 years for men and 81.8 years for women. Is this ‘preventable’? Perhaps all men over 50 should be forced to have their balls chopped off. Strangely, this policy recommendation is absent from NICE’s report.

But when we dig a little further into the various recommendations, the suggestion that the policies put forward could have any substantial impact on life expectancy is quickly revealed to be illusory. Let’s look at the evidence for the idea that if we avoid eating the wrong things we will live longer.

Salt

Poster campaigns and health professionals are forever telling us that we should reduce salt intake to lower our blood pressure and, in turn, cut cases of CVD. Yet while there may be some benefit in cutting salt intake in those who are already being medicated for high blood pressure or who have kidney disease, for most people there is no evidence that cutting salt is of any benefit at all. Indeed for some people it could be harmful.

There is a certain arrogance about the idea, repeated in the new report, that we should cut salt intake from an average of 8.5 grammes per day to six grammes per day by 2015, and then to three grammes per day by 2050. Firstly, the idea that high salt automatically equates to shortened lives is wrong: the Japanese have a very high-salt diet and enjoy longer lives than anyone else.

Secondly, our bodies are incredibly sensitive to the appropriate balance of salt and water in our blood, regulating it on a minute-by-minute basis to keep it within a very narrow range. Yet the groups and researchers proposing radical changes to our diet seem to believe that salt intake should be regulated by diktat from Whitehall rather than by our internal biology evolved over millions of years.

There is no consensus that such salt-reduction policies would be beneficial. A review in the British Medical Journal on the evidence connecting salt with high blood pressure, published in 2002, concluded: ‘Intensive interventions, unsuited to primary care or population prevention programmes, provide only small reductions in blood pressure and sodium excretion, and effects on deaths and cardiovascular events are unclear.’

Saturated fat

There has been plenty of evidence for a very long time that attempts to reduce saturated fat consumption have no effect on cardiovascular disease. For example, the Multiple Risk Factor Intervention Trial (MRFIT), which reported its findings in the early 1980s, encouraged a large number of middle-aged American men with high cholesterol to change their diet in an effort to reduce their saturated-fat intake and, therefore, their cholesterol. These test subjects were also encouraged to quit smoking and to treat their high blood pressure. Meanwhile, another large group of middle-aged men were left to their own devices. The result? Slightly more men in the low-fat diet group died than in the control group, but in reality there was no practical difference in outcomes.

Trans-fats

As for trans-fats, the evidence that reducing our intake will ‘save lives’ is once again weak. Trans-fats are a by-product of adding hydrogen to vegetable fats to make them stable at room temperature and give them a longer shelf-life, particularly in things like baked goods. While they’ve been around for decades, they became particularly popular among food manufacturers as an alternative to saturated fats.

So what’s the risk from trans-fats? A review in the New England Journal of Medicine in 2006 says: ‘In a meta-analysis of four prospective cohort studies involving nearly 140,000 subjects, including updated analyses from the two largest studies, a two per cent increase in energy intake from trans fatty acids was associated with a 23 per cent increase in the incidence of [coronary heart disease].’ That figure of 23 per cent sounds impressively high, but epidemiological studies are very blunt instruments.

As the US National Cancer Institute noted in 1994, ‘in epidemiological research, [increases in risk of less than 100 per cent] are considered small and are usually difficult to interpret. Such increases may be due to chance, statistical bias, or the effects of confounding factors that are sometimes not evident.’ As a comparison, the risk of getting lung cancer from being a regular smoker (over the course of decades, usually) is in the order of 2,000 per cent compared to non-smokers. While we can be pretty confident that active smoking significantly increases your risk of a variety of diseases, the small relative risk associated with trans-fats is much more ambiguous.

The other recommendations in the NICE report are a bunch of lame old hobbyhorses or, in the case of demanding that all government policy be assessed for its effect on CVD, they add up to a demand for a health-lobby veto on all lawmaking. Thanks, but no thanks.

But regardless of the evidence, there is a more principled basis on which we should object to these kind of policy proposals – namely, that we, and not NICE or anybody else, should have control over our own lives and our own, sometimes bad habits. Let us eat our junk, slob out on our sofas, smoke our fags and drink our booze. If these things turn out to shorten our lives, so be it (though the evidence that they will is usually as feeble as an old codger who’s avoided a ‘premature’ death). That’s surely a better way to live than to be endlessly subjected to the high-fibre, low-fat, salt-free dictatorship of Those Who Know What’s Good For Us.

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The myth of the smokefree health miracle

The evidence that bans on public smoking reduce the number of heart attacks is still woefully thin

Recent reports of a ‘dramatic’ fall in the number of heart attacks in England after July 2007 represented the latest in a long line of attempts to find immediate health benefits from smoking bans. But a serious examination of this body of evidence suggests that the effect of smoking bans is either tiny or non-existent.

The worldwide search began in 2004, when the British Medical Journal reported a 40 per cent decline in ‘acute myocardial infarction’ (AMI), the medical term for heart attack, in the small town of Helena, Montana. Subsequent ‘heart miracles’ claimed drops in AMI of 47 per cent (Bowling Green, Ohio), 27 per cent (Pueblo, Colorado) and 17 per cent (Scotland).

As previously reported on spiked, the widely touted Scottish figure of 17 per cent was at odds with hospital admissions data showing an eight per cent drop in the first year of the ban followed by an eight per cent rise in the second year. When this inconclusive evidence is combined with hospital admissions data from Wales, Denmark, New Zealand and Australia showing smoking bans having no effect on the heart attack rate (1), the most striking aspect of this field of research is the tendency to find dramatic results in small communities and practically nonexistent effects over large populations.

The counterintuitive conclusion was that secondhand smoke was ferociously lethal in one-horse towns in the mid-West, but strangely benign in whole nations. The alternative, if more cynical, explanation was that obscure destinations like Helena and Bowling Green were brought to the world’s attention because anti-smoking campaigners had dredged the data for unusual blips that roughly coincided with provincial smoking bans.

That question seemed set to be resolved when The Sunday Times announced in September 2009 that the smoking ban in England (population 49million) ‘caused a fall in heart attack rates of about 10 per cent’. The source of this claim was never disclosed and the anti-smoking campaign Action on Smoking and Health (ASH) quickly downplayed it, insisting that the 10 per cent figure was ‘not based on any research conducted to date’ (2). Nevertheless, the research was underway and it finally bore fruit a fortnight ago in the form of another British Medical Journal study.

Led by Dr Anna Gilmore, a member of ASH and the director of the Tobacco Control Research Group, the study found a post-ban drop in AMI of not 10 per cent, let alone the 40 per cent found in Helena, but of just 4.3 per cent. A welcome decline, to be sure, but since the final years of ‘smoky’ England saw similar declines of 3.2 per cent and 5.2 per cent, the evidence for a heart miracle in the most populous nation yet studied was less than compelling (11).


heart attack rates in England before and after smoking ban

Faced with data that unequivocally showed heart attacks falling at the same pedestrian rate as before the ban, Gilmore and her team turned to computer modelling. After making adjustments to the data, they concluded that, despite appearances, the smoking ban had a profound effect on the nation’s hearts. Of the 4.3 per cent drop in AMI admissions, Gilmore attributed more than half (2.4 per cent) to the smoking ban. The study concluded that ‘the implementation of smoke-free public places is associated with significant reductions in hospital admissions for myocardial infarction’. A press release was then issued, headlined ‘Smokefree legislation linked to drop in admissions for heart attacks’.

To make life simpler for busy journalists, the press release chose not to mention that this was a computer-generated estimate, instead flatly stating: ‘A 2.4 per cent drop in the number of emergency admissions to hospital for a heart attack has been observed following the implementation of smokefree legislation in England.’ As was helpfully pointed out, this 2.4 per cent drop equated to 1,200 heart attacks being ‘prevented’ by the 2007 legislation. There was no mention of the downward trend in AMI that long predated the smoking ban.

Since the 2.4 per cent figure exists only on a laptop at Bath University, the calculations that led to it can be neither verified nor debunked. The possibility that the smoking ban contributed to part of the drop in AMI admissions after July 2007 cannot be ruled out, particularly if it led to a significant drop in the number of smokers (the jury is still out on whether this happened). But since the number of heart attacks fell at a similar rate after July 2005 and July 2006, the burden of proof rests on Gilmore & Co. Without it, it is as if they were doing a rain dance in the middle of a thunderstorm and demanding credit for the rain. The onus is on them to convince us that the skies would have cleared if they hadn’t showed up, not the other way round.

Gilmore’s case rests on making adjustments for three relevant but hardly decisive confounding factors that might disguise the effect of the smoking ban: surface air temperature, population size and Christmas holidays. This is all good practice, but more significant risk factors such as smoking status, diet, statin use, exercise and stress go unaddressed. It could not be otherwise. Hospital admissions data reveal no personal information about any of the patients beyond their age and gender. This only highlights the immense difficulty of making specific assumptions from a mass of nameless aggregate data.

The only thing that can be said with any confidence is that there were 2,300 fewer heart attacks in 2007/08 than in the year before. With heart attacks and heart disease having hundreds of risk factors interacting with each other in complex and unpredictable ways, using raw data to single out any one of them is like listening out for a kazoo in a stadium full of vuvuzuelas. Any estimate made against this noisy statistical background can only be speculative to the point of wishful thinking.

Perhaps this underestimates the power of the team’s computer model, but if they have truly devised a formula that can predict the number of heart attacks by taking the temperature and seeing what day Christmas falls on, it is not one they are prepared to share with us. Effectively, the reader is told: ‘We know it doesn’t look like the smoking ban had any effect on AMI admissions but we’ve run it through a computer model and it has. Take it or leave it.’ In the context of the dubious and frequently bizarre history of ‘heart miracle’ studies, the reader could be forgiven for leaving it.

If it does nothing else, the English study confirms that the wilder claims of heart miracles in Helena and elsewhere were way off base. In the course of six years, the ‘smoking ban effect’ on heart attacks has fallen from over 40 per cent to less than five per cent. And since the heart attack rate was known to fall by more than five per cent in some years before smokefree legislation was introduced, attributing any part of the secular decline to the smoking ban becomes a matter of interpretation and conjecture.

Not that the hypothetical nature of Gilmore’s study ever impinged on the news coverage devoted to it. No one reading the newspapers two weeks ago could have gone away thinking anything other than that there were 1,200 fewer heart attacks after the smoking ban and that this decline in numbers was an unusual and remarkable event.

As was the case in Scotland two years ago, the statisticians who painstakingly collected admissions data from English hospitals might as well not have bothered. The true figures vanished, replaced by unseen adjustments and unspoken assumptions from the gatekeepers of knowledge at the UK Centre for Tobacco Control Studies. Once again we had findings erroneously leaked to the media months in advance, a press release which failed to get the most basic facts straight, and a study with no verifiable evidence to support its central conclusion. And all published just in time for the government’s review of the smoking ban. If this doesn’t warrant a little scepticism, what does?

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