Why the government can’t ‘cure’ obesity
There’s one major problem with the authorities’ obsessive focus on making us lose weight and shape up: it doesn’t work.
The authors of a new study on the myth of the childhood obesity epidemic, Patrick Basham and John Luik, argue that even if kids were ballooning in weight, that trend could not be reversed by lifestyle diktats from on high.
We have contended for some time that there is a dearth of evidence to substantiate the claim that the UK faces an epidemic of overweight and obese children. But let us assume, for a moment, that there is such a problem. The question then becomes: will the policies proposed, particularly those being implemented by the British government in its obesity strategy, address this problem?
We suggest that the answer to the question is that they will not.
The list of proposed remedies for pediatric overweight and obesity is extensive. The major ‘solutions’ include the following: advertising restrictions and bans; increasing and improving physical education; eliminating children’s access to unhealthy foods in schools and improving school meals; managing the time that children spend playing games online; weighing and measuring children and providing results to parents; and changing children’s eating patterns and managing their food consumption.
There are five general problems with these solutions. First, they assume that the so-called lifestyle interventions advocated by the health promotion community succeed in reducing weight, reducing disease, and increasing longevity. However, this assumption is not supported by the majority of the available evidence. For example, two recent clinical trials aimed at preventing cardiovascular disease failed to lower their subjects’ levels of low-density lipoprotein (LDL or ‘bad’) cholesterol and mortality (1).
These recent failures are not anomalies. Most lifestyle interventions around changing the composition of diet or the amount of food consumed have failed to find any significant benefit in terms of preventing multifactoral diseases, such as cancer, diabetes or heart disease, or, indeed, in increasing lifespan.
The Women’s Health Initiative Dietary Modification Trial, the largest and most extensive randomised controlled diet trial ever carried out, reported that, after eight years in which the subjects scrupulously followed the healthy eating regime, there were no statistically significant differences between the control and intervention groups in heart disease, stroke, diabetes, weight, 30 different cancers, or mortality. In other words, there were no important differences between those who ate a healthy diet and those who ate what they wished.
Second, supporters of health interventions assume that government-facilitated, population-wide behavioural change with respect to diet, weight and physical activity levels is, in fact, possible. The evidence for this is, however, extremely limited.
Interventions based on creating such behavioural change almost always rely on theories, such as cognitive learning and the theory of planned behaviour, in which changes in knowledge and beliefs lead to changes in intention and finally to changes in behaviour. These theories have rarely been subjected to rigorous evaluation, and where they have, they have generally been spectacular failures (2).
Part of the problem stems from ‘behaviour decay’, in which behavioural changes with respect to diet, exercise and weight persist for a short-time, but then gradually decay with little or no long-term impact. For example, even the most optimistic studies on dieting suggest a long-term success rate of less than 10 per cent. A recent study of behaviour decay that looked at improving diet and physical activity found that most of the change occurred by week six with significant decay at 18 months (3).
Third, they fail to conform to the standards of evidence-based medicine in that there is strikingly little evidence – particularly from the gold standard of research assessment, the randomised control trial – that any of these measures have reduced overweight and obesity in children and adolescents. It is now a commonplace requirement that proposed interventions rest only on rigorous clinical evidence of efficacy.
Yet there is an almost complete absence of even the most flimsy evidence of effectiveness for all of the measures proposed as solutions for childhood overweight and obesity. Even more worrying is the fact that the advocates of these solutions for overweight and obese children often dismiss evidence as unnecessary. Like so many advocates of lifestyle interventions, they believe that the usual standards of efficacy cannot be applied.
The fourth problem with these kinds of solutions is that they are based on the crucial assumption that overweight and obesity is caused in large measure by the environment in which children live. This assumption, however, is contradicted by the accumulating evidence on just how small the environmental contribution to obesity really is. A new study suggests that for twins the shared environment effect for both body mass index (BMI) and waist circumference is only 10 per cent (4).
This has significant, but generally unrecognised, implications for all obesity solutions, since it suggests both that the environment, whether the food environment or the wider environment, has little to do with childhood obesity and that changing that environment might well have an insignificant impact on childhood adiposity.
The final general problem with these sorts of solutions is that they violate the central canon of evidence-based medicine in that they are not connected with the cause of the problem. And because they are not connected with the root cause of the problem they are doomed both to be beside the point and to be unsuccessful.
Indeed, there is an almost complete lack of high-quality evidence about precisely what causes children to become overweight and obese. Yet the solutions typically advanced for childhood overweight and obesity confidently assume that we know not only what causes it but how to prevent it. Thus, we are told, if we can prevent food advertising to children, if we can control what they eat, particularly at school, if we can chart and follow their weight and increase their physical activity, we can prevent them from becoming overweight and obese.
However, it is precisely because the causal links between such things as advertising, eating patterns and types of food consumed, and physical activity and overweight and obesity are at best tenuous and, at worst, non-existent, that solutions such as those prescribed in the UK government’s obesity strategy are bound to fail.
Patrick Basham and John Luik are authors of Fat Kids? The Obesity Epidemic Myth, released on 6 February and available from the Democracy Institute, from which this article is adapted. They are previously authors, with Gio Gori, of Diet Nation: Exposing the Obesity Crusade, a Social Affairs Unit book. (Buy this book from Amazon(UK).)
Previously on spiked
Patrick Basham and John Luik reviewed a year of myths about smoking and obesity. They also examined new research which taught obesity hysterics a lesson and attacked the proposals to remove children from obese households.Dr Michael Fitzpatrick said we should stop bullying fat kids. Rob Lyons was sick of the endless diet of government intervention. Peter Marsh asked what’s behind the sensationalist child obesity headlines. Or read more at spiked issue Obesity.
(1) M Mitka ‘Lifestyle Modification and Heart Disease: Researchers Not Deterred by Trials Showing No Benefit’ Journal of the American Medical Association 2009 301: 150-151.
(2) A V Peterson et al ‘Hutchinson Smoking Prevention Project’ Journal of the National Cancer Institute 2000 92: 1979-1991; W Hardeman et al ‘Application of the Theory of Planned Behaviour Change Interventions: a Systematic Review’ Psychology and Health 2002 17: 123-158.
(3) R Merrill et al ‘Can Newly Acquired Healthy Behaviours Persist?’ Preventing Chronic Disease 2008 5: 1-13.
(4) J Wardle et al ‘Evidence for a Strong Genetic Influence on Childhood Adiposity Despite the Force of the Obesogenic Environment’ American Journal of Clinical Nutrition 2008 87: 398-404.
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