Teaching on an Evidence Based Practice workshop recently I came across a truly jaw-dropping projection. A participant used a clinical scenario about obesity to bring up a paper about the US Obesity epidemic.The study is three years old now, but the authors use data on adults and children from the National Health and Nutrition Examination Study (NHANES), between the 1970s and 2004. The projections are frightening for the burden and health-care costs of obesity and overweight in the US if current trends continue. By 2048, all American adults would become overweight or obese. Depending on your ethnic background it could even be worse with the authors stating that Black women and Mexican-American men are likely to reach that state even earlier. However, the authors point out that they make a number of assumptions. Firstly they assume that the increase in obesity will be at its current rate. They also ignore the effect that all future policy, environmental and behavioural changes may have. Finally they ignore the possibility that some individuals may be genetically protected from becoming obese.

In the UK the predictions are not that much better. A recent four part series on obesity in The Lancet journal included a paper co-authored by Professor Klim McPherson of The University of Oxford. Their study stated that by 2030 there would be an additional 11 million more obese adults in the UK. This would have a knock on effect of an extra 6-8 million cases of diabetes, 5—7 million cases of heart disease and stroke and approximately 600,000 additional cases of cancer. This sort of news travels fast with The Daily Mail being one of the first to report these finding to the public.

So is it all doom and gloom? Not necessarily. In the same paper the authors go on to suggest that a 1% reduction in BMI (equivalent to a 1kg loss) across the entire population could avoid up to 2 million incident cases of diabetes, nearly 2 million new cardiovascular disease cases, and 73 000–127 000 cases of cancer. The authors further infer that this could be achieved through a reduction of 20kcal/day sustained over 3 years i.e. less about a teaspoon of sugar a day. Better still, if we were all able to give up 200 to 400 kcal/day, obesity levels would drop to 1990 prevalence levels.

So small changes may be the best way to start beating this epidemic. Something to think about before adding that spoon of sugar to your next tea or coffee.

Today’s main news story is that obesity is on the up and will continue to rise if coordinated action is not taken at local, national and international levels. A Lancet series of articles examines the evidence for the growing burden and cost of obesity globally and the policy steps needed to prevent 65 million more adults in the USA and 11 million more adults in the UK becoming obese by 2030. Successive governments have allowed the food industry to self-regulate and the evidence clearly suggests that this does not work, since the industry’s interest are profits.

What strikes me is that instructive lessons learned from a strikingly similar case-in-point over the last 60 years, namely the tobacco industry, are not being put into practice. There was good medical evidence for smoking and its detrimental effects of health since the work of Richard Doll and Austin Bradford Hill showed the link with lung cancer in the early 1950s, but it was not until 2005 that the World Health Organization adopted the Framework Convention for Tobacco Control, the world’s first and only public health treaty. Our policymakers smugly talk about tobacco as a tackled problem, but it was less than 10 years ago that UK policy started moving in the direction of smoke-free public places.

We have an obese body of evidence (pun intended) to show that the pathophysiology and epidemiology of obesity is bad for our health, and we have enough evidence to show that current methods of tackling industry problems are not working. Governments are quick to say that the food industry is different but what are the incentives for the food industry to behave differently? Is it going to be acceptable to wait 50-60 years before governments and global health policymakers put evidence into practice? Evidence-based medicine aims, at the end of the day, to institute changes which make the health of individuals better. It seems that there are inequalities in the way evidence is put into practice, based not just on societal interests, but on conflicts of interest, particularly multi-billion dollar industries. If we are serious about EBM and evidence-based policy, we should take lessons learned from other sectors and apply them accordingly.

On both sides of the Atlantic, obesity, particularly in childhood, is a growing problem (no pun intended). So earlier this week, when new research claimed to associate a virus that causes the “common cold” with the development of obesity, the media took interest in both the UK and the US.

Jeffrey Schwimmer, lead researcher was quoted on the BBC:
"It is time that we move away from assigning blame in favour of developing a level of understanding that will better support efforts at both prevention and treatment. These data add credence to the concept that an infection can be a cause or contributor to obesity.”

That is big chat. Like all papers published in major journals, the abstract or summary of the paper is available on PubMed for free. I used the abstract to examine these claims a bit further.

The authors set out to compare blood levels of antibodies to adenovirus (AD36) in children who were obese versus those who were not. The first problem is that they did a “cross-sectional study”, which means they took a snapshot of their patients at a single point in time, rather than following them up over a length of time. That means that we deduce nothing about the virus (the “exposure”) causing obesity (the “outcome”) since we are not following the children up over time from the onset of the infection of the virus. At best, we can talk about an association or a link. Secondly, they have kids from 8-18 years of age. Children at eight are very different to children at eighteen and so you might expect the effect of infection at different stages of childhood to be different. So why are they lumping all kids of all ages together?

In the results, only 124 children were studied, and we have no idea how many patients were excluded from original recruitment. Half of the 124 children were obese. Before we go any further, the antibody (AD36) was present in 15% of the children. In other words, any comments made about the relationship between the antibody and obesity is based on 19 children. That does not seem a big enough number to be making any claims.

The paper’s main findings are: “The majority of children found to be AD36-positive were obese (15 [78%] of 19 children). AD36 positivity was significantly (P _ .05) more frequent in obese children (15 [22%] of 67 children) than nonobese children (4 [7%] of 57 children)”. Again, we are looking at only 19 children who had viral antibodies. In addition, the p-value is only just statistically significant (p=0.05). You do not have to read the whole paper to see the limitations of research. Bottom line: regular Big Macs and lack of exercise are still much more likely to cause obesity in childhood than the common cold.