‘Misleading’ to make fried food and fizzy drinks targets of anti-obesity drive

IT is misleading to focus public health campaigns on tackling obesity by targeting fried food and fizzy drinks, according to scientists.

As many seek to battle the festive bulge in January, a new study has challenged previous findings that any single aspect of diet or lifestyle can be addressed to reduce the risk of obesity in adults.

Researchers at the University of Exeter found instead many fattening aspects of the environment, lifestyle and behaviour interact with a person’s genes to influence his or her waistline – and the strongest influence is poverty.

In the UK, obesity affects around one in every four adults and one in every five children aged 10 to 11, according to the NHS.

Being obese increases risk of developing type 2 diabetes, coronary heart disease, some cancers and stroke.

The findings contradict some studies, which have concluded concentrating obesity policy on specific aspects such as the consumption of fizzy drinks or fried food could make a meaningful difference to help decrease waistlines, especially in those at high genetic risk of obesity.

The researchers said their study concluded it was premature to suggest specific aspects of behaviour or the environment can be targeted to reduce obesity levels effectively in people at high risk due to their genes.

Dr Jessica Tyrrell, who led the research, said: “There is no ‘silver bullet’ to reducing obesity risk.

“It is misleading to suggest public health measures should be targeted specifically at fried food reduction, fizzy drink consumption or TV watching in those genetically predisposed to obesity, as some previous studies in leading medical journals have suggested.

“Instead, the data are consistent with proposals that public health measures should aim to alter all aspects of these fattening factors in small ways to have more impact in lowering levels of obesity and type 2 diabetes.”

Dr Tyrrell said a person’s genes can mean they are more susceptible to becoming obese or developing type 2 diabetes in today’s modern world of plentiful food and sedentary lifestyles.

Until now little has been known about how genes interact with the modern environment and human behaviour to mean some people with this predisposition become obese, while others remain slim.

The study examined 120,000 volunteers who contribute health data to the UK Biobank and concluded poverty is likely to be related to many different factors, reflecting socio-economic influences on diet and activity levels.

Previous studies have shown in high income countries people from more deprived social backgrounds are more likely to be obese, but this study provides the strongest evidence yet that these effects are even stronger in people at the highest genetic risk of obesity.

The team found within the poorest half of the population carrying 10 additional genetic risk factors for obesity was associated with approximately 3.8kg extra weight in someone 1.73m tall.

In contrast, being of the same height and carrying the same number of obesity risk genetic factors was associated with just 2.9kg extra weight in the richest half of the population.

Professor Tim Frayling, who oversaw the study, added: “In order to inform evidence-based policy decisions around obesity, we need to understand more about the complex mix of genes, environment, behaviour and lifestyle.

“Our study suggests that genes and environment can interact to provide a ‘double whammy’ type effect, but, critically, it is really hard to narrow down which parts of the environment and lifestyle are the most critical.

“Large genetic datasets from resources like the UK Biobank are helping us pick the problem apart.”

The study, Gene-obesogenic Environment Interactions In The UK Biobank, is published in the International Journal Of Epidemiology.