11 December 2008

Obesity gene link to a preference for fattening foods

An obesity gene variant, present in 63% of the population, has been shown to cause people to eat 100 extra calories, on average, at a single meal.

A team at the University of Dundee conducted an eating test with 100 schoolchildren aged between 4 and 10 and found that the children with the common variant on the `obesity gene’ FTO consumed the extra 100 calories. These children chose to eat food types that contained more sugar and fats as opposed to more healthy options.

Results of the study are published in this week’s edition of the New England Journal of Medicine. The research was led by Professor Colin Palmer at the University of Dundee, and included colleagues who are now based at the Universities of St Andrews, Brighton and Glasgow Caledonian.

The study measured the metabolism, adiposity (fat distribution), exercise and eating behaviours in the schoolchildren. They were given a test meal at school, which included a mix of options: ham, cheese, crackers, crisps, raisins, grapes, cucumber, carrot, chocolate buttons, water, orange juice and bread rolls. Investigators recorded the food that remained on each child’s tray. Importantly, each child was tested with this meal on three occasions to increase the reliability of the results.

Researchers found the gene had no impact on metabolic rates or measures of physical activity. There was also no evidence that individuals carrying the obesity-related variant had any problem with satiety (knowing when to stop eating). However, they did find that there was an increased calorific intake from a greater consumption of the more fattening foods as opposed to the more healthy options.

'This work demonstrates that this gene does not lead to obesity without overeating and suggests that obesity linked to this gene could be modulated by careful dietary control,' said Professor Palmer, Chair of Pharmacogenomics in the Biomedical Research Institute at the University of Dundee.

'What it effectively shows is that the people with the relevant variants on the gene have a trait which may lead them to eat more unhealthy, fattening foods. I would stress that this is a trait, and not an absolute occurrence.

'The findings do not change the dietary and lifestyle advice to people, which would be to eat relatively healthily and take regular exercise. Doing this will still have a positive effect whether you carry this gene variant or not.

'But these findings do also reinforce the hypothesis that the increase in obesity seen in children over recent years may be largely attributable to the widespread availability of inexpensive and highly energy dense foods, which may be more attractive to the large proportion of the population who carry this genetic variant,' said Professor Palmer.

The results in the newly-published study are also consistent with studies in animals that have shown that feeding or fasting turns the expression of this gene on and off in the regions of the brain that are known to control eating behaviours.

Professor Palmer was part of the large group of scientists from around the UK that discovered the obesity gene, FTO, in 2007. They found that individuals carrying one copy of the variant (49% of the population) have an approximately 30% increased risk of obesity and individuals carrying two copies of the variant (14% of the population) have almost 70% increased risk of obesity. This effect has since been confirmed in many populations around the world.

Work has been continuing to further explore how the gene works.

'What we are doing with this work is debunking the old myths which are still often repeated in relation to obesity: ‘I have big bones’, or ‘I have a slow metabolism’, or indeed ‘it is in my genes’. While strong genetic effects have been found in extremely rare cases, most obesity is associated with rather weak genetic tendencies that are modifiable by diet and exercise,' said Professor Palmer.

'The genetics of obesity are complicated and it is likely that there are other genes which will have an effect. But we are now clearly seeing the effects of genetic variants like this one in FTO.'

NOTES TO EDITORS
Professor Palmer is available for interview.

The embargo terms are those of the New England Journal of Medicine and must be strictly adhered to.

A copy of the full paper, as published in the NEJM, is available, subject to the same embargo conditions.

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