A team at the University of Dundee in the UK conducted an eating test with 100 schoolchildren aged between 4 and 10 and found that the children with the common variant of the ‘obesity gene’ FTO consumed an extra 100 calories per meal, and chose to eat food types that contained higher levels of sugar and fats than other options.
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 that the gene had no impact on metabolic rates or measures of physical activity, and there was 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 doesn’t 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, 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.”
Published in 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.
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