Genetic mutations linked to childhood obesity
Scientists identify four DNA variations which may explain why some children become obese
Steve Connor is the Science Editor of The Independent. He has won many awards for his journalism, including five-times winner of the prestigious British science writers’ award; the David Perlman Award of the American Geophysical Union; twice commended as specialist journalist of the year in the UK Press Awards; UK health journalist of the year and a special merit award of the European School of Oncology for his investigative journalism. He has a degree in zoology from the University of Oxford and has a special interest in genetics and medical science, human evolution and origins, climate change and the environment.
Sunday 07 April 2013
The rise in the number of overweight children in Britain may be as much to do with their genes as their diet and exercise levels, according to a study that has identified a handful of genetic mutations linked with childhood obesity.
Scientists have discovered that children with the most severe kinds of obesity are more likely than other children to have one or more of four genetic variations in their DNA, which could influence such things as appetite and food metabolism.
The discovery is part of a wider search for the genes involved in increasing a person’s risk of becoming overweight when exposed to an “obesogenic environment” of high-calorie food and inactivity – which is known to affect some people more than others.
The study looked at 1,000 children with the most severe form of early-onset obesity, which is highly likely to result in obesity in adulthood. Some of the 10-year-olds in the study weighed between 80kg and 100kg (12.5st-15.7st).
Some of the genetic variations revealed by the study were rare but others are relatively common, suggesting an interaction between genetics and environment, which could explain why certain children become obese while others do not even when they share a similar upbringing.
Obesity among British children aged between two and ten has risen since 1995 from 10.1 per cent to 13.9 per cent in 2011. This rise cannot be due to a change in genes alone, because it takes many generations to alter the frequency of genetic mutations in the population.
However, it is clear that some children are predisposed to become obese when exposed to a high-calorie diet and lack of exercise. It is this genetic predisposition that scientists are trying to understand.
Professor Sadaf Farooqi of Cambridge University said: “Some children will be obese because they have severe mutations, but our research indicates that some may have a combination of severe mutations and milder-acting variants that in combination contribute to their obesity.
“As we uncover more and more variants and genetic links, we will gain a better understanding of obesity which in turn will open doors to areas of clinically relevant research.”
The latest study, published in the journal Nature Genetics and funded by the Wellcome Trust, identified four new genetic variants linked with severe childhood obesity. This brings the list of DNA variants associated with obesity to just over 50.
Professor Farooqi said: “There have always been some kids who are very heavy but this has in the past been a small number. Now, because of the environment they are growing up in, we are seeing many more children in this category.”
Some of the genetic variations linked with obesity are associated with genes involved in regulating leptin, a hormone known to act as an appetite suppressor. Variations of a gene known as FTO, for instance, are thought to increase the chances of obesity because of the gene’s effect on leptin levels in the body.
Eleanor Wheeler of the Wellcome Trust Sanger Institute in Cambridge, the lead author of the study, said: “We’ve known for a long time that changes to our genes can increase our risk of obesity. For example the gene FTO has been unequivocally associated with body-mass index, obesity and obesity related traits.
“In our study of severely obese children, we found that variations in or near two of the newly associated genes seem to have a comparable or greater effect on obesity than the FTO gene.”
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