Gene could be to blame for obesity

A common gene variant found in 16% of the population could be largely responsible for exploding rates of obesity, it has been revealed.

A common gene variant found in 16% of the population could be largely responsible for exploding rates of obesity, it has been revealed.

People with two copies of the gene are almost 70% more at risk of being obese than those having none, and three kilograms heavier on average.

Although the gene mutation only accounts for a modest weight increase, scientists believe it can tip the scales and lead to obesity in an already heavy population.

Obesity rates in the UK, where the research was carried out, have more than tripled since the 1980s. Around one in five adults is obese and more than half either obese or overweight – almost 24 million people.

By 2010 a third of all men and 28% of women in England will be obese, according to figures from the British Department of Health.

Obesity is defined by a Body Mass Index (BMI), a measurement relating weight and height, of 30 and over. People who are overweight have a BMI that is between 25 and 30.

The new findings are the first to identify a common, population-wide genetic link to obesity.

Experts hope the discovery will help them tackle rising levels of obesity, and the associated risk of type two diabetes. It might also point towards new drug treatments that stop people becoming grossly overweight.

Obesity greatly increases the risk of heart disease and diabetes, and has also been linked with cancer.

Each year it causes tens of thousands of premature deaths and costs the country an estimated £7 billion.

The obesity gene was identified by a population-wide screening study led by scientists from the Peninsula Medical School in Exeter and the University of Oxford.

DNA samples from more than 38,500 people from across the UK and Finland showed a strong association between a particular variation of a gene called FTO and obesity.

Genes come in pairs, and individuals carrying one copy of the FTO mutation were found to have a 30% higher risk of being obese than those with no copies.

The increased risk rose to 67% for people who had two copies of the gene variant. About one in six white Europeans have both copies.

Professor Andrew Hattersley, from the Peninsular Medical School, who led the research published yesterday in the journal Science, said: “As a nation, we are eating more but doing less exercise, and so the average weight is increasing, but within the population some people seem to put on more weight than others.

“Our findings suggest a possible answer to someone who might ask: ’I eat the same and do as much exercise as my friend next door, so why am I fatter?’ There is clearly a component to obesity that is genetic.”

The association between the FTO variant and obesity was seen in all age groups above seven years.

What the gene does and why it is linked obesity is still a mystery. One possibility is that it is merely a “marker” for other genes, inherited at the same time, which are genuinely responsible for excessive weight gain.

Co-author Professor Mark McCarthy, from the University of Oxford, said: “Even though we have yet to fully understand the role played by the FTO gene in obesity, our findings are a source of great excitement.

“By identifying this genetic link, it should be possible to improve our understanding of why some people are more obese, with all the associated implications such as increased risk of diabetes and heart disease.

“New scientific insights will hopefully pave the way for us to explore novel ways of treating this condition.”

The study was funded by the Wellcome Trust charity which is conducting one of the biggest searches ever undertaken for the genetic links to important diseases.

The Wellcome Trust Case Control Consortium programme played a major role in the new research.

Dr Mark Walport, director of the Wellcome Trust, said: “Obesity is one of the most challenging problems for public health in the UK.

“The discovery of a gene that influences the development of obesity in the general population provides a new tool for understanding how some people appear to gain weight more easily than others.

“This discovery, along with further results expected from the Wellcome Trust Case Control Consortium later this year, will open up a wealth of new avenues to understand and treat common diseases.”

Douglas Smallwood, chief executive of Diabetes UK, which also contributed to the study, said: “The discovery of a gene linked to obesity could open the door for new research into type two diabetes.

“Although type 2 diabetes can be genetic, being overweight is a leading factor in the development of the condition. If we can tackle obesity then we can make real in-roads into fighting type two diabetes and reducing the number of people living with the condition.

“Even though obesity may be genetic, it is vital that people who are overweight eat a well-balanced diet and take regular physical activity to reduce their chances of developing type 2 diabetes. It is important to note that obesity can not be attributed to genes in every case.”

Dr Susan Jebb, of the Medical Research Council Human Nutrition Research unit in Cambridge, said: “We have known for some time that there is a genetic susceptibility to obesity and some people are at greater risk of gaining weight than others.

“This research provides clear evidence of a biological mechanism which makes some people more susceptible to gaining weight in a world where food is plentiful and sedentary lifestyles the norm.

“By studying the action of this gene we may learn more about the detailed causes of obesity.

“People carrying a single copy of this gene are on average likely to be 1kg heavier than people who do not carry the gene and people with two copies are on average almost 3kg heavier.

“This is not a big difference, but, importantly, people who know they are carriers may be more motivated to adopt a prudent diet and healthy lifestyle to decrease their risk.

“Obesity is a complex disorder and there is no evidence from this research to suggest that carriers of the gene will not successfully lose weight by decreasing their energy intake and becoming more active.”

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