Childhood Obesity Risk Increased 50 Percent by new Genetic Mutations, Says Study
News Jan 21, 2009
Three new genetic mutations that together can increase a very young child's risk of becoming obese by 50 percent are revealed in a new study, published in the journal Nature Genetics.
Together with existing research, the new findings should ultimately provide the tools to predict which young children are at risk of becoming obese. Health professionals could then intervene to help such children before they develop weight problems, say the researchers from Imperial College London, the French National Research Institute CNRS and other international institutions.
In the UK, one four or five year old in every ten is obese, according to the Department of Health's National Child Measurement Programme 2007/08.
For today's ten-year study, scientists looked at the genetic makeup of obese children under six and morbidly obese adults, most of whom had been obese since childhood or adolescence, and compared this with age matched people of normal weight. The study reveals three previously unidentified genetic variations that increase the risk of severe obesity significantly, giving new insight into the reasons why some people become obese and others do not.
The mutation most strongly associated with childhood obesity and adult morbid obesity in the study is located near the PTER gene, the function of which is not known. Children with this mutation, called rs10508503, have a 34.1% increased risk of obesity, while adults with the same mutation are 20.6% more likely to be morbidly obese, according to the research.
The second mutation associated with child and adult obesity, called rs1805081, is found in the NPC1 gene. Previous studies in mice have suggested that this gene has a role in controlling appetite, as mice with a non-functioning NPC1 gene suffer late-onset weight loss and have poor food intake. The mutation in this gene increases the risk of childhood obesity by 9.6% and of adult morbid obesity by 13.6%.
The final mutation, rs1424233, is found near the MAF gene, which controls the production of the hormones insulin and glucagon, as well as chains of amino acids called glucagon-like peptides. These hormones and peptides are known to play key roles in people's metabolisms by metabolizing glucose and carbohydrates in the body.
In addition, glucagon and glucagon-like peptides appear to have a strong effect on people's ability to feel 'full' or satiated after eating. Children with the rs1424233 mutation have a 5.7% increased risk of early-onset obesity and adults have a 16.1% increased risk of becoming morbidly obese.
The increased risk of obesity is additive, so adults with all three mutations have a 50.3% increased risk of being morbidly obese and children with all three mutations have a 49.4% increased risk of early onset obesity.
Professor Philippe Froguel, the corresponding author of the study from the Department of Genomic Medicine at Imperial College London, said: "When young children become obese, their lives can be affected in a very negative way. Sadly, obese children are often unfairly stigmatized and they can suffer heart and lung problems, painful joints, diabetes and cancer as they grow up.
"Understanding the genetic basis of obesity is the first step towards helping these children. Once we identify the genes responsible, we can develop ways to screen children to find out who is most at risk of becoming obese. Hopefully we can then intervene with measures such as behavioral therapy, to make sure a child forms healthy eating habits and does not develop a weight problem," added Professor Froguel.
The researchers reached their conclusions by conducting a genome-wide association study of 1,380 Europeans with early-onset childhood obesity and adult morbid obesity, and 1,416 age-matched normal weight controls. The study revealed 38 genetic markers with a strong association to a higher than normal body mass index, which the researchers evaluated in 14,186 Europeans, identifying three mutations that are significantly linked to obesity.
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