International researchers have found that common childhood obesity has a genetic component apart from the usual causes like overindulgence and inactivity.
The team of researchers used genome-wide association techniques and found that several genetic variants associated with adult obesity are also active in childhood obesity, according to Struan Grant of the Children's Hospital of Philadelphia and colleagues. The analysis found two new genetic variants that had not been previously associated with obesity, Grant and colleagues reported online in Nature Genetics. The findings show that “there is indeed a genetic signature of childhood obesity,” Grant said. “It's not purely lifestyle.”
He cautioned that human genetics have not changed in the past few decades, during which childhood obesity has increased markedly, implying that the well-known environmental suspects of fast food and sedentary lifestyle also play a role. One of the next steps for the researchers, Grant said, is to try to “tease out the gene-environment interaction.”
Several genetic variants have been linked to adult obesity and a genetic underpinning is known for several syndromes that involve obesity, the researchers noted. But little is known about genetic influences on childhood obesity, they said. To help fill the gap, they conducted an analysis of 14 cohorts that had data from genome-wide association studies involving a total of 5,530 children. The participants body mass index (BMI) was at or above the 95th percentile and there were 8,318 controls with a BMI below the 50th percentile.
That analysis turned up seven genetic regions associated with obesity, all previously known from adult studies. “Some adult genes clearly impact early on in life,” Grant said. But when the researchers relaxed the significance level by a factor of 100, they turned up eight new signals. Grant and colleagues tested the eight new signals in nine independent data sets, including 2,818 cases and 4,083 controls, and found two signals that reached genome-wide significance.
Grant said one advantage of studying children, rather than adults, is that long-term confounders -- such as a lifetime of overeating - have less time to obscure genetic links. He said that studies in adults have needed data from hundreds of thousands of participants in order to find signals, while he and colleagues had only about 21,000 volunteers. And when the researchers went back to look at an adult cohort, the 123,864-strong participants in the GIANT Consortium, they found that both of their new signals were present. “They were there, but they were not as strong as in the kids,” Grant said.
Keith-Thomas Ayoob of Albert Einstein College of Medicine in New York City, who was not part of the study, said this study increases scientific knowledge about obesity but the clinical picture is unchanged. “We may know more about childhood obesity, but until there's a magic bullet, the treatment will be the same,” Ayoob said. “Kids still need to have better diets and they really need to be more active.”
“Obesity is the result of a complex interplay among biological, behavioral, cultural, environmental and economic factors,” said Karen Winer, a program director at the Eunice Kennedy Shriver National Institute of Child Health and Human Development, part of the National Institutes of Health, which helped fund the new study. “Obesity is recognized as a highly heritable condition, but the underlying genetic factors associated with common obesity, until today, have remained a mystery,” she said.
Ruth Loos, director of the Genetics of Obesity and Related Metabolic Traits Program at Mount Sinai School of Medicine in New York, was not involved in this study but says this research, like previous work, “shows that the genetic susceptibility to obesity begins at an early age. However, this does not mean that those who are genetically susceptible are destined to become obese adults, because a healthy lifestyle remains an important factor that can reduce one's genetic susceptibility.” This study suggests “that trying to fight this genetic susceptibility should start early in life,” Loos said.
She said gene research may provide insight into the biological pathways that contribute to obesity. “If some of these genes turn out to be drug-able targets, then maybe this could lead to new medication. But that is indeed years away, it will require much more detailed physiological research,” Loos said.
Further research to identify the mechanism of action might lead to better understanding of obesity, Grant said. “We're going to continue to look for more genes, and the more information we get, the more accurately we will eventually make lifestyle decisions for children based on their genetic makeup,” Grant said. “This is giving us new insights to the biology of obesity, which could potentially one day lead to both more efficient medications and more specific diet and exercise advice for kids who are genetically predisposed to obesity.”
Currently, about a third of kids are obese or overweight. Roughly 17% of children and adolescents ages 2 to 19 are obese. Children are considered obese if they are in the 95th percentile or above, based on standard national pediatric growth charts.
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