Common childhood obesity -- the kind we usually blame on overindulgence and inactivity -- also has a genetic component, an international collaboration of researchers has concluded.
Using genome-wide association techniques, the researchers showed 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.
As well, the analysis found two new genetic variants that had not been previously associated with obesity, Struan and colleagues reported online in Nature Genetics.
The findings show that "there is indeed a genetic signature of childhood obesity," Grant told MedPage Today. "It's not purely lifestyle."
But he noted 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."
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While the findings increase scientific knowledge about obesity, the clinical picture is unchanged, commented Keith-Thomas Ayoob of Albert Einstein College of Medicine in New York City, who was not part of the study.
"We may know more about childhood obesity, but until there's a magic bullet, the treatment will be the same," Ayoob said in an email to ABC News/MedPage Today. "Kids still need to have better diets and they really need to be more active."
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.
One research implication of the findings, he said, is that it might help identify new pieces of the obesity puzzle. For instance, neither of the new regions has been implicated in obesity before, Grant said, and little is known about them, other than that they both act in the gut.
Research to identify the mechanism of action might lead to better understanding of obesity, he said.