Some children get severely obese because they lack particular chunks of DNA, which kicks their hunger into overdrive, researchers report.
The British researchers checked the DNA of 300 children who'd become very fat, on the order of 220 pounds by age 10. They looked for deletions or extra copies of DNA segments.
They found evidence that several rare deletions may promote obesity, including one kind they studied further and found in less than 1 percent of about 1,200 severely obese children.
That deletion, on chromosome 16, apparently causes trouble because it removes a gene that the brain needs to respond to the appetite-controlling hormone leptin, said Dr. Sadaf Farooqi of Cambridge University.
In her study, children with a chromosome 16 DNA deletion "have a very strong drive to eat," said Farooqi, who co-led the research. "They're very, very hungry, they always want to eat."
The work, reported online Sunday by the journal Nature, has already produced a real-world payoff. Farooqi said four children with the chromosome 16 deletion had drawn the attention of British child welfare authorities, who blamed the parents for overfeeding them.
"We were able to intervene" and get the parents of two children off the hook, and the other two cases are under discussion, she said.
That's happened before when the scientists uncovered genetic causes for severe childhood obesity, she said, ABC News informs.
Scientists at Cambridge University found that certain types of genetic mutation were present in those suffering from severe obesity.
"This is the first evidence that copy number variants have been linked to a metabolic condition such as obesity," said Dr Matt Hurles from the Wellcome Trust Sanger Institute, one of the leaders of the study.
Dr Sadaf Farooqi from Cambridge University added: "This study shows that severe obesity is a serious medical issue that deserves scientific investigation.
"It adds to the growing weight of evidence that a wide range of genetic variants can produce a strong drive to eat, Telegraph.co.uk informs.
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