The obesity epidemic has become a major public health concern. The phenomenon is typically attributed to changes in diet and lifestyle, and socioeconomic factors like poverty and poor education.
Genetic factors have been known play a role as well, but a recent study by UK-based scientists suggests they play much more prominent role, at least in a subset of people who become morbidly obese at a young age.
In the study, Sadaf Farooqi of the University of Cambridge and colleagues showed that many such kids are missing a large chunk of DNA, known as SH2B1, from chromosome 16.
The missing genetic code had been known to play a role in regulating weight and blood sugar levels. Kids with the chromosomal abnormality tended to overeat on a massive scale, and gain weight easily.
To reach these conclusions, the scientists scanned the genomes of 300 morbidly obese kids in search of copy number variants (CNVs), which are lengthy strands of DNA that are either duplicated or missing.
The scientists compared their findings with information from healthy controls.
In their write-up, which appears in Nature, the scientists wrote, “we identified several rare copy number variants that were recurrent in patients but absent or at much lower prevalence in controls.”
“Part of chromosome 16 can be deleted in some families. People with this deletion have severe obesity from a young age,” Farooqi told Medical News Today: “One particular gene on chromosome 16 called SH2B1 plays a key role.”
The finding may have broad social implications, since it is common to blame parents or guardians for morbid obesity in kids. The scientists noted for example, that some kids in the study had been handed over to Social Services because their parents were assumed to have been deliberately overfeeding them.