The discovery, noted in tomorrow's edition of The New England Journal of Medicine, may eventually lead to new targets for obesity drugs. But it doesn't mean that obesity is all about genetics -- lifestyle still counts.
The new report links gaps in the BDNF gene to greater likelihood of obesity, at least in children with a rare genetic disorder called the WAGR syndrome, which includes a certain type of kidney tumor, no iris in the eye, genitourinary problems, and mental retardation.
The researchers -- who included Joan Han, MD, of the Eunice Kennedy Shriver National Institute of Child Health and Human Development -- studied 33 children (average age: 11) with WAGR syndrome.
Most people have two copies of the BDNF gene. But 19 of the patients in Han's study -- 58% -- were missing part or all of one of their BDNF copies. That left them with low levels of a brain chemical called brain-derived neurotrophic factor (BDNF), which is made by the BDNF gene.
All of the patients with gaps in their BDNF gene were obese by age 10, compared with 20% of patients with intact BDNF genes.
Those findings don't prove that the BDNF gene gaps caused obesity. But the researchers note that BDNF may help regulate energy (calorie) intake, based on studies in animals.
Further studies are needed in people, but the BDNF gene "may have potential for the treatment of obesity," states an editorial published with the study.
BDNF isn't the only gene involved in obesity; additional obesity genes "should be revealed soon, opening new avenues for prevention and clinical care," write the editorialists, who included Philippe Froguel, MD, PhD, chairman of the department of genomic medicine at Imperial College London's Hammersmith Hospital.
They note that intersection of genetic vulnerability and the "current Western lifestyle" may make certain people "particularly susceptible to weight gain." In other words, it's not just about the genes, or just about diet and activity, but the combination of all those factors.