Nevertheless, the study itself is a tour de force because the researchers used a combination of modern techniques, including experimenting on both human and mouse cells as well as taking advantage of publicly available data, to figure out the inner workings of the FTO gene. It turns out that all of us have various “colors” of fat cells. White fat cells tend to store energy. Brown fat burns it. A version of white fat cells, called beige fat, works more like brown fat in its ability to burn energy. In the study, cells from people and mice with the obesity-prone version of the FTO gene preferentially shunted the precursors of fat cells to developing into white rather than beige fat.
Responding to these results, Clifford Rosen, an editor at NEJM who wrote an accompanying editorial, said, “A lot of people think the obesity epidemic is all about eating too much but our fat cells play a role in how food gets used… you now have a pathway for drugs that can make those fat cells work differently.” While we surely need effective and safe weight-loss medicines, this statement is perilous because some people will infer that food intake is irrelevant. Even among people with more obesogenic gene types, however, better eating and physical activity are fruitful.
Another important lesson can get lost in the shiny promise of “new pathway, new drugs.” Unraveling the underlying machinery of FTO could lead us to something more profound: non-pharmaceutical ways to prevent this machinery from turning on in the first place during early human development. Treating obesity will always be hard. Early life prevention holds promise for avoiding the need for treatment later on.