The most horrifying news story I’ve read this spring wasn’t about terrorism or war but about a hormone called leptin, known for its role in regulating appetite and metabolism. Since its discovery in 1994, leptin has become the holy grail of anti-obesity crusaders, a miraculous substance that could suppress appetite at the source: in the brain. In this society, anything’s better than being fat.
Leptin’s superhero status was enhanced last year when a study in the American Journal of Physiology showed that infant rats who were fed lots of leptin never got fat or developed diabetes, no matter how much fat they ate. The idea, explained one of the study’s researchers, was to change the way the body uses and stores energy. In utero and/or early exposure to leptin apparently makes the body metabolically inefficient—not just for a little while but for good.
This finding made leptin the A-bomb of the War on Fat, at least according to a group of researchers at the University of Buckingham. They’re developing a line of baby foods and formula laced with leptin. The goal: to make children thin for life.
Before you start cheering, remember fen-phen, the miracle drug that was supposed to make people thin? It damaged their hearts, and has inspired thousands of lawsuits, many still ongoing 10 years later.
Even if leptin-laced formula does what it’s supposed to, even if there are no immediate negative side effects, it’s still a worrisome proposition. The nifty little feedback loop we call metabolism serves us well. Human beings are designed to get hungry and eat. It’s a matter of survival.
Witness what happens when the link between appetite and behavior weakens or breaks. My husband and I watched our 14-year-old daughter nearly starve to death after developing anorexia. For two long years, she never felt hungry. She was hungry, of course; many of the behaviors associated with the illness—obsession with cooking, cutting food into tiny bites, pouring mustard on everything—proclaimed this appetite, despite the fact that she herself didn’t feel hunger pangs. But the connection between her brain and her body had been disrupted by the illness.
For my daughter, recovery from anorexia meant gaining quite a bit of weight. What if she’d been a leptin baby, her metabolism engineered to make weight gain difficult or impossible? No matter how many calories a day we fed her, she might not have survived. Some researchers believe that breakdowns in leptin regulation and processing might be part of what causes anorexia in the first place. Certainly an important step in my daughter’s recovery has been learning to recognize feelings of hunger and fullness again—feelings she would never have access to, if the Birmingham researchers have their way.
As a recent UCLA study showed, 98 percent of diets fail, causing a rebound effect that winds up making people fatter. Ditto the no-fat craze of the 1980s, which may well have something to do with the current rise in obesity.
No matter how well-intentioned, our attempts to micro-manage our metabolisms usually cause more harm than good. Better to teach kids to eat when they’re hungry and stop when they’re full, and to accept the fact that humans come in different shapes and sizes, than to mess up the next generation’s neurochemistry in the name of thinness.