The Secret of Feeling Full

Monday, Aug. 19, 2002 By CHRISTINE GORMAN

Article Tools

Reprints

It sounds like a weight watcher's dream come true: a simple hormone, long thought to play an obscure function in the pancreas, turns out instead to be a powerful appetite suppressant--the body's way of telling the brain it's time to push the plate away. If a pharmaceutical company could put it in a pill and sell it at the drugstore, you might, just might, never again have to count calories or wrestle with your willpower. Just pop one of these things before a meal, and your stomach says--entirely on its own--"No, thank you, I've had quite enough."

The scientific name for this remarkable substance is PYY3-36, or PYY for short, but the researchers who discovered its new function have dubbed it, appropriately enough, the fullness hormone. "If you give it prior to a meal, it switches off the appetite," says Dr. Stephen Bloom, an endocrinologist at Hammersmith Hospital in London. "PYY is what makes you less hungry after a meal."

But don't break out the cartons of Ben & Jerry's just yet. For one thing, the research reported in Nature last week was just a modest first step. A dozen volunteers in London were injected at various times with either the hormone or a placebo. Then they were led to an Indian-food buffet and invited to pack away all they could eat. Result: while on PYY, the grazers voluntarily consumed one-third fewer calories.

But getting results like this under lab conditions and making a drug that's safe and effective are two very different matters. For one thing, nobody is going to brave a hypodermic needle just to avoid eating a third helping of tandoori chicken; yet if you put PYY in a simple pill, it will quickly be destroyed by stomach acids. For another, nobody knows what the side effects of ingesting this hormone for months or years might be. It's quite possible, as with so many other biologically active substances, that the body will quickly build a tolerance to any excess PYY, rendering it ineffective.

After all, we have been down this road before. When scientists reported in the mid-1990s that the absence of a hormone called leptin triggered the development of some very fat mice, it seemed that a cure for obesity was finally at hand. If these fat mice didn't make enough leptin, the reasoning went, then maybe fat people didn't make enough either. Would giving them leptin make them thin? The logic was so compelling that the pharmaceuticals firm Amgen reportedly paid tens of millions of dollars for development rights. It turned out, however, that most fat people--and fat mice--produce plenty of leptin. Their bodies, for reasons that are poorly understood, just aren't very sensitive to its effects.

Even if PYY proves to be no miracle, it sheds light on how hunger works, and this comes at a time when Americans seem to be particularly confused about what makes us fat. The old arguments--is it too much fat, too many carbohydrates or too many calories?--were stirred up once again last month by an article in the New York Times Magazine suggesting that low-fat diets may be making us fatter. While the new information about PYY won't help you choose between a high-protein or low-fat diet, it goes a long way toward explaining how the brain and the digestive system conspire to keep the pounds on.