Nutrition: The Owner's Manual

Leptin, secreted by fat cells, suppresses appetite. Leptin deficiency is associated with overeating in rats, but leptin supplements in humans have not led to the predicted appetite suppression. In a complex balance, the hypothalamus contains two opposing types of cells: NPY cells, which, when activated, stimulate appetite, and POMC cells, which suppress appetite. Both are constantly active, and the dominance of one or the other determines feeding urges. Leptin deficiency activates the NPY cells, which is why losing weight makes you hungry. This appears to be at least one aspect of the “set point” theory. The trick for researchers is to learn how to lose fat, and hence leptin, without in turn activating the NPY cells.

Food is more than physical nourishment—it forms the basis of bonding between mother and child and, according to recent research, between friends. Eating sets off two (at least) processes: oxytocin and cholecystokinin are released to the brain. We’ve known for a while that oxytocin was released during maternal nursing (and during sexual orgasm in both sexes, and in nest building, and in uterine contraction during childbirth, and in response to massage), thus helping to cement the bond between mother and child. But we now know that nursing and eating in general not only set off oxytocin, but also cholecystokinin, the latter of which sends a message from the intestine to the brain that says, “Food has now gotten where it needed to! Thanks, system, you’re working just fine.”

Chemical players that shut down appetite include enterostatin (produced by the stomach and pancreas in response to the ingestion of fat), serotonin, dopamine, cholecystokinin (CCK), and leptin (from the Greek leptos, “thin”), a protein produced by the newly discovered “obesity gene” on chromosome 6. After you’ve eaten, cholecystokinin is released in the intestines to tell the brain you’re full. Leptin tells the body whether to burn fat you’re eating or store it as fat.

At a spring 1998 meeting of the Society of Behavioral Medicine in New Orleans, Yale University researchers reported that high levels of cortisol are associated with high cravings for fatty snacks. When given a choice, high-cortisol snackers head for the nachos, low-cortisol snackers for lower-fat snacks. Cortisol levels are increased by stressful experiences

Two primary chemical actors head the complex cast of characters in the tense drama of appetite control: chemicals that trigger hunger and chemicals that trigger satiety. If these are in good order, much of the rest of one’s chemical makeup will have a minimal effect on appetite and weight control