Why Can’t We Stop Eating? Rats Can Develop ‘Immunity’ to Fat

PULLMAN, Wash. — When you see a picture of a grizzly bear in the fall, round and ready for hibernation, you probably think you’re looking at one fat animal. You are, but . . .
“There’s a good chance that you are as fat as that bear,” says Robert Ritter, a professor in the Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology at Washington State University. According to the National Institutes of Health, about 33 percent of us are overweight and 34 million of us are obese. By hibernation time, that bear may be about 40 percent fat. However, according to Caroline M. Pond, an internationally known expert on obesity, even a lean, non-obese human female in her 50s may be as much as 38 percent fat.
Granted, bears are not an accurate standard for human fitness. However, says Ritter, “Something seems to have gone wrong with our ability to control our eating.” The internal signals that tell us we’re feeling full and should stop eating don’t seem to be working.
Why? It may be because the world we live in is not the same as the world we evolved in, at least as far as food is concerned. Most of our evolutionary development has been through times when food was not consistently available. When it was, people feasted and stored the energy so that they might survive the periods when it was not.
“Now high calorie foods are always available,” says Ritter, especially food that is high in fat.
Normally, a variety of signals contribute to feelings of satiation, of being full. They include signals that depend on the amount of each type of major nutrient that’s been eaten, whether it’s sugar, protein or fat. They also include signals that are the result of the stomach being stretched as it fills with food.
Ritter put together our collective weight and our high fat diets and asked, “Is there a connection?” If we eat a high fat diet, does our body lose its ability to become satiated by fat?
For rats, the answer appears to be “yes.” Mihai Covasa, a research assistant professor in Ritter’s lab, has found that after rats adapt to a high fat diet, fat has only half its usual ability to make the rats feel satiated. Scientists in England have found a similar effect in humans.
While the mechanism for this change is not yet known, it may involve a molecule Ritter has worked with for much of his scientific career, cholecystokinin or CCK. CCK is a hormone that is released from cells in the small intestine in response to the presence of fat or protein. It activates sensory nerves that connect the gut with the brain and ultimately results in a reduction of the amount of food eaten at the meal currently being consumed.
Covasa has found that the rats on the high fat diet secrete ample CCK, but their brains do not respond to it as well as the brains of rats on low fat diets. He and Ritter also have found that the rats on the high fat diets have a normal response to sugar in the diet, suggesting that specific controls relating to fat are involved in the change. Future experiments should explain how this happens as well as how other processes are involved in the decreased response to dietary fat.
But one of Ritter and Covasa’s most interesting results, though still preliminary, suggests that if the rats eat a high fat diet that is also high in fiber, they do not gain weight. If they eat a high fat diet that is low in fiber, they gain weight.
The bottom line may be that what we already know is true: We’re more likely to do well if we eat a varied diet. This translates into eating a diet that can turn on a variety of signals that tell us it’s time to stop.