Eating when you're not hungry--especially high-calorie, high-fat foods--may not always rise to the newly broadened clinical definition of an eating disorder. But the behavior that for many Americans is a routine pastime certainly contributes to excess weight gain, with its implications for health. And it is considered "disordered eating" by most mental health professionals.
A study published Thursday in the journal Science adds to evidence that binge eating--and overeating generally--may have a biological basis. The new research, conducted on mice, suggests a target in the brain that drug developers should consider in exploring treatments for such disordered eating.
Not surprisingly, researchers focused their attention on the hypothalamus, one of the brain's most primitive structures, a key node in the brain circuitry that drives us to eat and drink, to seek out sexual partners, and generally to crave more of what makes us feel good. From its seat in the brain's deepest recesses, the lateral hypothalamus is lashed up to the amygdala, where basic, powerful emotions such as fear, anger and love are processed.
As part of the limbic system, these structures evolved early in the rise of mammals to ensure that the necessities for survival and reproduction got top billing in behavior.
In the 1960s, neuroscientists electrically stimulated the lateral hypothalamus and saw that it played a key role in feeding behavior, and in the reinforcement of feeding behavior. But how it did that remained a mystery.
To explore how the lateral hypothalamus governs eating behavior, a group of researchers from the University of North Carolina used mice and a relatively new technique: To discern how certain cells work, they genetically engineered the cells to respond to light; then, they turned those cells on and off, essentially, with a miniature flashlight, and watched the resulting behavior.
The researchers applied the on-off treatment to a group of cells in the amygdala and their projections into the lateral hypothalamus. They hypothesized that the cells, called the bed nucleus of the stria terminalis, interact with the hypothalamus to regulate eating.
Sure enough, when they "turned on" these unique cells in mice who were well fed, the result was rapid and striking: The animals immediately launched into "voracious feeding behavior." And the mice clearly enjoyed the impulse to pig out: They showed a clear preference for being in the space they associated with having the cells turned on.
Moreover, given the choice, the animals made a beeline to high-fat, high-calorie foods.
The trick worked more dramatically when the mice's food was restricted and they were then allowed to eat at will. But even when the mice were well fed, those with the targeted cells turned on continued to eat well after they would have been filled up.
Research has suggested that stress, genes and environmental factors, such as the ubiquity of high-calorie, high-fat foods, all may trigger overeating. But if future therapies aim to fortify the vulnerable against those triggers, they might well focus on the special cells targeted here, the researchers said.
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