Feedback
Health

Study Explains Why Your Brain Makes You Snack

Image: Energy bars

Does these snacks make your mouth water? Your brain may be tricking you. Getty Images

You've tried every diet. You know to never eat standing at the fridge, you know to cut back on sugar, fat and other calorie-dense foods. You know to only eat when you are hungry and to stop when you're full.

But people are still driven to snack - even when they aren't hungry any more. It's fueling the obesity epidemic and helps explain why virtually every diet fails and why two-thirds of Americans are overweight or obese.

Now, researchers may have found one little piece of the puzzle. It turns out your brain may have a system for making you want to snack.

There's a whole class of neurons that motivate animals to eat.

The tests are done in mice, and humans almost certainly have more complex brain systems controlling appetite and eating behavior. Nonetheless, the findings could provide important clues about why people overeat.

Two separate teams of researchers have identified the brain systems that might motivate animals - including people - to eat even if they're not really hungry.

One team at the Howard Hughes Medical Institute's Janelia Research Campus found a batch of brain cells called AGRP neurons that seemed to send an annoying signal until they were shut off. Mice could shut these neurons off by eating, but also by seeing food, or even by going to a place where they had found food before, the team reports in the journal Nature.

"We suspect that these neurons are a very old motivational system to force an animal to satisfy its physiological needs. Part of the motivation for seeking food is to shut these neurons off," Scott Sternson, a group leader at Janelia, said in a statement.

They found a similar group of neurons called the subfornical organ or SFO neurons that controlled drinking behavior.

"There's a similar motivational quality to hunger and thirst," Sternson says. "You want them to end."

A second team at Beth Israel Deaconess Medical Center and the National Institute of Diabetes and Digestive and Kidney Diseases made similar findings.

"When these AGRP neurons are 'turned on,' either by fasting or by artificial means, laboratory animals eat voraciously," said Dr. Bradford Lowell of Beth Israel Deaconess, who helped lead the study.

Lowell says the AGRP neurons sense the low energy reserves, activate, and release brain-signalling chemicals called neurotransmitters that shut off brain cells that make an animal feel full.

And they think they found a way to turn off the circuit.

"One reason that dieting is so difficult is because of the unpleasant sensation arising from a persistent hunger drive," said Lowell. "Our results show that the artificial activation of this particular brain circuit is pleasurable and can reduce feeding in mice, essentially resulting in the same outcome as dieting but without the chronic feeling of hunger."

While tasty food and hunger both drive animals to eat, Lowell says there's another mechanism, also. "There is a major hypothesis called 'Drive Reduction' that proposes that you eat to get rid of the unpleasant feeling of hunger," he said.

His team genetically engineered mice that had this system turned on, and whose brains were also altered so that a blue light activated nerve cells that 'told' the mice they had eaten. Normal mice moved around a cage system randomly, but the genetically engineered mice sought out a little room where the blue light turned off their hunger drive, they report int he journal Nature Neuroscience.

"Our findings suggest that the therapeutic targeting of these cells may reduce both food consumption and the aversive sensations of hunger - and therefore may be an effective treatment for obesity," Lowell said.

Obviously, it's not possible to genetically engineer people in the same way as mice, but it might be possible to find a drug that activates the same switches.