A Chinese worker sat in front of a huge billboard advertising the opening of a fast food restaurant in Shanghai.
A Chinese worker sat in front of a huge billboard advertising the opening of a fast food restaurant in Shanghai.PHILIPPE LOPEZ/AFP/Getty Images

We’ve all been there. What starts as a handful of chips or a spoonful of ice cream ends with an empty container and dread of the bathroom scale. But what it is it about overeating that makes even the most disciplined person occasionally lose control?

For years, researchers have been probing the possibility that obesity and addiction overlap, with emerging evidence suggesting that the same reward circuits in the brain that are activated by drugs also respond to calories. Obese people, the thinking goes, may overindulge because their brains’ reward circuitry, which responds to the pleasure of eating, is out of whack.


Now, Yale University researchers have found evidence that high-fat foods have the ability to alter and interfere with the reward circuitry in the brain -- and that injecting a particular molecule can restore the normal reward response in the brain. Administering that molecule can cause mice to find a low-fat meal satisfying.

“The idea is that if the brain adapts to a drug or calories in such a way that your reward response is deficient, then these individuals would need to consume more of the same,” said Ivan de Araujo, a professor of psychiatry at Yale University School of Medicine, who led the study published in the journal Science. “When the reward system is weak, you do more to obtain the same reward.”

In the research published Thursday, researchers wanted to first test how calories from high-fat food activated reward circuits in the brain, independent of the pleasure animals experience from tasting and smelling food. They used a catheter to infuse high- and low-fat foods directly into the animals’ guts, and found that the high-fat calories caused deficient responses in the brains’ reward circuitry.

Then, they tried injecting a molecule called oleoylethanolamine into mice, and found that they could restore normal levels in the brain of the chemical messenger, dopamine, that signals reward. Mice given the molecule were also able to find low-fat meals more appetizing.


Now, they hope to monitor the brain activity of human subjects using imaging scans, to see if they can detect altered brain activity that can then be reversed through a similar treatment. They are also interested in studying whether some of bariatric surgery’s positive effects may be explained by alteration of this brain-gut signaling pathway. They have yet to study whether other components of diet, such as sugar, act through the same mechanism.

Dr. Nora Volkow, director of the National Institute on Drug Abuse, who was not involved in the research, said it was a fascinating elucidation of the ways in which a peripheral organ is linked to the reward pathways in the brain. She said that a multitude of signals that promote eating or fullness all appear to work by triggering the brain’s reward system -- the same one that is activated by drugs.

“What has been surprising is that there’s been such a reticence to recognize this,” Volkow said. “You have different levels of severity. ... I lose control once in awhile with candies or with chocolate -- it does not mean I am addicted. Drugs activate and hijack the neurocircuitry that is in our brain to respond to natural rewards like food.”

Carolyn Y. Johnson can be reached at cjohnson@globe.com. Follow her on Twitter @carolynyjohnson.