You probably know the feeling of having a hearty meal at a restaurant, and feeling full and satisfied … only to take a peek at the dessert menu and decide the cheesecake looks just irresistible.
So why is it that you just absolutely couldn’t have another bite, but you somehow make an exception for a sweet treat? Or as Jerry Seinfeld might put it back in the day “Whhaaaat’s the deal with dessert?!”
Scientists now have a better understanding of the neural origins of this urge thanks to a recent study published in the journal Science.
Working with mice, researchers tried to set up a scenario similar to the human experience described above. They started by offering a standard chow diet to mice who hadn’t eaten since the previous day. That “meal” period lasted for 90 minutes, and the mice ate until they couldn’t eat any more.
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Then it was time for a 30-minute “dessert” period. The first round of the experiment, researchers offered mice more chow for dessert, and the mice ate just a little bit more.
The second time around, during the “dessert” period, they offered a high sugar feed to the mice for 30 minutes. The mice really went for the sugary feed, consuming six times more calories than when they had regular chow for dessert.
In the mice, researchers monitored the activity of neurons that are associated with feelings of fullness, called POMC neurons. They’re located in a part of the brain called the hypothalamus, which is “very important for promoting satiety,” says Henning Fenselau, one of the study authors and a researcher at the Max Planck Institute for Metabolism Research in Cologne, Germany.
The scientists found that when the mice were eating the high sugar diet, the neurons released beta-endorphin, an endogenous opioid — one generated within your body. This chemical bonded to opioid receptors in the mice’s brains and triggered a feeling of reward.
“When we taste something sweet, it’s not just the sugar we’re consuming — it’s triggering a system in the brain that associates that sweet taste with pleasure, which makes us want to keep eating,” says Dr. Paule Joseph, a researcher who studies metabolism at the National Institutes of Health and was not associated with the study.
When the team then blocked this opioid pathway, the mice stayed away from the sugar.
The researchers found the same neural mechanism in humans when studying donated brain tissue and scanning the brains of volunteers, who sat in an fMRI machine and were fed a sugar solution through a tube.
This led the scientists to conclude, says Fenselau, that in humans like in mice “the opiate action in this part of the brain drives that consumption of high-sugar containing foods.”
Fenselau says the results suggest that people’s brains evolved to love sugar in excess.
Other research has found a link between sugar consumption and the dopamine system in our brain; some research even suggests sugar’s effect on the brain in the long-run can be similar to addictive drugs.
The study at the Max Plank Institute was short-term — researchers didn’t keep the diet going over time to see if the mice gained weight or experienced other metabolic changes.
Joseph says a follow-up study, “to look at how these circuits function over the long term, particularly with chronic sugar exposure,” could be important to understanding the development of compulsive sugar consumption.
Fenselau says studying this neural reward pathway further could shed light on how sugar overconsumption may contribute to the development of obesity.
So could a weight loss medication that blocks opiate receptors along with suppressing appetite be effective? There is one such product on the market, naltrexone bupropion, sold in the U.S. under the brand name Contrave. It’s a combination of bupropion, an antidepressant that can also suppress appetite, and the opioid-blocker naltrexone, which is often prescribed on its own to treat addiction.
But it’s not as effective as the newer weight loss drugs like Ozempic and Wegovy, says Fenselau.
This story originally appeared on NPR’s Short Wave. Listen here.
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