Why You Always Have Room for Dessert, According to Science

Ever had a meal so large you thought you’d burst, only to hear those magical words, “Would you like to see the dessert menu?” and respond, “Yes, yes I would.” People often joke about having a “second stomach” that’s just for dessert, and it turns out that’s not too far from the truth.

In February, researchers from the Max Planck Institute for Metabolism Research in Cologne, Germany, published a new report in the journal Science that examined the effects of sugar consumption after we already feel full. They discovered that hypothalamic pro-opiomelanocortin (POMC) neurons in the hypothalamus — the part of the brain that regulates our hormones and creates feelings of hunger, thirst, sleepiness, and a sense of fullness after eating—are responsible for this effect. 

It’s all thanks to our neurons

“We discovered that POMC neurons not only promote satiety in fed conditions but concomitantly switch on sugar appetite, which drives overconsumption,” the researchers explained. 

In simple terms, the Institute explained that the same nerve cells that make us feel full also trigger our cravings for sweets afterward. In fact, they noted that even the “mere perception” of having sweets releases the “opiate ß-endorphin, which makes evolutionary sense because sugar provides quick energy” — and this is true for mice and humans. 

Here’s how the scientists figured out we really do have a dessert stomach

To reach this conclusion, the team first investigated mice’s reaction to sugar after they were full and found that, yes, they, too, still wanted dessert after dinner. The study noted that the mice were given a regular “chow” diet, which they could access for 90 minutes. Then, they were given access to either more of the same food or a “high-sugar-containing diet,” aka “dessert,” for a 30-minute window.

The team observed that when the mice were given chow during the dessert window, they only ate a small amount, but when they were offered the “dessert,” their caloric intake increased by more than sixfold. “This vigorous stimulation of consumption of the high sugar–containing food was consistent across all mice,” the team added.

“When mice are full and eat sugar, these nerve cells not only release signaling molecules that stimulate satiety but also one of the body’s own opiate: ß-endorphin,” the Institute shared. “This acts on other nerve cells with opiate receptors and triggers a feeling of reward that causes the mice to eat sugar even beyond fullness.” 

The team added that this specific opioid pathway was activated only when the mice ate additional sugar, not when they ate “normal or fatty food.” But when the researchers blocked the specific neural pathway the mice chose not to eat additional sugar. The researchers found that the “same region of the brain reacted to the sugar in humans” when they conducted scans on human volunteers. 

“From an evolutionary perspective, this makes sense: sugar is rare in nature but provides quick energy. The brain is programmed to control the intake of sugar whenever it is available,” Henning Fenselau, the research group leader at the Max Planck Institute for Metabolism Research and head of the study, shared in a statement. 

Here’s why this study matters 

As for how they hope their research will be used, the team noted that it could be useful in the treatment of obesity. “There are already drugs that block opiate receptors in the brain, but the weight loss is less than with appetite-suppressant injections,” Fenselau said. “We believe that a combination with them or with other therapies could be very useful. However, we need to investigate this further.”