Over a year ago, some of my faculty colleagues and I started a tradition in which we try out different restaurants in the Austin area. This quickly became a highlight worth looking forward to, an informal dinner club, if you will, where we explore Austin’s vibrant food scene. Each outing has been filled with great food, engaging conversations, and lively debates. The outings allow for unfiltered conversations that only happen when academics step away from their offices, everything from university policies, stories about our research, and sometimes we’ve even entered into philosophical discussions about the nature of consciousness. But no matter what the evening’s discussion, one thing is a constant, no matter how full we feel after the main course, we always order dessert.

We’ll sit there, intently glance at the dessert menu, pretend to consider skipping it this time, only for someone to suggest sharing something “just to taste.” That suggestion quickly spirals into a round of orders, and before we know it, we are digging into a chocolate cake, or some perfectly caramelized something or other. And then comes the inevitable realization that we were stuffed just moments before, but yet somehow we found more room for dessert.

We laugh at ourselves, calling it a mystery of human nature. But being neuroscientists, we know there must be a deeper explanation. And as it turns out, there is, as evidenced in a recently published study in the journal Science [1], which has finally given us the answer.

Satiety, the feeling of being full after eating, is a fundamental biological process. It helps regulate body weight and prevents us from overeating. When we eat a meal, the brain receives signals that say, “Enough,” you don’t need more food. And yet, mysteriously, that same state of fullness seems to trigger our desire for sweet foods. This contradiction has long puzzled both neuroscientists and anyone who has ever found themselves reaching for dessert despite feeling full.

A team of researchers led by Marielle Minère and Henning Fenselau, along with colleagues, set out to investigate why this happens. Their findings revealed a surprising brain mechanism at play, one that helps explain why sugar cravings persist even when we are no longer hungry.

Central to their discovery are pro-opiomelanocortin (POMC) neurons, a group of cells that live in the brain’s hypothalamus that have long been known to regulate appetite and satiety. Traditionally, POMC neurons are believed to work by promoting fullness. They release a neuropeptide called α-melanocyte-stimulating hormone (α-MSH), which signals to the brain that it’s time to stop eating. But Minère and colleagues discovered something unexpected, which is that not all POMC neurons function this way.

Instead of suppressing appetite, some POMC neurons actually stimulate it, but only for sugar! These neurons project to a brain structure called the paraventricular thalamus (PVT), a region in the brain involved in motivation and reward processing. But rather than releasing α-MSH, these particular POMC neurons produce β-endorphin, which is an opioid peptide that activates µ-opioid receptors (MORs) in the PVT. Effectively, this opioid signaling, the researchers found, is what drives the desire for sugar when we are in a state of satiety.

In other words, while the body signals that it has had enough food, the brain simultaneously activates a pathway that specifically encourages sugar consumption.

To test this, researchers used various state-of-the-art techniques, including optogenetics and chemogenetics, which allowed precise control of brain activity in mice. When they blocked opioid signaling from POMC neurons to the PVT, sugar intake dropped significantly. The mice, despite being fed, no longer exhibited a strong preference for sweet foods. Interestingly, this effect was specific to sugar, blocking the pathway had no impact on the consumption of fatty foods.

This finding suggests that our brain treats sugar differently from other foods. While satiety suppresses general appetite, it appears to reinforce the drive to consume sugar. This explains why, even after a heavy meal, desserts still look so good!

So, while my colleagues and I always joked about our inability to resist dessert, something that likely occurs at many dinner tables throughout the world, we now have a neuroscientific explanation for this yearning. So, next time we gather for one of our restaurant outings and inevitably find ourselves ordering something sweet, I know we won’t be able to resist pointing it out: it’s not just us, it’s our POMC neurons talking.

Of course, this study also has wider implications beyond just explaining our after-dinner excess. Understanding how this brain circuit functions might have real implications for tackling binge eating and obesity, where sugar consumption often continues despite signals of satiety. If researchers can develop ways to modulate this opioid-driven system, then it could lead to new treatments to help curb excessive sugar intake without impacting normal appetite regulation.

In the meantime, next time I sit with my colleagues, watching us justify dessert choices, I’ll take comfort in knowing that neuroscience is literally on our side.