Scientists Discover Why It's So Hard to Stop Eating Even When Our Bodies Are Full

"You don't actually need those calories, but those calories taste so good."

eating

For some people, overeating is a personal challenge. But scientists are on a mission to understand why we continue to eat after we’ve had our fill. A few chips are delicious; a whole bag is a disaster waiting to happen — but somehow we can’t help ourselves. In a study released Wednesday in the journal Neuron, scientists argue that our need to overfeed doesn’t stem from inherent gluttony. Instead, it is linked to a newly identified network of mammalian brain circuitry that drives us to consume tasty calories.

First author Andrew Hardaway, Ph.D., is a research assistant professor at the University of North Carolina, Chapel Hill who is fascinated by the neurobiology of eating. He acknowledges to Inverse that the topic is “a big can of worms.” There are multiple processes, multiple signaling pathways, and multiple brain regions that control the act of eating.

What Hardaway is most interested in is understanding what’s so special about tasty foods: We know that mammals are motivated to get what’s yummy, but we didn’t know how exactly the brain reacts and drives us toward tasty foods. But we do have some clues: Previous experiments have shown that hedonic eating — eating for pleasure rather than necessity — involves the engagement of nociceptin, a small protein that works as a signaling molecule in the mammalian nervous system.

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Mouse central amygdala containing prepronociceptin (green) and PKC delta (magenta) neurons.

Most research on why we eat, designed primarily as a way to figure out how to stop obesity, focuses on a type of feeding called homeostatic eating. Hardaway says one way to think about homeostatic eating is that it’s what happens when you’ve slept all night, you wake up, you exercise, you have low blood sugar, and you just need to feed to fulfill your caloric deficit. It’s completely triggered by hunger, and it keeps our energy levels up.

“Hedonic feeding is when you’ve already had your dinner, you’re sitting on your coach, and you just want to feed for reward, and you grab that pint of Ben & Jerry’s,” Hardaway says. “You don’t actually need those calories, but those calories taste so good.”

To study the role nociceptin has on hedonic feeding, the team genetically engineered mice to produce a fluorescent molecule along with nociceptin, which literally illuminated the pathways that the protein travels. While there are multiple nociceptin circuits in the brain, the scientists saw that one specific one in the central nucleus of the amygdala became ignited when the mice were fed tasty alternatives to their plain old lab chow.

Subsequently, when the team genetically removed half of the nociceptin-making neurons in this circuit, the mice became less interested in binging on calorie-rich food. It was an unusual find for Hardaway, because typically when you find a brain circuit involved in eating, it contributes to a variety of processes. It was interesting that this particular pathway didn’t connect at all to homeostatic eating.

“In the study, we find that when we take these neurons away we get reduced consumption of palatable foods, arguing that these neurons are necessary for tasty food consumption,” Hardaway says.

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A circuit in the brain drives us to eat calorie rich food.

To see this specific contribution to tasty food, Hardaway explains, adds credence to the idea that, in the brains of mice and hypothetically in people, there’s this a moment-to-moment process in the amygdala where the brain dynamically judges whether or not you should eat something because it tasty.

The amygdala is a very evolutionarily conserved brain structure — which is why scientists suspect a study like this on mice can hold true for humans. It’s also usually studied for its contributions to fear learning. What’s unique about this study is that they are finding it has a role in positive affective behavior.

“Food consumption could be a rewarding form of behavior,” Hardaway says. “Our data underscore that there’s maybe a broader function of the central amygdala with contributions to emotional processing.”

An accepted and governing school of thought is that hedonic eating exists because it’s a byproduct of a time when large calorie-rich meals were scarce — hence the circuit that drives it in our brains. Scientists hypothesize that we evolved to over-consume when we came across calories, and that over-consumption is in part driven by circuitry that tells us something is tasty.

This hardwiring is now unnecessary in an era when we have reduced physical activity and an abundance of calorically cheap, readily available food. More than 35 percent of Americans are obese, endangering their health. The team here hopes that now that we know what part of the brain drives tasty food consumption, it can perhaps help scientist develop more effective obesity interventions.

“Neurons in the central nucleus of the amygdala in mice can provide us with a new therapeutic entry point into targeting this circuitry in people,” Hardaway says. “That could be behavioral therapy, it could be a useful biomarker, or we can actually find ways to drug these specific neurons. These preclinical studies have set the stage, and now its time to learn more about how this circuit works.”

Partial summary:

Food palatability is one of the many factors that drives food consumption and the hedonic drive to feed is a key contributor to obesity and binge eating. In this study, we identified a population of prepronociceptin-expressing cells in the central amygdala that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of Pnoc-CeA cells reduces high-fat-diet-driven increases in bodyweight and adiposity. Pnoc-CeA neurons project to the ventral bed nucleus (PBN), and nucleus of the solitary tract (NTS), and activation of cell bodies in the central amygdala (CeA) or axons on the vBNST, PBN, and NTS produces reward behavior but did not promote feeding of palatable food.