By Lois Zoppi, BA

Reviewed by Kate Anderton, B.Sc. (Editor)

Scientists at the UNC School of Medicine have revealed that the reason we eat more than we need to may be caused by cellular communication originating in the emotion-processing center of the brain. The research was published in the journal Neuron yesterday.

Indulging in cravings for calorific foods when we already feel full is not an uncommon occurrence. While it could be put down to how easy it is to obtain great tasting (but often unhealthy) food is in modern society, the urge to binge on our favorite foods may actually be aby-product of evolution.

Scientists have identified two types of eating: homeostatic eating, which is brought on by hunger and serves to replenish energy levels, and hedonic eating, which is eating motivated by the pleasure brought on by eating calorie-rich food.

Binge-eating is ‘wired’ into our brains

Obesity increases the risk of diabetes, heart disease, and certain cancers, and is a condition that affects approximately 40 percent of American adults.

In ancient environments, humans would have consumed calorie-rich foods in large amounts in preparation for possible famines, which were a regular occurrence over the evolutionary period. That same instinct to fill up on calorific foods in modern society, where there is a rich abundance of foods regularly available, often leads to obesity.

There’s just so much calorically dense food available all the time now, and we haven’t yet lost this wiring that influences us to eatas much food as possible.”

Thomas Kash, Lead Author

This “wiring”, in Kash’s opinion, “seems to be the brain’s way of telling you that if something tastes really good, then it’s worth whatever price you’re paying to get to it, so don’t stop.”

Kash and his fellow researchers found a network of cellular communication stemming from the emotional center the brain, which caused the  mice in the study to continue eating food despite the fact that they had already met their energy needs.

Investigations into brain cells and cellular circuits have been plentiful over the past few decades, but success in finding anti-obesity remedies derived from these sources has been scant. These investigations have usually centered on homeostatic eating.

Kash’s experiment involved engineering mice to produce a fluorescent molecule with nociceptin, a signaling molecule that has been found to havea number of effects on the stomach and intestines, as well as stimulating the urge to over-eat.This allowed them to clearly see the cells that were stimulating the nociceptin circuits.

Emotional responses to food

One circuit stood out to the researchers; a circuit that runs to areas of the brain that regulate eating, among others. This circuit originates in the amygdala, the portion of the brain that is responsible for processing and regulating emotions.

Scientists have studied the amygdala for a long time, and they’ve linked it to pain and anxiety and fear, but our findings highlight that it does other things too, like regulate pathological eating.”

First author J. Andrew Hardaway PhD, research assistant professor of pharmacology at the UNC School of Medicine, said:

“Our study is one of the first to describe how the brain’s emotional center contributes to eating for pleasure. It adds support to the idea that everything mammals eat is being dynamically categorized along a spectrum of good/tasty to bad/disgusting, and this may be physically represented in subsets of neurons in the amygdala.

Blocking the nociception receptor  limited the consumption of calorific food, but had no effect on homeostatic eating.

The behavioral effects of blocking nociception activity probably involve multiple mechanisms in the brain. But on the whole, blocking nociception seems to stabilize behavior, bringing it closer to normal.”

A weight-loss solution?

Depleting the number of nociceptin neurons in these cellular circuits reduced weight gain, suggesting nociception receptor antagonists could represent an attractive route for drug developers investigating anti-obesity and anti-binge-eating medication.

However, Kash’s study concludes by advising “caution in interpreting sufficiency (not necessity) of the contribution of specific neural circuits to feeding when their optogenetic activation produces motor patterns of eating across a broad consummatory spectrum.”

The scientists will now explore whether nociceptin antagonists could be possible treatments for depression, pain, and substance abuse.