Breaking News: Two independent studies, published today, use new technology to isolate the neural circuit that controls compulsive sugar consumption, shedding light on binge eating disorders.

Warning: this article may make you want to eat—and not because you are hungry.

Using rays of light and tiny, mouse-sized imagining, two teams of neuroscientists have found a clear distinction between the neurons that signal true hunger and the neurons that cause us to seek candy-coated pleasure.

The research, conducted at the Massachusetts Institute of Technology and the University of North Carolina at Chapel Hill, was published today in the journal Cell. These teams identified a reward-related neural circuit that specifically controls compulsive sugar consumption in mice without preventing feeding necessary for survival, generating a novel target for the safe and effective treatment of compulsive overeating in humans.

What this means is that appetite suppression, whether it be through medications or willpower, may not actually lead to weight loss.

Obesity Is Pervasive

Overeating and obesity have been subjects of study for psychologists, physicians, nutritionists, and neuroscientists for decades. Despite this study, the worldwide prevalence of obesity nearly doubled between 1980 and 2008.

The fundamental cause of obesity is an imbalance between the number of calories consumed and the number of calories expended through the activities of daily living. Globally, our consumption of energy-dense, high-fat foods has increased while we have become more sedentary. In 2014, more than 1.9 billion adults were overweight. Of these, over 600 million were obese, according to the World Health Organization.

Increases in BMI increase the risk for noncommunicable diseases, such as cardiovascular disease, musculoskeletal disorders like osteoarthritis, and some cancers.

We Know Sugary Treats Aren’t Good for Us… And Yet…

Research teams from MIT and the University of North Carolina have attempted to tease out the primary cause of obesity – unhealthy eating habits.

“Our findings, says says senior study author Kay Tye of MIT, “are exciting because they raise the possibility that we could develop a treatment that selectively curbs compulsive overeating without altering healthy eating behavior.”

Compulsive overeating is a type of reward-seeking behavior, similar to drug addiction. Whether we are grazing on chips because they are in the house, or consuming an entire bag of licorice in one sitting, we eat this food because it feels good—not necessarily because we are hungry.

Tye and her team used a technique called optogenetics to distinguish between the brain circuits involved in compulsive overeating and those involved in normal feeding. The MIT researchers tested their hypothesis that a neural pathway from the lateral hypothalamus to the ventral tegmental area—also implicated in other reward-related behaviors, such as sexual activity and drug addiction—might play an important role in compulsive overeating.

Optogenetics involves genetically modifying specific populations of neurons to express light-sensitive proteins that control neural excitability, and then delivering either blue or yellow light through an optic fiber to activate or inhibit those cells, respectively. Activation of the pathway from the lateral hypothalamus to the ventral tegmental area caused well-fed mice to spend more time feeding and increased the number of times mice poked their nose into a port to receive a sugar reward, even when they had to cross a platform that delivered foot shocks to get to the reward.

By contrast, inhibition of the same pathway reduced this compulsive sugar-seeking behavior without decreasing food consumption in hungry mice, suggesting that different neural circuits control feeding in hungry animals.

“In our modern day society, there is no scarcity of palatable foods, and high-sugar or high-fat foods are often even more available than fresh produce or proteins,” Tye says. “We have not yet adapted to a world where there is an overabundance of sugar, so these circuits that drive us to stuff ourselves with sweets are now serving to create a new health problem. The discovery of a specific neural circuit underlying compulsive sugar consumption could pave the way for the development of targeted drug therapies to effectively treat this widespread problem.”

Implanted Device Allows University of North Carolina Researchers to See the Neurons of Mice as They Search for Food

Garret Stuber, from the University of North Carolina School of Medicine, and his team similarly used an optogenetic approach in mice to identify neurons in the lateral hypothalamus that control both feeding and reward-seeking behavior. The UNC team visualized the neural circuit dynamics in freely moving animals using nVistaHD by Inscopix, a unique, miniature, integrated fluorescence microscopy device.

For the first time ever scientists watched as one neuron was activated when a mouse searched for food while a nearly identical neuron next to it remained inactive; instead, the second neuron only became activated when the mouse began eating.

This work suggests that manipulating an entire genetically defined subtype of neurons to treat a condition, such as binge-eating, might be too broad of an approach. Drug developers might have to focus on one type of cell within the subset in order to avoid potentially serious side effects.

“This is important to know because if we want to create a drug treatment for obesity, for instance, then you wouldn’t want to affect cells involved in appetite because you might affect cells involved in other aspects of motivated behavior,” said Stuber. “But if we could target only the cells involved in consumption, then maybe we could modulate only those cells without affecting motivation.”


Jenn Lonzer has a B.A. in English from Cleveland State University and an M.A. in Health Communication from Johns Hopkins University. Passionate about access to care and social justice issues, Jenn writes on global digital health developments, research, and trends. Follow Jenn on Twitter @jnnprater3.