By CYNTHIA M. BULIK, PhD
Published: September 26, 2013
What better way to stop decades of misattribution of binge eating to willpower, sloth, or gluttony than actually identifying precise cellular connections in the brain that cause a mouse to eat, whether hungry or not! That is exactly what Garret Stuber, his neurobiology graduate student Josh Jennings, and colleagues have done in a study published in Science on September 27th.
Hang on while I walk you through some of the science. Back in the 1950s, when scientists electrically stimulated a region of the brain called the lateral hypothalamus and triggered mice to eat, they knew that they were stimulating many different types of brain cells. Not until now did scientists learn exactly what they were stimulating.
Stuber and Jennings focused on one cell type in the part of the brain called the BNST (bed nucleus of the stria terminalis), an outcropping of the amygdala, which is associated with emotion. The BNST also forms a bridge between the amygdala and the lateral hypothalamus, the brain region that drives primal functions such as eating, sexual behavior, and aggression.
Stuber’s team stimulated parts of those cells by using an optogenetic technique, an intricate process that ends with shining light on the synapses of those cells.
As soon as the light hit BNST synapses the mice began to eat way more than normal even though they had already been well fed. Moreover, the mice showed a strong preference for high-fat foods.
Stuber said, “They would essentially eat up to half their daily caloric intake in about 20 minutes. This suggests that the BNST pathway could play a role in food consumption and pathological conditions such as binge eating.”
I saw how the mice reacted to the light. It was like a switch going on and off. Light on…eat voraciously…light off…indifferent to the food. When I saw this, I knew that these guys were on to something big.
Stimulating the BNST also led the mice to exhibit behaviors associated with reward, suggesting that shining light on BNST cells enhanced the pleasure of eating. On the flip side, shutting down the BNST pathway caused mice to show little interest in eating, even if they had been deprived of food.
The study, which uses technologies highlighted in the new National Institutes of Health Brain Initiative, suggests that faulty wiring in BNST cells could interfere with hunger or fullness cues and contribute to human eating disorders, leading people to eat even when they are full or to avoid food when they are hungry.
“The study underscores that obesity and eating disorders have a neurological basis,” said Stuber, a researcher at UNC’s School of Medicine and the UNC Neuroscience Center. “With further study, we could figure out how to regulate the activity of cells in a specific region of the brain and develop treatments.”
This is a game-changer.
The bottom line is that we know precious little about the biology of eating disorders and until we do, our treatments will remain less than satisfactory. There are no medications that are effective in the treatment of anorexia nervosa, and only about half of people with bulimia nervosa and binge eating disorder respond to existing treatments.
Back in 1996, the FDA approved fluoxetine (Prozac) for the treatment of bulimia nervosa. That is the last and only medication that has won FDA approval for the treatment of any eating disorder. Not that there is ever going to be a magic pill to treat eating disorders, but research like Stuber and Jenning’s might help us identify treatment targets that are specific to the symptoms of binge eating and restrictive eating. Until now, just about every medication that we have tried has focused on a secondary symptom like mood or anxiety.
These results bring clarity to the field. Parents, partners, and patients often wonder why recovery from eating disorders can be so difficult. For years I have explained that sufferers face an uphill battle against their biology. Until now, the nature of that biology has been an unknown. This innovative work literally shines a light on the biology that they are fighting against.