After six months of therapy, the patients reported significantly reduced binge episodes and weight loss.
A pilot study demonstrates that an implanted brain stimulator significantly reduced bingeing episodes and aided patients in losing weight.
Researchers at the University of Pennsylvania's Perelman School of Medicine discovered that a small device that detects food craving-related brain activity in an important brain region and reacts by electrically stimulating that region had promise in a pilot clinical study in two patients with loss-of-control binge eating disorder (BED).
The experiment, described in a paper published in the journal Nature Medicine, followed the two patients for six months as the implanted device—of a sort commonly used to treat drug-resistant epilepsy—monitored activity in a portion of the brain known as the nucleus accumbens.
The nucleus accumbens is involved in pleasure and reward processing and has been linked to addiction. When the device detected nucleus accumbens signals that had previously been shown to predict food cravings, it activated that brain region, interrupting the craving-related signals. Over the course of six months, the patients reported significantly fewer binge episodes and lost weight.
“This was an early feasibility study in which we were primarily concerned with safety, but certainly the substantial clinical benefits these patients gave us are really remarkable and exciting,” said study senior author Casey Halpern, who is an associate professor of neurosurgery at Penn Medicine and the Corporal Michael J. Crescenz Veterans Affairs Medical Center.
The binge eating disorder is thought to be the most common eating disorder in the United States, affecting at least a few million individuals. It is typically linked to obesity, and often involves binge-eating episodes without the purging of bulimia. The bingeing person has a feeling of losing control over eating, therefore he or she continues to eat beyond the usual level of satisfaction.
Cravings for particular foods precede BED episodes. Halpern and colleagues discovered evidence that specific low-frequency electrical activity in the nucleus accumbens emerges shortly before these cravings—but not before normal, non-binge eating. The mice ate considerably less of a tasty, high-calorie meal than they would have otherwise ate.
The device developed by the researchers to capture signals from and stimulate the mice's brains is commercially available and approved for the treatment of drug-resistant epilepsy. It's surgically implanted under the scalp, with wires extending across the skull to each brain hemisphere's nucleus accumbens.
The researchers used the same brain-stimulation technique and strategy in humans. For six months, the participants monitored their binge eating episodes in the lab, and when they returned home, they reported the time of their episodes.
The brain-stimulation devices automatically sent high-frequency electrical stimulation to the nucleus accumbens whenever low-frequency craving-associated signals occurred. During this six-month period, the patients reported significant reductions in their feelings of loss-of-control, and in the frequency of their bingeing episodes—each lost more than 11 pounds. One of the subjects improved so much that she no longer met criteria for binge-eating disorder. There appeared to be no significant adverse side-effects.
"This was a wonderful demonstration of how translational science may function in the best of situations," said study co-lead author Camarin Rolle, PhD, a postdoctoral researcher with Halpern's group.
The researchers have continued to follow the subjects for another six months, and have begun enrolling new patients for a larger study. They argue that the same therapy technique might also be applied to other loss-of-control conditions, such as bulimia.
Rajat S. Shivacharan, Camarin E. Rolle, Daniel A. N. Barbosa, Debra L. Safer, Cara Bohon, Vivek P. Buch, Dan E. Azagury, Mahendra T. Bhati, Robert C. Malenka, and Casey H. Halpern, Nature Medicine, 29 August 2022 DOI: 10.1038/s41591-022-01941-w.
The National Institutes of Health sponsored the research.