A brain-stimulating implant interrupts craving-related signals and decreases bingeing episodes

According to researchers at the Perelman School of Medicine at the University of Pennsylvania, a small device that detects food craving-related brain activity in a key brain region and responds by electrically stimulating that region showed promise in a pilot clinical trial involving two patients with loss-of-control binge eating disorder (BED).

The research, which is described in a paper published today in Nature Medicine, monitored the activity of the nucleus accumbens in two patients for six months using an implanted device that is often used to treat drug-resistant epilepsy. The nucleus accumbens processes pleasure and reward and has been associated with addiction.

When the gadget detected signals from the nucleus accumbens that had been demonstrated to predict food cravings in previous studies, it immediately stimulated that brain region to disrupt the craving-related signals. Over the course of six months of treatment, patients reported significantly fewer binge episodes and weight loss.

BED is the most prevalent eating disorder in the United States, impacting several million individuals. It is characterized by numerous episodes of binge eating without purging, and is frequently associated with obesity. The binge eater feels as though he or she has lost control over eating, therefore he or she continues to eat past the normal threshold of feeling full.

BED episodes are preceded by a yearning for particular meals. In a 2018 study including mice and people, Halpern and colleagues found evidence that specific low-frequency electrical activity emerges in the nucleus accumbens right before these cravings, but not before normal, non-binge eating. The researchers activated the nucleus accumbens in mice to interrupt this craving-related activity whenever it happened. They discovered that the mice consumed considerably less of a delectable, high-calorie diet than they would have otherwise.

The device used by the scientists to record and stimulate the brains of mice is commercially accessible and licensed for the treatment of drug-resistant epilepsy. It is surgically implanted beneath the scalp, with wires extending through the skull to each hemisphere’s nucleus accumbens.

The current study was a preliminary examination of the same equipment and method on human volunteers. Two highly obese BED patients were implanted with brain-stimulation devices by Halpern’s team, and for six months, the researchers monitored signals from the devices. Occasionally, the patients were at the laboratory, where they were offered buffets of their favorite foods — fast food and candy were prevalent — but they spent the majority of their time at home, going about their normal activities.

The researchers were able to videotape the patients’ binge-eating episodes in the laboratory, and the patients self-reported the timings of their bouts at home. As in their previous work, the researchers noticed a characteristic low-frequency signal in the nucleus accumbens in the seconds preceding the patients’ initial bites of their binge meals.

In the subsequent phase of the trial, the brain-stimulation devices automatically gave high-frequency electrical stimulation to the nucleus accumbens whenever craving-associated signals of low frequency were detected. During this six-month period, the patients reported significant improvements in their feelings of loss of control and the frequency of their bingeing episodes; each also lost over 11 pounds. She no longer fit the criteria for binge eating disorder. It appeared that there were no substantial harmful effects.

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