A new case study offers an unusually close look at how tirzepatide, a medication used for type 2 diabetes and weight loss, may influence the brain activity behind “food noise,” the nonstop thoughts about food that many people with obesity or binge eating experience. The findings are based on a single participant, but they highlight how complex eating behavior can be and why medications may not completely resolve intrusive cravings.
Researchers at the University of Pennsylvania were able to gather this data because the participant was enrolled in a clinical trial involving implanted electrodes, a procedure sometimes used in research on difficult-to-treat neurological conditions. The participant, a 60-year-old woman referred to as “Participant 3,” had severe, treatment-resistant obesity and long-standing loss-of-control eating. She had tried multiple treatments, including bariatric surgery, behavioral therapy and medications, but continued to struggle.
She also had significant “food noise,” reporting intense preoccupation with both sweet and salty foods. Before entering the trial, she was prescribed tirzepatide for type 2 diabetes. Because this happened shortly before her neurosurgery, researchers were able to observe how her brain responded to the medication before any stimulation was delivered.
After the electrodes were implanted, tirzepatide appeared to quiet electrical activity in the brain’s reward center, the nucleus accumbens, which helps regulate motivation, pleasure-seeking and impulses. That quieting matched her experience: for a period of time, she reported no food preoccupation.
But several months later, the same brain region began showing the elevated activity typically seen in people with obesity and binge-eating tendencies. Her food noise returned as well. The shift suggests the medication’s effect on her eating-related brain activity was temporary or incomplete.
The researchers emphasize that this study cannot be used to generalize about tirzepatide in the broader population. The insights come from a single person with highly complex medical and neurological needs, and her experience does not reflect typical use. But the work offers clues about why GLP-1–based medications may help reduce intrusive food thoughts for some people, why those effects may vary and why medications alone may not fully address eating behaviors rooted in the brain’s impulse and reward circuits.
“This study offers major insights into how these drugs may work inside the brain and will guide us as we explore new indications,” said senior author Casey H. Halpern, MD. He cautioned, however, that “it’s far too soon to call GLP-1 and GIP inhibitors miracle drugs for more conditions beyond type 2 diabetes and obesity.”
Study investigators said the observations should encourage more research into how these medications influence the neural pathways involved in food preoccupation and binge eating, and whether new treatments might more directly target those circuits.
The research was published in Nature Medicine and supported by the National Institutes of Health. The authors report no personal financial conflicts related to the study.