Imagine the smell of a savory steak sizzling in a jus of garlic and butter, or the decadent texture of tiramisu inside your mouth. The sensations of taste, smell, texture, and sight merge in the brain to give us the encapsulating experience of flavor, which forms a place from where all humans derive pleasure. But for millions of American adults on GLP-1 medication, is the drug muting this sense of joy by rewiring how we perceive food?

GLP-1 is the abbreviated form of Glucagon-like Peptide-1, a naturally occurring hormone that has discrete functions in the brain and body. GLP-1 drugs like the FDA-approved weight loss and anti-diabetic drugs Wegovy and Ozempic are considered medical miracles. With over eight million prescriptions written since 2018, GLP-1 drugs are successfully reducing weight in obese patients, improving cardiac health, and regulating insulin levels in the body. Scientists are also discovering additional benefits, from preventing certain types of cancer to curbing addiction. With burgeoning trends for the epidemics of obesity and diabetes, GLP-1 drugs are being celebrated as being profoundly effective in tackling these sinister conditions.

Analysis of posts from the subreddit r/WegovyWeightLoss, and personal interviews with patients using Semaglutide have reported common themes of these drugs making the patient feel more ‘normal,’ with a person claiming that it "saved their life." However, a growing chorus of patients has reported something more fundamental and central to using these drugs—emotional flatness and altered food perception, which in turn leads to reduced food intake.

The science behind it is complex. Food intake is an orchestrated process that requires communication between the brain and the body to signal cycles of hunger and satiation. Sensory inputs converge onto specialized regions of the brain to regulate when and how much to eat and help us decide if the bite feels irresistible or forgettable, and GLP-1 plays a salient role in this medley. Though it is naturally produced in the gut, research has shown the prevalence of GLP-1 receptors in key brain areas regulating behaviors related to appetite control and how we perceive something as ‘rewarding.’  GLP-1 drugs can also bind to these receptors and, in extension, modulate the communication between brain cells, leading to an altered valuation of food.

Dynamic cross-talk between neurons of the brain generates behaviors which are guided by perception generated in the mind. Studies using rodent models report that GLP-1 drug-induced alterations in perception initiate at the level of the sensory systems—they can tune the processing of smell and/or taste, leading to a chain reaction of altered signals up to the higher brain areas. Thus, it is not that users don’t want the tiramisu; at a cellular level, the brain is no longer receiving the "yum" signal.

This discovery is a critical distinction that should change how we approach obesity treatment. It reframes the condition not just as a failure of metabolic signaling, but as a disease influenced by an individual’s sensory perception. If the joy of food is a key driver of overconsumption for some, then understanding how the brain processes pleasure on GLP-1 drugs is as important as understanding how it processes glucose.

GLP-1 suppresses hunger, but also potentially pleasure pathways. This creates a responsibility on the clinicians’ part to provide appropriate counsel to patients on potential neuropsychological and sensory shifts that follow GLP-1 use. Of course, research directed towards investigating these shifts is of essence. After all, as Virginia Woolf aptly wrote, “to think well and love well, the most important thing is to dine well.”