Binge eating disorder affects millions of adults and carries serious cardiometabolic consequences, yet the pharmacological toolkit remains limited — lisdexamfetamine, SSRIs, and topiramate each come with meaningful tolerability trade-offs. The emerging application of GLP-1 receptor agonists to eating-disorder pathology represents a conceptual shift: rather than targeting neurotransmitter systems directly, these agents work upstream through appetite, satiety, and reward circuitry, potentially addressing the biological drivers of loss-of-control eating.
This PROSPERO-registered systematic review, conducted under PRISMA 2020 guidelines, screened 1,125 records from five major databases — MEDLINE, Embase, PsycINFO, Scopus, and Cochrane CENTRAL — ultimately identifying 12 eligible human studies. Included trials evaluated GLP-1 receptor agonists (GLP-1 RAs) and the dual GIP/GLP-1 agonist class in patients with confirmed binge eating disorder or clinically significant binge eating behaviors. Outcomes captured included binge episode frequency, psychiatric symptom burden, body weight, and cardiometabolic markers, providing a multi-dimensional portrait of treatment response.
The mechanistic rationale here is compelling and deserves careful unpacking. GLP-1 receptors are expressed not only in the pancreas and gut but throughout mesolimbic reward regions, including the nucleus accumbens and ventral tegmental area — precisely the circuits implicated in compulsive food-seeking. Animal models have demonstrated that GLP-1 agonism attenuates dopamine-driven reward responses to palatable foods, suggesting a neurobiological mechanism beyond simple appetite suppression. That said, the evidence base remains early-stage: 12 studies is a modest corpus, and the heterogeneity in study design, drug type, dose, and binge eating ascertainment methods likely limits firm conclusions. Most included studies were not powered specifically for eating-disorder endpoints, and none appear to be large Phase III trials targeting BED as a primary indication. This review therefore reads as confirmatory of a promising direction rather than practice-changing — a signal that warrants dedicated randomized controlled trials before incretin therapies can be formally positioned within BED treatment algorithms.