What if Your Food Cravings Are More Than Habit?

The same drugs that curb overeating may also blunt addictive urges.

Posted May 28, 2026 | Reviewed by Margaret Foley

Finding the late Bart Hoebel [1,2] at a neuroscience meeting was never difficult. He was exceptionally tall and rose above the sea of scientists not only in stature but also in vision, a commanding presence in every sense of the word. He was known for his pioneering work on the neurobiology of motivation , feeding, and addiction , subjects that have fascinated me since my early undergraduate years.

Much of Prof. Hoebel’s legacy lies in making the case that highly palatable foods, particularly sugar, recruit the brain’s reward systems in ways that resemble addictive processes [3,4,5,6]. That idea resonated with me at more than an academic level. I had seen others around me struggle to stop eating high-fat, high-carbohydrate processed foods despite earnest efforts to do so, and the notion that some foods might be addictive felt less like speculation than lived truth. Still, the idea remained a subject of controversy in the scientific community. To be clear, behavioral neuroscientists agreed that highly palatable foods engage neural reward systems. The debate was whether this justified the language of addiction, especially in humans. Some questioned how well animal models of sugar bingeing translated to human eating behavior, while others argued that obesity was too complex to be framed through an addiction lens. Yet the central question Prof. Hoebel raised never disappeared: Are some forms of overeating driven by mechanisms that overlap with those involved in substance use disorders?

That question is what makes Richard O’Connor’s recent review article in Frontiers in Behavioral Neuroscience so interesting [7]. O’Connor argues that the emergence of GLP-1 receptor agonists has given new life to the debate over food addiction. These drugs, best known for their effects on weight loss, appear to do more than reduce hunger. They may also act on reward and motivation circuits that overlap with those involved in substance use disorders, returning the field to questions Hoebel helped place on the scientific map.

GLP-1, or glucagon-like peptide-1, is a hormone that helps regulate blood sugar, slows the emptying of the stomach, and promotes satiety after eating [8]. Medications that mimic this hormone, called GLP-1 receptor agonists, were initially developed for diabetes but are now mostly known for their effects on weight loss. O’Connor argues that the importance of these medications may go deeper. In addition to their effects on metabolic processes, they may also influence reward and the “pull” of highly palatable foods. It is this overlap that makes them so relevant to the questions that Hoebel began asking decades ago.

O’Connor moves beyond the broad claim that GLP-1 drugs reduce appetite and instead highlights their effects within specific neural systems. He underscores that GLP-1 receptors are found not only in the pancreas and gastrointestinal tract, but also in the brain, including the brainstem, hypothalamus, ventral tegmental area, striatum, and other limbic regions involved in motivation and reward. Particularly noteworthy is the paper’s emphasis on the overlap between GLP-1 signaling and the mesolimbic dopamine system, the circuitry long implicated in reinforcement, craving, and addiction. The review discusses evidence that GLP-1 receptor agonists can reduce motivation for sucrose, dampen food reward, attenuate cue-evoked dopamine responses, and decrease alcohol -, cocaine-, and nicotine-related behaviors in animal models. In humans as well, the review points to findings that exenatide (one of many GLP-1 receptor agonists now available) can reduce food-related neural responses in regions such as the insula, amygdala, putamen, and orbitofrontal cortex.

The review also underscores that GLP-1 drugs may alter not just the amount of food consumed, but, importantly, the motivational value of food itself. It summarizes evidence that semaglutide, liraglutide, and tirzepatide (all widely prescribed GLP-1 drugs) reduce cravings for sweet, fatty, savory, and highly processed foods, while in some cases shifting preference toward less energy-dense alternatives. In rodent studies, similar effects appear in reduced intake of candy, lipid-rich foods, and sucrose solutions, along with decreased operant responding for palatable food rewards. This is important because it suggests that GLP-1-based treatment acts not only through satiety and gastric mechanisms, but through central reward-related mechanisms that influence which foods are wanted, sought, and repeatedly consumed.

What makes this emerging literature on GLP-1 drugs especially powerful is that it reveals shared mechanisms and shared therapeutic possibilities. Consider, for example, a 2026 BMJ cohort study by Washington University researchers of more than 600,000 U.S. veterans with Type 2 diabetes in which treatment with a GLP-1 receptor agonist was associated with lower risks of new substance use disorders across alcohol, cannabis, cocaine, nicotine, and opioids, as well as with fewer overdoses, hospitalizations, and drug-related deaths among those already carrying such diagnoses [9]. Of course, observational findings do not amount to direct proof, but they suggest that GLP-1 drugs may be targeting a common neurobiology of craving rather than a single substance-specific pathway. That same interpretation dovetails nicely with an earlier 2022 review [10] arguing that GLP-1’s effects in addictive disorders are mediated centrally, at least in part through dopamine signaling. If that is right, then the implications are significant: Drugs developed to quiet overeating may also help quiet addictive urges more broadly, bringing Prof. Hoebel’s framework closer to clinical relevance than ever before.

The new GLP-1 literature does not settle the food-addiction debate, but it does make one thing harder to ignore: Hoebel may have recognized, early on, how deeply feeding, reward, and compulsion are intertwined. Science evolves, methods improve, and terminology changes, but some ideas endure because they were asking the right question all along. Bart Hoebel asked one of those questions.

Aronson E. 2011. Renowned psychologist Bart Hoebel - who studied addiction, behavior - dies. Princeton University. Available at: https://www.princeton.edu/news/2011/06/14/renowned-psychologist-bart-ho…
Leibowitz SF. 2012. Obituary for Bart Hoebel. Psychopharmacology. doi:10.1007/s00213-011-2614-8
Woods SC, Ramsay DS. 2011. Food intake, metabolism and homeostasis. Physiology & Behavior. doi:10.1016/j.physbeh.2011.04.026
Bartoshuk L. 2011. Addicted to Food: An Interview with Bart Hoebel. Association for Psychological Science. Available at: https://www.psychologicalscience.org/observer/addicted-to-food-an-inter…
Avena NM, Rada P, Hoebel BG. 2007. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience & Biobehavioral Reviews. doi:10.1016/j.neubiorev.2007.04.019
Hoebel BG. 1985. Brain neurotransmitters in food and drug reward. American Journal of Clinical Nutrition. doi:10.1093/ajcn/42.5.1133
O’Connor RM. 2026. Revisiting food addiction in the era of GLP-1–based obesity pharmacotherapy via neural reward pathways linking feeding and substance use. Frontiers in Behavioral Neuroscience. doi:10.3389/fnbeh.2026.1805953
Collins L, Costello RA. 2026. Glucagon-Like Peptide-1 Receptor Agonists. In: StatPearls. Available at: https://www.ncbi.nlm.nih.gov/books/NBK551568/
Cai M, Choi T, Xie Y, Al-Aly Z. 2026. GLP-1RA and risks of substance use disorders among US veterans with type 2 diabetes: A cohort study. The BMJ. doi:10.1136/bmj-2025-086886
Klausen MK, Thomsen M, Wortwein G, Fink-Jensen A. 2022. The role of glucagon-like peptide 1 (GLP-1) in addictive disorders. British Journal of Pharmacology. doi:10.1111/bph.15677

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Juan Dominguez, Ph.D. , is a professor at the University of Texas.

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