Diet
Obesity Actually Changes Your Brain
New studies show that brain changes may persist even after weight loss.
Updated May 19, 2025 Reviewed by Tyler Woods
Key points
- Brain imaging study showed obesity reduced dopamine D2 receptors, supporting overeating.
- Structural brain changes in regions corresponding to the mouth, lips, and tongue reinforce overeating.
- Western high-fat, high-sugar diets rewire neural circuits but GLP-1s may reverse brain changes.
Researchers have found that eating highly processed, sugary, fat-filled foods not only changes your body but also your brain. Dr. Dana Small, Canada Excellence Research Chair in Metabolism and the Brain at McGill University, conducted pioneering research over the past decade on modern diets and their effects on the brain. In a 2023 study, Dr. Small and colleagues demonstrated that habitual consumption of high-fat and high-sugar foods changes the brain’s reward processing so that healthy low-fat foods are ignored.
Ashley Gearhardt, Ph.D., a Professor at the University of Michigan, and others have found that combinations of artificial sweeteners and fats/sugars are “hyper-palatable”, leading to addictive eating behaviors. Research led by Gene-Jack Wang, M.D., and colleagues has demonstrated that obesity is linked to alterations in the somatosensory cortex.
Science has established that overeating changes the brain, and the brain changes accompanying overeating are not easily reversible. Interestingly, bariatric surgery to decrease weight has been associated with only a partial reversal of brain changes. These findings suggest that liking and wanting highly processed, fatty, and sugar-filled foods may persist and compromise recovery from obesity. Much of this process is unconscious.
Neuroimaging Technology Shows “Toxic” Brain Changes
Gene-Jack Wang, M.D., and Nora Volkow, M.D. at the National Institute on Drug Abuse (NIDA) conducted brain imaging studies showing obesity is associated with structural and functional changes in the brain. Wang’s group used positron emission tomography (PET) and MRI imaging to examine brain activation in obese individuals. The most striking finding was increased activation and structural prominence of the somatosensory regions associated with the mouth and lips in obese individuals. This finding suggests the brain’s representation of the mouth may be hyper-responsive, potentially leading to greater attention to oral sensations and an intensified reward response during eating. Alarmingly, the brain’s “real estate” becomes dominated by food-related processing in obese people. Wang proposed this brain change undermines willpower and restraint as it relentlessly reinforces habitual and compulsive overeating.
Translational Scientists like University of Buffalo Professor Dr. Peter Thanos, working with Gene Jack Wang, Nora Volkow, and others, have shown a strong relationship between obesity and D2 deficiency, D2 hypersensitivity underlying obesity, and response to high-fat diets. Thanos has even developed an animal bariatric surgery model, which has predicted human brain recovery, especially in response to high-fat diets after bariatric surgery.
Wang and Volkow use drug addiction analogies to describe this “hijacking” of brain circuits to favor feeding behaviors over other stimuli. Structural somatosensory cortex changes are not easily reversible, especially in individuals who are obese for extended periods, indicating a persistent neurobehavioral imprint. So, even after weight loss, the person’s brain continues to crave food as if they were still obese.
Note that Weight Watchers members often failed, despite high motivation. For example, in their study of 700 “lifetime members” who reached goal weight and maintained it at least six weeks, most regained the lost pounds over the next five years. They were eating because their brains convinced them they were hungry.
2025 Findings in Adolescents and Adults
Recent research by Huiling Zhou and colleagues extends the foundational work of Volkow and Wang by providing a detailed analysis of progressive brain changes associated with obesity. Zhou studied 258 overweight or obese participants and 74 individuals with normal weight and showed the progressive impact of obesity on brain structure, such as decreased gray matter in multiple parts of the brain. Reductions in gray matter in the prefrontal cortex and hippocampus may contribute to impairments in executive function, memory, and decision-making.
A finding from a study of thousands of teenagers in the US raises concerns that obesity affects not only physical health but also learning, memory, and emotional control, according to lead researcher Dr Augusto César F. De Moraes, of UT Health Houston School of Public Health in Austin, Texas.
On 5/10/25 at the European Association for the Study of Obesity, Dr. De Moraes presented the data and said, “This is particularly alarming, given that the teenage years are such an important time for brain development.”
De Moraes and colleagues analyzed data from 3,320 participants to see the effects of obesity on brain development and health. Several brain regions were larger in adolescents with abdominal obesity than peers without abdominal obesity. The biggest changes were in the hippocampus, which is involved in memory and learning, and the amygdala, which regulates emotions, including fear, happiness, anger, and anxiety. The amygdala was particularly large in teenagers with very high levels of abdominal fat. Dr. De Moraes concluded, “Our findings suggest that obesity, particularly abdominal obesity, can impair teenagers’ learning, memory, and control of emotions. I worry about how these changes, which are occurring at the age of 13 or 14, might affect them later in life.” In the US, it’s estimated that more than one in three children aged 5 to 14 (36.2% of boys and 37.2% of girls) are overweight or obese—more than 15 million children.
Do Brain Changes Reverse After Weight Loss?
After weight loss, dopamine receptor availability may increase, and prefrontal and somatosensory cortex metabolism may improve, especially after bariatric surgery or long-term lifestyle changes. However, many brain alterations persist, even after bariatric surgery, especially in those with long-term obesity or repeated cycles of weight loss and gain (“yo-yo dieting”).
The widespread adoption of glucagon-like peptide-1 (GLP-1) agonists (think Ozempic) could change things by inducing significant changes in food consumption and preferences. In a soon-to-be-released study, four consumer groups were surveyed to understand how GLP-1s may affect food consumption and preferences. The research study, to be published in June 2025, showed that patients currently taking a GLP-1 medication ate significantly fewer calories, processed foods, sugar-sweetened beverages, refined grains, and beef than other groups.
Summary
Obese individuals show increased neural responses to the food they try to avoid. Their responses to palatable food cues (taste, smell, appearance) are coded in the insula, orbitofrontal cortex, and somatosensory cortex, creating a feedback loop encouraging overeating. Western diet-related brain changes often leave consumers searching for hedonic and highly palatable food, eating for pleasure rather than nutritional needs. This means recovery from obesity is possible, but it’s partial and slow, especially when structural brain changes and altered sensory mapping have become entrenched. However, recent research offers hope. For example, patients taking GLP-1s report actual changes in food preferences, suggesting reorganizing the brain and its relationship to fatty and sugary foods is possible, at least while medications are being taken. Adding GLP-1 agonists after bariatric surgery or other treatments is becoming more commonplace. Prevention, early intervention, and effective treatment of obesity are critically important.
References
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Dilley, A., Adhikari, S., Silwal, P., Lusk, JL.k McFadden, BR . Characteristics and food consumption for current, previous, and potential consumers of GLP-1 s, Food Quality and Preference, Volume 129, 2025, 105507, ISSN 0950-3293, In Press. https://doi.org/10.1016/j.foodqual.2025.105507. (https://www.sciencedirect.com/science/article/pii/S0950329325000825)
Saeed S, Bonnefond A, Froguel P. Obesity: exploring its connection to brain function through genetic and genomic perspectives. Mol Psychiatry. 2025 Feb;30(2):651-658. doi: 10.1038/s41380-024-02737-9. Epub 2024 Sep 5. PMID: 39237720; PMCID: PMC11746128.
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Thanos PK, Michaelides M, Piyis YK, Wang GJ, Volkow ND. Food restriction markedly increases dopamine D2 receptor (D2R) in a rat model of obesity as assessed with in-vivo muPET imaging ([11C] raclopride) and in-vitro ([3H] spiperone) autoradiography. Synapse. 2008 Jan;62(1):50-61. doi: 10.1002/syn.20468. PMID: 17960763.