Food Noise, Dopamine, and the GLP-1 Brain: How Semaglutide and Tirzepatide Rewire Reward Pathways
If you've ever been on a diet and spent half your workday thinking about food — what you'll eat next, whether that snack counts, bargaining with yourself at 3pm — you already know what food noise is, even if you've never heard the term. For millions of people living with obesity, this mental chatter isn't just occasional hunger. It's relentless, intrusive, and exhausting. And then something extraordinary happened: people started taking GLP-1 drugs like semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro, Zepbound), and the noise went quiet. Not "quieter." Quiet. The science behind that silence is one of the most fascinating stories in modern neuroscience — and it starts deep inside the brain's reward circuitry.
What Is "Food Noise"? Defining the Mental Chatter
"Food noise" isn't a formal medical diagnosis. It's a patient-coined term that captures something clinicians have long struggled to put into words: the near-constant, involuntary mental preoccupation with food, eating, cravings, and body weight that many people with obesity experience.
It sounds like this: What's for lunch? Should I eat that? I shouldn't have eaten that. I want something sweet. Why can't I stop thinking about food? It's not ordinary hunger. It doesn't go away when you eat. It's background radiation in the brain — always humming, always pulling at attention, always sapping cognitive and emotional resources.
Clinically, this maps onto what researchers now call maladaptive prospection — a failure of the brain's default mode network (DMN) to regulate reward-seeking mental simulation. Instead of planning useful futures, the brain loops on short-term food rewards. A 2026 review in Cureus described food noise as "a form of maladaptive prospection: a faulty way of thinking about the future, characterized by repetitive, cue-driven mental simulation of short-term reward at the expense of long-term goals."
What makes GLP-1 drugs remarkable isn't just that they suppress appetite. It's that they seem to turn off the mental radio station playing food content 24/7. Users describe it as a cognitive unburdening — suddenly having mental bandwidth to think about other things.
The Neuroscience of Food Noise: Why Some Brains Can't Stop Thinking About Food
The Dopaminergic Reward System in Obesity
To understand food noise, you need to understand dopamine — but probably not in the way you've heard about it before. Dopamine is less about pleasure and more about wanting and motivation. It's the neurochemical that makes you reach for things, chase rewards, and repeat behaviors. In the context of food, dopamine is what drives you toward the fridge, not necessarily what makes you enjoy what's inside it.
The key brain circuit here is called the mesolimbic pathway, and it runs from a small midbrain region called the ventral tegmental area (VTA) to the nucleus accumbens (NAc) in the forebrain. This VTA → NAc highway is the brain's core reward highway. When you eat something calorie-dense — a slice of pizza, a handful of chips — this pathway floods with dopamine. Your brain registers: that was important. Do it again.
In people with obesity, this system becomes hyperactivated. High-calorie, ultra-processed foods trigger larger dopamine releases and create addictive-like behavioral patterns. The brain starts treating food the way it treats drugs: prioritizing it, fixating on it, and struggling to stop despite consequences. Neuroimaging studies confirm that obese individuals show increased activation in appetite and reward-related brain regions (the insula, amygdala, putamen, and orbitofrontal cortex) when exposed to food images — even before eating a single bite. The brain is already in anticipation mode, already wanting, already noisy.
The Default Mode Network and Food Rumination
Beyond the mesolimbic pathway, food noise also involves the default mode network (DMN) — the brain's "idle" mental activity system that activates when you're not focused on an external task. In people with obesity, the DMN appears dysregulated, spending its idle cycles generating food-related thoughts rather than more neutral mental content. GLP-1 drugs appear to modulate DMN activity. The Cureus review noted that in studies blocking endogenous GLP-1, the DMN was more activated — and that those with the biggest GLP-1-driven changes in DMN connectivity also reported the greatest reductions in hunger. The drug may literally be reorganizing the brain's resting-state mental content.
Where GLP-1 Receptors Live in the Brain
Here's the key insight: GLP-1 isn't just a gut hormone. It's a brain signal.
GLP-1 receptors (GLP-1Rs) are expressed throughout the central nervous system, positioned in exactly the regions you'd want to modulate if your goal was quieting food noise:
- Area postrema: A circumventricular organ at the base of the brainstem — one of the few places where the blood-brain barrier is naturally permeable. A key site for sensing circulating GLP-1 and triggering nausea and satiety signals.
- Nucleus tractus solitarius (NTS): Located in the brainstem, the NTS is sometimes called the "emergency brake" on eating. It integrates signals from the gut and sends satiety messages upward into the brain.
- Hypothalamus (arcuate nucleus): The master regulator of hunger and energy balance. GLP-1 signaling here suppresses appetite by modulating pro-opiomelanocortin (POMC) neurons that signal fullness.
- VTA and nucleus accumbens: The core of the mesolimbic reward pathway. As research published in Endocrinology confirmed, GLP-1-producing neurons in the NTS project directly to the VTA and NAc — meaning the brain's own GLP-1 system has a dedicated connection to the reward circuitry.
- Hippocampus: Involved in memory formation around food cues. GLP-1 signaling here may reduce the motivational salience of food memories.
This wide distribution isn't accidental. It means GLP-1 is doing more than just saying "you're full." It's restructuring the entire value system the brain places on food.
Two Roads to the Brain: How GLP-1 Drugs Get Past the Blood-Brain Barrier
GLP-1 receptor agonist drugs like semaglutide and tirzepatide are large peptide molecules. The brain is normally protected by the blood-brain barrier (BBB), a tight cellular seal that keeps most molecules out. So how do these drugs reach brain reward centers? There are two main pathways:
Pathway 1: Vagal Afferent Nerve Signaling
The vagus nerve runs from the gut to the brainstem, acting as the body's primary gut-to-brain communication cable. GLP-1 drugs activate GLP-1 receptors on vagal nerve endings in the gut wall, sending electrical signals up to the NTS and brainstem. This is fast signaling — within minutes of a meal or drug action. Think of it as a phone call from your stomach directly to your brain's appetite control center.
Pathway 2: Circumventricular Organs (CVOs)
Certain regions of the brain — the area postrema, subfornical organ, and organum vasculosum of the lamina terminalis — have no blood-brain barrier. They're specifically designed to sense circulating hormones and drugs. GLP-1 drugs can access the brain through these "windows," entering and diffusing into adjacent brain regions. This is likely the major route by which pharmacological doses reach the VTA and nucleus accumbens.
The combination of these two pathways gives GLP-1 drugs broad access to the brain's appetite and reward architecture in ways that simple dietary changes or willpower cannot achieve.
The NTS: The Brain's Emergency Brake on Eating
The nucleus tractus solitarius deserves its own moment of attention. It sits at the back of the brainstem and is essentially the brain's primary "stop eating" center. It receives signals from:
- The stomach (stretching, fullness)
- The intestines (nutrient sensing)
- The vagus nerve (chemical signals from the gut)
- Circulating hormones including GLP-1
When the NTS is activated — by a large meal, by GLP-1 release, or by a GLP-1 drug — it fires signals upward to the hypothalamus and downward to motor circuits that control eating behavior. Think of it as a circuit breaker. In people with obesity, this circuit breaker may be sluggish or desensitized. GLP-1 drugs are essentially resensitizing it — turning up the gain on satiety signaling so the brake engages sooner and more powerfully.
Neuroimaging Evidence: What Happens in the Brain on GLP-1
The clearest proof that GLP-1 drugs change the brain comes from functional MRI (fMRI) studies that watch brain activity in real time as participants look at images of food.
van Bloemendaal et al. (2014)
This landmark study placed obese T2DM patients and normoglycemic obese and lean individuals (n=48) in an fMRI scanner and showed them pictures of food. The key finding: obese individuals showed increased brain responses to food pictures in appetite- and reward-related regions (insula, amygdala). When the GLP-1 receptor agonist exenatide was administered intravenously, it decreased food-related brain responses in the insula, amygdala, putamen, and orbitofrontal cortex — and participants subsequently ate less at a buffet meal. Blocking GLP-1 receptors with exendin 9-39 reversed these effects. The drug wasn't changing their willpower. It was changing their brain's response to food cues.
ten Kulve et al. (2016)
A follow-up study used fMRI to examine the physiological role of endogenous GLP-1 after a meal. In obese T2DM patients, blocking endogenous GLP-1 (using exendin 9-39) prevented the normal meal-induced reduction in brain activation to food pictures — particularly in the insula and orbitofrontal cortex, regions involved in food craving and reward evaluation. In other words, natural GLP-1 released after eating normally helps "switch off" food-reward brain activation. In obesity, this switch may be partially broken. GLP-1 drugs essentially force it back on.
The Brain Reward Anticipation Study (2015)
Ten Kulve and colleagues also examined anticipatory vs. consummatory reward. They found that GLP-1 receptor activation decreased anticipatory food reward (the "wanting") while increasing consummatory food reward (the satisfaction of actually eating). This is clinically important: the drug doesn't make food taste bad. It reduces the desperate wanting that drives food noise, while letting people actually enjoy what they eat. The result: smaller portions feel more satisfying.
Dopamine Modulation: Quieting the "Wanting" System
Now here's where the science gets truly interesting. Research from Science Advances (2025) reveals the precise cellular mechanism behind GLP-1's dopamine modulation. GLP-1 receptors in the VTA are expressed primarily on GABA neurons — inhibitory interneurons that pump the brakes on dopamine neurons. When GLP-1 activates these GABA neurons, they suppress dopamine neuron firing. The result: less dopamine release in the nucleus accumbens in response to reward stimuli, including food and drugs.
This elegant circuit means GLP-1 doesn't eliminate dopamine signaling (which would be catastrophic — dopamine is essential for motivation, movement, and mood). Instead, it dials down the magnitude of the dopamine spike triggered by hyper-palatable foods. The brain still enjoys food. It just doesn't go into hyperdrive about it.
Using the language of addiction science: GLP-1 reduces both the wanting (incentive salience driven by dopamine) and partially modulates the liking (hedonic response). High-fat, high-sugar foods become less neurologically compelling. The brain stops treating them as exceptional events worth obsessing over.
The Decision Fatigue Reduction Effect
One of the less-discussed but enormously meaningful effects patients report is this: making healthy food choices becomes easier. Not because they want pizza less (though they often do), but because they're not exhausted from constantly fighting off food thoughts all day.
Decision fatigue is real and well-documented in psychology. Willpower operates like a muscle — the more you use it, the more depleted it becomes. People who spend all day fighting food cravings have less cognitive and emotional resources left for everything else. When food noise goes quiet on GLP-1 therapy, this cognitive load is lifted. Suddenly, the healthy choice isn't a heroic act of discipline. It's just... what happens. This may be one of the underappreciated behavioral mechanisms through which GLP-1 drugs produce sustained weight loss in ways that diets alone never could.
STEP Trial Evidence: What Patients Actually Report
The STEP (Semaglutide Treatment Effect in People with Obesity) clinical trial program included patient-reported outcome measures alongside weight loss data. The Control of Eating Questionnaire (CoEQ), validated in obesity research, was used to capture subjective food craving experience.
Results from the STEP trials showed significant improvements across multiple CoEQ domains in semaglutide-treated patients compared to placebo, including:
- Reduced craving for sweet foods
- Reduced craving for savory/fatty foods
- Reduced hunger intensity
- Improved fullness after eating
- Reduced positive mood toward eating
These findings match what patients describe anecdotally: the drug changes the emotional and motivational relationship with food, not just the mechanical hunger signal. The food noise reduction is a measurable phenomenon, not just anecdote.
GLP-1 and Addiction: The Same Reward Pathway
The mesolimbic dopamine system doesn't just care about food. It's the same circuit that underlies addiction to alcohol, nicotine, opioids, and other substances. If GLP-1 drugs modulate dopamine signaling in this circuit, you'd expect them to affect addictive behaviors too — and that's exactly what researchers (and users) are finding.
The Grigson lab at Penn State conducted the first randomized controlled trial testing liraglutide (a GLP-1 RA) in opioid use disorder. Among 20 patients, those on liraglutide experienced a 40% reduction in opioid cravings over three weeks — at even the lowest doses. A 2025 JAMA Psychiatry trial found that semaglutide significantly reduced alcohol craving and weekly alcohol consumption in adults with alcohol use disorder. The same quieting of dopaminergic reward drive that silences food noise also appears to silence the call of addictive substances.
This isn't a side effect. It's the same mechanism operating across all reward-seeking behaviors. The GLP-1 system evolved as a broad satiety and reward-modulating system. Modern GLP-1 drugs are tapping into that breadth.
Microdosing and Food Noise: The Neurological Dose Question
An emerging clinical observation is that some patients find lower doses of semaglutide (0.25–0.5 mg/week, far below the therapeutic 2.4 mg weight-loss dose) achieve the food noise reduction effect even when they produce minimal weight loss. This matters because:
- The neurological effects of GLP-1 (food noise quieting, craving reduction) may require a lower receptor occupancy threshold than the metabolic effects (insulin secretion, gastric emptying).
- Some patients tolerate microdoses far better than standard doses — with fewer GI side effects.
- For patients whose primary goal is mental wellness around food (not substantial weight loss), microdosing may be a reasonable clinical discussion.
This is still early and mostly observational. But the pattern suggests that the brain reward modulation of GLP-1 drugs may operate through a different pharmacodynamic curve than their metabolic effects — a meaningful distinction for future prescribing and research.
Why Some People Don't Experience the Food Noise Effect
Not everyone describes the "quiet" experience. Some patients report modest appetite reduction but no dramatic change in food preoccupation. Several explanations exist:
GLP-1 receptor density variation: Individual differences in GLP-1R expression in reward-relevant brain regions may determine how strongly the drug modulates dopamine circuits. People with fewer receptors in the VTA/NAc may experience less central effect.
Genetic variants in dopamine signaling: Polymorphisms in the DRD2 gene (dopamine receptor D2) and other reward-pathway genes are known to influence obesity risk and behavioral response to reward stimuli. These same variants may modulate GLP-1 responsiveness.
Baseline dopamine tone: People with higher baseline dopamine activity may show more dramatic dampening effects, while those with already-blunted dopamine responses may notice less change.
Comorbid psychiatric conditions: Depression, ADHD, and anxiety disorders all involve dopamine and the DMN in complex ways that may interact with GLP-1 drug effects unpredictably.
Dose insufficiency: The neurological dose-response curve may require higher doses than the patient is currently taking. Dose escalation sometimes awakens the food noise benefit that lower doses didn't produce.
Long-Term Neuroplasticity: What Happens to a Brain Freed from Food Noise
This is the frontier question. When food noise is suppressed for months or years, what happens to the brain?
The good news is that chronic suppression of hyperactive food-reward signaling may allow maladaptive neural circuits to normalize. Neuroplasticity — the brain's ability to rewire itself based on experience — works in both directions. Just as repeated exposure to hyper-palatable foods can sensitize reward circuits over time, reduced reward-seeking activity may allow them to desensitize back toward baseline. Some researchers hypothesize that sustained GLP-1 therapy could produce lasting changes in reward circuitry that persist even after the drug is stopped — though this remains speculative and the rebound in appetite after discontinuation suggests the circuits snap back quickly without ongoing drug action.
The Cureus review describes GLP-1s as "nudging the DMN in the direction of balance" — not permanently resetting it, but creating an extended period of neurological quietude in which patients can rebuild healthier behavioral patterns. Whether those patterns become self-sustaining is one of the most important questions in obesity medicine right now.
Comparison Table: GLP-1 Brain Regions and Their Functions
| Brain Region | GLP-1R Present | Primary Function | Effect of GLP-1 Activation |
|---|
| Area Postrema | Yes | Detects circulating hormones/toxins; triggers nausea | Amplifies satiety signal; contributes to nausea side effect |
| Nucleus Tractus Solitarius (NTS) | Yes (dense) | Satiety integration; vagal signaling hub | Fires "stop eating" signals; reduces food intake |
| Hypothalamus (Arcuate Nucleus) | Yes | Master hunger/energy regulator | Suppresses hunger via POMC neuron activation |
| Ventral Tegmental Area (VTA) | Yes (on GABA neurons) | Reward motivation; dopamine production | Inhibits dopamine neurons via GABA interneurons; reduces reward salience |
| Nucleus Accumbens (NAc) | Yes | Reward processing; "wanting" center | Reduces dopaminergic reward response to food |
| Hippocampus | Yes | Memory; food cue associations | May reduce motivational salience of food memories |
Frequently Asked Questions
Q: What is "food noise" and is it a real medical phenomenon?
A: Food noise refers to the persistent, involuntary mental preoccupation with food, cravings, and eating that many people with obesity experience throughout the day. While not a formal diagnostic term, it reflects measurable dysfunction in the brain's reward and default mode networks, where food-related thoughts intrude on daily cognitive function. Neuroimaging studies confirm that obese individuals show heightened brain activation in reward regions in response to food cues, providing a biological basis for this experience.
Q: How do GLP-1 drugs like semaglutide reduce food noise?
A: GLP-1 drugs activate GLP-1 receptors in the brain's reward circuit — particularly in the VTA and nucleus accumbens — where they stimulate GABA inhibitory neurons that pump the brakes on dopamine release. This reduces the dopaminergic "wanting" signal for food, making hyper-palatable foods neurologically less compelling. Additionally, GLP-1 drugs modulate the default mode network, reducing the brain's tendency to generate food-related rumination during idle mental states.
Q: Does semaglutide make food taste bad?
A: No. Research shows that GLP-1 receptor activation reduces anticipatory food reward (the craving and wanting) while actually maintaining or slightly increasing consummatory food reward (the satisfaction of eating). People on semaglutide often find smaller portions genuinely satisfying — the drug doesn't remove pleasure from food, it removes the frantic, obsessive quality of food desire.
Q: What brain imaging evidence exists for GLP-1's effects on food cravings?
A: Multiple fMRI studies demonstrate GLP-1's central effects. Van Bloemendaal et al. (2014) showed that intravenous GLP-1 receptor agonist reduced activation in the insula, amygdala, putamen, and orbitofrontal cortex when obese patients viewed food images. Ten Kulve et al. (2016) confirmed that blocking endogenous GLP-1 prevented meal-induced suppression of food-reward brain activation. Participants who received active GLP-1 drug also consumed significantly less food at a subsequent buffet meal.
Q: Why do GLP-1 receptors exist in reward-processing brain regions?
A: GLP-1 is produced not only in the gut but also by neurons in the nucleus tractus solitarius of the brainstem, which project directly to the VTA and nucleus accumbens. This reflects GLP-1's evolutionary role as a broad satiety and reward-modulating signal — the body evolved to reduce reward drive for food when nutrient needs are met. GLP-1 drugs amplify and extend this natural satiety signal.
Q: Does GLP-1 work through the blood-brain barrier?
A: GLP-1 drugs reach the brain through two routes: (1) activating GLP-1 receptors on vagal afferent nerve endings in the gut, sending electrical signals to the brainstem; and (2) accessing the brain through circumventricular organs (like the area postrema) where the blood-brain barrier is naturally permeable. These pathways allow pharmacological GLP-1 to influence central brain regions despite the barrier.
Q: Can lower (micro) doses of semaglutide still reduce food noise?
A: Clinical observations suggest that some patients experience meaningful food noise reduction at doses below the standard therapeutic range (0.25–0.5 mg/week vs. the 2.4 mg weight-loss dose). This may reflect a lower activation threshold for central reward modulation compared to full metabolic effects. However, this area lacks robust clinical trial data, and microdosing is not an FDA-approved or standard-of-care approach.
Q: Why doesn't everyone experience food noise reduction on GLP-1 drugs?
A: Individual variation in GLP-1 receptor density in brain reward regions, genetic differences in dopamine signaling pathways (particularly DRD2 receptor polymorphisms), baseline dopamine tone, and comorbid psychiatric conditions all influence how dramatically a person experiences the central appetite-quieting effects of GLP-1 drugs. Not everyone who takes these medications reports the dramatic "silence" of food thoughts — the effect appears to vary considerably.
Q: Does GLP-1 drug-induced food noise suppression carry neurological risks?
A: There are no established neurological harms from GLP-1-mediated dopamine modulation at therapeutic doses. Unlike drugs of abuse that deplete or overwhelm dopamine systems, GLP-1 drugs work through a physiological receptor pathway with natural feedback regulation. Some clinical trials have shown mixed mental health signals (including rare reports of mood changes), but these are not definitively linked to dopamine pathway modification and require further research.
Q: What happens to food noise when you stop taking GLP-1 drugs?
A: Most patients report that food noise returns within days to weeks of stopping GLP-1 medication, consistent with the drug's pharmacological half-life (approximately 1 week for semaglutide). This suggests the brain reward changes are driven by active drug presence rather than lasting neuroplastic rewiring. This is a key argument for long-term maintenance therapy in most patients rather than short-term treatment.
Q: Is the food noise effect related to GLP-1's anti-addiction properties?
A: Yes — they appear to share the same mechanism. The mesolimbic dopamine circuit that drives food noise is identical to the one that drives cravings for alcohol, nicotine, and opioids. GLP-1's dampening of dopaminergic reward signaling in the VTA and nucleus accumbens is likely why patients on semaglutide report not just quieter food thoughts, but also reduced desire for alcohol, nicotine, and other compulsive behaviors.
Q: What role does the default mode network play in food noise?
A: The default mode network (DMN) is the brain's "idle" system — active during mind-wandering, self-referential thought, and prospection. In people with obesity, the DMN appears to generate a disproportionate amount of food-related mental content. GLP-1 drugs appear to modulate DMN activity, correlating with patients' subjective reports of a "quieter" mental landscape. Those with the largest GLP-1-driven DMN changes also show the greatest appetite reductions.
Key Takeaways
- Food noise is a neuroscientifically real phenomenon — hyperactivated dopamine reward circuits make some brains treat food as a high-priority, ever-present concern rather than a background need.
- GLP-1 receptors are expressed throughout the brain's reward and satiety systems, including the VTA, nucleus accumbens, NTS, hypothalamus, and hippocampus — giving these drugs direct access to reward circuitry.
- Two pathways carry GLP-1 drug signals to the brain: vagal nerve afferents from the gut and circumventricular organs where the blood-brain barrier is permeable.
- fMRI studies (van Bloemendaal 2014, ten Kulve 2016) provide direct neuroimaging evidence that GLP-1 receptor activation reduces brain responses to food cues in reward-related regions.
- The cellular mechanism: GLP-1 activates GABA inhibitory interneurons in the VTA, which suppress dopamine neuron firing — reducing food's neurological "pull."
- Decision fatigue is reduced: quieter food thoughts free up cognitive resources, making healthy choices less effortful.
- The food noise effect is not universal — GLP-1 receptor density, dopamine genetics, and baseline mental health all modulate the central response.
- The same mechanism explains GLP-1's anti-addiction effects on alcohol, opioids, and nicotine — identical dopamine reward circuitry.
- Food noise returns when the drug is stopped, supporting long-term maintenance therapy for most patients.
Citations & References
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Van Bloemendaal L, et al. "GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans." Diabetes. 2014. https://pubmed.ncbi.nlm.nih.gov/25071023/
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Ten Kulve JS, et al. "Endogenous GLP-1 mediates postprandial reductions in activation in central reward and satiety areas in patients with type 2 diabetes." Diabetologia. 2016. https://pmc.ncbi.nlm.nih.gov/articles/PMC4630252/
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Ten Kulve JS, et al. "Brain reward-system activation in response to anticipation and consumption of palatable food is altered by glucagon-like peptide-1 receptor activation in humans." Diabetes Obes Metab. 2015. https://pubmed.ncbi.nlm.nih.gov/26094857/
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Alhadeff AL, et al. "GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake." Endocrinology. 2012. https://pmc.ncbi.nlm.nih.gov/articles/PMC3275387/
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Roth K, et al. "Quieting 'Food Noise': How GLP-1s and Mindfulness Rewire the Overactive Mind." Cureus. 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC12770913/
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Avila C, et al. "An endogenous GLP-1 circuit engages VTA GABA neurons to control cocaine seeking." Science Advances. 2025. https://www.science.org/doi/10.1126/sciadv.adr5051
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Grigson PS, et al. "Use of a GLP-1 agonist to treat opioid use disorder in rats and man." Penn State Research Project. https://pure.psu.edu/en/projects/use-of-a-glp-1-agonist-to-treat-opioid-use-disorder-in-rats-and-m-7/
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Fella Health. "What Part of the Brain Does GLP-1 Affect? Key Regions Explained." 2025. https://www.fellahealth.com/guide/what-part-of-the-brain-does-glp-1-affect
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Callondoc. "GLP-1 Microdosing and Food Noise: What's Actually Changing in the Brain." 2026. https://www.callondoc.com/en/blogs/glp-1-microdosing-and-food-noise-whats-actually-changing-in-the-brain
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Amsterdam UMC. "Brain reward-system activation in response to anticipation and consumption of palatable food is altered by GLP-1 receptor activation." https://pure.amsterdamumc.nl/en/publications/brain-reward-system-activation-in-response-to-anticipation-and-co/
