Food Noise Explained: What Brain Scans Actually Show

What Is "Food Noise"?

The term "food noise" has exploded into public awareness alongside GLP-1 medications, but until recently it lacked a formal scientific definition. Researchers have now provided one.

Earlier work by Hayashi et al. in Nutrients (2023) defined food noise as "heightened and/or persistent manifestations of food cue reactivity, often leading to food-related intrusive thoughts and maladaptive eating behaviors." The researchers proposed the CIRO model (Cue–Influencer–Reactivity–Outcome) as a framework for understanding how environmental food cues trigger these responses.

The distinction matters: everyone thinks about food. Food noise refers specifically to thoughts that are unwanted, intrusive, and interfere with daily life—more akin to rumination than normal appetite signals.

Survey Data: How Many People Experience Food Noise?

A survey presented at EASD 2025 (the INFORM study) by Novo Nordisk and Market Track LLC examined food noise in 550 U.S. adults taking semaglutide for weight loss. The results were striking:

Food Noise Metric	Before Semaglutide	During Treatment
Constant thoughts about food throughout the day	62%	16%
Spent too much time thinking about food	63%	15%
Food noise disrupts daily life	60%	20%

Participants also reported improvements in mental health (64%), self-confidence (76%), and healthier habits (80%) after starting treatment. Some 81% had been on semaglutide for at least four months. The study used a validated 22-question Food Noise Questionnaire.

A separate survey by Moser and colleagues examined 411 adults on GLP-1 medications for at least 3 months and found that 58% reported feeling less hungry and 64% reported feeling fuller sooner. About one-fifth reported changes in taste perception: food tasting sweeter (21%) or saltier (23%).

The Brain Imaging Evidence

The 2025 Tirzepatide fMRI Trial

The most rigorous recent evidence comes from a randomized Phase 1 trial published in Nature Medicine (June 2025) by Martin et al. at Pennington Biomedical Research Center. This study used functional MRI to examine brain activity in real-time.

The primary outcome was change in energy intake at an ad libitum lunch at week 3. The results:

Outcome	Tirzepatide vs Placebo
Energy intake reduction at week 3	−524.6 kcal (95% CI: −648.1 to −401.0)
Percent reduction from baseline	72%
Statistical significance	P < 0.0001

The fMRI results showed that tirzepatide decreased brain activation in response to images of high-fat, high-sugar foods in several key regions:

• Medial frontal gyrus — involved in decision-making and reward evaluation
• Cingulate gyrus — linked to emotion and craving
• Orbitofrontal cortex — encodes the pleasantness and reward value of food
• Hippocampus — involved in memory and contextual associations

Critically, the study found that tirzepatide did NOT increase "cognitive restraint"—meaning participants weren't consciously trying harder to restrict their eating. The reduction in intake appeared to happen without volitional effort, suggesting the medication works by reducing the brain's drive toward food rather than increasing willpower.

Earlier Exenatide Studies

These findings build on earlier work with first-generation GLP-1 medications. A 2014 study by van Bloemendaal et al. in Diabetes examined 48 subjects (lean, obese, and obese with T2DM) using fMRI during intravenous exenatide infusion.

The researchers found that exenatide decreased food-related brain responses in:

• Insula — taste perception and interoception
• Amygdala — emotional and aversive processing
• Putamen — part of the striatum, involved in reward
• Orbitofrontal cortex — reward valuation

Importantly, these effects were observed specifically in obese subjects and T2DM patients—the groups who showed increased baseline activation compared to lean controls. The medication appeared to normalize the heightened reward response.

The First-in-Human Brain Electrode Study

Perhaps the most remarkable recent finding comes from a case study published in Nature Medicine (November 2025) that recorded electrical activity directly from inside the human brain.

Researchers at the University of Pennsylvania were conducting a trial of deep brain stimulation for loss-of-control eating. They implanted electrodes in the nucleus accumbens (NAc)—the brain's central reward hub—of three patients with severe obesity and binge eating disorder. One participant happened to be taking tirzepatide for diabetes management.

In the two participants NOT taking tirzepatide, the researchers identified a specific electrical signature—increased "delta-theta" frequency power (≤7 Hz) in the nucleus accumbens—that correlated with episodes of severe food preoccupation. This brain signal appeared just before or during moments of intense food craving.

In the participant taking tirzepatide at maximum dose:

• Initially, the delta-theta activity in the NAc was quiet
• She reported NO food preoccupation during months 2-4 after dose escalation
• Brain signals reflected this silence

The Effect Didn't Last

After approximately five months on maximum dose tirzepatide, something changed:

The study authors emphasize this is a single case, and the findings cannot be generalized. However, it suggests that tirzepatide's effects on food preoccupation may involve tolerance or adaptation in the brain's reward circuitry over time.

How Do GLP-1s Reach the Brain?

GLP-1 (glucagon-like peptide-1) is secreted by intestinal L-cells after eating. Pharmaceutical GLP-1 receptor agonists mimic this hormone. But how do these large peptide molecules affect brain function?

According to research published in the International Journal of Obesity:

The circumventricular organs are specialized brain regions that lack a complete blood-brain barrier, allowing them to sense circulating hormones directly. From these entry points, GLP-1 signals can activate a distributed network of brain regions involved in appetite regulation.

The vagus nerve also plays a role: studies in rodents show that peripherally injected exendin-4 (a GLP-1 analog) caused neural activity in the hypothalamus and limbic structures, and these effects were partially abolished by vagotomy—cutting the vagus nerve.

Beyond Food: Implications for Addiction

If GLP-1 medications dampen the brain's reward response to food, could they work for other rewarding substances? The same neural circuitry—insula, amygdala, striatum, orbitofrontal cortex—responds to alcohol, nicotine, opioids, and other drugs.

According to a December 2025 feature in Nature:

• A small trial of liraglutide in 20 patients with opioid-use disorder reduced craving by approximately 40%
• fMRI studies showed exenatide produced "muted activity in reward-related regions when participants viewed images of alcoholic drinks"
• Multiple clinical trials of semaglutide for alcohol dependence are underway, with fMRI to capture brain changes

The anecdotal reports are intriguing: one man wrote to researchers that after years of addiction to opioids, "he was drug- and alcohol-free for the first time in his adult life" after starting semaglutide. Clinical trials will determine if this translates to broader populations.

Key Limitations and Open Questions

The science of "food noise" is still early-stage. Critical limitations include:

Definition still evolving. The RAID-FN Inventory (Ro Allison Indiana Dhurandhar-Food Noise Inventory) for measuring food noise was only recently developed. Different studies use different measures.

Survey data is retrospective. Asking people to recall their pre-treatment experiences introduces memory bias. Prospective studies measuring food noise before and during treatment are needed.

Tolerance question unresolved. The NAc electrode case study suggests effects may wane, but this was n=1. Larger, longer studies are required.

Weight loss vs. drug effect. It's unclear how much "food noise reduction" comes from the medication directly versus from weight loss itself. Disentangling these effects is challenging.

Not FDA-approved for food preoccupation. GLP-1 medications are approved for diabetes and obesity. Their effects on eating disorders or food preoccupation have not been formally studied for regulatory approval.