Food Noise Isn’t Hunger — and Why Broccoli Never Fixed the Brain

Food noise does not announce itself politely. Instead, it hums in the background, persistent and exhausting. For years, patients tried to describe it. Meanwhile, medicine largely ignored it. Recently, however, GLP-1 receptor agonists forced the conversation into the open.

I did not understand food noise myself until it stopped.

About twelve hours after my first GLP-1 injection, I stood in my kitchen waiting for baked salmon to finish cooking. Nothing dramatic happened. No emotional moment followed. Still, something felt different. The internal commentary was gone. The negotiations disappeared. For the first time, my brain felt quiet.

At that moment, I finally understood what patients had been telling me for years.

First, Define the Problem Clearly

Food noise is not hunger. Hunger serves a biological purpose. In contrast, food noise describes persistent, intrusive thoughts about food that occur regardless of energy needs. People experience rumination, preoccupation, cravings, and mental fatigue—even when they are physiologically full.

Importantly, this phenomenon is now measurable. The Food Noise Questionnaire validates what patients already knew. Specifically, it assesses the frequency of food thoughts, difficulty controlling them, interference with daily activities, emotional distress, and craving intensity. In other words, food noise exists independently of willpower.

Consequently, advice that targets hunger alone inevitably fails.

Next, Address the Broccoli Myth

I eat vegetables. Nevertheless, I have never liked broccoli.

Frankly, if broccoli is air-fried to the edge of carbonization, I will tolerate it. That concession, however, does not transform broccoli into a neurological intervention. Fiber increases fullness. Protein improves satiety. Vegetables slow digestion. None of those actions quiet the reward centers of the brain.

Put simply, broccoli fills the stomach. Food noise lives elsewhere.

Because of that distinction, the “just eat for satiety” argument collapses under scrutiny.

Then, Follow the Science Where It Leads

Food noise arises from heightened food-cue reactivity. Visual cues, smells, availability, and anticipation activate reward pathways long before food reaches the stomach. Ultra-processed foods amplify this response. Their engineered combinations of refined carbohydrates, fats, salt, and flavor compounds reliably stimulate the mesolimbic dopamine system.

As a result, ultra-processed foods increase wanting rather than liking.

However—and this matters deeply—removing ultra-processed foods does not automatically restore normal appetite signaling. Once reward circuitry becomes dysregulated, dietary virtue alone cannot reset it. At that stage, telling someone to “just eat whole foods” resembles telling someone with tinnitus to “enjoy the silence.”

Therefore, ultra-processed foods contribute to the problem, but they do not explain it entirely.

Now, Enter GLP-1 Receptor Agonists

GLP-1 receptor agonists act centrally and peripherally. While many people fixate on gastric emptying, the central mechanisms explain the lived experience.

In the hypothalamus, GLP-1 receptor agonists activate satiety-promoting POMC/CART neurons while inhibiting hunger-promoting NPY/AgRP neurons. This dual action reduces homeostatic hunger. Meanwhile, in the brainstem—particularly the nucleus tractus solitarius—GLP-1 signaling integrates gut-brain communication and sustains appetite suppression.

More importantly, GLP-1 receptor agonists modulate reward circuitry. In regions such as the ventral tegmental area and nucleus accumbens, these agents dampen dopamine signaling. Consequently, food becomes less compelling rather than forbidden.

Functional imaging studies confirm this effect. After GLP-1 treatment, brain responses to food cues decrease in the insula, amygdala, orbitofrontal cortex, and related regions. The brain still recognizes food. It simply stops obsessing.

As a Result, Behavior Changes Without Force

Once food noise quiets, people do not suddenly become disciplined saints. Instead, they become selective.

In my own case, wine lost its appeal. I did not swear it off. I simply stopped wanting it. Eventually, I quit five wine clubs. When a glass tastes mediocre, I put it down and choose iced tea. That behavior reflects altered reward signaling, not moral growth.

Similarly, food choices shift without struggle. People stop eating things merely because they are available. They stop drinking because something is poured. The absence of compulsion creates space for intentional eating.

That distinction explains why GLP-1 therapy feels different from appetite suppression.

Finally, Place Diet Back Where It Belongs

The Mediterranean diet improves health. I recommend it. I eat it. Still, it does not cure food noise.

Diet supports metabolic health once interference disappears. GLP-1 therapy removes that interference. Together, they work better than either alone. Pretending otherwise leads to fat shaming disguised as nutritional advice.

Obesity is a disease. GLP-1 receptor agonists treat that disease. Food then becomes nourishment rather than negotiation.

So, What Actually Matters

Ultra-processed foods worsen food noise, yes. Yet removing them does not repair dysregulated reward circuitry. Satiety fills the stomach. GLP-1 therapy quiets the brain. Once the noise fades, nutrition finally has a fair chance.

In the end, broccoli keeps my mother from returning from the grave. GLP-1s keep my brain quiet. Both have their place. Only one treats the disease.

REFERENCES:

1. Medications for Obesity: A Review.

The Journal of the American Medical Association. 2024. Gudzune KA, Kushner RF.

2. The Arcuate Nucleus Mediates GLP-1 Receptor Agonist Liraglutide-Dependent Weight Loss.

The Journal of Clinical Investigation. 2014. Secher A, Jelsing J, Baquero AF, et al.

3. Direct and Indirect Effects of Liraglutide on Hypothalamic POMC and NPY/­AgRP Neurons - Implications for Energy Balance and Glucose Control.

Molecular Metabolism. 2019. He Z, Gao Y, Lieu L, et al.

4. On the Pleiotropic Actions of Glucagon-Like Peptide-1 in Its Regulation of Homeostatic and Hedonic Feeding.

International Journal of Molecular Sciences. 2025. Sayers S, Wagner E.New

5. Glucagon-Like Peptide 1 (GLP-1) Action on Hypothalamic Feeding Circuits.

Endocrinology. 2025. Hwang E, Portillo B, Williams KW.New

6. GABA Neurons in the Nucleus Tractus Solitarius Express GLP-1 Receptors and Mediate Anorectic Effects of Liraglutide in Rats.

Science Translational Medicine. 2020. Fortin SM, Lipsky RK, Lhamo R, et al.

7. GLP-1 Receptor Activation Modulates Appetite- And Reward-Related Brain Areas in Humans.

Diabetes. 2014. van Bloemendaal L, IJzerman RG, Ten Kulve JS, et al.

8. Glucagon-Like Peptide 1 and Its Analogs Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight.

Diabetes. 2017. Anderberg RH, Richard JE, Eerola K, et al.

9. of GLP-1 Therapies for Addiction and Mental Health Comorbidities—Quo Vadis?.

JAMA Psychiatry. 2026. Farokhnia M, Leggio L.New

10. GLP-1 and Weight Loss: Unraveling the Diverse Neural Circuitry.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 2016. Kanoski SE, Hayes MR, Skibicka KP.

11. Mechanisms of GLP-1 Receptor Agonist-Induced Weight Loss: A Review of Central and Peripheral Pathways in Appetite and Energy Regulation.

The American Journal of Medicine. 2025. Moiz A, Filion KB, Tsoukas MA, et al.New

12. GLP-1 Physiology and Pharmacology Along the Gut-Brain Axis.

The Journal of Clinical Investigation. 2026. Beutler LR.New