Fork U with Dr. Terry Simpson podcast

How GLP-1 Quiets Food Noise

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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...

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