How Zepbound and Ozempic Quiet Food Noise
And why you should get a cat who eats broccoli
Food Noise Isn’t Hunger — and the Lack of Empathy in Medicine Is Making Obesity Worse
For years, patients tried to describe something medicine struggled to name. Meanwhile, clinicians often redirected the conversation toward discipline, diet plans, or personal responsibility. Eventually, however, GLP-1 receptor agonists forced a long-overdue reckoning. As a result, food noise finally entered the medical conversation.
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. Nevertheless, something unmistakable changed. The internal commentary vanished. The negotiations ended. For the first time, my brain felt quiet.
Only then did patient stories fully make sense.
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. Specifically, 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. It assesses frequency of food thoughts, difficulty controlling them, interference with daily activities, emotional distress, and craving intensity. Consequently, food noise moved from anecdote to data.
Because of that distinction, advice aimed solely at hunger inevitably fails.
However, Patients Face a Bigger Problem Than Biology
Before we go deeper into neurobiology, we need to confront something uncomfortable: many patients encounter judgment instead of care when they seek help.
Recently, two physicians publicly dismissed GLP-1 therapy as a “crutch” and framed obesity as a failure of discipline rather than a disease. One is Jack Wolfson, who brands himself online as The Natural Heart Doctor. The other is Whitfield Lewis, who promotes a personally branded dietary framework as a substitute for medical treatment.
Both arguments followed the same predictable pattern.
First, they reduced GLP-1 medications to “appetite suppressants.”
Next, they insisted that satiety alone should replace pharmacologic therapy.
Finally, they ignored the central nervous system entirely.
That pattern matters.
Not because it is shocking, but because it is common. More importantly, it shows exactly what people with obesity are up against. Instead of empathy, they receive moral judgment. Instead of physiology, they get ideology. Instead of treatment, they get lectures.
Crucially, neither argument acknowledges obesity as a disease.
Instead, both rely on moralized eating narratives. If a patient struggles, they “lack discipline.” If medication helps, it “doesn’t count.” If biology intervenes, it is dismissed as weakness.
That approach is not evidence-based medicine. It is belief layered onto physiology.
As a result, patients delay care.
Consequently, shame replaces treatment.
Over time, trust in medicine erodes.
This is not a patient failure.
This is a professional failure.
Next, Understand Why “Just Eat Better” Falls Apart
Predictably, the conversation turns to satiety. Fiber increases fullness. Protein helps appetite control. Vegetables slow digestion. All of that is true. However, none of those interventions address reward circuitry.
Here, broccoli inevitably enters the chat.
For honesty’s sake, I do not like broccoli. Frankly, if broccoli is air-fried to the edge of carbonization, I will tolerate it. Even so, tolerating vegetables never rewired my brain. Therefore, while vegetables support health, they do not silence intrusive food thoughts.
Put differently, satiety fills the stomach. Food noise lives elsewhere.
Meanwhile, Ultra-Processed Foods Complicate the Picture
At this point, many people argue that ultra-processed foods explain everything. To a degree, they are right. Ultra-processed foods reliably activate reward pathways. Their engineered combinations of refined carbohydrates, fats, salt, and flavor compounds stimulate the mesolimbic dopamine system.
As a result, ultra-processed foods increase wanting rather than liking.
However, this explanation remains incomplete. Although ultra-processed foods worsen food noise, removing them does not automatically normalize appetite signaling. Once reward circuitry becomes dysregulated, dietary virtue alone cannot reset it. Consequently, telling someone to “just eat Mediterranean” resembles telling someone with tinnitus to enjoy silence.
Thus, ultra-processed foods matter, but they do not fully explain food noise.
Therefore, the Brain Must Enter the Conversation
GLP-1 receptor agonists change the discussion because they act centrally, not just peripherally. While many people fixate on slowed gastric emptying, the lived experience comes from the brain.
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 set it down and choose iced tea.
That shift reflects altered reward signaling, not moral growth.
And this is the point: GLP-1 therapy removes interference. Diet then has a chance to work.
A Brief, Necessary Digression About Broccoli, My Cat Suzie, and Magical Thinking
At this point, someone always says, “But if people just ate better food, wouldn’t that solve most of this?”
This is where broccoli enters the story.
Let me start with a confession. I have never liked broccoli. I eat it, yes, but enjoyment is a strong word. If broccoli is air-fried to the edge of crispness—somewhere between “vegetable” and “char”—I will tolerate it. That is the extent of our relationship.
As a child, however, I attempted a workaround.
We had a cat named Suzie. I discovered early on that if I pushed broccoli far enough to the edge of my plate, Suzie might take care of it for me. Unfortunately, my mother noticed that Suzie, a creature with excellent instincts, would not eat broccoli either.
Mom closed that loophole quickly.
Suzie understood something important: broccoli is not magic.
And neither is “eating great food.”
Now, to be fair, whole foods do some of what GLP-1s do. Fiber slows gastric emptying. Protein increases satiety. Volume and texture can enhance fullness. In that sense, food can partially mimic peripheral GLP-1 effects.
That’s real physiology.
However, here’s the part lost in the wellness translation.
Broccoli does not act on the arcuate nucleus of the hypothalamus.
Broccoli does not inhibit NPY/AgRP neurons.
Broccoli does not dampen dopamine signaling in the nucleus accumbens.
And broccoli does not quiet food cue reactivity at 10 p.m.
In other words, broccoli fills the stomach.
Food noise lives in the brain.
That distinction explains why people can eat beautiful, Mediterranean, high-fiber, protein-forward meals—and still spend the rest of the evening thinking about food. The food did its job. The brain simply didn’t get the message.
GLP-1 therapy changes that conversation.
It doesn’t replace good food. It removes interference, so good food finally has a chance to work.
Suzie never ate broccoli.
I still don’t like broccoli.
And neither of us ever found that vegetables alone fixed the noise.
I still eat vegetables, mostly because if I didn’t my mom would return from the grave. Trust me, it's better to live with a category 5 hurricane.
Medicine exists for the parts food cannot reach.
And that’s not weakness. That’s biology.
Biology beats willpower.
Obesity is a disease.
Get a cat who likes vegetables.
In the Paid section, we go into depth about the role of the brain in food noise. My paid folks love nerdy stuff - I think.
