Asking this as a poll because the anecdotes are plentiful and the distribution is not.
The food noise came back three weeks after I reduced my dose, well before the weight moved, which tells me something about which effect tracks what.
What would genuinely help is knowing whether the quiet is the same mechanism as the appetite suppression or a separate one, because they seem to come and go on different schedules.
Roughly, people seem to land in one of these:
- Held where they were and waited it out
- Changed one variable and kept everything else fixed
- Changed several things at once and cannot now attribute the result
- Stopped and reassessed from a clean baseline
Say which and say why — the why is the useful half.
mike_mod said:The food noise came back three weeks after I reduced my dose, well before the weight moved, which tells me something about which effect tracks what.
"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants. Now certain foods — especially sweets — literally repulse me.
It's not just reduced appetite; it's an active disgust response. My therapist says this is common and likely related to the reward pathway modulation. It's mostly a positive change, but I do miss enjoying food the way I used to.
Dr.NateNeph said:"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants.
The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related hospitalizations in GLP-1 agonist users[1].
The mechanism is plausible: GLP-1R is expressed in the mesolimbic reward pathway (VTA, nucleus accumbens). Agonism at these receptors may reduce the reinforcing properties of alcohol, similar to the reduction in "food noise."
RCTs for GLP-1 agonists in AUD are now underway. If positive, this would be a paradigm-shifting repurposing of existing medications.
[1] Wang W, et al. Nat Med. 2024;30:574-584.
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Browse GL Biochemmike_mod said:The food noise came back three weeks after I reduced my dose, well before the weight moved, which tells me something about which effect tracks what.
Adding a me-too, because a thread of one person's experience is not much use. I had assumed I was the exception until I read this.
From the other side of the consultation, briefly.
Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80% of the weight loss effect is centrally mediated[1].
The key brain regions: arcuate nucleus (appetite), area postrema (nausea), NTS (satiety), VTA/NAc (reward). Peripheral effects (gastric emptying, insulin secretion) contribute but are secondary for weight loss.
This has implications for next-gen drugs: optimizing brain penetration and CNS receptor occupancy may be more important than systemic exposure.
[1] Secher A, et al. J Clin Invest. 2014;124(10):4473-4488.