Counting rather than debating, for once. The debate can happen underneath.
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.
So the question, as narrowly as I can put it: 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.
SteveThurs 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.
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.
LipidDoc_ATL said:The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…
Rebound hunger after missed dose of food noise: I missed my injection by 3 days due to a shipping delay and the hunger came ROARING back. Like a switch flipped. It was eye-opening to feel the difference.
This experience actually reinforced my understanding of what the medication does — it's not just "suppressing appetite," it's normalizing dysregulated hunger signaling. When the drug wears off, you feel the full force of what it was managing.
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Browse GL BiochemSteveThurs 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.
Same pattern here, and in the same order. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads.
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.