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 narrow version of the question is 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.
Happy to be told the question itself is wrong.
wanda_boise 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.
Alcohol relationship change with food noise: I used to drink cocktails most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 7 months.
The "food noise" reduction seems to extend to other reward-seeking behaviors, including alcohol. My liver enzymes have improved, my sleep is better, and I've saved roughly $237/month on alcohol. Triple win.
BethLabQueen said:Alcohol relationship change with food noise: I used to drink cocktails most nights.
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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Shop Reference Standardswanda_boise 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.
This is my experience too, for whatever a second data point is worth. The detail I would add is minor and it is already implied above.
Clinical perspective, offered as context rather than as advice.
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.