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.
Practical detail welcome, however dull — the duller the better.
kevin_tulsa 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.
kevin_tulsa said:...regarding food noise mechanism of action...
To build on this — the mechanism is more complex than "it makes you less hungry." GLP-1 agonists:
- Activate hypothalamic satiety centers (appetite reduction)
- Delay gastric emptying (prolonged fullness)
- Potentiate glucose-dependent insulin secretion
- Suppress glucagon secretion
- Modulate reward pathway dopaminergic signaling
- Reduce hepatic lipogenesis
- Have direct cardiovascular protective effects
It's a multi-target drug with systemic metabolic effects. Understanding the mechanism helps us predict and manage side effects.
NurseKim_ATL said:kevin_tulsa said: ...regarding food noise mechanism of action...
Alcohol relationship change with food noise: I used to drink 2 glasses of wine most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 11 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 $197/month on alcohol. Triple win.
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Browse GL Biochemkevin_tulsa 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.
Mine went the same way, slower. Nothing to add that would improve it.
From the other side of the consultation, briefly.
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.