The thing that changed for me was not hunger, it was that the constant background negotiation about food simply stopped, and I had not realised it was constant until it was not.
What I actually want to know 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.
Tell me what I have not thought of.
TrialNerd_Beth said:The thing that changed for me was not hunger, it was that the constant background negotiation about food simply stopped, and I had not realised it was…
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.
Dr.SleepRoch said:The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…
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 $161/month on alcohol. Triple win.
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Browse GL BiochemTrialNerd_Beth said:The thing that changed for me was not hunger, it was that the constant background negotiation about food simply stopped, and I had not realised it was…
This matches mine closely enough to be worth saying so out loud. The detail I would add is minor and it is already implied above.
Adding the clinical framing, because it changes how the question reads.
Neuroscience perspective on food noise:
GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area postrema, and — critically — the mesolimbic reward pathway[1].
This is directly relevant to food noise because the central effects of GLP-1 agonists extend far beyond simple appetite suppression. The reduction in "food noise" that patients describe is likely mediated by modulation of dopaminergic signaling in the VTA and nucleus accumbens.
The emerging data on reduced addictive behaviors (alcohol, gambling) further supports this mechanism. food noise should be understood in this broader neurobiological context.
[1] Merchenthaler I, et al. J Comp Neurol. 1999;403(2):261-280.