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 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.
I have searched first, so if this is covered somewhere point me at it and I will read it.
gary_naperville 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.
kate.chem said:The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…
Phantom hunger vs real hunger on food noise: learning to distinguish between the two has been a revelation. Real hunger: gradual onset, physical stomach sensation, any food sounds good. Phantom hunger: sudden, emotionally triggered, specific food cravings, occurs right after eating.
The GLP-1 agonist suppresses real hunger beautifully. Phantom hunger still pops up but I can now recognize it for what it is — an emotional signal, not a physical need. Mindfulness training helped enormously with this distinction.
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Browse GL Biochemgary_naperville 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…
Adding a me-too, because a thread of one person's experience is not much use. 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.