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.
The bit I cannot resolve on my own 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.
I have searched first, so if this is covered somewhere point me at it and I will read it.
ChrisMacros 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…
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.
JennaRN said: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.
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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Shop Reference StandardsChrisMacros 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…
Can confirm. Same sequence, different timescale.
From the other side of the consultation, briefly.
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.