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 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.
I have searched first, so if this is covered somewhere point me at it and I will read it.
ingrid_STO 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…
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 8 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 $162/month on alcohol. Triple win.
sarah.morrison said:Alcohol relationship change with food noise: I used to drink 2 glasses of wine most nights.
sarah.morrison 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.
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Shop Reference Standardsingrid_STO 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…
Same pattern here, and in the same order.
Clinical perspective, offered as context rather than as advice.
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.