BenResearch_OR said:"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants.
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.
NauseaFreeNow 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.
NauseaFreeNow 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.
Dr.LipidDallas said:Neuroscience perspective on food noise: GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area…
Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80% of the weight loss effect is centrally mediated[1].
The key brain regions: arcuate nucleus (appetite), area postrema (nausea), NTS (satiety), VTA/NAc (reward). Peripheral effects (gastric emptying, insulin secretion) contribute but are secondary for weight loss.
This has implications for next-gen drugs: optimizing brain penetration and CNS receptor occupancy may be more important than systemic exposure.
[1] Secher A, et al. J Clin Invest. 2014;124(10):4473-4488.
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Shop Reference StandardsA narrower follow-up, since the general answer is now clear:
How would you tell the difference between that and the alternative explanation?
VendorMark said:Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80%…
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.