DanielChem_CHI 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.
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.
KristenIndy 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 cocktails most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 6 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 $200/month on alcohol. Triple win.
COA_Karl said:The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…
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:
Did your prescriber agree with that reading, and if not what was their objection?
Dr.BariatricHTX said:Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80%…
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.