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.
lisa_labSD 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 3-4 beers most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 9 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 $179/month on alcohol. Triple win.
Dr.PeteFamMed said:Alcohol relationship change with food noise: I used to drink 3-4 beers most nights.
"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants. Now certain foods — especially red meat — literally repulse me.
It's not just reduced appetite; it's an active disgust response. My therapist says this is common and likely related to the reward pathway modulation. It's mostly a positive change, but I do miss enjoying food the way I used to.
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Browse GL Biochemlisa_labSD 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…
This is my experience too, for whatever a second data point is worth. Nothing to add that would improve it.
From the other side of the consultation, briefly.
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.