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.
What I actually want to know 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.
Tell me what I have not thought of.
WendyG_ATL 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 $167/month on alcohol. Triple win.
Dr.RenalNash said:Alcohol relationship change with food noise: I used to drink 3-4 beers most nights.
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.
Sigma-Aldrich — Research-Grade Standards
Certified reference materials, analytical reagents, and research-grade standards for peptide verification. Trusted by laboratories worldwide.
Shop Reference StandardsWendyG_ATL 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.
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.