Counting rather than debating, for once. The debate can happen underneath.
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.
What I am trying to establish 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.
Roughly, people seem to land in one of these:
- Held where they were and waited it out
- Changed one variable and kept everything else fixed
- Changed several things at once and cannot now attribute the result
- Stopped and reassessed from a clean baseline
Say which and say why — the why is the useful half.
SteveThurs 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.
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 $207/month on alcohol. Triple win.
LarryQC_SD 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.
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Browse GL BiochemSteveThurs 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.
Same pattern here, and in the same order.
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.