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.
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.
Tell me what I have not thought of.
ingrid_STO 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 2 glasses of wine most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 5 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 $231/month on alcohol. Triple win.
labquiet_amy said:Alcohol relationship change with food noise: I used to drink 2 glasses of wine 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 Biochemingrid_STO 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 experience, arrived at from the opposite direction. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads.
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.