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 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.
Practical detail welcome, however dull — the duller the better.
ChrisMacros 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.
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. Like a switch flipped. It was eye-opening to feel the difference.
This experience actually reinforced my understanding of what the medication does — it's not just "suppressing appetite," it's normalizing dysregulated hunger signaling. When the drug wears off, you feel the full force of what it was managing.
julia.endo 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.
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 BiochemChrisMacros 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.
Second this. I had assumed I was the exception until I read this.
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.