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 would genuinely help is knowing 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.
pete_nash 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.
The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related hospitalizations in GLP-1 agonist users[1].
The mechanism is plausible: GLP-1R is expressed in the mesolimbic reward pathway (VTA, nucleus accumbens). Agonism at these receptors may reduce the reinforcing properties of alcohol, similar to the reduction in "food noise."
RCTs for GLP-1 agonists in AUD are now underway. If positive, this would be a paradigm-shifting repurposing of existing medications.
[1] Wang W, et al. Nat Med. 2024;30:574-584.
DebRD_ATL said:The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…
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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Shop Reference Standardspete_nash 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.
Can confirm. Same sequence, different timescale.
Clinical perspective, offered as context rather than as advice.
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.