KevinCompounds said:Phantom hunger vs real hunger on food noise: learning to distinguish between the two has been a revelation.
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 4 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 $170/month on alcohol. Triple win.
LondonLisa 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.
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.
Dr.ReproEndo said:Alcohol relationship change with food noise: I used to drink 2 glasses of wine most nights.
Neuroscience perspective on food noise:
GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area postrema, and — critically — the mesolimbic reward pathway[1].
This is directly relevant to food noise because the central effects of GLP-1 agonists extend far beyond simple appetite suppression. The reduction in "food noise" that patients describe is likely mediated by modulation of dopaminergic signaling in the VTA and nucleus accumbens.
The emerging data on reduced addictive behaviors (alcohol, gambling) further supports this mechanism. food noise should be understood in this broader neurobiological context.
[1] Merchenthaler I, et al. J Comp Neurol. 1999;403(2):261-280.
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Shop Reference StandardsA narrower follow-up, since the general answer is now clear:
What did you change at the same time, and can you separate the two now?
james_edin said:Neuroscience perspective on food noise: GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area…
james_edin said:...regarding food noise mechanism of action...
To build on this — the mechanism is more complex than "it makes you less hungry." GLP-1 agonists:
- Activate hypothalamic satiety centers (appetite reduction)
- Delay gastric emptying (prolonged fullness)
- Potentiate glucose-dependent insulin secretion
- Suppress glucagon secretion
- Modulate reward pathway dopaminergic signaling
- Reduce hepatic lipogenesis
- Have direct cardiovascular protective effects
It's a multi-target drug with systemic metabolic effects. Understanding the mechanism helps us predict and manage side effects.