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.
Not looking for reassurance. Looking for the part I have got wrong.
Dr.MetabolicMD 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.
Dr.MetabolicMD 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.
BethLabQueen said:Dr.MetabolicMD said: ...regarding food noise mechanism of action...
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 11 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 $213/month on alcohol. Triple win.
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Shop Reference StandardsDr.MetabolicMD 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.
From the other side of the consultation, briefly.
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.