DebRD_ATL said:

"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants.

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.

fiona_VT 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.

fiona_VT 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:

1. Activate hypothalamic satiety centers (appetite reduction)
2. Delay gastric emptying (prolonged fullness)
3. Potentiate glucose-dependent insulin secretion
4. Suppress glucagon secretion
5. Modulate reward pathway dopaminergic signaling
6. Reduce hepatic lipogenesis
7. 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.

JennaRN 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.

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.

One thing that is still open after AttorneyGrant’s answer:

What would you measure differently if you were starting again?

TinaHashiRN said:

The GLP-1 and alcohol use disorder connection, relevant to food noise: observational data from Scandinavian registries shows reduced alcohol-related…

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.