PharmacoVig_BOS 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 cocktails most nights. Since starting GLP-1 therapy, I have zero interest in alcohol. Haven't had a drink in 10 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 $216/month on alcohol. Triple win.

WendyG_ATL said:

The thing that changed for me was not hunger, it was that the constant background negotiation about food simply stopped, and I had not realised it was…

WendyG_ATL 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.

Dr.RaviCardio said:

Alcohol relationship change with food noise: I used to drink cocktails most nights.

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.

Following on from jason_sac26 — and this may be the naive question:

How would you tell the difference between that and the alternative explanation?

andrew_nyc 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.