Non-scale victories thread — celebrate everything

labquiet_amy 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.

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 5 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 $199/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…

"Food aversion" side effect of food noise that I wasn't prepared for: I used to LOVE cooking and trying new restaurants. Now certain foods — especially fried foods — literally repulse me.

It's not just reduced appetite; it's an active disgust response. My therapist says this is common and likely related to the reward pathway modulation. It's mostly a positive change, but I do miss enjoying food the way I used to.

mike_nyc 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.

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

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

anders_CPH 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.