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ForumsOff-TopicGardening on GLP-1 — need advice Page 2

Gardening on GLP-1 — need advice

RetaRick_CA Wed, Jan 24, 2024 at 6:23 AM 15 replies 2,176 viewsPage 2 of 3
LibrarianMeg
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Jan 24, 2024 at 7:31 PM#6
LipidDoc_ATL 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.

References:
[1] Wang W, et al. Nat Med. 2024;30:574-584.
33 3Dr.NateNeph, PharmD_Rodriguez, julia.endo and 30 others
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Dr.RaviCardio
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Jan 25, 2024 at 12:43 AM#7
RetaRick_CA 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.

"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 sweets — 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.

Last edited: Jan 25, 2024 at 1:43 AM
32 2anna.melb_AU, mark_tokyo, hans_munich and 29 others
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Dr.GastroMayo
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Jan 25, 2024 at 5:55 AM#8
LibrarianMeg 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.

References:
[1] Secher A, et al. J Clin Invest. 2014;124(10):4473-4488.
Last edited: Jan 25, 2024 at 10:55 AM
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hans_munich
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Jan 25, 2024 at 11:07 AM#9

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

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

30 0tammy_FL, Dr.LipidDallas, alex_tucson and 27 others
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RetaRick_CA
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Jan 26, 2024 at 12:05 PM#10
Dr.GastroMayo said:
Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80%…

Phantom hunger vs real hunger on food noise: learning to distinguish between the two has been a revelation. Real hunger: gradual onset, physical stomach sensation, any food sounds good. Phantom hunger: sudden, emotionally triggered, specific food cravings, occurs right after eating.

The GLP-1 agonist suppresses real hunger beautifully. Phantom hunger still pops up but I can now recognize it for what it is — an emotional signal, not a physical need. Mindfulness training helped enormously with this distinction.

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