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Evidence-based GLP-1 & peptide discussion since 2023
ForumsOff-TopicPet photos thread — looking for input

Pet photos thread — looking for input

Dr.EndoEP Thu, May 30, 2024 at 10:39 AM 61 replies 3,097 viewsPage 1 of 13
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Dr.EndoEP
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Oct 2024
El Paso, TX
May 30, 2024 at 10:39 AM#1

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 constant until it was not.

What I am trying to establish 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.

Tell me what I have not thought of.

5 0NicoleRaleigh, james_edin, FranDenver and 2 others
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LabKate
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Jan 2024
Oregon
May 30, 2024 at 11:30 AM#2
Dr.EndoEP 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…

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.
4 24laura_annarbor, JenMemphis, pat_auckland and 1 other
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bri_stats
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May 2024
Seattle, WA
May 30, 2024 at 12:21 PM#3
LabKate said:
Central vs peripheral GLP-1R signaling in food noise: elegant studies using brain-penetrant vs peripherally-restricted GLP-1 agonists show that ~80%…

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.
3 23TomFromTexas, mike.trainer_LA, sarah_nash92
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PeptideSynthNJ
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Aug 2024
Princeton, NJ
May 30, 2024 at 1:12 PM#4
Dr.EndoEP 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…

This is my experience too, for whatever a second data point is worth. The detail I would add is minor and it is already implied above.

2 22MikeKY_noInsulin, Dr.RaviCardio
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PeptideChemSF
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Jan 2024
San Francisco, CA
May 30, 2024 at 6:03 PM#5

From the other side of the consultation, briefly.

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.

1 21BrianDallas92
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