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ForumsNutrition & SupplementationMeal prepping when you have zero appetite is so weird — what worked for you? Page 2

Meal prepping when you have zero appetite is so weird — what worked for you?

dave_SLC Thu, Sep 18, 2025 at 11:57 AM 51 replies 1,950 viewsPage 2 of 11
sarah.morrison
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Sep 18, 2025 at 1:58 PM#6
Dr.ObesityMed 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.

Neuroscience perspective on food noise:

GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area postrema, and — critically — the mesolimbic reward pathway[1].

This is directly relevant to food noise because the central effects of GLP-1 agonists extend far beyond simple appetite suppression. The reduction in "food noise" that patients describe is likely mediated by modulation of dopaminergic signaling in the VTA and nucleus accumbens.

The emerging data on reduced addictive behaviors (alcohol, gambling) further supports this mechanism. food noise should be understood in this broader neurobiological context.

References:
[1] Merchenthaler I, et al. J Comp Neurol. 1999;403(2):261-280.
30 0josh_phd_bmore, roxy_nash, tony_orlando and 27 others
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stefan_berlin
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Sep 18, 2025 at 2:45 PM#7
dave_SLC 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…

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.
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NurseAsh_DET
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Sep 18, 2025 at 3:32 PM#8
sarah.morrison said:
Neuroscience perspective on food noise: GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area…
sarah.morrison 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.

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fiona_VT
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Sep 18, 2025 at 4:19 PM#9

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

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

Last edited: Sep 18, 2025 at 5:19 PM
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dave_SLC
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Sep 18, 2025 at 8:03 PM#10
NurseAsh_DET said:
sarah.morrison said: ...regarding food noise mechanism of action...

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.
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