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ForumsOff-TopicHas anyone dealt with showed my before photo to my hairdresser and she gasped?

Has anyone dealt with showed my before photo to my hairdresser and she gasped?

DerekSJ_a1c Tue, Sep 24, 2024 at 1:02 PM 10 replies 1,746 viewsPage 1 of 2
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DerekSJ_a1c
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Sep 24, 2024 at 1:02 PM#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 after 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.

Not looking for reassurance. Looking for the part I have got wrong.

36 6adam_van, Dr.SurgeonPGH, rachel_ABQ and 33 others
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LibrarianMeg
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Sep 24, 2024 at 2:04 PM#2
DerekSJ_a1c 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…

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.
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ricardo_MIA
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Sep 24, 2024 at 3:06 PM#3
LibrarianMeg said:
Neuroscience perspective on food noise: GLP-1 receptors are expressed throughout the CNS, with high density in the hypothalamic arcuate nucleus, area…

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: Sep 24, 2024 at 8:06 PM
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steve_okc
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Sep 24, 2024 at 4:08 PM#4
DerekSJ_a1c 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…

Same experience, arrived at from the opposite direction. I had assumed I was the exception until I read this.

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Dr.DermMIA
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Sep 24, 2024 at 10:01 PM#5

From the other side of the consultation, briefly.

DerekSJ_a1c 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.

Last edited: Sep 25, 2024 at 12:01 AM
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