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ForumsOff-TopicFitness tracker recommendations — 12 month update

Fitness tracker recommendations — 12 month update

adam_van Sat, Aug 17, 2024 at 3:07 PM 11 replies 1,925 viewsPage 1 of 3
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adam_van
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Aug 17, 2024 at 3:07 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.

The narrow version of the question 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.

Numbers rather than impressions, if you have them.

41 11FranDenver, Dr.BariatricHTX, LindaRN_retired and 38 others
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NurseKim_ATL
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Aug 17, 2024 at 3:16 PM#2
adam_van 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.
40 10raj_cambridge, ingrid_STO, pete_nash and 37 others
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Dr.ObesityLA
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Aug 17, 2024 at 3:25 PM#3
NurseKim_ATL 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.
39 9tampaLisa73, KarenAZ_mom, zoe_NC and 36 others
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PeptideSynthNJ
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Aug 17, 2024 at 3:34 PM#4
adam_van 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.

38 8MikeKY_noInsulin, Dr.RaviCardio, jennifer_SEA and 35 others
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Dr.KarenChen
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Aug 17, 2024 at 4:21 PM#5

Clinical perspective, offered as context rather than as advice.

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.

Last edited: Aug 17, 2024 at 10:21 PM
37 7sarah_nash92, FitDadDave, RunnerRach and 34 others
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