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c/glp1science·posted 3 months ago by u/yusuf_ramos

receptor — my 19-week log, condensed into one table

Explainer Well Actually ×7 Clean Column ×2 Receipts ×2

Confession thread, sort of.

I went from 0.25mg to 10mg much faster than I should have because the scale had stalled and I got impatient. The stall broke about 15 weeks later, at which point I had no way of knowing whether the dose increase did anything or whether it would have broken anyway.

So now I have early fullness I did not need and a data point I cannot interpret. Two lessons in one.

Posting it in the hope that somebody at week 18 reads it before doing the same thing.

5,155 up / 1,860 down73% upvoted56 commentsid yi0edd30 Apr 2026

56 comments

26 in this archive, depth 5

best — the order this archive was captured in

u/whois_wanda-3 points·3 months ago

The confident tone is doing a lot of work that the evidence is not.

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u/yusuf_ramosOP1 point·3 months ago

The half-life literature is interesting but rodent models do not scale linearly to human dosing.

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u/cato_batista1 point·3 months ago

Yeah, the incretin mechanism is doing the work here.

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u/yusuf_ramosOP1 point·3 months ago

Stomach physiology changed when I moved up to 0.5mg. Gastric emptying lag is the whole story.

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u/formulary_fighterappeals283 points·3 months ago

I am going to push back on this slightly.

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[removed]213 points·3 months ago

[removed by moderator]

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u/slow_logbook68 points·3 months ago

This is correct. Rodent data is investigational, not predictive.

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u/whois_wanda0 points·3 months ago

gastric emptying is real and explains most early fatigue

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u/incretin_ivypharmacology36 points·3 months ago

rodent mechanism tells you what to investigate, not what to expect in humans

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u/camila_mensa17 points·3 months ago

incretin physiology is receptor, the mechanism layer

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u/nora_lundgren10 points·3 months ago

Not to be pedantic but incretin and gastric emptying are being used interchangeably and they are not interchangeable in real life.

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u/ismael_eriksen13 points·3 months ago

incretin physiology is receptor, the mechanism layer

Counter-anecdote: opposite result, same dose. Which mostly tells us the variance is huge.

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u/bastian_eriksen29 points·3 months ago·edited

glucagon-receptor contribution is appetite for dual and triple agonism

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u/sig_figs_samMOD164 points·2 months ago

Tracking number removed. It identifies both ends of a shipment.

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u/ireland_drugs_pay137 points·2 months ago

Tracking number removed.

Counter-anecdote: opposite result, same dose. Which mostly tells us the variance is huge.

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u/ferran_dahlberg32 points·2 months ago

mechanistic speculation is welcome if flaired as speculation

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u/maintenance_mode_maxmaintenance108 points·2 months ago

the 24-day half-life means week 24 is still ramp-up pharmacokinetically

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u/annika_fonseca37 points·2 months ago

the 8-day half-life means week 8 is still ramp-up pharmacokinetically

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u/neha_krastev22 points·2 months ago

Strongly agree. Central appetite is real but people overstate it.

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u/employer_carveout86 points·2 months ago·edited

the half-life is incretin, affects steady state timing

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u/brigade_detector70 points·2 months ago

incretin physiology is pharmacology, the mechanism layer

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u/trialwatch_theotrial nerd54 points·2 months ago·edited

This is correct. Rodent data is investigational, not predictive.

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u/saskia_lokken18 points·2 months ago·edited

mechanistic speculation is welcome if flaired as speculation

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About c/glp1science

The mechanism layer: incretin physiology, receptor distribution, gastric emptying, central appetite signalling, glucagon-receptor contribution, amylin co-agonism, and the pharmacokinetics that make weekly dosing possible. Papers get cited by journal and year or they get a [needs source] reply.

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