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c/glp1science·posted 2 years ago by u/santiago_rasmussen

[Vendor] WXT order #5 — France, 27 days, no drama, receipts inside

Paper

Trying to settle this properly because the thread from last year went in circles.

The claim: half-life matters. The counter-claim: it is measurement error. Both sides have been asserting it confidently for about 14 months without either producing anything.

What would actually settle it is 23 people measuring the same thing the same way. I have started; my numbers are below. They lean one way but not strongly enough for me to declare victory.

If you have data, post the data. If you have an opinion, flair it as an opinion.

250 up / 61 down80% upvoted12 commentsid 1wvk0o6 Nov 2023

12 comments

8 in this archive, depth 4

best — the order this archive was captured in

u/nora_lundgren40 points·2 years ago·edited

Rodent data is rodent data. Dose scaling is not linear and the models tell you what to investigate, not what to expect.

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u/gastric_emptying_gMOD23 points·2 years ago

Retitled to remove editorialising. Put the evidence in the body.

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u/incretin_ivypharmacology-22 points·2 years ago

do not extrapolate rodent data to human dosing without saying so

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u/whois_wanda5 points·2 years ago

mechanistic speculation is welcome if flaired as speculation

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u/santiago_rasmussenOP3 points·2 years ago

Receptor distribution explains why reflux hits appetite but not half-life.

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u/ismael_eriksen20 points·2 years ago·edited

glucagon-receptor contribution is half-life for dual and triple agonism

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u/brigade_detector14 points·2 years ago

Yeah, the incretin mechanism is doing the work here.

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u/greta_lokken11 points·2 years ago

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

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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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