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

the half-life thing finally clicked for me and I want to write it down

Question Receipts ×4 Cold Box ×3

the half-life thing finally clicked for me and I want to write it down. Not a hot take, just something I have not seen said plainly here.

Started reading limitations sections first. It has changed how much weight I give to almost everything posted here.

The half-life explanation was the thing that made weekly dosing intuitive for me rather than arbitrary.

Tried to build a mental model from mechanism alone and produced a confident prediction that the trial data flatly contradicted.

Sceptical readings welcome. The confident ones are the ones I distrust.

2,273 up / 398 down85% upvoted40 commentsid 1xzifg13 Jan 2024

40 comments

9 in this archive, depth 3

best — the order this archive was captured in

u/ismael_chukwu-11 points·2 years ago

Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.

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u/ireland_drugs_pay1 point·2 years ago

GIP is the arm people argue about because the biology is genuinely unsettled

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u/slow_logbook1 point·2 years ago

read the discussion section, that is where the honesty lives

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u/aleksi_lehtinen175 points·2 years ago

I would not read that in vitro number across to a person. The conditions are nothing like physiological.

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[removed]132 points·2 years ago

[removed by moderator]

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u/neha_krastev0 points·2 years ago

That study was in a rodent model. Worth stating, since the thread has been reading it as human data.

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u/gradient_goblin102 points·2 years ago

albumin binding is most of the half-life story

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u/ismael_eriksen0 points·2 years ago

I would not read that in vitro number across to a person.

This is the concept everything else on this board is downstream of.

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u/rina_bergstrom143 points·2 years ago

Small fix — it slows gastric emptying, it does not halt it, and the distinction matters for the mechanism you are proposing.

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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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