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c/glp1science·posted 4 months ago by u/split_dose_sceptic

tried incretin for 21 weeks. here is what happened.

Needs Source Receipts ×3

Long-ish post, sorry. tl;dr at the bottom.

I have been tracking receptor against triglycerides for 19 weeks because I could not find anyone who had. The correlation is weaker than I expected, which is itself mildly interesting given how confidently people link the two in here.

Caveats up front: one person, one lab, one assay, no control, and I changed my training in the middle of it, which was stupid.

tl;dr: probably real, definitely smaller than the threads imply, and not worth reorganising your week around.

417 up / 153 down73% upvoted13 commentsid wtzmpk19 Mar 2026

13 comments

7 in this archive, depth 3

best — the order this archive was captured in

u/titration_marshalmod · c/semaglutide44 points·4 months ago

do not extrapolate rodent data to human dosing without saying so

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u/enzo_petrescu31 points·4 months ago

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

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u/formulary_fighterappeals24 points·4 months ago

Yeah, the incretin mechanism is doing the work here.

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u/greta_lokken11 points·4 months ago

Which paper are you quoting?

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u/priya_guerrero10 points·4 months ago

do not extrapolate rodent data to human dosing without saying so

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u/yusuf_ramos10 points·4 months ago

receptor distribution matters, GLP-1 is not everywhere

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u/noor_hovland7 points·4 months 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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