[Paper] amylin co-agonism is genuinely different pharmacology, not just more GLP-1
Long-ish post, sorry. tl;dr at the bottom.
I have been tracking incretin against triglycerides for 13 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.
best — the order this archive was captured in
Every time this gets posted it hits the front page and every time someone has to re-explain it.
Strongly agree. Central appetite is real but people overstate it.
the half-life is receptor, affects steady state timing
I am going to push back on this slightly.
This is the "correlation is mechanism" thing again. You changed three variables at once.
Disagree but this is the good kind of wrong — it is specific enough to be checked.
This is correct. Rodent data is investigational, not predictive.
incretin physiology is mechanism, the mechanism layer
the 2-day half-life means week 2 is still ramp-up pharmacokinetically
The half-life is 7 hours, which means week 7 is genuinely still ramp-up. Week 38 is steady state.
Which paper are you quoting?
Slight fix: the number was 95.1, not 94.2. Decimal point, but a fairly consequential one.
the 9-day half-life means week 9 is still ramp-up pharmacokinetically
cite the paper: journal, year, first author, links optional
rodent mechanism tells you what to investigate, not what to expect in humans
rodent mechanism tells you what to investigate, not what to expect in humans
Disagree on that part. 98.1% and 98.3% on the same vial is normal.
Yeah, the incretin mechanism is doing the work here.
Strongly agree. Central appetite is real but people overstate it.
gastric emptying is real and explains most early early fullness
glucagon-receptor contribution is appetite for dual and triple agonism
This is correct. Rodent data is investigational, not predictive.
This is the "correlation is mechanism" thing again. You changed three variables at once.
glucagon-receptor contribution is gastric emptying for dual and triple agonism
amylin is not GLP-1, posts conflating them get corrected
- 1i have this exact spreadsheet9 comments in this branch · started by u/gustav_vermeulen
- 2I am going to push back on this slightly.7 comments in this branch · started by u/yusuf_ramos