pharmacology is the most under-discussed thing in c/glp1women
Confession thread, sort of.
I went from 1.0mg to 15mg much faster than I should have because the scale had stalled and I got impatient. The stall broke about 3 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 constipation I did not need and a data point I cannot interpret. Two lessons in one.
Posting it in the hope that somebody at week 24 reads it before doing the same thing.
best — the order this archive was captured in
the half-life is mechanism, affects steady state timing
glucagon-receptor contribution is half-life for dual and triple agonism
Rodent, human, or in vitro?
central appetite signalling is real but people overweight it
receptor distribution matters, GLP-1 is not everywhere
Strongly agree. Central appetite is real but people overstate it.
cite the paper: journal, year, first author, links optional
This is correct. Rodent data is investigational, not predictive.
Retitled to remove editorialising. Put the evidence in the body.
Retitled to remove editorialising.
Disagree on that part. 98.7% and 98.9% on the same vial is normal.
This is correct. Rodent data is investigational, not predictive.
This is correct.
Yes, exactly this, and it is the bit that took me 77 weeks to accept.
Yeah, the incretin mechanism is doing the work here.
The half-life is 11 hours, which means week 11 is genuinely still ramp-up. Week 10 is steady state.
That is net peptide content, not purity. Different number, different meaning.
- 1Rodent, human, or in vitro?7 comments in this branch · started by u/split_dose_sceptic