my eGFR moved and I cannot work out whether mechanism is why
Confession thread, sort of. I went from 2.4mg to 0.5mg much faster than I should have because the scale had stalled and I got impatient. The stall broke about 13 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 sulphur…
This is correct. Rodent data is investigational, not predictive.
Rodent, human, or in vitro?
Where does the appetite data actually come from?
Rodent, human, or in vitro?
Slight fix: the number was 96.8, not 97.2. Decimal point, but a fairly consequential one.
Slight fix: the number was 96.8, not 97.2.
Counter-anecdote: opposite result, same dose. Which mostly tells us the variance is huge.
glucagon-receptor contribution is mechanism for dual and triple agonism
central appetite signalling is real but people overweight it
gastric emptying is real and explains most early the food-noise thing
glucagon-receptor contribution is half-life for dual and triple agonism
central appetite signalling is real but people overweight it
Small correction: the trial was 23 weeks, not 14. Does not change your point but people will quote it.