BariatricNurseD said:Albumin binding above 99% is the whole reason weekly dosing works, and it is also why the trough matters more than the peak.
I will push back on the "any working dose is fine" framing. The maintenance evidence sits overwhelmingly at the top studied dose, and the extension data shows regain tracking dose reduction rather than tracking stopping. Holding low is reasonable; pretending it is evidentially equivalent is not.
If somebody has the primary source to hand I would rather cite it than paraphrase it.
One concrete data point for the thread. Worth knowing that the injection site changes very little. Abdomen, thigh and upper arm are bioequivalent for semaglutide, so a site change is not a plausible explanation for a bad week.
DebRD_ATL said:I will push back on the "any working dose is fine" framing.
Adding the part of the answer the thread has not reached. The liver data is among the strongest non-weight findings in the class. The semaglutide MASH programme reported a large advantage over placebo on MASH resolution, with a substantial minority also achieving fibrosis improvement — and fibrosis is the endpoint that predicts outcomes. Mechanistically it is reduced hepatic lipogenesis, increased fatty-acid oxidation, less hepatic inflammation, and possibly a direct effect on stellate-cell activation.
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Browse GL BiochemFollowing on from MASHdoc_SA — and this may be the naive question:
Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?
Closing the loop on my own question.
Following this thread I went back and re-read the extension data properly. The point about trough rather than peak explains the pattern I was seeing on day six, which I had been blaming on the vial.