COA_Karl said:The mechanism that matters here is not stomach emptying, it is central.
Filing a mild objection. Mild because I might be wrong; an objection because nobody has addressed the case that does not fit. The trial means are being read too generously in this thread. STEP populations were selected, supported, and titrated by protocol, and the real-world curves are consistently a few points worse. That difference is not noise, it is what happens when you remove the study infrastructure.
The figures, for anyone assembling their own picture. 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.
anders_CPH said:The trial means are being read too generously in this thread.
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.
Worth separating that from liver and MASH, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.
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Shop Reference StandardsOne thing that is still open after AmyNC_wife’s answer:
Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?
OP back with an update, since a thread like this is useless without one.
Update. I did go to 2.4mg in the end, and the honest report is that it bought me less than the step before it and cost me two bad weeks. Worth knowing rather than worth repeating.