This one has a reasonably settled answer, so here it is. 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.
Two drinks now land like five, and I found that out in a way I would rather not repeat.
What would genuinely help is knowing whether the change in tolerance is the smaller stomach, the smaller body, or something central, and whether it settles.
If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
PharmD_Rodriguez said:The liver data is among the strongest non-weight findings in the class.
Agreed, and ALT falling is not the same as fibrosis improving. Enzymes are a crude proxy; FIB-4 or elastography is what tells you about the thing that matters.
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Browse GL BiochemSallyK_inj said:Two drinks now land like five, and I found that out in a way I would rather not repeat.
This is my experience too, for whatever a second data point is worth.
Adding the clinical framing, because it changes how the question reads. There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.