Short answer first, then the reasoning. 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.
The bit I cannot resolve on my own is whether the change in tolerance is the smaller stomach, the smaller body, or something central, and whether it settles.
Happy to be told the question itself is wrong.
mike.trainer_LA 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.
That is the short version; the long version is somebody else's post.
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Browse GL Biochemmatt_MKE said:Two drinks now land like five, and I found that out in a way I would rather not repeat.
Same pattern here, and in the same order. I had assumed I was the exception until I read this.
Clinical perspective, offered as context rather than as advice. Start from the measurement rather than the conclusion. Almost every disagreement here turns out to be two people measuring different things and comparing the numbers anyway.
Ask again with the specifics and you will get a better answer than this one.