pete_nash said:Dr.GutHealth said: ...but the FDA says semaglutide...
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.
pete_nash said:Dr.GutHealth said: ...but the FDA says semaglutide...
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.
Clinical perspective, offered as context rather than as advice. Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the correction. That is slower than asserting, and it is the only version that survives being wrong.
rachel_ABQ said:Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the…
Second this. I had assumed I was the exception until I read this.
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Shop Reference Standardsrachel_ABQ said:Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the…
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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