From the other side of the consultation, briefly. If two explanations both fit, the useful question is which one predicts something the other does not. That is answerable; arguing about which sounds more plausible is not.
ingrid_STO said:If two explanations both fit, the useful question is which one predicts something the other does not.
Same pattern here, and in the same order.
ingrid_STO said:If two explanations both fit, the useful question is which one predicts something the other does not.
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.
Correct me if the detail matters more than I have assumed.
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Browse GL BiochemThe figures, for anyone assembling their own picture. Give anything pharmacological four weeks before you judge it, and give anything measured weekly a four-point rolling average before you call it a trend.
Following on from ingrid_STO — and this may be the naive question:
Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?