rick_sfbay ↑ said:

ALT was mildly raised at baseline, normalised at month five, and I now have no idea whether anything happened to the fibrosis that actually matters.

NASH/MAFLD therapeutic landscape and liver and MASH: GLP-1 agonists are emerging as potential first-line NASH therapy. The Phase 2b data for semaglutide showed 59% NASH resolution (vs 17% placebo) with 43% achieving fibrosis improvement[1].

Mechanism: GLP-1R activation reduces hepatic lipogenesis, increases fatty acid oxidation, reduces hepatic inflammation, and may directly reduce hepatic stellate cell activation (fibrosis pathway).

With resmetirom (thyroid hormone receptor agonist) recently approved for NASH, the field is evolving rapidly. Combination approaches (GLP-1 + resmetirom) are being explored.

LibrarianMeg ↑ said:

Liver ultrasound comparison for liver and MASH: my hepatologist ordered serial ultrasounds to track NAFLD regression.

Adding the part of the answer the thread has not reached. Take it one variable at a time. Almost every unanswerable question in these threads is unanswerable because three things changed in the same fortnight, and no amount of subsequent argument can untangle them after the fact.

A narrower follow-up, since the general answer is now clear:

What would you measure differently if you were starting again?

Reporting back.

For the archive: it took about six weeks rather than the two I expected, and the difference between those two numbers was the whole of my problem.