This is a continuation of a long topic, addressed by post number rather than by page. Start at post 1.
Adding thanks rather than a view. I do not have a view worth the space.
Where the honest answer is "nobody knows", giving it plainly is more useful than a confident synthesis of mechanism and anecdote.
A partial answer, offered because a partial answer beats none.
I read post #32 twice before replying, because I had assumed the opposite.
A condition being an exclusion criterion in a trial does not mean the treatment is contraindicated. It frequently means the trialists wanted a cleaner population.
Reading it back, the second half matters more than the first.
The useful distinction on hepatic steatosis is between what was measured and what was inferred from it. Both end up in the same sentence and only one of them has error bars.
Hepatic steatosis and MASH: a phase 2 trial in semaglutide for steatohepatitis showed resolution was more frequent on treatment. Histological resolution is a surrogate for long-term clinical outcomes like cirrhosis.
Post #34 is right about the mechanism and I think understates the practical bit.
A request rather than an answer: could whoever has the primary source for hepatic steatosis post it? I have seen the claim three times this month and each version had lost a qualifier.
Coming back to post #36, because the follow-up matters more than the original answer.
Bariatric surgery history: altered anatomy after surgery affects absorption. That matters for oral medications and for reconstituted solutions. Discussing specific medications and doses with a clinician familiar with bariatric surgery is prudent.
The short version is the first sentence; the rest is why.
Agreed, and I will stop repeating the version of this I had been repeating.
Worth separating two things that post #37 runs together.
Gastrointestinal conditions interact with a mechanism that slows gastric emptying in ways that are plausible and largely unstudied.
Marking that as an opinion rather than a finding.
Adding a reference point for hepatic steatosis. Mine is a single case, collected without controls, and I am posting the method alongside it so it can be discounted appropriately.
I would call the community position on hepatic steatosis likely rather than established, and I would be comfortable defending that hedge.
Obstructive sleep apnoea: SURMOUNT-OSA used an objective endpoint, the apnoea-hypopnoea index. Reduction was substantial. Whether the benefit is weight loss or a direct drug effect is not resolved by the trial.
I would be glad to be shown a cleaner way of putting this.
The honest answer to most questions here is that the trial population did not include the case being asked about, and that saying so is more useful than filling the gap with mechanism.
The version of hepatic steatosis that circulates here is a simplification of a simplification. It is not wrong, but it has lost the conditions under which it holds, and those conditions are where the interesting cases live.
Genuine question rather than a rhetorical one: has anyone here actually observed hepatic steatosis, as opposed to read about it? The thread is long and I cannot tell.
Right, and stated more narrowly than I would have dared to state it.
Source for the hepatic steatosis figure, since it was asked for. It is in the discussion rather than the abstract, which is why the version circulating is stronger than the paper is.
Reading the surrounding paragraph is worth the two minutes. The authors are more careful than their summarisers.
Post #50 describes the usual case. This is about the unusual one.
Registry and observational data covering excluded populations is accumulating and is weaker evidence than a trial and better than nothing.
It is one reading of the data and not the only reasonable one.
Seconded. It reads as careful rather than confident, which is the right register.
Where a condition is well controlled and where it is not are different questions and the published data rarely distinguishes them.
I keep a log for hepatic steatosis specifically because my memory of it turned out to be systematically wrong in one direction. Six weeks of notes cost nothing and settled it.
Post #56 is the version of this I will quote in future. One addition.
Type 2 diabetes: the population with the largest evidence base for these compounds. The SURPASS and SUSTAIN programmes established glycaemic benefit. The renal and cardiovascular benefit evidence is separate from the glycaemic benefit evidence.
I have said this before in a thread nobody could find, so it is worth repeating.
Where I part company with post #54, and it is a narrow parting.
Hepatic steatosis is one of those subjects where the general answer and the answer for a specific case diverge, and the thread will go in circles until someone says which one is being asked for.
Bariatric surgery history: altered anatomy after surgery affects absorption. That matters for oral medications and for reconstituted solutions. Discussing specific medications and doses with a clinician familiar with bariatric surgery is prudent.
I would put this at better than even and not much better.
On hepatic steatosis, the part that usually goes wrong is that the question is asked as though it has one answer. It has a range, and the width of the range is the interesting bit.
If you can post the two or three numbers you are working from, several people here will check the arithmetic rather than argue about the conclusion.