u/signe_boateng

The incretin effect is the observation that oral glucose provokes a larger insulin response than intravenous glucose at matched glycaemia, and the difference is mediated by gut hormones. That is the foundation the whole class sits on.

Correcting my own comment: I attributed that to the GIP arm and the paper attributes it to the GLP-1 arm.

Is there any human data on that mechanism yet?

Is that from a human study or a preclinical model?

the review page nobody can find on any other site is a warning

Yes. The discussion section is where the authors say what they actually think, and almost nobody here reads it.

pressure to decide today is the oldest signal there is

Tolerance to the gastric effect develops with continued exposure while the appetite effect largely persists. That single fact explains most of the "it settles but it still works" pattern the side-effect board reports.

Small fix — it slows gastric emptying, it does not halt it, and the distinction matters for the mechanism you are proposing.

Right, and the group-buy structure is the underrated risk here. One person holds everything and there is no recourse designed in.

the pattern repeats because it works, not because people are stupid

Same view. Tolerance developing to the gastric effect while the appetite effect persists explains most of what the side-effect board reports.

I would separate the two claims. The site being newly registered is checkable. The motive you are inferring is not.

Correction: that is glucose-dependent insulin secretion, which is why hypoglycaemia risk is low as monotherapy. Not the same claim as you made.

Agreed.

Disagreeing here: that is a delay, and this board has to keep delay and intent in separate columns.

That is a report count, not a test count, and it changes how thin the evidence base actually is.

What was the exposure in that experiment relative to therapeutic?

Careful. What you are describing is a delayed shipment, and this board should not turn that into an accusation without more.

no names without evidence, that is the sidebar rule and it is a good one

The directory deliberately separates "we have nothing on this name" from "this went badly". Collapsing the two is how boards like this generate false certainty.

Glucose-dependent insulin secretion is why hypoglycaemia risk is low as monotherapy: the effect scales with glycaemia rather than acting unconditionally.

Careful. What you are describing is a delayed shipment, and this board should not turn that into an accusation without more.