Adding the clinical framing, because it changes how the question reads. The useful move here is to separate what is established from what is widely repeated. Those two sets overlap less than the confident tone of most write-ups suggests, and the second set is where nearly all the disagreement on this board comes from.
One concrete data point for the thread. The boring version of this is the one that works, and the boring version is: measure a baseline, change one variable, wait, measure again under the same conditions. Nobody wants that answer and it is still the answer.
One thing that is still open after Dr.NateNeph’s answer:
How long did you give it before you decided it was working?
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Browse GL BiochemBethLabQueen said:The boring version of this is the one that works, and the boring version is: measure a baseline, change one variable, wait, measure again under the…
This is where I part company with the consensus forming above. The mechanism that matters here is not stomach emptying, it is central. GLP-1 receptor agonism in the arcuate nucleus stimulates POMC neurons and suppresses AgRP/NPY signalling, which is why the effect is appetite and food salience rather than physical fullness. Delayed gastric emptying largely tachyphylaxes over the first months; the appetite effect does not.
Happy to go further on any of that.