Dr.KarenChen said:The dose-response is real but shallow at the top.
Filing a mild objection. Mild because I might be wrong; an objection because nobody has addressed the case that does not fit. The "earlier than weight loss explains" argument is weaker than this thread makes it sound. Blood pressure and inflammatory markers move fast and are downstream of early weight loss, so the mechanism is not as cleanly separable as the summaries imply.
Adding the numbers, since they settle part of this. For anyone assembling their own picture: Tmax is one to three days, terminal half-life about 165 to 170 hours, steady state at four to five weeks, and subcutaneous bioavailability near 89%. Those four numbers explain most of the questions people ask about timing.
If somebody has the primary source to hand I would rather cite it than paraphrase it.
COA_Karl said:The "earlier than weight loss explains" argument is weaker than this thread makes it sound.
Adding the part of the answer the thread has not reached. 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.
Worth separating that from semaglutide, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.
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Browse GL BiochemOne thing that is still open after emma_london’s answer:
How much of the between-person variation is pharmacokinetic and how much is just adherence measured badly?
Reporting back.
Update. I did go to 2.4mg in the end, and the honest report is that it bought me less than the step before it and cost me two bad weeks. Worth knowing rather than worth repeating.