Clinical perspective, offered as context rather than as advice. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.

Worth separating that from the pharmacology, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.

From the other side of the consultation, briefly. Start from the measurement rather than the conclusion. Almost every disagreement here turns out to be two people measuring different things and comparing the numbers anyway.

PharmHunterJen said:

Start from the measurement rather than the conclusion.

Can confirm. Same sequence, different timescale. The detail I would add is minor and it is already implied above.

PharmHunterJen said:

Start from the measurement rather than the conclusion.

Coming at PharmHunterJen’s question from a different direction. The mechanism is more central than most summaries suggest. Receptor agonism in the arcuate nucleus activates POMC neurons and inhibits AgRP/NPY signalling, and the downstream MC4R pathway is the same one disrupted in monogenic obesity — convergent genetic evidence that the target is the right one. Peripherally there is glucose-dependent insulin secretion, glucagon suppression and delayed gastric emptying, but the gastric component largely adapts over months while the central effect persists, which is why the durable effect is appetite rather than fullness.

If somebody has the primary source to hand I would rather cite it than paraphrase it.

Moderator note: the sourcing question belongs in the vendor section and has been split out.