raj_cambridge said:

Give anything pharmacological four weeks before you judge it, and give anything measured weekly a four-point rolling average before you call it a…

Agreed, and one caution: a single measurement is not a measurement. Anything that moves day to day needs a trend before it means anything at all.

raj_cambridge said:

Give anything pharmacological four weeks before you judge it, and give anything measured weekly a four-point rolling average before you call it a…

Bookmarking. The distinction being drawn above is the one nobody else makes. Taking it to my next appointment.

Clinical perspective, offered as context rather than as advice. If two explanations both fit, the useful question is which one predicts something the other does not. That is answerable; arguing about which sounds more plausible is not.

Dr.EndoEP said:

If two explanations both fit, the useful question is which one predicts something the other does not.

Same pattern here, and in the same order.

Dr.EndoEP said:

If two explanations both fit, the useful question is which one predicts something the other does not.

Coming at Dr.EndoEP’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.

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

Correct me if the detail matters more than I have assumed.