[Question] how do you actually verify satiety
Genuine question, and the title is the question: how do you actually verify satiety.
Bought small deliberately because the evidence base is thin. That felt like the only defensible approach.
Asked a question here that turned out to be based on a mechanism confusion. Three people untangled it patiently.
Kept a log purely because so few people are logging this one. It is one person and it is not data.
Would rather be corrected in public than confident in private.
best — the order this archive was captured in
Independent purity data on this compound is sparse compared with the older molecules, simply because far fewer members have paid for testing. Sparse data means wide uncertainty, not a verdict.
Independent purity data on this compound is sparse compared with the older molecules, simply because far fewer members have paid for testing.
Agreed, and the combination arms are where the interesting numbers actually live.
Agreed that the monotherapy numbers look modest out of context and that the context is the whole story.
Cosigning on the thin independent data. Fewer members test this, so the bands are wider and should be treated that way.
Yes. Anyone reading this board should hold their conclusions loosely until phase 3 reports.
How many separate lots has anyone here tested?
The tolerability tables were more informative than the headline numbers, which is usually the case and never how it gets summarised.
Which receptor family are you attributing that effect to?
Nothing containing this compound is approved as a standalone product, and research-use-only material is not approved for human use.
Amylin is co-secreted with insulin and acts on satiety and gastric emptying through its own receptor complexes. An amylin analogue is therefore not a variant of an incretin agonist — it is a different signalling axis.