Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
What would genuinely help is knowing why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Not looking for reassurance. Looking for the part I have got wrong.
This one has a reasonably settled answer, so here it is. There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.
NurseKim_ATL said:There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.
That is correct as far as it goes, and here is where it stops going. The phase 2 numbers were about 24% mean weight loss at 48 weeks on the top dose, with the curve still descending at the end of the study. A curve that has not flattened is a real finding, but it also means the true plateau is unknown, and phase 2 populations are small and selected.
Correct me if the detail matters more than I have assumed.
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Browse GL BiochemJakeBK_lifts said:Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
Second this.
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.