Reading the retatrutide phase 2 data properly rather than the headline, and the 24% figure is doing a lot of work that the confidence interval does not support as firmly as people think.
What I am after is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Practical detail welcome, however dull — the duller the better.
This one has a reasonably settled answer, so here it is. Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the correction. That is slower than asserting, and it is the only version that survives being wrong.
Dr.GutHealth said:Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the…
No disagreement with Dr.GutHealth. One condition attached. The glucagon component looks paradoxical and is not. Glucagon receptor agonism raises energy expenditure and drives hepatic fatty-acid oxidation, and its hyperglycaemic tendency is offset by the GLP-1 arm's insulin secretagogue effect. Net result: intake down from GLP-1/GIP, expenditure up from glucagon, glycaemia neutral or improved. It is a balancing act, and it is why the liver-fat results are the most interesting part of the dataset.
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Browse GL Biochemmona_PHX said:Reading the retatrutide phase 2 data properly rather than the headline, and the 24% figure is doing a lot of work that the confidence interval does…
Can confirm. Same sequence, different timescale.
From the other side of the consultation, briefly. Worth answering the question that was asked rather than the one behind it. The narrow version usually has an answer; the broad version usually does not, and answering the broad one is how a thread stops being useful.