This one has a reasonably settled answer, so here it is. It is worth asking what the claim would look like if it were false. If nothing would look different, it is not a claim about the world and no amount of discussion will settle it.
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.
So the question, as narrowly as I can put it: why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Numbers rather than impressions, if you have them.
PharmD_Rodriguez said:It is worth asking what the claim would look like if it were false.
PharmD_Rodriguez has the substance of this right. The condition it depends on is worth stating. 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 Biochemnick_SD_fit 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.
Adding the clinical framing, because it changes how the question reads. 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.