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.
The narrow version of the question is 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.
Answering the narrow version, because the broad one does not have a single answer. The useful move here is to separate what is established from what is widely repeated. Those two sets overlap less than the confident tone of most write-ups suggests, and the second set is where nearly all the disagreement on this board comes from.
labquiet_amy said:The useful move here is to separate what is established from what is widely repeated.
Agreeing with labquiet_amy, and the qualification matters more than the agreement. 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 BiochemBethLabQueen 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…
This matches mine closely enough to be worth saying so out loud. The detail I would add is minor and it is already implied above.
Adding the clinical framing, because it changes how the question reads. 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.