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 bit I cannot resolve on my own is 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.
Short answer first, then the reasoning. 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.
TirzTom said:Start from the measurement rather than the conclusion.
TirzTom 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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View Resultsadam_van 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…
Adding a me-too, because a thread of one person's experience is not much use. I had assumed I was the exception until I read this.
Adding the clinical framing, because it changes how the question reads. 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.