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 would genuinely help is knowing why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Tell me what I have not thought of.
Taking the question as asked, rather than the general version of it. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.
amsterdam_pete said:The distinction that resolves most of these threads is between what is true on average and what is true for one person.
amsterdam_pete 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 Biochemrick_sfbay 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…
Second this. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads. The version of this that has an answer is narrower than the version being asked. Narrow it and it becomes tractable; leave it broad and the thread will produce nine confident and incompatible replies.