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.
This one has a reasonably settled answer, so here it is. 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.
Dr.AddMedPHL said:Start from the measurement rather than the conclusion.
Dr.AddMedPHL 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_newbie 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…
Same experience, arrived at from the opposite direction. The detail I would add is minor and it is already implied above.
Clinical perspective, offered as context rather than as advice. 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.