TrialNerd_Beth said:The glucagon component looks paradoxical and is not.
Careful with treating an unchanged LDL-C as a failure. If ApoB and triglycerides both fell, the particle picture improved regardless of what the calculated LDL says.
Worth separating that from retatrutide, which this thread keeps folding into the same question. They behave differently and the advice does not transfer.
Adding the numbers, since they settle part of this. For anyone tracking the class: GLP-1 alone gets you appetite, GLP-1 plus GIP adds tolerability and lipid handling, and adding glucagon adds expenditure and liver-fat reduction. Each addition also adds a receptor system that can generate side effects.
RetaRick_CA said:Careful with treating an unchanged LDL-C as a failure.
Omega-3 index improvement on the lipid panel: often overlooked but my omega-3 index went from 4.4% to 8.9% over 13 months. I supplemented with 2g EPA+DHA daily.
This matters because omega-3s are anti-inflammatory and cardioprotective, complementing the GLP-1 benefits. Target omega-3 index is >8%. Combined with the triglyceride reduction from the medication, my lipid profile is the best it's been in decades.
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Browse GL BiochemA narrower follow-up, since the general answer is now clear:
Why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose?
Closing the loop on my own question.
Rereading it with the dropout table open changed my view. I still think it is the most interesting molecule in the pipeline; I no longer think the 24% is the number that will end up on a label.