Why? ‘EET-A will show temporary benefits as an anti-ageing therapy (70% as above) and will work “better” than* senolytics in that it will actually reverse ageing rather than needing to be taken at higher concentrations over time (40%).’
How would you obtain and how would you dose if you were performing a human study?
(and why 3 separate parts?)
Perhaps I am being too confident in it. I didn’t have time to cite sources but the biology of AD seems to be a microcosm of the biology of ageing overall, and EET-A has shown a bunch of random unconnected benefits in mouse models (regenerating blood vessels after a heart attack etc.).
I do not know how I would obtain it (one would probably need free access to a chemical lab to synthesize it, just looking at EET and other analogues they seem relatively synthesize-able) as for dosing I would dose at comparable ppm levels to the rodent models.
I did 3 separate parts partially because I thought they seemed rather unconnected, and mostly because I was concerned about posting a very long and cumbersome post. Now that I look at it, it didn’t really need to be three parts at all, it just felt a lot longer when I was writing it.