I have tried researching this and can not seem to be able to get a satisfying answer!
What are the mechanisms that prevents aromasin from having a negative affect on lipid profile?
How does it differ from fremara and arimidex?
I seem to recall reading somewhere that aromasin works by not allowing estrogen to attach to receptors (much moreso than nolvadex) - that way, estrogen can exert its positive effects on lipids.