That's all very good info....the studies showing so and so reduces or increases
IGF-1 levels by X% are misleading though. There are several studies that show both increases and decreases in
IGF-1 levels with all three AIs and nolva. I wouldn't conclude anything regarding their abilities to affect IGF-1 levels at this point.
A similar issue with HDL levels, as there have been studies that have shown each of the AIs can lower HDL levels, but there have also been studies showing that HDL levels are unaffected by the AIs. Nolvadex (tamoxifen) is pretty consistently shown to increase both HDL and IGF-1 levels, from what I've seen.
As for
winstrol preventing the conversion of
deca or fina to progestins, I'm not sure I buy that. If someone can explain how that works, I'd appreciate it. I also don't understand chasteberry, as it increases progesterone levels....progesterone can be a prolactin receptor agonist, hence prog/prolactin gyno.
I also don't get how
exemestane would be the most beneficial AI (being type I, steroidal) on lipid levels. It reduces plasma estrogen more than other AIs, so how would it not affect HDL the most?
If anybody can answer these questions, you'll have my eternal gratitude.
Demeur??