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Originally Posted by einstein1905 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?? |
I wouldn't be surprised in
Winny prevents the some progestin-like activity of
deca/fina. My guess would be competitive inhibition of 5-alpha reductase; with the androgenic potential of
Winny being much less than deca/fina. Furthermore, the aromatization of deca/fina is also enzyme mediated but likely one of the liver cytochromes not typical aromatase activity. That means that something as simple as grapefruit juice might increase or decrease the anabolic (and side effects). Another option is that
Winny acts like
Clomid. The androgenic effects of
Winny are so weak in comparison to Deca/Fina that it essentially blocks the activity.
I had no idea people were using chasteberry for gyno. Last I heard it was almost useful for PMS. I saw one reference that said it binds to the estrogen receptor and stimulates the PRODUCTION of progesterone receptors but it doesn't activity the progesterone receptor. So it's conceivable that chasteberry may block the estrogen and progesterone receptors.
Exemestane can have a negative influence on estrogen and boost HDL at the same time by acting through different pathways. Although estrogen is important for HDL it clearly isn't the sole determinant of HDL. In fact, Pfizer has a drug in development that has doubled HDL levels in early trials.