Hey I have been taking 4-AD and am planning to be taking more in the future. I of course don’t want to get ‘gyno’ since I already have it slightly. I would take Chrysin but since I am trying to grow a beard, I want the DHT. I was thinking about taking Nolvadex. It says it deactivates the estrogen in the breasts and activates it in the bones. I was wandering if this was a good idea or if my hips would become wider, etc.
Estrogen levels do not increase with 4-AD use so there is no issue here anyway. This was
seen in our Androsol studies and also, I’m told, has been seen by some other people in their studies. Anyhow there is no issue and
if 4-AD is all you are using, you don’t need
More precisely, Nolvadex (and Clomid) do
not “activate estrogen” in the bones, but
rather act as estrogens themselves.
Yes, but doesn’t an excess in testosterone cause some of it to turn into estrogen?
Matt, you’re right that one would first guess
that since 4-AD raises testosterone, that
estrogen levels should rise also; but when
there is repeated observed evidence that it
doesn’t happen then it’s time to stop worrying about it. Measurements trump hypotheses.
I would suppose that the reason estrogen levels
do not rise is that while T levels are higher so there is more substrate for the aromatase enzyme, the 4-AD competes for binding, but
cannot itself aromatase, so net rate of
aromatization does not increase. That is
just a theory. The important thing is that
the measurements show no increase, both those
commissioned by Biotest and some done by others.
If you’ve reached maturity then estrogenic effect of Nolvadex on bone is not an issue, except as a good thing (improving bone density) but if you are still growing, then
I’d consider it a poor idea. Pelvic widening,
I’m dubious of, but earlier closure of the epiphyseal plates (causing bone growth to end sooner) is a very reasonable possibility. I
don’t think anyone has shown yet whether tamoxifen is an estrogen or antiestrogen at the epiphyseal plates, but since it’s an estrogen
in bone, I’d bet on it being estrogenic with
regard to plate closure as well.
Ok, you say 4-AD doesn’t raise estrogen levels, what about DHT levels?
We have not measured changes in DHT and I don’t think anyone else has. You’d expect some increase since testosterone increases, but since testosterone does not increase outside the normal range, it doesn’t follow that DHT would either (4-AD itself does not convert to DHT but must first be converted to testosterone.)