Prohormones by Patrick Arnold
I thought Dharkham's article was a pretty good review of prohormones.
However there are a few discrepancies that I would like to clear
up, since I am given the chance to by QFAC.
1) Nandrolone and norandrostenedione CAN convert
to estrogens. It is a complex reaction that is different than the
conversion that testosterone and androstenedione undergo, and it
is slower and less efficient. While it does involve an interaction
of the nors with the aromatase enzyme, the actual aromatization
mechanism is not the same as that seen with test and a-dione. Technically
it involves a hydroxylation at the beta position of Carbon 1, followed
by a spontaneous rearrangement to either estrone (from norandrostenedione)
or estradiol (from norteststerone). The conversion for norandrostenedione
is more efficient than that of nortestosterone, and perhaps not
too surprisingly, I am quite aware of cases of gynecomastia from
norandrostenedione usage.
2) 4-androstenediol was never an unapproved drug.
This is most likely due to the fact that researchers at the time
were looking for steroids with a greater anabolic effect and a lesser
androgenic affect. 4-AD was therefore not a good candidate as it
assayed out as slighlty more androgenic than anabolic. BTW, I first
came across 4-AD when I saw it was an interesting by product in
the synthetic production of testosterone from androstenedione. I
then ran across it again in a German language androgen review book
and saw it could behave as a prohormone.
3) LPJ Research Inc. got the name "androdiol"
approved as a trademark from the USPTO a couple of years ago. It
did seem at first that androdiol was already trademarked for 5-AD,
but it turned out it had just been used as a lay term for that compound
and so was not relevant to our trademark approval.
4) We actually don't know the origin of 4-AD in
the body, just that it is there in small amounts. It is either a
weird testosterone metabolite in tissues with low 5-alpha reductase
activity (i.e. placenta), or a product of incomplete conversion
of 5-AD to testosterone.
5) Is 4-AD active in its unconverted form? I used
to say it was without question. However after giving it thought
it is not completely apparent that it is. It does have considerable
activity when given to rats by injection or when rubbed on a capon's
comb (an indicator of androgenic activity). But does this indicate
it is directly active? Not neccesarily, because we don't know whether
the activity observed is from direct interaction of the 4-AD, from
testosterone that it metabolizes into, or from combination of the
two. If someone could determine what sort of binding 4-AD has to
androgen receptors than we would have a better picture of what is
happening. The same situation, as far as I know, exists for nor-4-AD;
we just don't know if it is active directly from the evidence that
exists.
6) Although SHBG receptors are present on muscle
cell membranes, there is absolutely no indication that they are
responsible for any anabolism in this tissue. At this point the
preponderance of evidence suggests that SHBG will reduce the activity
of androgens, as more SHBG will reduce the fraction of bioavailable
androgen in the system. Contrary to what Dharkam indicates, SHBG
will not extend the activity of testosterone and nortestosterone.
The binding of these androgens to SHBG is so strong that they essentially
all remain associated in the complex form and the steroids will
not be able to break away to diffuse into cells. SHBG seems to be
emerging as a possible risk factors in disorders of the prostate
as well.
The Anabolic Steroid Control Act of 2004 was signed into law by President Bush on October 22, 2004. It will be effective on approximately January 20, 2005. After that date, just possessing these banned substances will be a crime. This law makes ALL steroid precursors (prohormones) except DHEA "controlled substances" in the United States.
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