You are correct, Anavar is metabolized in the kidneys unlike other orals that are broken down in the liver (winstrol). However liver function is still slightly effected, Var is RX'd to patients in long term use without any liver problems. Approx at 10mg ED over a year+ time
And Nelson, no offense, but please do show some studies to back the "Think of taking 10 shots of liquor a day non stop for 2 months straght."... I find this bogus and I also don't think it's good as a board sponser, where new guys are taking everything you say serious, to be reading such a unprovable statement and then have it passed throught the grapevines.
I would like to see some documentation that anavar is metabolised in the kidney.
It doesn't make sense that there is only one exogenous steroid that is metabolised in the kidney when all steroid hormones are metabolised in the liver.
http://www.clinchem.org/cgi/reprint/42/7/1001
The metabolism of testosterone can be discussed as a basic
metabolic pathway for all synthetic AAS. The enzymes that
convert testosterone to its distinct metabolites are also active
towards AAS when similar groups and configurations are
present.
I think this is where the confusion arises: They are referring to secondary and tertiary metabolism, not the initial metabolism of steroids.
Oxandrolone (17/3-hydroxy-l7a-methyl-2-oxa-5a-androstan-
3-one; Fig. 28) was synthesized in 1962 by Pappo and
Jung [89]. In 1989 Masse et al. [47] published a GC-MS
investigation of oxandrolone metabolism in men. Oxandrolone
is excreted unchanged and metabolized to its 17-
epimer (4), which has already been explained as a urinary
rearrangement product of an excreted 17/3-sulfate. In this
degradation process the 18-nor-!7,17-dimethyl product (5) is
also formed. Excretion of further 16-hydroxylated metabolites
(2) of oxandrolone have been confirmed, but in low
concentrations.
3) Sulfatation of the secondary 17(3-hydroxy group. Sulfatation
at the 17(3-hydroxy group in AAS is possible and is
described in the metabolism of testosterone [55] (Fig. 8, right).
Sanaullah and Bowers discussed detection of epitestosterone and
testosterone sulfates in urine by liquid chromatography/MS in
1995 [56].
4) Sulfatation of the tertiary 17(3-hydroxy group in 17(3-
hydroxy-1 7 a-methyl steroids and 17-epimerization. Sulfatation
at the 17(3-hydroxy group in 17(3-hydroxy- 17a-methyl steroids
was first described for metandienone in horses by Edlund et al.
[57]. The 17(3-sulfate of the tertiary hydroxy group is sterically
influenced and decomposes in urine to yield several dehydration
products and the corresponding 17-epimeric isomer (17ahydroxy-
l7(3-hydroxy; Fig. 9). 17-Epimerization has been demonstrated
for several 17(3-hydroxy- 17 a-methyl steroids [26, 58-
60]. The distribution of reaction products has been similar in
several studies of AAS excretion.
Studying fluoxymesterone metabolism, Horning and I were
able to isolate the assumed sulfate conjugate of fluoxymesterone
and to compare it with synthesized fluoxymesterone 17/3-sulfate
(unpublished). The urinary compound had the same HPLC
retention time and ultraviolet absorbance spectrum as the
synthesized fluoxymesterone sulfate. When the isolated metabolite
and the synthesized product were dissolved in water, they
showed the same route of hydrolysis (t112 -4 h) and the same
distribution of reaction products. From these results we concluded
that the precursor of 17-epimeric steroids is the corresponding
17/3-sulfate conjugate.