Pub. L. 101–647, title XIX , § 1903, Nov. 29, 1990 , 104 Stat. 4853 , as amended by Pub. L. 108–358 , § 2(c), Oct. 22, 2004 , 118 Stat. 1663 , provided that: “(a) Drugs for Treatment of Rare Diseases.— If the Attorney General finds that a drug listed in paragraph (41) of section 102 of the Controlled Substances Act (as added by section 2  of this Act) is— “(1) approved by the Food and Drug Administration as an accepted treatment for a rare disease or condition, as defined in section 526 of the Federal Food, Drug , and Cosmetic Act ( 21 . 360bb ); and “(2) does not have a significant potential for abuse, the Attorney General may exempt such drug from any production regulations otherwise issued under the Controlled Substances Act as may be necessary to ensure adequate supplies of such drug for medical purposes. “(b) Date of Issuance of Regulations.— The Attorney General shall issue regulations implementing this section not later than 45 days after the date of enactment of this Act [ Nov. 29, 1990 ], except that the regulations required under section 3(a) [former 1903(a)] shall be issued not later than 180 days after the date of enactment of this Act.”
It is interesting to note that oxymetholone does exhibit some tendency to convert to dihydrotestosterone in the body, although this does not occur via the 5-alpha reductase enzyme. Oxymetholone is already a dihydrotestosterone-based steroid, so no such alteration can take place. Aside from the added c-17 alpha alkylation (discussed below), oxymetholone differs from DHT only by the addition of a 2-hydroxymethylene group. This grouping can be removed metabolically, reducing oxymetholone to the potent androgen 17alpha-methyl dihydrotestosterone (mestanolone). 387 There is little doubt that this biotransformation contributes at least on some level to the androgenic nature of this steroid. Note that since 5-alpha reductase is not involved, the relative androgenicity of oxymetholone is not affected by the concurrent use of finasteride or dutasteride.
Oxandrolone is most certainly a hepatotoxic steroid. It does not carry the strongest level of hepatotoxicity among anabolic steroids, but it is stronger than most. This is due to it being a C17-aa anabolic steroid. All C17-aa steroids are hepatic, but the level of toxicity varies greatly between them. Due to this steroid’s strong hepatotoxicity, this is why total use must be limited (see administration section).
Due to use, those who supplement with Anadrol will find their liver enzyme values increase. An increase in values is not a sign of damage but rather a sign of stress that can lead to damage if responsible practices are not followed and the stress is allowed to remain. Proper dosing and duration of use protocols are imperative when it comes to this steroid. Further, it is important the individual avoids excess alcohol consumption when supplementing with this steroid due to the liver stress such consumption will cause. In fact, most will find avoiding all alcohol to be best during use. If this is a problem and you are supplementing for the purpose of performance enhancement remember there is nothing on earth that is as anti-performance as alcohol. Those who supplement are also encouraged to limit their use of Over the Counter (OTC) medications. Many OTC medications carry strong hepatic natures, and the added stress can be extensive when coupled with Anadrol. Use should be limited to when only absolutely needed. If these rules can be followed, once use is discontinued liver enzyme values will return to normal and no damage will be done. As a final note, Anadrol should not be used if the liver is unhealthy.