This blog post contains citations referenced in my video, which you can watch here.
A. A review of the literature failed to discover any androgen receptor binding studies for methenolone. How websites report an androgenic to anabolic ratio is unclear.
B. Human liver function:
a. It was originally thought that methenolone enanthate and acetate (and nandrolone phenoproprionate) would not produce liver stress, in contrast to 17-alkylated steroids.
b. Methenolone enanthate appears to have improved albumin turnover in cirrhotic patients.
C. Human female breast cancers:
a. Methenolone enanthate was (ineffectively) used to treat females with breast cancers. It was shown to produce virilization and not to convert to estrogen.
b. In a group of 28 cancerous women given methenolone enanthate, 12 developed dyslipidemia that regressed upon discontinuation.
D. Human anemia:
a. The acetate version has been used to treat female anemics at 20 mg.
b. It produced cholestatic jaundice in some anemics at 1-2 mg/kg.
E. Human metabolism:
a. In men, a single dose of methenolone acetate produced methenolone in urine for up to 90 hours after administration, totaling to 1.6% of the oral dose.
b. Several other metabolites were found, consequent to oxidation of the 17-hydroxyl group and a reduction of the A-rings.
c. The major metabolite is 3alpha-hydroxy-1-methylen-5alpha-androstan-17-one, which can be detected in urine up to 5 days after a single ingestion of the drug.
d. Methenolone sulfate and other sulfated metabolites form a core component of the metabolism of methenolone in man.
a. There is a US patent on the use of methenolone or nandrolone to treat dry eyes.
a. Methenolone acetate was shown to increase erythropoietic activity of bone marrow cells, either by increasing the sensitivity of erythropoietic cells or their numbers.
b. When compared to testosterone, oxymetholone, and metholone, methenolone produced a more erythropoietic effect than testosterone (though metholone produced the most). This indicates that the virilization and erythropoietic effects work through different mechanisms.
c. A study found that halotestin (fluoxymesterone) and methenolone similarly increased hematopoiesis in rodents, as well as iron uptake into blood.
H. Bone development:
a. Like other AAS, methenolone enanthate was shown to increase bone development in growing female rodents and decrease it in male rodents.
b. It halts the growth of young rodents.
c. In rodents, methenolone produced a favorable healing profile for fractured bones despite its less androgenic nature. Early calcium callus concentrations were raised less than with testosterone, but later repair was comparable.
d. Via agonism of the androgen receptor, DHT, fluoxymesterone (halotestin), and methenolone are mitogenic on in vitro bone cells, meaning they cause bone cell division and proliferation.
I. Renal function:
a. Even without improving muscular development, methenolone enanthate was shown to increase kidney weights in growing male rodents.
J. Cardiac function:
a. It was shown to produce left ventricular hypertrophy in pubertal rodents, with more pronounced effects occurring among the female rodents.
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