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Why Primobolan is Primo 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[1]. b. Methenolone enanthate appears to have improved albumin turnover in cirrhotic patients[2]. 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[3]. b. In a group of 28 cancerous women given methenolone enanthate, 12 developed dyslipidemia that regressed upon discontinuation[4]. D. Human anemia: a. The acetate version has been used to treat female anemics at 20 mg[5]. b. It produced cholestatic jaundice in some anemics at 1-2 mg/kg[6]. 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[7]. 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[8]. d. Methenolone sulfate and other sulfated metabolites form a core component of the metabolism of methenolone in man[9]. F. Vision: a. There is a US patent on the use of methenolone or nandrolone to treat dry eyes[10]. G. Erythropoiesis: a. Methenolone acetate was shown to increase erythropoietic activity of bone marrow cells, either by increasing the sensitivity of erythropoietic cells or their numbers[11]. b. When compared to testosterone, oxymetholone, and metholone, methenolone produced a more erythropoietic effect than testosterone (though metholone produced the most)[12]. 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[13]. 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[14]. b. It halts the growth of young rodents[15]. 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[16]. 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[17]. I. Renal function: a. Even without improving muscular development, methenolone enanthate was shown to increase kidney weights in growing male rodents[18]. J. Cardiac function: a. It was shown to produce left ventricular hypertrophy in pubertal rodents, with more pronounced effects occurring among the female rodents[19].