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However, nandrolone decanoate remains available from compounding pharmacies in the United States, for instance AnazaoHealth. It is only available from this particular pharmacy at a very high concentration of 200 mg/mL however, which although a potentially workable concentration for use in transmasculine people, is likely completely impractical for use in transfeminine people. Compounding pharmacies might be able to do custom concentrations upon request though. Testosterone is aromatized in small amounts into estradiol, and for this reason, testosterone has estrogenic activity. It may have positive effects on sexual desire in men as well (Wibowo & Wassersug, 2013).
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There are case reports of severe and complete masculinization of the voice in women treated with excessive doses of nandrolone (Damsté, 1964; Brodnitz, 1971; Baker, 1999). Voice changes have also been seen with nandrolone derivatives like normethandrone (Feldman et al., 1960). The dosage of nandrolone for use in androgen replacement therapy in women and men hasn’t been established. Hence, we don’t completely know what the appropriate dose is for use in transfeminine and transmasculine hormone therapy. Another potential means of delivering nandrolone is via an orally active nandrolone androgen prohormone like 19-nordehydroepiandrosterone (19-nor-DHEA).
In experimental animal models, nandrolone is synthesized endogenously through a mechanism distinct from DHT (25). Furthermore, the metabolism of nandrolone in animal models yields compounds completely unrelated to DHT (15,26). It has also been proven that the actions of 5AR on nandrolone produce a compound that has decreased affinity and activity at the androgen receptor (15). Given that nandrolone is not converted to DHT it seems logical to assume that it would have less effect on hair loss than exogenous testosterone (with its subsequent conversion to DHT). Thus, nandrolone may be beneficial in treating hypogonadal men concerned about alopecia in the setting of TST. The molecular mechanism underlying this altered tendon activity may be related to collagen synthesis 60,110.
The results highlighted an increase of plasma levels of liver necrosis markers, an increase in collagen deposition in liver parenchyma, portal space, and centro lobular vein 113,114. The mechanism involved in collagen deposition could be the increase in the number and in the activity of Kuppfer cells. During this time, there was no need for a black market or underground laboratories (UGL) since these drugs were readily available from health professionals. However, the situation dramatically changed after the introduction of the Anabolic Steroid Control Act in 1990, and subsequently reinforced by the Anabolic Steroid Control Act of 2004.
The chronic effects of AAS abuse, aside from neuropsychiatric and behavioral effects, include a wide range of somatic consequences. Consequently, AASs may exert negative effects on reproductive, hepatic, musculoskeletal, endocrine, renal, immunologic, cardiovascular, cerebrovascular, and hematological systems 19,20,21,22. They can cause androgenic and masculinizing effects like oily skin, acne, seborrhea, facial/body hair growth, scalp hair loss, and voice deepening, among others.
Individuals with 5α-reductase type 2 deficiency undergo masculinization of the genitals at puberty such that a small and near-functional penis develops (Peterson et al., 1977; Marks, 2004; Hiort, 2013; Photos). This is so striking that males with 5α-reductase type 2 deficiency in the Dominican Republic are referred to as “guevedoces”, which is said to literally mean “penis at 12”. We’ve made all possible efforts to ensure that the information provided here is accurate, up-to-date and complete, however, it should not be treated as a substitute for professional medical advice, diagnosis or treatment. Practo only provides reference source for common information on medicines and does not guarantee its accuracy or exhaustiveness. The absence of a warning for any drug or combination thereof, should not be assumed to indicate that the drug or combination is safe, effective, or appropriate for any given patient. Practo does not assume any responsibility for any aspect of healthcare administered with the aid of information provided above.
To sum up, inflammatory cytokines, oxidative stress, protein synthesis alteration, and apoptosis are common mechanisms involved in AAS-related damage. Supra-physiologic doses of common AASs alter immune function by influencing the production of certain cytokines. In fact, the users of AASs have abnormal immunoglobulin (Ig) concentrations; the lowest levels of immunoglobulin G (IgG), immunoglobulin M (IgM) and immunoglobulin A (IgA), “significantly lower” than controls for IgA and IgM 129. Kanda and coauthors 130 showed that spontaneous IgM and IgG production in humans was inhibited by exposure to 1 nM testosterone, which is nearly a physiological dose, suggesting that high doses would potentially adversely affect the immune system. Some studies suggest that AASs are immune suppressive and depend on the type of AAS used and the dose and timing of administration.
Hassager and colleagues concluded that anabolic steroids stimulate type III collagen synthesis, which affects muscular tissues as well as bone tissues 111. ND has important effects on the hypothalamic—pituitary—adrenal Axis (HPAA) and on lipid metabolism. In a study by Gårevik et al., cholesterol level, steroid synthesizing enzymes in the adrenal gland (HMGCR) mRNA and Apo-lipoprotein B (ApoB) appeared to increase after a single dose of ND in humans, and this effect was persistent after 14 days 47.