Testosterone is the primary natural male androgen. Many people have argued that because it is natural that it is the best. The body has several elaborate systems to prevent what it sees as an overload of testosterone in the system. As you add more testosterone, enzymes such as aromatase and 5-alpha reductase work harder to keep a state of equilibrium and therefore to lower testosterone levels1. This produces more estrogen and DHT. Testosterone binds very well to SHBG and only a small fraction circulates in the free state2,3.
As with nandrolone, all esters of testosterone result in the same drug being delivered to the muscle after the ester is stripped off. The ester controls how slowly testosterone will be released into the body. Several things can influence the release of testosterone from an ester depot including the size of the depot, the concentration of the steroid in the oil vehicle, the type of oil used for vehicle, the injection site (gluteus, deltoid) and others4. Also, as the size of the ester increases, its percentage of the total molecular weight also increases. This means that you get less testosterone per 100 mg of testosterone enanthate (72 mg) than you would with 100 mg of testosterone acetate (87 mg). Testosterone is also available as a water-based suspension. Suspension is very short acting requiring frequent (daily) injections. Many people will use suspension in drug-tested competitions because it is cleared quickly. As this is a water-based injection, it is more prone to bacterial contamination, so extra care must be taken to not contaminate multi-use vials.
As discussed previously, testosterone inhibits 11-beta hydroxylase resulting in decreased levels of free and total cortisol levels as well as decreased CBG levels5. This results in increased levels of deoxycorticosterone which can cause sodium and water retention and increased blood pressure6. Testosterone does not affect TBG and TBPA in the manner described for some of the synthetic AAS5.
1. Bergink EW, Geelen JA, Turpijn EW: Metabolism and receptor binding of nandrolone and testosterone under in vitro and in vivo conditions. Acta Endocrinol Suppl (Copenh). 271:31-7, 1985
2. Saartok T, Dahlberg E, Gustafsson JA: Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. Jun;114(6):2100-6, 1984
3. Pugeat MM, Dunn JF, Nisula BC: Transport of steroid hormones: interaction of 70 drugs with testosterone-binding globulin and corticosteroid-binding globulin in human plasma. J Clin Endocrinol Metab. Jul;53(1):69-75, 1981
4. Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ: Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther. Apr;281(1):93-102, 1997
5. Barbosa J, Seal US, Doe RP: Effects of anabolic steroids on hormone-binding proteins, serum cortisol and serum nonprotein-bound cortisol. J Clin Endocrinol Metab. Feb;32(2):232-40, 1971
6. Uygur MC, Arik AI, Altug U, Erol D. Effects of the 5 alpha-reductase inhibitor finasteride on serum levels of gonadal, adrenal, and hypophyseal hormones and its clinical significance: a prospective clinical study. Steroids. Apr;63(4):208-13, 1998
Adapted with permission from Seth Robert’s Anabolic Pharmacology, all rights reserved.