Nandrolone is the common name given to the C-19 demethylated derivative of testosterone, 19-nortestosterone. While this seems like a minor alteration, its effects on the actions of the molecule are profound. First of all, nandrolone is a more potent binder of the androgen receptor with approximately 50% greater binding affinity than testosterone1,2,3. Secondly, since the 19-methyl group plays a pivotal role in the aromatization process, the conversion to estrogenic metabolites is reduced to about twenty percent with nortestosterone and its derivatives of the rate of testosterone4. Thirdly, the 5-alpha reduction of nortestosterone and its derivations results in dihydronandrolone metabolites which are considerably weaker than the parent compound5,6. Finally, binding to SHBG is significantly reduced with nortestosterone compared to testosterone7.
Nortestosterone is actually produced in small quantities in mammals, including man. Nortestosterone is considered to be a derivative of progesterone and it does, in fact, have some level of progestational activity, about twenty percent of the binding of progesterone1,3. Much has been made of this fact, especially with regard to nandrolone’s ability to induce gynecomastia. Since nandrolone does not convert to estrogen in nearly the same quantities as testosterone, all sorts of explanations have been concocted to account for the apparent ease with which it causes gynecomastia. The fact is that while nandrolone does convert to a smaller degree, significant increases in estrone have been observed in the literature with nandrolone therapy4. Estrone is sulfated to form estrone sulfate which has a very long half-life in the body and can act as a reservoir of estradiol through back conversion. The main contributing factor is the fact that nandrolone is not very androgenic. In fact, because of the formation of less potent, dihydronandrolone metabolites, the total androgenic stimulation is much reduced with the use of nandrolone. This, combined with the formation of estrone, results in a significant shift in the androgenic to estrogenic ratio. This is also the largest reason for the major shutdown in natural testosterone production seen with nandrolone and its derivatives8. The fact that there is a small progestational activity does further impact the shutdown of natural testosterone production but likely has minimal to no effect on the propensity of nandrolone to cause gynecomastia. However, nortestosterone has been shown to have mixed agonist/antagonist activity at the progesterone receptor and antagonism of the progesterone receptor may increase estrogen receptor concentration in the breast and hypothalamus which may contribute to the estrogenic effects that some notice with nandrolone9.
Used in reasonable doses, nandrolone is almost the perfect steroid. The major drawbacks to nandrolone are its reduced androgenic activity and its conversion to estrogen. Nandrolone is known to dramatically affect libido in a negative fashion due to its reduced androgenic activity and results in a condition known as “deca dick”. This is due to the suppression of natural testosterone levels and the lack of androgenic stimulation in DHT target tissues (such as the prostate). Many people will add testosterone to nandrolone to help counteract the negative effect on libido. Others will add a source of androgen such as mesterolone or dromostanolone to maintain androgenic tissues. Another alternative is to use small doses of a 5-alpha reductase inhibitor which will maintain some of the more potent nandrolone in androgen target tissues – this would of course also increase the risk of androgenic side effects. This is the opposite effect that 5-alpha reductase inhibitors have when combined with other reducible steroids. Nandrolone, unlike most other androgens, actually increases TBG and TBPA levels slightly resulting in reduced levels of free thyroid hormones10. One study showed nandrolone to be the most potent stimulator of red blood cell production compared to testosterone and oxymetholone11.
While many steroids (such as testosterone) inhibit the production of cortisol through the inhibition of 11-beta hydroxylase activity and the formation of hypertensinogenic deoxycorticosterone, nandrolone has been shown to have little to no hypertensinogenic effect due to a lack of inhibition of 11-beta hydroxylase12. On the other hand, nortestosterone has been shown to inhibit cortisol production through the inhibition of 21 hydroxylase. This is demonstrated by the reduction in non-plasma bound cortisol shown in the literature10. This reduction in cortisol is likely due to chronic dosing because increases in cortisol have been shown to occur early in therapy with nandrolone and may account for the relief in joint soreness that some have attributed to nandrolone13.
Different esters are attached to this molecule to change the rate at which they are absorbed from the injection site. That is the only thing that the different esters change. Once the ester is removed you have just plain nandrolone. Nandrolone is well known for causing positive test results. In fact, most tested athletes will avoid nandrolone because it can be detected for extended periods of time. Why this is so is somewhat of a mystery but much of it has to do with the habits of the user. Most nandrolone esters tend to have a long half-life. When injected on a period shorter than the half-life, nandrolone levels in the blood will rise to very high levels which take a long time to be metabolized and cleared from the body14,15
1. Ojasoo T, Delettre J, Mornon JP, Turpin-VanDycke C, Raynaud JP: Towards the mapping of the progesterone and androgen receptors. J Steroid Biochem. 27(1-3):255-69, 1987
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. Loughney DA, Schwender CF: A comparison of progestin and androgen receptor binding using the CoMFA technique. J Comput Aided Mol Des. Dec;6(6):569-81, 1992
4. Yoshiji S, Yamamoto T, Okada H. [Aromatization of androstenedione and 19-nortestosterone in human placenta, liver and adipose tissues]. Nippon Naibunpi Gakkai Zasshi. 62(1):18-25, 1986
5. Schanzer W: Metabolism of anabolic androgenic steroids. Clin Chem. Jul;42(7):1001-20, 1996
6. 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
7. 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
8. Bijlsma JW, Duursma SA, Thijssen JH, Huber O: Influence of nandrolondecanoate on the pituitary-gonadal axis in males. Acta Endocrinol (Copenh). Sep;101(1):108-12, 1982
9. Reel JR, Humphrey RR, Shih YH, Windsor BL, Sakowski R, Creger PL, Edgren RA. Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives. Fertil Steril. 31(5):552-61, 1979
10. 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
11. Gorshein D, Murphy S, Gardner FH. Comparative study on the erythropoietic effects of androgens and their mode of action. J Appl Physiol. 35(3):276-8, 1973
12. Hall CE, Hungerford S. Similarities and differences between effects of testosterone and 19-nortestosterone in rats, with particular reference to hypertensogenic potency. J Steroid Biochem. 16(4):581-5, 1982
13. Bergink EW, Janssen PS, Turpijn EW, van der Vies J: Comparison of the receptor binding properties of nandrolone and testosterone under in vitro and in vivo conditions. J Steroid Biochem. Jun;22(6):831-6, 1985
14. Schlussman SD, Zhou Y, Johansson P, Kiuru A, Ho A, Nyberg F, Kreek MJ: Effects of the androgenic anabolic steroid, nandrolone decanoate, on adrenocorticotropin hormone, corticosterone and proopiomelanocortin, corticotropin releasing factor (CRF) and CRF receptor1 mRNA levels in the hypothalamus, pituitary and amygdala of the rat. Neurosci Lett. Apr 28;284(3):190-4, 2000
15. van der Vies J: Implications of basic pharmacology in the therapy with esters of nandrolone. Acta Endocrinol Suppl (Copenh). 271:38-44, 1985
Adapted with permission from Seth Robert’s Anabolic Pharmacology, all rights reserved.