Trenbolone is a derivative of nandrolone in that it lacks the methyl group at position 19. Trenbolone binds strongly to both the androgen receptor and the progesterone receptor1. This strong binding likely makes trenbolone an agonist of the progesterone receptor. Though people generally believe progesterone agonists to cause gynecomastia, progesterone agonists actually result in the downregulation of estrogen receptors. This strong progesterone receptor binding is also believed to be the source of the severe shutdown and loss of libido in a good portion of trenbolone users. As mentioned, trenbolone binds strongly to the androgen receptor (stronger than any commercially available androgen) and is not metabolized to 3-alpha metabolites in skeletal muscle delivering rapid strength and size gains2.
Trenbolone appears to have an antiglucocorticoid effect in animals but there is no reason to believe that this does not occur in humans as well3,4. Trenbolone cannot be converted to estrogens and although it is commonly believed that trenbolone is not 5-alpha reduced, there is a paper in the literature that shows trenbolone to be less potent in tissues with high levels of 5-alpha reductase4. This is exactly the same thing that is seem with nandrolone and since trenbolone is also a 19-nor steroid it is reasonable to assume, based on this evidence that trenbolone is in fact 5-alpha reduced to less potent metabolites. This would also partly explain the reports of gynecomastia as well as the shutdown that are seen with trenbolone even though it does not convert to estrogen. The decreased androgenic stimulation as a result of the production of less potent 5-alpha reduced androgens upsets the androgen to estrogen balance that results in greater net estrogenic signaling in the breast and hypothalamus.
The main problem with trenbolone is that it is very difficult (if not impossible) to find in a preparation that is made for human consumption. Trenbolone used to be available as Parabolan but if it is made anymore (which no one seems to be in agreement about) it is not readily available. Most of the tren that is currently available on the black market is made from cattle implants called Finaplix®. Several underground labs have created injectable versions of this drug by dissolving the pellets in a solvent and bottling the solution. Kits are also available through many sources that allow a person to make their own injectable at home from the pellets. The problem with these underground versions and homemade concoctions is that they are not produced in a sterile fashion. This can lead to abscess, sepsis, and even anaphylactic shock followed by death. Also, the solvents used to dissolve the pellets are not meant to be injected and can cause the same problems with the additional possibility of poisoning. Trenbolone is available with acetate, enanthate or occasionally the hexahydrobenzylcarbonate esters. The acetate ester is injected daily or every other day and was previously available in a veterinary product called Finaject that is no longer produced. The enanthate ester is produced by underground labs and could be injected every 7-10 days but is probably injected more frequently by AAS users. The hexahydrobenzylcarbonate ester was originally produced as a pharmaceutical grade human-use product with the name Parabolan but hasn’t been made in a long time. It seems to pop up in underground preparations from time to time and has a similar half-life as the enanthate ester and therefore is injected weekly or biweekly.
Trenbolone is a very potent anabolic that can produce dramatic increases in weight and strength, especially when combined with other anabolics. Along with this potency comes the likelihood for androgenic side effects such as high blood pressure, acne and hair loss among others. This steroid also has a reputation for being toxic to the kidneys. There is no direct evidence for this side effect in the scientific literature but since the kidneys do respond to androgenic stimulation and trenbolone can cause hypertension which can also damage the kidneys, care should be taken.
233. Ojasoo T, Delettre J, Mornon JP, Turpin-VanDycke C, Raynaud JP: Towards the mapping of the progesterone and androgen receptors. J Steroid Biochem. 1987:27(1-3):255-69.
235. Schanzer W: Metabolism of anabolic androgenic steroids. Clin Chem. 1996:42(7):1001-20.
286. Jones SJ, Johnson RD, Calkins CR, Dikeman ME: Effects of trenbolone acetate on carcass characteristics and serum testosterone and cortisol concentrations in bulls and steers on different management and implant schemes. J Anim Sci. 1991:69(4):1363-9.
287. Wilson VS, Lambright C, Ostby J, Gray LE Jr: In vitro and in vivo effects of 17beta-trenbolone: a feedlot effluent contaminant. Toxicol Sci. 2002:70(2):202-11.
Adapted with permission from Seth Robert’s Anabolic Pharmacology, all rights reserved.