I went to the trouble of writing one of the foremost experts on trenbolone. He provided with me with a wealth of information on trenbolone. I asked about trenbolone gynecomastia. Both he and I agree that it is not described in the literature. Further, any association would be worthy of publication. [Doing whatever it takes for Meso readers!]
Here are his thoughts on the interactions of trenbolone with the progesterone receptor (PR). The literature indicates that 17beta-trenbolone has a high affinity for the bovine PR (Bauer ER et al 2000); while its primary metabolites 17alpha-trenbolone and trendione do not (~1-2% of the affinity of progesterone). The ED50 (effective dose) of trenbolone to produce activity at the PR in a yeast bioassay (40nM) is approximately 10-fold higher than progesterone (4.5nM) and 57-fold higher than THG (0.7nM), a highly progestogenic AAS
(Death AK et al 2004). Similarly, others have shown that trenbolone has a high ED50, with a relative potency at the PR near that of testosterone (i.e., almost non-existent) using yeast bioassays (McRobb L et al 2008). Together, these results appear to suggest that trenbolone does in fact bind to the PR, but that it requires a relatively high dose to induce biologic activity (compared with progesterone or THG for example). This would seem to agree with previous reports that trenbolone is either non-progestogenic or only weakly progestogenic (Neumann F 1976).
As a side note, I would invite you to write a Letter to the Editor of the journal Steroids, in response to our recently published report, regarding your clinical experiences with trenbolone induced gynecomastia. I believe this would be of great interest to other clinicians, especially considering the preponderance of evidence suggesting that trenbolone is only a weak progestin and only weakly estrogenic (see our review for discussion).
Braunstein GD. Aromatase and gynecomastia. Endocr Relat Cancer 1999;6:315-24.
Bauer ERS, Daxenberger A, Petri T, Sauerwein H, Meyer HHD. Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and the bovine gestagen receptor. APMIS 108:838-46 (2000).
Death AK, McGrath KCY, Kazlauskas R, Handelsman DJ. Tetrahydrogestrinone Is a Potent Androgen and Progestin. J Clin Endocrinol Metab 2004;89(5):2498-500.
McRobb L, Handelsman DJ, Kazlauskas R, Wilkinson S, McLeod MD, Heather AK. Structure-activity relationships of synthetic progestins in a yeast-based in vitro androgen bioassay. J Steroid Biochem Mol Biol. 2008 May;110(1-2):39-47.
Neumann F. Pharmacological and endocrinological studies on anabolic agents. Environ Qual Saf Suppl 1976(5):253-64.
Yarrow JF, McCoy SC, Borst SE. Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity.
Recently, the development of selective androgen receptor modulators (SARMs) has been suggested as a means of combating the deleterious catabolic effects of hypogonadism, especially in skeletal muscle and bone, without inducing the undesirable androgenic effects (e.g., prostate enlargement and polycythemia) associated with testosterone administration. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone; 17beta-TBOH), a synthetic analog of testosterone, may be capable of inducing SARM-like effects as it binds to androgen receptors (ARs) with approximately three times the affinity of testosterone and has been shown to augment skeletal muscle mass and bone growth and reduce adiposity in a variety of mammalian species. In addition to its direct actions through ARs, 17beta-TBOH may also exert anabolic effects by altering the action of endogenous growth factors or inhibiting the action of glucocorticoids. Compared to testosterone, 17beta-TBOH appears to induce less growth in androgen-sensitive organs which highly express the 5alpha reductase enzyme (e.g., prostate tissue and accessory sex organs). The reduced androgenic effects result from the fact that 17beta-TBOH is metabolized to less potent androgens in vivo; while testosterone undergoes tissue-specific biotransformation to more potent steroids, dihydrotestosterone and 17beta-estradiol, via the 5alpha-reductase and aromatase enzymes, respectively. Thus the metabolism of 17beta-TBOH provides a basis for future research evaluating its safety and efficacy as a means of combating muscle and bone wasting conditions, obesity, and/or androgen insensitivity syndromes in humans, similar to that of other SARMs which are currently in development.