As for trenbolone supposedly causing gyno: Back when I did consultations for a lot of people, there were hundreds of cases of those using trenbolone made from Fina or a then-known-good product (namely Ttokkyo), not using Deca, and either using aromatizing steroids at so moderate a dose as to make gyno no issue, or using Nolvadex or Clomid at sufficient dose to keep estrogenic gyno from being an issue, or just using HCG at appropriately low dose to keep estrogen levels from going too low as well as to maintain testicular function.
Not one case of gyno, or one case of existing gyno being aggravated.
I don’t believe that trenbolone causes gyno. That is my opinion. Any alleged case seems always to fall into one of these categories:
Questionable product was used that may not have been trenbolone.
Deca was used.
Aromatizing steroids at sufficient dose to explain gyno used at the same time without use of SERM or antiaromatase.
Anadrol used under high-estrogen conditions.
Psychological gyno. (Meaning, no physical evidence, just “I did my first injection yesterday and today I’ve got nipple pain!”)
Here’s an abstract supporting Trenbolone as a progestin.
1: APMIS. 2000 Dec;108(12):838-46.Links
Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor.
Bauer ER, Daxenberger A, Petri T, Sauerwein H, Meyer HH.
Institut für Physiologie, Research Center for Milk and Food Weihenstephan, Technical University Munich, Germany.
For the steroidal growth promoters trenbolone acetate (TBA) and melengestrol acetate (MGA) neither the complete spectrum of biological activities nor the potential endocrine disrupting activity of their excreted metabolites in the environment is fully understood. The potency of these substances in [3H]dihydrotestosterone ([3H]-DHT) displacement from the recombinant human androgen receptor (rhAR) and from human sex-hormone binding globulin (hSHBG) was evaluated. In addition, the potency for [3H]-ORG2058 displacement from the bovine uterine progestin receptor (bPR) was tested. For comparison, different anabolics and synthetic hormones were also tested for their binding affinities.
For 17beta-trenbolone (17beta-TbOH), the active compound after TBA administration, an affinity the rhAR similar to dihydrotestosterone (DHT) and a slightly higher affinity to the bPR than progesterone were demonstrated.
The affinity of the two major metabolites, 17alpha-trenbolone and trendione, was reduced to less than 5% of the 17beta-TbOH-value. The affinity of these three compounds and of MGA to the hSHBG was much lower compared with DHT. MGA showed a 5.3-fold higher affinity than progesterone to the bPR but only a weak affinity to the rhAR. The major MGA metabolites have an affinity to the bPR between 85% and 28% of the affinity of progesterone. In consequence, MGA and TBA metabolites may be hormonally active substances, which will be present in edible tissues and in manure. We conclude that detailed investigations on biodegradation, distribution and bio-efficacy of these substances are necessary.
Since Trenbolone has a higher affinity for the progesterone receptor than progesterone itself, it’s highly suggestive that increased prolactin will result.
No, it does not support the claim that trenbolone is a progestin, in the slightest.
You could just as well say a study showing tamoxifen binds the estrogen receptor (which it does) supports that it is estrogenic in that tissue and thus supports some silly claim that it can cause gyno.
Or say that a study showing that spironolactone, cimetidine, or flutamide bind the androgen receptor and can displace DHT or testosterone supports that these are anabolic/androgenic, and thus supports some silly claim that you can take Tagamet to get huge, when in fact they are anti-androgenic.
Binding does not prove activity. Most hormone antagonists work by binding the receptor and will be seen to displace the endogenous ligand.
Try looking for studies where they assay activity and you will find consistently no progestagenic activity for trenbolone.
The second part (“for all we know”) from that study, yes. From other studies that do evaluate activity, we know that in the animals studied there was no detectable progestagenic activity.