This is a cut-and-paste form one of the studies I have confidence in regarding deca:
..Synthetic nandrolone metabolite, named estren (19-Nor-4-androstene-3α,17β-diol)11. Estren was found to only weakly bind the estrogen receptor, showing no real activity at that site and possessing a 300-fold lower binding affinity. Yet it mimicked the actions of estrogens in osteoblasts. Estren was however shown to be as active as DHT at activating certain androgen receptor related transcripts. The same study also demonstrated that estren was capable of activating estrogen specific constructs in the DNA through the androgen receptor. Estren is a metabolite of nandrolone through the 3α-HSD enzyme. So in first instance one might suggest we start looking for something that blocks this enzyme. However I mentioned that this steroid was synthetic. Nandrolone is a natural androgen. So why does estren not appear naturally in the body ? Well mostly because it is a very labile structure, that is quickly converted back to nandrolone. The problem however is that the researchers noted that despite similar activity on several constructs as DHT, it bound with a 200-fold lower activity to the androgen receptor. The researchers found that the high androgenic potency of estren resulted in its conversion to the more stable molecule nandrolone, almost 50% in 4-6 hours, and no less than 95% within 24 hours. From this it can be concluded that the effects of estren via the AR are mediated by its metabolite nandrolone, and it is in fact nandrolone that activates estrogen specific transcripts via binding and activating the androgen receptor. Now the study also noted that binding of DHT activated estrogen-related transcripts, so this is not uncommon, but DHT did so with a 30 to 100-fold lower potency than estren. The authors concluded :
“Finally, the unexpected estren-dependent activation(and by extension nandrolone-dependent activation) of ERE-driven gene expression in cells that express AR, which occurs with far greater potency relative to DHT, predicts the possibility of some troublesome feminizing effects in males, which still await examination."
This is indeed a further blow to nandrolone’s already damaged image as being a safe steroid. As my co-author astutely pointed out, one could potentially treat this problem with the addition of chemicals that block the estrogen response element, such as piperidinediones12. However I’m not aware of any commercial preparations with such products, and finding them may prove difficult. So until further notice the only way to block nandrolone’s very potent estrogenic effects is to block the androgen receptor, and with it any and all anabolic effect the drug may have.
