The thing is that gyno occurs quite frequently with nandrolone, whereas I've yet to witness a confirmed case of trenbolone gyno. This despite the fact that both the progestagenic capacity is greater and the difference between AR and PR activation is smaller than for nandrolone. With nandrolone however we've been able to elucidate the mechanism of its effect. Whereas tren clearly shows the effects of a progestin in its action, nandrolone seems to exert none of the typical progestagenic effects. In fact it seems to perfectly fit the bill of an estrogenic steroid, something that was widely believed and accepted before people had access to medline. Nandrolone does aromatize, but to a much lesser degree [19]. It's also been shown to bind the estrogen receptor, but doesn't seem to activate it unless at micromolar doses in vitro [20], something that would take massive consumption to mimic in vivo. One study however did estimate nandrolone's estrogenic potential at 60% that of estradiol [21]. With those figures a higher prevalence of gyno with this steroid than with testosterone isn't that hard to imagine, especially when you know that the same enzyme that converts testosterone to DHT (5-alpha-reductase), the metabolite with the most profound effect on estrogen inhibition in the breast also converts nandrolone to DHN, which is a significantly WEAKER androgen (thus causing a massive A:E imbalance). But where does the estrogenic action come from ? Researchers already established [22] that aromatase, PR and ER did not play a role because the co-administration of inhibitors for each compound had no significant effect on the estrogenic potential. The elucidation of its mechanism came through a study on the synthetic steroid estren, a direct precursor to nandrolone [23]. It showed that estren was able to mediate estrogenic effects by binding the AR and activating Estrogen Response Elements (ERE's) in the DNA. Consider ERE's like little signs that say "hey estrogen receptor, bind here and do your thing". Apparently estren causes the AR to confuse itself with an ER. Estren however is a highly unstable metabolite, which rapidly converts to nandrolone under physiological circumstances. The time-frame of estrens effect (increased ERE activation while it is increasingly metabolized to nandrolone) and estrens low RBA to the AR compared to nandrolone clearly shows that this effect is mediated by nandrolone. So nandrolone causes estrogenic effects by binding the androgen receptor.
This causes a huge problem in treatment, since the only way to stop this effect is to block the AR, and with it the anabolic effect of nandrolone. Technically there is some evidence that ERE's can be blocked using piperedinediones [24] but I'm not aware of any formulations containing such products, nor is there any data on their safety. This is crucial : THE ONLY WAY TO STOP NANDROLONE'S ESTROGENIC EFFECT IS TO NOT USE IT. While I would think its logical that if a certain compound gives you more problems, or harder to treat problems, that you cease use of that product, especially since there are plenty of other products available that offer the same benefits, I would stress this extra for nandrolone. It's easily replaced with a drug like boldenone, which is completely different, but produces the same outward results, probably a little leaner. But it's easy to see why this compound would be great food for all the alternate "theory" guru's, and their primary proof for "estrogen-management doesn't work in every case". Fact is it does, but in this case the only way to manage it is not to take it.
