Is this still your current evaluation in terms of AAS ranking regarding cardiovascular risk factors?
Three things I am curious about:
1) Why there are no human studies of trenbolone since it was used for humans in the 80s?
2) Why current research (my first post) is done on trenbolone with a possible use for humans?
3) Regarding these studies trenbolone seems to be not that androgenic, therefore maybe it is not a strong CNS stimulant?
(1) When it was synthesised back in the 1960s, standards for drug approval were much less stringent than they are nowadays. If the mechanism of action was comparable to other compounds in a class, and there were animal studies demonstrating general safety, that would sometimes be sufficient.
(2) Tren's an interesting compound, but all kinds of compounds, some of which are notoriously dangerous, are still researched with an eye to potential future applications. Thalidomide's repurposing to other uses is an example.
(3) Tren has been demonstrated to be rather androgenic in most animal and cell-culture studies, and those aren't really disputed by anyone, not even the study you're quoting. There is only really one relevant paragraph from the paper relating to your quote above:
To this effect, TREN is a promising candidate to reduce the incidence of androgenic and/or estrogenic side effects associated with androgen administration because TREN (1) reduces serum testosterone [104,105,237] and DHT (unpublished laboratory results) presumably through pituitary or hypothalamic feedback inhibition [93,106], (2) does not appear to undergo 5-a reduction or aromatization [58,68], and (3) is metabolized to less potent androgens in vivo [39,58,68]. Ultimately, research examining the prevalence of androgen- and/or estrogen-mediated side effects associated with TREN administration and the mechanisms through which TREN reduces prostate growth is warranted.
As you can see, all they're really saying is that it doesn't convert to DHT or E2, but it's hardly unique among AAS in that regard. And their assumption that DHT is the main or only mechanism for virilization or androgenicity in AAS is patently misleading and myopic. I would say, having read the paper, that they're just trying to drum up interest in the compound to justify the research they're already undertaking. Which is not to say their research isn't helpful (it is, and they've done quite a lot before and since), merely that many scientists attempt to create self-justifying cycles of related research in order to keep themselves happily employed and (most importantly) to get it published
Having said that, any study which can claim that prostate cancer is the only really 'serious risk' for AAS-using bodybuilders demonstrates a concerning lack of knowledge on the part of the authors
