Guys, have you ever experienced E2 decrease with boldenone (if yes, where’re you from)? In Central Europe our UG boldenone cuts E2 even more than Mast, so much that 400 mg of TE with 700 mg BU isn’t often sufficient w/o an AI. Literature & evidence from studies indicate the presence of a metabolite structurally similar to atamestane, so it’s not surprising. What’s surprising is a fact that you guys from USA/GB never complain about that.
Literature shows ATD (arimistane) is a metabolite of boldenone, said drug is a potent steroidal (suicidal) aromatise inhibitor. At what concentration this metabolite is produced im unsure, I’d hypothesise it depends on individualistic metabolism of the drug
I was going to try boldenone, but worried about effects on gabaergic transmission and worried about lack of efficiency. It appears this is one of those compounds with an incredibly wide level of discrepancy regarding results. Some can take 1-2 grams of the stuff and notice absolutely nothing, bloodwork also remains entirely unchanged, others say “anything below 600mg is a waste” and some say “I took 2-300 mg and it was the best compound ever”… why??
Ive seen varying rates of tolerability to different compounds, but not quite to the extent of “this has NO pharmacologic effect on me vs this is the best shit ever”
Reference please. Haven’t seen any study with androsta-3,5-diene-7,17-dione as a boldenone metabolite.
Plus it’s “unique apetite-stimulatory property” - BS. There’s no evidence or any premise from deduction that it should act in other way than T in those regards.
I’ll send reference after dinner, give me an hour or so
I apologise, it appears Boldenone is a metabolite of ATD, btw I’m not talking about this
Theres two supps marketed as arimistane I believe, there’s this one and androsta-1,4,6-triene-3,17-dione, of which boldenone appears to be a metabolite of
It’s not entirely out of the question to speculate perhaps this compound would also be a metabolite of boldenone itself
The quick answer is “yes, it absolutely does”.