Triple B Solutions

What’s the deal with DHB anyway? The only thing consistent in the reports I’ve read is the PIP lol some people say it’s like Tren without sides, others say it’s nothing special.
I didn’t care for it because it was unusable the way it was brewed. The lab way overdosed it and it arrived crashed. I remade it down to a lower mg/ml and it still would crash between shots. I gave up on it. But the pip wasn’t bad at all once it was down to 100mg/ml in MCT.
 
I didn’t care for it because it was unusable the way it was brewed. The lab way overdosed it and it arrived crashed. I remade it down to a lower mg/ml and it still would crash between shots. I gave up on it. But the pip wasn’t bad at all once it was down to 100mg/ml in MCT.
Did it effect e2 at all? In your opinion, would masteron be a good addition to test/dhb/low npp, or redundant?
 
DHB has always piqued my interest, but if it carries the same trait of raising HCT to the extent that EQ does, then it's a no go for ol' MSG.
 
don't expect hct to be raised as @Type-IIx posted a study claiming dhb is an essentially trivial metabolite of EQ (in terms of amount produced) but worth checking, no?
Wait, that's the exact opposite of what I said. DHB is a misnomer, it's 1-Testo with no relationship (it is not a metabolite of boldenone) to boldenone. I never said DHB/1-Testo is non-hematopoieitic, if anything, the opposite is likely given its being of the same class as Stenbolone and Primobolan which are quite potent hematinic agents.
 
I never said DHB/1-Testo is non-hematopoieitic, if anything, the opposite is likely given its being of the same class as Stenbolone and Primobolan which are quite potent hematinic agents.
Oh . . . I say, with knowing nod, before I go to Google and start searching for those big words starting with the letter h
 
I misspoke - I understood what you meant that boldenone doesn't metabolize to dhb. Meant structurally they are quite similar - boldenone with the one reduced pi bond = boldenone + two hydrogens. Obviously small structural changes can drastically alter aas function (mast and superdrol, dbol and eq) but given the paucity of studies on dhb, aas in general (excuse me, 1-testo) isn't it worth considering?
@Type-IIx, Not being rhetorical /smartass, these are genuine questions, I work in research (not biology, clearly) so I'm genuinely curious. Trying to take a step beyond bro science.
Wait, that's the exact opposite of what I said. DHB is a misnomer, it's 1-Testo with no relationship (it is not a metabolite of boldenone) to boldenone. I never said DHB/1-Testo is non-hematopoieitic, if anything, the opposite is likely given its being of the same class as Stenbolone and Primobolan which are quite potent hematinic agents.
 
E.g. Definitely notice cardio boost from 300 mg eq, but did not with 700 primo or 350 sten. In your opinion, will I get one from hematopoesis of 1-testo?
 
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