injectable Dianabol

[CensoredBoardsSuck]

Was injectable dianaol ever really used in animals?

Or in 3 mg dbol pills for 5 - 6 lb roosters. You ever try to give a chicken a pill?

 

[Wunderpus]

Or in 3 mg dbol pills for 5 - 6 lb roosters. You ever try to give a chicken a pill?

Wait, are these those pills that make your cock grow?? Are the gains mostly water weight/ temporary? Can I run an oral only cycle for my cock?

Thanks.

 

[BBC3]

Oh my bad. I thought that things we eat go thru the liver like food.

FOR FUKING GID DAMN FREAK SAKES THANK FUKING YOU..!!!!!

Oh and another point of emphasis should be made.

Essentially ALL AAS must pass thru the liver whether they are ingested of injected.

That's bc the liver is responsible for catabolizing all drugs (some more than others) into byproduct forms that are capable of renal excretion.

Finally just bc a 17-methyl AAS becomes available in an injectable rather than a pill form, does NOT in any way imply it's less hepatotoxic.

MethyTren and MethyTest both fit the aforementioned categories and BOTH are quite hepatotoxic.

It's possible these agents undergo considerable "second pass" hepatic metabolism OR the absence of an ester allows for an abrupt accumulation of "toxic peak levels" which simply overwhelms the livers detoxification capabilities OR some combination of both.

 

[BBC3]

And was NOT AT JIM

 

[PenisSurfer]

Oh and another point of emphasis should be made.

Essentially ALL AAS must pass thru the liver whether they are ingested of injected.

That's bc the liver is responsible for catabolizing all drugs (some more than others) into byproduct forms that are capable of renal excretion.

Finally just bc a 17-methyl AAS becomes available in an injectable rather than a pill form, does NOT in any way imply it's less hepatotoxic.

MethyTren and MethyTest both fit the aforementioned categories and BOTH are quite hepatotoxic.

It's possible these agents undergo considerable "second pass" hepatic metabolism OR the absence of an ester allows for an abrupt accumulation of "toxic peak levels" which simply overwhelms the livers detoxification capabilities OR some combination of both.

PO admin causes a concentration spike at the portal vein while IM admin into a depot allows for slow release. Yes it all goes through the liver eventually, but PO admin all of it goes through liver at the same time in the same place.

c17 alkylation prevents enzymatic attack of the 17 hydroxyl. I suspect c17 alkylation also increases affinity of the steroid for GCRs, which is part of the cause of hepatoxicity. Search glucocorticoid hepatoxicity...