11-18-2002, 02:29 PM #1
17aa - Is it not a question of dose?
Why is it when 17aa drugs are spoken of people seem to make greater inference to the drug rather than the doseage? I constantly hear things being said like 'anavar is easy on the liver but dbol , winny and anadrol will fuck up your liver in no time'
Maybe I'm a retard but here's my understanding:
All things remaining the same, each molecule of substance must have an additional carbon atom which replaces the H atom at position 17 in the ring. This molecule prevents the breakdown of the compound during oral administration. So what gives? I realize that if you have one compound and add another one to it it is no longer the same but maybe someone can explain how this would affect liver toxicity. Why is 50mg Anadrol more liver toxic than 50mg Anavar?? This seems to be the prevailing logic on this forum and many others.
Maybe someone could shed some light on this.
11-18-2002, 02:36 PM #2Junior Member
- Join Date
- Oct 2002
no idea but interesting none the less iv never looked at it that way i hope this gets cleard up, im eager to see a response on this one
11-18-2002, 03:44 PM #3
While you are correct that turning a parent compound into a 17 AA always renders that compounds metabolites 17 AA (whatever the parent breaks into) their is still a difference in the parent itself. Like any drug their are different half lives, different amounts of time it passes through the liver before being rendered inactive, binding affinities, speed through the system. All these help determine the overall effect it has on the liver.
11-18-2002, 04:39 PM #4
i may be the retard here, but for me, the bottom line is this:
there are some 17 aa's that are hard on your liver and other organs, and some that arent no matter what the dosage. this goes for oils as well, as they do have an effect on liver function. most people seem to think that since the 1st pass theory is eliminated with injecting oils, that they are easier on liver function. this is true to an extent, but they still affect the liver and other internal organs as well.
most guys are going to run a decent dose of any 17aa to get results. anadrol , dbol , and halo are three that come to kind as being extremely harsh. andriol (which for me is basically worthless) and anavar are 2 of easiest on the body.
11-18-2002, 04:39 PM #5
If that line of reasoning were true to any extent then why would trenbolone produce an effect any different from methenolone or boldenone ? The alkylation prevents the liver from totally destroying the substance on the first pass. It does not dictate the effects of the substance on the body nor on the liver itself. The process of breaking the substance down, the effects it has on body chemistry and the effect of it's metabolites differ from one substance to the next and along with it the degree of hepata-toxicity.
11-18-2002, 04:44 PM #6Originally posted by hammerhead
If that line of reasoning were true to any extent then why would trenbolone produce an effect any different from methenolone or boldenone?
i could be way off here, as im no chemist, but maybe it has something to do with tren being an acetate? this makes tren extremely soluble and therefore its easily broken down.
11-18-2002, 07:20 PM #7
I'm trying to follow the line of reason here - my first post was a direct response to the original post - not to anyone else's replies.
The acetate part of it doesn't have a whole lot of effect on potency. Boldenone acetate would not be as powerful as trenbolone acetate. The ester of an injectable oil-dissolved steroid determines how long it takes the body to absorb the compound from the injection site. An injection of sustenon-250 takes about 3 to 4 weeks for most of the testosterone to be aborbed from the injcetion site whereas with trenbolone acetate it's a matter of days. Any way you take it - the trenbolone molecule once bound to an androgen receptor produces way more (i'm going to have to get technical on you here) "stuff" than say, boldenone.
Andriol is not C17-alpha-alkylated nor is Primobolan tabs. They are both harmless to the liver.
Why are some C17AA's more hepatatoxic than others? That's the original question here right? Rickson did a pretty good job of explaining that one.
11-18-2002, 11:16 PM #8
Thanks for the input guys.
11-19-2002, 07:26 AM #9Member
- Join Date
- Aug 2002
One theory about the harshness to the liver is how much processing the liver does on the gear. Anavar is broken down the least of any of the 17aa's, which means less processing of the 17aa which means less damage to the liver.
11-19-2002, 01:08 PM #10
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