posted May 24, 2000 03:57 PM            

For example Abombs and dbol??..

Ive been looking like a bitch for the answer to this with no luck..

posted May 25, 2000 04:18 PM         

Any replies!

posted May 25, 2000 04:46 PM            

This quiestion was answered a while back. Do a search and look for "receptor question".

Good info.

posted May 25, 2000 05:45 PM            

For example Stacking something like 1000mg (or more) per week of Sustanon with almost any amount of winny would be a waste of winny. But stacking something like Deca with winny could be seen as 'complimentary'. Notice I haven't distinguised between the 17-AA orals and any other A/S because ther really is no difference on their receptor affinities (the 17-AA merely stabilizes the A/S so it can pass through the gut without getting degraded. The alky group is removed in the liver before the steroid becomes active).

posted May 25, 2000 06:49 PM            

more later..........

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MP

posted May 25, 2000 07:36 PM            

Here's 2 studies off of the top of the pile that will put you all to sleep for the night.

The effect of anabolic-androgenic steroids on aromatase activity and androgen receptor.

Abstract

The level of aromatase is transcriptionally regulated through a specific androgen-receptor mediated mechanism and can be used as a measure of central androgenic effect. Therefore, several commonly abused anabolic-androgenic steroids (AAS) were tested for their ability to induce aromatase activity. In addition, we determined the relative binding affinities of these compounds for the androgen receptor, as well as their ability to bind androgen receptor in vivo following subcutaneous injections. All of the AAS compounds tested significantly stimulated aromatase activity above castrate levels. The compounds that produced the greatest stimulation of aromatase activity were those that bound most avidly to the androgen receptor in vitro (i.e., testosterone, dihydrotestosterone and
nandrolone). In contrast, the 17-Alpha alkylated compounds that were tested (stanozolol, danazol, methandrostenolone) modestly stimulated aromatase and were weak competitors for the androgen receptor. The subcutaneous injection of AAS compounds increased the concentrations of occupied nuclear androgen receptors in the brain, but the magnitude of effect was not related to their potency for inducing aromatase or their relative binding affinity for the androgen receptor suggesting that androgen receptor occupancy is not correlated with the action of androgen on aromatase. The present results help explain the behavioral effects of AAS.

Record 2

Metabolism and receptor binding of nandrolone and testosterone under in vitro and invivo conditions.

Abstract

The metabolism and receptor binding of nandrolone (N) and testosterone (T) were studied under in vitro and in vivo conditions. The results of both in vitro incubation studes with 3H-N and 3H-T in tissue homogenates and in vivo infusion studies with 3H-N and 3H-T show the importance of the enzymes 5 alpha-reductase and 3 alpha/beta-hydroxysteroid-oxidoreductases in the prostate and the importance of the enzyme 17 hydroxysteroid dehydrogenase in the kidney for the effects of N and T on these tissues.
Following infusion of a combined dose of 3H-N and 3H-T there is a preferential retention at the receptor of 5 alpha-dihydrotestosterone (DHT) over 5 alpha-dihydronandrolone (DHN), N and T (DHT much greater than DHN greater than N greater than T) in the prostate because T is a better substrate than N for 5 alpha-reductase and because DHT binds more strongly to the androgen receptor than DHN, N and T. In the kidney 5 alpha-reductase is not important; there is a preferential retention of N in T (DHN and DHT were only present in small amounts) because N is less susceptible than T for metabolic inactivation by the enzyme 17 beta-hydroxysteroid dehydrogenase and N binds strongly to the androgen receptor. Both in vitro and in vivo studies
show that N and T were relatively stable in spleen, thymus and muscular tissue (only shown in vivo) and, as a result, the same amount of N and T was bound to the receptor in these tissues in the in vivo infusion experiment.

The short of it all is that steroid biochemistry is not a simple case of it binds or it doesn't bind!!

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The Mad Scientist

posted May 25, 2000 08:15 PM            

First of all this abstract said that D-bol is less likely to cause aromatase activity than testosterone. I have made that observation myself.

Lets see, d-bol is methandrostenolone. Unless thats anadrol forget this paragraph. So what happens in aromatase. Does androstenolone convert?does that methyl group prevent it?

One question for you, it just don't seem to me that the methyl(17A) group is ever removed from oral 17AA compounds once inside the body-I know this is the opposite of what every expert out there says but they have been wrong so many times that its not even funny.

Two observations: the methyl group switches the activity from AR to non-AR methods; the methyl group also makes the molecule more estrogenic whether that is due to increased aromatase activity or greater estrogenic properties. It would be good to know which on that last point.

posted May 25, 2000 09:32 PM            

And yes, methandrostenolone is dbol, and it is not as strong at inducing reductase enzymes as the non-17-AA roids.

I didn't know that the methyl group increased the estrogenic activity. If you come across a reference or two, could you please email me. I'm always looking to learn more. I'm also not sure why you say that winny has very little non-AR activity? Below is another abstract (apologies to all of you that are just hear to be told how much of what to stack with what!!), and I think the last few lines of it are important. In a nutshell, even though all of the 17-AA roids are weak at the androgen receptor, their "myotrophic potency" (ie ability to stimulate new muscle growth) are very similar to the much stronger androgens.

Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

ABSTRACT:
It is unclear whether anabolic steroids act on skeletal muscle via the
androgen receptor (AR) in this tissue, or whether there is a separate
anabolic receptor. When several anabolic steroids were tested as
competitors for the binding of [3H]methyltrienolone (MT) to the AR and skeletal muscle and prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than
methenolone greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol ,
methanedienone, and fluoxymesterolone. Other compounds had
RBAs too low to be determined (e.g. oxymetholone and ethylestrenol . The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction to metabolites, which did not bind to the AR. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most
cases.

posted May 26, 2000 01:31 PM            

Great info though..I would like to hear Mac's thought on this when the bro has time to type the shit out..

Thanx for the help bros, my answer has pretty well been resolved, which is good considering it pertained alot to my next cycle.

Thanx,
WCP

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"Man doth not yeild himself unto the Angels, nor unto Death utterly......save only through the weakness of his feeble will"
--Joseph Glanvill

posted May 27, 2000 11:09 AM         

Methylation at the 17-alpha position does not inhibit aromatization. Methandrostenolone, methylandrostenediol, 17-MENT, 17-methyltestosterone all aromatize.

"One question for you, it just don't seem to me that the methyl(17A) group is ever removed from oral 17AA compounds once inside the body-I know this is the opposite of what every expert out there says but they have been wrong so many times that its not even funny."

Who stated that the methyl group is removed? Or that it makes a difference?

"Two observations: the methyl group switches the activity from AR to non-AR methods; the methyl group also makes the molecule more estrogenic whether that is due to increased aromatase activity or greater estrogenic properties. It would be good to know which on that last point."

Examples that disagree with your idea that 17-methylation affects AR binding are: 17-methyltestosterone, methyltrienolone, and 17-MENT. Also, there is no evidence that methyltest is more capable of aromatization or has greater estrogenicity than testosterone.

"the methyl group also makes the molecule more estrogenic whether that is due to increased aromatase activity or greater estrogenic properties."

posted May 27, 2000 12:23 PM            

I thought the binding to the AR happens at the 17 alpha position, i might be wrong. A methyl would hinder that. If you say methyltest has significant AR activity in humans fine, but I never thought so. Is that beta or alpha position? I think it would make a big difference.

"This statement contradicts your original statement that methandrostenolone gives
you less estrogen problems and the study abstract shows that D-bol is a weaker
inducer of aromatase than testosterone."

I'm comparing same structure molecules with the only difference in the added methyl group(ex. d-bol ; EQ). You are comparing testosterone to d-bol. not valid. I should have been more clear, my fault.

Also this study did not say how exactly they measured that aromatase activity, aromatase on test due to added aas or a system only composed of that aas. makes a very big difference. And let me just say that their are a million other factors that most studies don't even think about like SHBG aas interaction that makes the results completely different. So the only valid studies can only be done useing complete human systems otherwise results don't mean much..thats why I like real world results.

posted May 28, 2000 03:10 PM            

I'm going to side with the last statement in the last post and state that 'stacking' as it's done by you guys has never been studied scientifically. If I were you, I would read all I can on this and other boards, and take advice from knowledgeable and experienced people. Hundreds of thousands of people all over the world have been using themselves as human experimental systems. It's just never been written up in a medline style paper.There will be a lot of misinformation, but other peoples experiences are (for now) the best info we have. I'm certainly NOT saying to ignore the research, just don't get hung up on it.

posted May 28, 2000 10:38 PM            

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I say no to drugs...they just don't listen!
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