Bodybuilders?

[triton2]

Nice point global. I would tend to agree with you as far as cutting is concerned; when you are cutting it's best to avoid aromatizing steroids such as testosterone, because they tend to bloat you and no one would surely want to go on-stage bloated. Besides, some compounds such as trenbolone and oxandrolone tend to help you shed bodyfat.

However, as far as building skeletal muscle is concerned, I don't think that anyone can say things like "You cannot use primo for bulking, its main use is that of cutting". If you use primo you won't see a "mass explosion" as you'd tend to see with testosterone mainly because primo doesn't promote water weight gains; that's all. Mg per mg test would be more anabolic than primo, I agree. But let's say you use primo at 1000mg/week and compare it to testosterone at 600-700mg/week, do you honestly think that primo is going to promote less anabolism than test? I think not... People would usually say they made more gains with test because they get bloated, but that's all; I very much doubt they acquire any more skeletal muscle mass with test than they'd do with primobolan at equipotential dosages.
On the other hand, I also think that all that pseudoscientific theories that assure stacking many types of AAS is the best approach, as far as bulking is concerned, don't make much sense. If you combine 300 mg testosterone + 300 mg winstrol + 300 mg primobolan, do you really think you are going to gain more muscle than using just 700 mg winstrol? I don't think so... Of course, you can say that test also works via ER but:

1) I don't think ER anabolism has been clearly demonstrated

2) Many people just don't want to have supraphysiological levels of E in their bodies, so they use an antiE. Taking this premise ("We don't want E levels to reach supraphysiological levels") into account, I don't think that stacking many compounds has any added benefit (as far as building skeletal muscle mass is concerned) above using just a bigger dose of a single compound.

 

[losin_it]

On the other hand, I also think that all that pseudoscientific theories that assure stacking many types of AAS is the best approach, as far as bulking is concerned, don't make much sense. If you combine 300 mg testosterone + 300 mg winstrol + 300 mg primobolan, do you really think you are going to gain more muscle than using just 700 mg winstrol? I don't think so... Of course, you can say that test also works via ER but:



2) Many people just don't want to have supraphysiological levels of E in their bodies, so they use an antiE. Taking this premise ("We don't want E levels to reach supraphysiological levels") into account, I don't think that stacking many compounds has any added benefit (as far as building skeletal muscle mass is concerned) above using just a bigger dose of a single compound.

I think the only reason why most people perfer stacking different compunds is that they want to feel the effect of the drugs faster and the amount of times they have to administer the drug. For example: taking Test Propinate to kick start the cycle because of its fast release effect and continuing using Cypionate with it after the 4th week so you wouldnt need to jab your self as frequently as you would with a drug like Porp/Winny.

Although its has nothing to do with ahir, I just wanted to add that diet has alot to do with how bloated you get while taking testosterone. It makes a HUGE difference between eating clean and cramming your face with all kinds of crap. Alot of readers dont know that pro's take T3, Clenbuterol, and dieretics to look shredded, so I wouldnt flollow their diets for my needs and expect to look lean. I ve never had to use anti e's either, guess Im just lucky.

Some good intelligent conversations going on here besides the few stupid posts, but its nice to see members engaged in something that is offering some very useful imformation for those tempted to use steroids but arent familiar with its effects.

Triton, you sound like one of trainers that wrote for MuscleMedia back in the day. That writer had alot of excitment for Ru58841 as do you from the sounds of it but so far the response from users has been less then stellar.

 

[ronaldkia]

anybody who says steroids make our hair fall is an ultra dumb idiot...and anybody who uses steroids is even worse.

 

[stax]

Just look at Hulk Hogan and Randy Savage.

 

[Dave001]

Nandrolone (N) -> dihydronandrolone (DHN) via 5alpha-reductase.
N is more potent than DHN. Therefore, finasteride increases the androgenic potency of N in the hair follicle by preventing its metabolism into the less potent DHN.

 

[triton2]

Nandrolone (N) -> dihydronandrolone (DHN) via 5alpha-reductase.
Affinity for androgen receptor: DHN < N.

Therefore, finasteride increases the androgenic potency of N in the hair follicle by preventing its metabolism into the less potent DHN.

Are you sure?

Note: 19norT = 19nortestosterone = nandrolone

"The results of AR binding studies revealed that 5alpha-reduction of T and ET significantly enhanced their affinities, and that the 5alpha-derivative of 19norT displayed a similar binding affinity to that exhibited by 19norT. In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency[...]"

J Steroid Biochem Mol Biol. 1997 Jan;60(1-2):121-9.
5alpha-reduction of norethisterone enhances its binding affinity for androgen receptors but diminishes its androgenic potency.
Lemus AE, Enriquez J, Garcia GA, Grillasca I, Perez-Palacios G.

 

[ronaldkia]

stax
Junior Poster



Joined: 14 Feb 2005
Posts: 311

Posted: Sun Nov 13, 2005 12:14 am Post subject:

--------------------------------------------------------------------------------

Just look at Hulk Hogan and Randy Savage.



Look at Ronnie coleman, Flex Wheeler, Kevin Levrone... The Rock, none of them are bald. and by the way everybody knows hulk hogan and macho man, started off with front receiding hairline, not male pattern baldness... youll never find an assertive person with male pattern baldness..its impossible! im not arguing with you, im telling you!

 

[SE-freak]

RONALDKIA???? WHY DID YOU CHANGE YOUR AVATAR???NOOOOOOOOOOOOOOOOOOOOOOOOOO

 

[Dave001]

Nandrolone (N) -> dihydronandrolone (DHN) via 5alpha-reductase.
Affinity for androgen receptor: DHN < N.

Therefore, finasteride increases the androgenic potency of N in the hair follicle by preventing its metabolism into the less potent DHN.

Are you sure?

About its androgenic potency? Yes, I'm fairly certain. However, my concluding statement above is somewhat of a non sequitur, and I'm not entirely certain what I was thinking when I wrote it. Nandrolone is a more potent androgen than its 5alpha-reduced metabolite, dihydronandrolone (DHN), but it may not have a higher binding affinity. I don't know for sure how their binding affinities compare. IIRC, reported binding affinities were somewhat inconsistent. Thanks for asking about that. I will edit my original post to avoid confusing anyone.

Please see the following review article:

Cellotti, F. and P. N. Cesi (1992). "Anabolic steroids: A review of their effects on the muscles, of their possible mechanisms of action and of their use in athletics." The Journal of Steroid Biochemistry and Molecular Biology 43(5): 469.

See also:

Bergink, E. W., P. S. Janssen, et al. (1985). "Comparison of the receptor binding properties of nandrolone and testosterone under in vitro and in vivo conditions." Journal of Steroid Biochemistry 22(6): 831-6.

.... "The present results explain the relatively strong effect of nandrolone compared to that of testosterone on target tissues devoid of 5 alpha-reductase activity (e.g. muscular tissue) compared to its relatively weak effect on tissues with a relatively high 5 alpha-reductase content (e.g. prostate)."

 

[mon]

One of your fellow bodybuilders has died, Eddie Guerrero. The steroid abuse had taken its toll. Stay away from that rubbish. Build your body naturally.

 

[triton2]

About its androgenic potency? Yes, I'm fairly certain. However, my concluding statement above is somewhat of a non sequitur, and I'm not entirely certain what I was thinking when I wrote it. Nandrolone is a more potent androgen than its 5alpha-reduced metabolite, dihydronandrolone (DHN),

Dave, I think that what the study you have posted proves, if anything (because it seems to be somewhat at odds with the study I posted), is that DHN has a lower AR binding affinity than that of nandrolone.
You say that nandrolone is a more potent androgen than DHN, but the study you posted doesn't state that. However, the quote I posted proves that not only DHN's androgenic EFFECTS aren't lower than those of nandrolone, but they are indeed HIGHER.

"In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency,"

 

[Dave001]

Dave, I think that what the study you have posted proves, if anything (because it seems to be somewhat at odds with the study I posted), is that DHN has a lower AR binding affinity than that of nandrolone.
You say that nandrolone is a more potent androgen than DHN, but the study you posted doesn't state that. However, the quote I posted proves that not only DHN's androgenic EFFECTS aren't lower than those of nandrolone, but they are indeed HIGHER.

"In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency,"

I don't think that quote *proves* anything. Did you read the review article I referenced? It's generally a good idea to start with a recent review type of article before looking at individual research studies, because a review will summarize the most pertinent research in a field (complete with references to individual studies, of course), and it will be written by someone involved in that discipline, and who will be trained at interpreting results from the respective research protocols. That's not meant to sound condescending; I don't know you or what you know.

I'm not completely ruling out the *possibility* that the previously accepted understanding of nandrolone's pharmacology has changed, but I haven't seen anything to indicate that it has, and I think it's very unlikely. Combing through all of the potentially relevant research from the last few years or so is not the way I want to invest my time right now, so I'm afraid I can't offer you but another recommendation to read the review article I referenced earlier.

 

[triton2]

. Did you read the review article I referenced?

Only the abstract is available, I cannot access the whole review.

I'm not completely ruling out the *possibility* that the previously accepted understanding of nandrolone's pharmacology has changed,

And where does that 'previously accepted understanding of nandrolone', at least as far as DHN androgenity, stem from? In order to arrive at the conclusion that DHN is less androgenic than nandrolone, I think there should be some studies which corroborated that idea, don't you think? Perhaps that just stems from a myth created by some 'erroneous' in vitro study or something... I'd like to see the evidence which proves that DHN is less androgenic than nandrolone.

but I haven't seen anything to indicate that it has,

What about the study I quoted? Doesn't this indicate that nandrolone is no more androgenic than DHN is?

""In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency,"

It clearly states that 5-alpha-reduction of 19norT (conversion of N to DHN) increases its androgenic potency, IN TERMS OF BIOLOGICAL ACTIVITY, not just in terms of AR binding, where both (N's and DHN's) tend to be quite similar in the study I quoted

and I think it's very unlikely.

Why would it be any more unlikely than the thesis you support? Are there a larger number of scientific studies to support your thesis than to support mine? If so, I'd like to see them to know whether or not they are in vivo and whether or not they measure physiological androgenic activity and not only AR binding.
By the way, don't think that I'm trying to be harsh or something. I'm not. It's just that I think we all learn more if we discuss things intensively like this and, at the same time, we can also have fun. Peace.

 

[Dave001]

Did you read the review article I referenced?

Only the abstract is available, I cannot access the whole review.

The whole review is available. You'll need to get it from the library.

Cellotti, F. and P. N. Cesi (1992). The Journal of Steroid Biochemistry and Molecular Biology 43(5): 469.

Perhaps that just stems from a myth created by some 'erroneous' in vitro study or something... I'd like to see the evidence which proves that DHN is less androgenic than nandrolone.

A decent library will have that evidence.

What about the study I quoted? Doesn't this indicate that nandrolone is no more androgenic than DHN is?

One sentence isn't enough context to mean much of anything. I'd have to see the whole paper. You have to view it in consideration of all of the studies.

 

[Dave001]

""In terms of biological activity, the results showed that 5alpha-reduction of T and 19norT significantly increased their androgenic potency,"

It clearly states that 5-alpha-reduction of 19norT (conversion of N to DHN) increases its androgenic potency, IN TERMS OF BIOLOGICAL ACTIVITY, not just in terms of AR binding, where both (N's and DHN's) tend to be quite similar in the study I quoted

I just grabbed the full text of the above study. You need to keep in mind that what the authors mean by "biological activity" may not be quite what *you* mean. ;-) My position remains.

 

[Dave001]

Here are a couple more references, along with their respective abstracts:

Sundaram, K., N. Kumar, et al. (1995). "Different patterns of metabolism determine the relative anabolic activity of 19-norandrogens." The Journal of Steroid Biochemistry and Molecular Biology 53(1-6): 253.

Abstract: Testosterone, the principal androgen secreted by Leydig cells, exerts a wide range of actions including growth of the male reproductive tract (androgenic effects) and growth of non-reproductive tissues such as muscle, kidney, liver, and salivary gland (anabolic effects). As androgenic steroids were discovered some were found to have relatively more anabolic than androgenic activity. The results reviewed in this report suggest that these differences result, in part, from the differential metabolism of the steroids in individual tissues and the varied activities of the individual metabolites. In the accessory sex organs (e.g. the prostate) testosterone is 5alpha-reduced to dihydrotestosterone (DHT) which, due to its higher affinity for androgen receptors (AR), amplifies the action of testosterone. In contrast, when 19-nortestosterone (NT) is 5alpha-reduced, its affinity for AR decreases, resulting in a decrease in its androgenic potency. However, their anabolic potency remains unchanged since significant 5alpha-reduction of the steroids does not occur in the muscle. 7alpha-methyl-19-nortestosterone (MENT) does not get 5alpha-reduced due to steric hindrance from the 7alpha-methyl group. Therefore, the androgenic potency of MENT is not amplified as happens with testosterone. These metabolic differences are responsible for the increased anabolic activity of NT and MENT compared to testosterone. Part of the biological effects of testosterone are mediated by its aromatization to estrogens. The fact that MENT is also aromatized to 7alpha-methyl estradiol, a potent estrogen, in vitro by human placental and rat ovarian aromatase suggests that some of the anabolic actions of MENT may be mediated by this estrogen.

Comments: Perhaps the most telling observation is what happens when you administer testosterone and nandrolone in combination with a 5alpha-reductase inhibitor. They did just that in the above study. That is one of the studies I remember reading a long time ago, and it supports my contention that it would be a *bad* idea to use finasteride in conjunction with nandrolone. I can send you a copy of the full text (as a scanned PDF) if you would like.


Kumar, N., K. Sundaram, et al. (1995). "Feedback regulation of gonadotropins by androgens in rats: is 5alpha-reduction involved?" The Journal of Steroid Biochemistry and Molecular Biology 52(1): 105.

Abstract: The action of testosterone (T) on the sex accessory organs, such as ventral prostate (VP) and seminal vesicles (SV) is amplified by its 5alpha-reduction to dihydrotestosterone (DHT). This does not happen in the case of muscle (levator ani, LA) which contains little or no 5alpha-reductase activity. It has been suggested that the regulation of gonadotropins by T may also be mediated by its 5alpha-reduced metabolites. We investigated this question by utilizing two types of androgens: (1) T and 17alpha-methyl-testosterone (17MT), whose potency increases following 5alpha-reduction; and (2) 19-nortestosterone (NT) and 17alpha-methyl-19-nortestosterone (17MNT) whose potency decreases following 5alpha-reduction. Castrated rats were used to investigate the ability of these androgens to stimulate VP, and SV (androgenic action) and LA growth (anabolic action) and to suppress the post-castration rise in LH levels. In addition, modification of these actions by a 5alpha-reductase inhibitor (5alpha-RI) was studied. Compared to T, NT was approximately 5 times less potent in stimulating VP and SV. By contrast, it was twice as potent as T in stimulating LA growth. Similarly, 17MNT was 5 times less androgenic but twice as anabolic as 17MT. The antigonadotropic potency of both the 19-nor compounds was 2-3 times greater than that of their respective 19-methylated parent compounds. The similarity in their anabolic and antigonadotropic potency suggested that 5alpha-reduction is not a factor in their antigoanabolic and antigonadotropic potency suggested that 5alpha-reduction is not a factor in their antigonadotropic action. This was confirmed by the use of the 5alpha-RI. Treatment of rats receiving the androgens with 5alpha-RI showed that it decreases the androgenic activity of T and 17MT while it increases the androgenic activity of NT and 17 MNT. In all cases the anabolic activity and the antigonadotropic potency remained unchanged. It is concluded that the regulation of pituitary gonadotropin secretion by T does not depend upon its 5alpha-reduction to DHT.

Comments: I have not read the full text of the above study, but it appears to support the same conclusion.

 

[ronaldkia]

omg! reading you guys talk about steroids is disgusting! you guys are sick. its really sick reading all this sh*t..imagine if your girlfriends/ wives/ children read what your writing.. omg..id rather eat my own s__t then read anymore of your s___t.

i hope all of you who take steroids not only get ill, but have your hairs falloff, your muscles and testicles too. You guys must be the stupidest people walking on the face of this earth. geez (gone to puke).

 

[triton2]

omg! reading you guys talk about steroids is disgusting! you guys are sick. its really sick reading all this $#iT..imagine if your girlfriends/ wives/ children read what your writing.. omg..id rather eat my own s__t then read anymore of your s___t.

i hope all of you who take steroids not only get ill, but have your hairs falloff, your muscles and testicles too. You guys must be the stupidest people walking on the face of this earth. geez (gone to puke).

There are far worse things than getting bald and sick or having testicular shrinkage. One of those things is having your IQ.

Somebody please ban this troll.

Thanks.

 

[triton2]

Dave, it would be very kind of you if you sent me the full text of those studies we are discussing. I think it would be very interesting, so I'd like you to send them to me if you wish.

thank you.

 

[Dave001]

There doesn't seem to be any controversy surrounding the issue, if that's your concern. Send me a PM with an e-mail address to which to send the documents if you're still interested in reading some of the studies.