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Topic starter 11/12/2018 7:09 am
How can you in good conscience suggest that nandrolone is better for muscle building than testosterone ?
Nandrolone has often been the drug used by many athletes throw the world, not only for bodybuilding purposes with good results to increase lean mass and to improve atheltic performances. It's an effective drug even at reasonnable doses. Because its higher affinity for the AR, we can think that it is more effective on mg for mg basis.
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Nandrolone does so with an almost threefold higher efficiency than test or DHT. And yes it does have something to do with it, by-products created in a certain reaction usually have some type of function in that regard, if there is one thing research teaches us, it is that is unwise to assume that things in biology happen for random reasons, everything has a function. Likely the function of nandrolone in that regard is to be an intermediate androgen/estrogen that regulates certain estrogenic target genes via a non-concensus receptor, namely the androgen receptor.
Actually, there is no specific function for 19-Nor in the human body. Natural production of 19-Nor is anecdotal.
I see that here you say :"certain estrogenic target genes", that's very different that to claim : Nandrolone is 60% as estrogenic as E2.
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And did the test also exclude AR activation of ERE's? that seems doubtful ...
The study is too old to have considered this but they have excluded progestational and estrogenic activity.
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Actually that's not entirely true. Studies done on nandrolone decanoate pharmacokinetics comparing ester, injection volume and injection site demonstrate that even a gluteal decanoate injection of high concentration doesn't yield more than 7-8 days of half-life. Testosterone Enanthate injections given in the same concentration (200 mg/ml), dose and injection site, yield 6-7 day half-lives. The difference is not as big as suggested. Some studies on longer test esters suggests that comparatively testosterone is more likely to have an equal or longer half-life time, compare test undecanoate to laurabolin for instance.
With long ester the injection volume will greatly influence the duration of release, here you speak about a single injection of 200mg, if we use a bigger volume, the difference between the enanthate and decanoate ester will be more significant.
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Its never funny to worry about supressive effects. Compromising recovery, considering most athletes do not get blood results to confirm recovery, is not a wise idea. I find the idea that against better knowledge you are trying to promote nandrolone as less supressive a scary idea.
Firstly, what I write is only for theoretic purpose. Secondly, we know that we can achieve HPTA, endogenous T production and spermatogenesis suppression with T alone. So, where the devil ?
To conclude, my goal has never been to say that nandrolone is a safe and non-suppressive drug, just to evaluate its suppressive potency in regards of the scientific litterature and studies.
11/12/2018 7:49 am
oth, in the case of someone with permanently suppressed hpta, nandrolone has some speculative benefits that i have injoyed. I do a cycle periodically for my joints and it seems to help. I also find it to be as anabolic as test. This is all purely subjective of course. I think the conventional wisdom now is for tested athletes to avoid it due to the long halflives of the metabolites and others be cautious because of it suppressive characteristics.
jb
11/12/2018 8:32 am
[B]Nandrolone has often been the drug used by many athletes throw the world, not only for bodybuilding purposes with good results to increase lean mass and to improve atheltic performances. It's an effective drug even at reasonnable doses. Because its higher affinity for the AR, we can think that it is more effective on mg for mg basis.
By now you should know two things :
1.The in vitro RBA does not correlate with the in vivo RBA
2.RBA is not a good indicator of anabolic efficiency.
Nandrolone use is very widespread, since the 70's, but not for its anabolic efficiency, but because it has been wrongfully portrayed as a safe drug based on its therapeutical profile. The argument is even further made irrelevant since the statement can be made for Dbol,winny and a handful of other drugs as well, none of which are more potent than testosterone.
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Actually, there is no specific function for 19-Nor in the human body. Natural production of 19-Nor is anecdotal.
I see that here you say :"certain estrogenic target genes", that's very different that to claim : Nandrolone is 60% as estrogenic as E2.
The latter claim is not disproven, there is no data on how many ERE's it binds. If it binds concensus ERE's its pretty safe to assume its pretty much acting as an estrogen. And the presence of nandrolone naturally in the body has been documented so many times, that even the entire academic body adopts the notion that nandrolone is a naturally occuring metabolite, which is also why doping detection limits are built with a margin of error. At least two of the three proposed mechanisms of action of aromatisation also support the production of nandrolone during this process, and the level of nandrolone in the body correlates positively with E2 and E2:T levels, but not with T levels. All this evidence makes it hard to maintain that nandrolone is not naturally produced, or it would not correlate to endogenous steroid synthesis.
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The study is too old to have considered this but they have excluded progestational and estrogenic activity.
Well therein lies the difficulty since the very nature of this discussion is about the ability of drugs to cause estrogenic effects separate from aromatization and unaltered ER binding. This, as well as the Holterhus study, strongly support differential modulation of target genes by varied recruitment of corepressors and coactivators, that can perfectly explain the differential effects of steroids under different circumstances, such as for instance the binding on non-concesus RE's, like ERE's by the AR.
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With long ester the injection volume will greatly influence the duration of release, here you speak about a single injection of 200mg, if we use a bigger volume, the difference between the enanthate and decanoate ester will be more significant.
True, and if people were using 50 mg/ml maybe that would hold true, as clinical trials point out. But you and I both know that bodybuilders use large amounts and therefor large concentrationsof 200 mg/ml or more, to minimize injection volume, thereby reducing the retention pocket for steroid, which is what i was attempting to point out by referring to the Minto study, which is an excellent study at pointing out these half-life discrepancies that plagues message board discussions so much.
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Firstly, what I write is only for theoretic purpose. Secondly, we know that we can achieve HPTA, endogenous T production and spermatogenesis suppression with T alone. So, where the devil ?
If supression is greater, recovery is more difficult. Its not a hard concept to grasp. And we all write for theoretic purpose, but you can't lose track of the fact that many people looking for practical advice roam these boards who don't get that nuance. We may be theoreticist, but we have a responsibility to members as well to make that clear.
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To conclude, my goal has never been to say that nandrolone is a safe and non-suppressive drug, just to evaluate its suppressive potency in regards of the scientific litterature and studies. ]
If everyone stuck to a perfect PCT it wouldn't really be an issue, I remember one study on medibolics that showed 12 week use with test and deca followed by HCG/Nolva/clomid PCT that showed recovery was complete. Nonetheless we know that is not the case, which is why I choose to stress rather than relativate the supressive ability of deca, and always recommend cessation of supressive drugs one week prior to less supressive drugs.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
11/12/2018 9:17 am
oth, in the case of someone with permanently suppressed hpta, nandrolone has some speculative benefits that i have injoyed. I do a cycle periodically for my joints and it seems to help. I also find it to be as anabolic as test. This is all purely subjective of course. I think the conventional wisdom now is for tested athletes to avoid it due to the long halflives of the metabolites and others be cautious because of it suppressive characteristics.jb
well that really sums it up, as a therapeutic drug nandrolone is rightly the number one. For cycling for a healthy male, itis however very far from the drug of choice, and that is the most important nuance we need to make.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
Topic starter 11/12/2018 10:14 am
[B]By now you should know two things :1.The in vitro RBA does not correlate with the in vivo RBA
You have only one study to support this idea and here it is :
Everyone can make his own opinion to estimate how much it is informative ...
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2.RBA is not a good indicator of anabolic efficiency.
The RBA in rat muscle is often used as an estimate of the myotrophic potency of the compound.
But I agree, other parameters like nitrogen retain and protein synthesis and/or decreased breakdown are more relevant. Do you have some scientific studies where T is better than 19-Nor in this regard ?
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The latter claim is not disproven, there is no data on how many ERE's it binds. If it binds concensus ERE's its pretty safe to assume its pretty much acting as an estrogen. And the presence of nandrolone naturally in the body has been documented so many times, that even the entire academic body adopts the notion that nandrolone is a naturally occuring metabolite, which is also why doping detection limits are built with a margin of error. At least two of the three proposed mechanisms of action of aromatisation also support the production of nandrolone during this process, and the level of nandrolone in the body correlates positively with E2 and E2:T levels, but not with T levels. All this evidence makes it hard to maintain that nandrolone is not naturally produced, or it would not correlate to endogenous steroid synthesis.
No please, don't make me say what I have not said ! Of course, 19-Nor can naturally occuring in human body, it is well documented. I am french, I have follow up with lot of attention the Djamel Bouras affair, and I know the line of defence of many athletes in terms of nandrolone abused. But I repeat natural nandrolone remain anecdotal, no specific role has been identified.
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Well therein lies the difficulty since the very nature of this discussion is about the ability of drugs to cause estrogenic effects separate from aromatization and unaltered ER binding. This, as well as the Holterhus study, strongly support differential modulation of target genes by varied recruitment of corepressors and coactivators, that can perfectly explain the differential effects of steroids under different circumstances, such as for instance the binding on non-concesus RE's, like ERE's by the AR.
In my opinion, really too early to make this sort of conclusions. Actually, no proof that 19-Nor is able to promote gyno or other undesirable estrogenic effects via an AR-mediated manner.
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True, and if people were using 50 mg/ml maybe that would hold true, as clinical trials point out. But you and I both know that bodybuilders use large amounts and therefor large concentrationsof 200 mg/ml or more, to minimize injection volume, thereby reducing the retention pocket for steroid, which is what i was attempting to point out by referring to the Minto study, which is an excellent study at pointing out these half-life discrepancies that plagues message board discussions so much.
In legal gear, I do not know deca at 200mg/ml, only 100mg/ml, so if you want to get more mg you will have to inject more volume too. By the way it is not very important, just to say that the long ester used often in nandrolone preparation could have an impact on nandrolone bad reputation.
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If supression is greater, recovery is more difficult. Its not a hard concept to grasp.
Sorry but it's difficult to understand to me ... If you used heavy T dose, you shut down your HPT axes, considerably reduce your T production and inhibit your spermatogenesis. So, because you are in a suppressive state, how it can be worst ? If your LH become undetectable, it is undectable, by the way if it has been caused by nandrolone or T abused.
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And we all write for theoretic purpose, but you can't lose track of the fact that many people looking for practical advice roam these boards who don't get that nuance. We may be theoreticist, but we have a responsibility to members as well to make that clear.Nonetheless we know that is not the case, which is why I choose to stress rather than relativate the supressive ability of deca, and always recommend cessation of supressive drugs one week prior to less supressive drugs.
No I am not in this sort of considerations. I only want to open the debate with a scientific approach to distinguish the rational believes to the myths. I absolutely decline all responsability. I write here with all my honesty and hope to make a contribution to a better AAS understanding. Nothing else.
11/12/2018 10:53 am
You have only one study to support this idea and here it is :Everyone can make his own opinion to estimate how much it is informative ...
Its also the only study done on in vivo RBA, with not a single remark, let alone a study to disprove it ...
Along with that it doesn't take a rocket scientist to see that a drug with low RBA like anadrol is a very potent anabolic. So it would be a very naive thing to believe that RBA is an efficient predictor of anabolic activity.
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The RBA in rat muscle is often used as an estimate of the myotrophic potency of the compound.
But I agree, other parameters like nitrogen retain and protein synthesis and/or decreased breakdown are more relevant. Do you have some scientific studies where T is better than 19-Nor in this regard ?
Again, those are flawed arguments since they are rarely determined in conjuction to give a total idea of net anabolism, and they are subject to quite a lot of variables.
To correctly determine anabolic potency we need data on which genes play a role in myotrophy, and to what extent each AAS activates said genes, by recruitment of coregulators. That data is not available.
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No please, don't make my say what I have not said ! Of course, 19-Nor can naturally occuring in human body, it is well documented. I am french, I have follow up with lot of attention the Djamel Bouras affair, and I know the line of defence of many athletes in terms of nandrolone abused. But I repeat natural nandrolone remain anecdotal, no specific role has been identified.
Oh, then it went lost in translation. May have been wiser to state that the role of nandrolone was anecdotal, not that natural nandrolone was anecdotal. That is true, no actual role for natural nandrolone has been elucidated to date, but what I said was that it would be foolish to assume that it had no use. And given that it is a product of aromatisation, it probably plays a role somewhere along those lines as an androgen/estrogen intermediate.
I agree, its a moot point on my account, since there is no additional data to add to this discussion. Just pointing out that you shouldn't suggest that it isn't a functional metabolite.
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In my opinion, really too early to make this sort of conclusions. Actually, no proof that 19-Nor is able to promote gyno or other undesirable estrogenic effects via an AR-mediated manner.
Well, most athletes bloat up, get mood swings and several have developed gyno while on nandrolone. This despite the fact that even in vitro it only aromatizes at 20% of test (in vivo is likely even less) and only binds the ER in millimolar ranges. Progesterone is also not an option, as trenbolone is a more potent progestin and doesn't cause these problems to the same extent. The majority of athletes using 500-750 mg per week of testosterone do not even develop gyno. Its a fairly rare condition with other drugs.
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In legal gear, I do not know deca at 200mg/ml, only 100mg/ml, so if you want to get more mg you will have to inject more volume too. By the way it is not very important, just to say that the long ester used often in nandrolone preparation could have an impact on nandrolone bad reputation.
Its about the amount of steroid versus the size of the retention pocket, hence the concentration is what matters. 100 mg/ml will have a longer half-life than 200 mg/ml, that is true. But most athletes given the choice will opt for the latter as they prefer to inject less volume. which also reduces half-life.
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Sorry but it's difficult to understand to me ... If you used heavy T dose, you shut down your HPT axes, considerably reduce your T production and inhibit your spermatogenesis. So, because you are in a suppressive state, how it can be worst ? If your LH become undetectable, it is undectable, by the way if it has been caused by nandrolone or T abused.
Depends on the detection limits of what you are using, if you ask for a specific LH determination you get more sensitive results, that are exact. And you can definitely see a difference in normally used doses. Aside from that, and probably more important is the length of supression and the dose over the course of coming off. recovery will be faster and more complete if your drug of choice has a fast drop in serum levels after cessation. This depends on both half-life and on the clearance of the drug and its metabolites. In the latter area nandrolone scores pretty bad, with detectable metabolites up to 24 months after last use.
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No I am not in this sort of considerations. I only want to open the debate with a scientific approach to distinguish the rational believes to the myths. I absolutely decline all responsability. I write here with all my honesty and hope to make a contribution to a better AAS understanding. Nothing else.
i'm just saying, be careful. You may not wish to consider it, but you should. Others read your messages.
And this debate will not likely lead to much better understanding of AAS. Which does not make the discussion any less interesting, but most of what we state here can hardly be deemed fact. We are only dealing with what is most likely.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
Topic starter 11/12/2018 11:36 am
Its also the only study done on in vivo RBA, with not a single remark, let alone a study to disprove it ...
Comparison between the binding of 19-nortestosterone, 5alpha-dihydrotestosterone and testosterone in rat prostate and bulbocavernosus/levator ani muscle.
"Comparing these in-vitro data with in-vivo findings from the literature, in both organs there is a positive correlation of the extent of binding in vitro to the stimulation of growth in vivo"
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Along with that it doesn't take a rocket scientist to see that a drug with low RBA like anadrol is a very potent anabolic. So it would be a very naive thing to believe that RBA is an efficient predictor of anabolic activity.
Yes but anadrol has to be given in bigger amounts due to its low binding affinity to the AR.
But that's true, in vivo bioactivity of androgens could be influenced not only by binding affinity to receptors but also by factors such as absorption, binding to serum proteins and metabolism. However, the potency of 19-Nor is primarily related to its higher affinity to AR.
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Again, those are flawed arguments since they are rarely determined in conjuction to give a total idea of net anabolism, and they are subject to quite a lot of variables.
To correctly determine anabolic potency we need data on which genes play a role in myotrophy, and to what extent each AAS activates said genes, by recruitment of coregulators. That data is not available.
Yes, that data is not available. But i think that a simple study which compare LBM increase between a T and a N group, could be enough for most physical trainers and steroid users.
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Oh, then it went lost in translation. May have been wiser to state that the role of nandrolone was anecdotal, not that natural nandrolone was anecdotal. That is true, no actual role for natural nandrolone has been elucidated to date, but what I said was that it would be foolish to assume that it had no use. And given that it is a product of aromatisation, it probably plays a role somewhere along those lines as an androgen/estrogen intermediate.
I agree, its a moot point on my account, since there is no additional data to add to this discussion. Just pointing out that you shouldn't suggest that it isn't a functional metabolite.
Endogenous nandrolone production is refered as a side reaction to enzymatic aromatisation, it can only be found in low amounts. Even in pregnant women whose are known to have higher 19-nor and its metabolites levels, the 2 ng/mL limit is unlikely reached.
I have not wanted to say that natural 19-nor is an unfuctionnal metabolite, only that its role is not major in the man endocrinal equilibrium.
About the role of endogenous nandrolone :
"To the best of our knowledge, these studies are the first to examine the effect of Nandrolone on endometrial mitogenesis and gene expression and to evaluate its possible actions during pregnancy. Although the concentrations of Nandrolone in uterine luminal fluids have not been accurately quantified, the recent report that a major steroid product of the stably expressed porcine P450arom type III (blastocyst) isoform is Nandrolone suggests physiological relevance for this androgen. Nandrolone can bind to the ER� isoform, albeit with low affinity. However, our findings that Nandrolone behaves more like an androgen than an estrogen and the limited ER� expression in the pig endometrium during early pregnancy (unpublished data), suggest that the functional effects of Nandrolone in vivo are likely to be mediated via AR."
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Well, most athletes bloat up, get mood swings and several have developed gyno while on nandrolone. This despite the fact that even in vitro it only aromatizes at 20% of test (in vivo is likely even less) and only binds the ER in millimolar ranges. Progesterone is also not an option, as trenbolone is a more potent progestin and doesn't cause these problems to the same extent. The majority of athletes using 500-750 mg per week of testosterone do not even develop gyno. Its a fairly rare condition with other drugs.
Gynecomastia and many other side effects have been reported by physicians, scientists and users at therapeutical doses of TE. Nandrolone is generally said to have less side effects.
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Its about the amount of steroid versus the size of the retention pocket, hence the concentration is what matters. 100 mg/ml will have a longer half-life than 200 mg/ml, that is true. But most athletes given the choice will opt for the latter as they prefer to inject less volume. which also reduces half-life.
I agree. But because real Deca-durabolin (100mg/ml or less) has strongly been used by the past, it could have played a role in the nandrolone's bad reputation.
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Depends on the detection limits of what you are using, if you ask for a specific LH determination you get more sensitive results, that are exact. And you can definitely see a difference in normally used doses. Aside from that, and probably more important is the length of supression and the dose over the course of coming off. recovery will be faster and more complete if your drug of choice has a fast drop in serum levels after cessation. This depends on both half-life and on the clearance of the drug and its metabolites. In the latter area nandrolone scores pretty bad, with detectable metabolites up to 24 months after last use.
Metabolites detection time is not a relevant information to compare steroids potency in term of HPT axes suppression. This detection time is linked to the ester which has been used in conjonction whith the parent drug. How long do you think we could find detectable metabolites after a testosterone decanoate cycle in a castrated and adrenalectomized subject ? There is no reason to think that slight steroid's traces are able to delay HPTA recovery.
Primobolan-depot is detectable for months too and no-one worries about its suppressive effect.
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You may not wish to consider it, but you should. Others read your messages.
And I hope they do, I wish other opinions too.
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i'm just saying, be careful.
This remark disturbs me. When I have written that what I say is only for theoretic purpose, it's not only to preserve me against legal action, it's because it is the simple truth. I want to write with all my honesty and write what I think without to be scared by how people will interpret it. I think this board is made for adults, clevers and educated guys whoses are able to make their own opinions. When Nandi has written his excellent article about thyroid hormones and reveals the truth about the irrational fear commonly carried in the bodybuilding's world, it was not to promote their use. The same thing for me when I say that nandrolone is maybe not as suppressive as it is often believed.
And nandrolone's suppressive effect (like the other androgens) has been proven to be totally reversible.
11/12/2018 12:20 pm
wrt suppression, BB, why have you not availed yourself of the minto study. There is fertile ground there.
http://jpet.aspetjournals.org/cgi/content/full/281/1/93
jb
Topic starter 11/12/2018 1:09 pm
I know it and I have read it many and many times, and so what ?
In this study we can see that an injection of 100mg nandrolone decanoate lowers endogenous T from 18 nM (baseline) to 5nM at day five. Then the recovery processus starts at day ten and total recovery is achieved between days 25 and 30.
That's mean that nandrolone is suppressive ... someone has claimed the opposite ? When we speak about the suppressive effect of androgens, we deal with a relative concept, that's mean to learn comparative datas.
Nandrolone is suppressive but in the light of this thread we can think that its potency in this regard could be comparable to testosterone (or slighty lesser, slighty greater), not the terrifying stuff sometimes described.
11/12/2018 1:52 pm
Just my 2 cents here, Deca Durabolin has been widely used in Brazil for several decades, it's a kind of living legend here, it is stacked with Sustanon 250 (Durateston) and generally I don't see such negative reports that I have read in the international forums.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
11/12/2018 2:44 pm
actually i was thinking that the rates of recovery supported your position that nandrolone was not as suppressive as some think! Just trying to help out here....
jb
11/12/2018 3:29 pm
When I said international forums, I was meaning when compared to some important Brazilian ones, besides the word from streets as well.
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
11/12/2018 4:02 pm
when i first entered the scene deca was a mainstay, lately it seems to have lost some of the attraction.
jb
11/12/2018 4:45 pm
Why's that?
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
11/12/2018 5:43 pm
for basically the issues we have been discussing here, reports that is is very suppressive and pct is very difficult.
jb