After cessation of cetrorelix injections in week 12, gonadotrophins and Testosterone increased significantly despite continued 19NT-HPP injections. In parallel, spermatogenesis was restimulated in five of six volunteers.
CONCLUSIONS: Combined administration of cetrorelix and 19NT-HPP leads to azoospermia within 3 months. However, complete azoospermia cannot be maintained by continued injections of the non-aromatizable 19NT-HPP alone.
i think the more likely conclusion from this study is that 200mg injections of 19nt-hpp every three weeks is not sufficient to completely suppress hpta and sprematogenesis.
In this study, 19nt-hpp caused persisten azoospermia. Of course the doses were a little higher.
jb
=========
19-nortestosterone for male fertility regulation.
POPLINE Document Number: 035527
Author(s):
Knuth UA
Behre H
Belkien L
Bents H
Nieschlag E
Source citation:
In: Male contraception: advances and future prospects, edited by Gerald I. Zatuchni, Alfredo Goldsmith, Jeffrey M. Spieler [and] John J. Sciarra. Philadelphia, Pennsylvania, Harper and Row, 1986. :320-8. (PARFR Series on Fertility Regulation)
Abstract:
Male fertility control requires a slow-release androgen formulation devoid of high-peak concentrations after injection. Nandrolone (19-nortestosterone, 19 NT) and its esters provide this characteristic and have been used widely as anabolic substances with no toxic side effects. On the basis of data for half-life and peak formulation, nandrolone hexyloxyphenylpropionate (19NT-HPP) was selected as the androgen ester suitable for further use in clinical trials for a male antifertility agent and a pilot study was conducted in 5 volunteers. Participants received 100 mg/week injections of 19NT-HPP for 3 weeks, followed by 200 mg/week for the next 10 weeks. By week 13, all subjects were azoospermic and this condition persisted for 4-14 weeks after treatment. There were no apparent side effects, and no evidence of impaired libido or impotence despite severely reduced testosterone values. Given these results, the antifertility potential of 19NT-HPP was investigated in greater detail in 12 volunteers. Again, 19NT treatment suppressed serum gonadotropins below detection limits and testosterone levels were in the castrate range. Complete suppression persisted up to week 28 (3 weeks after conclusion of treatment). Normalization occurred 15-28 weeks after the last injection. 83% of subjects attained azoospermia or severe oligospermia by the end of the treatment. The formulation did not affect liver enzymes, creatinine, uric acid, serum electrolytes, or serum lipids; however, hemoglobin, erythrocytes, hematocrit, and mean corpuscular volume were significantly elevated after 13 weeks of treatment. Because of its long half-life, 19NT-HPP offers a considerable advantage over available testosterone esters. The antifertility effectiveness of this agent seems to depend largely on the unique binding characteristics of the parent substance and its reduced metabolite to the androgen receptor. Future studies using different dose regimens or combinations with other substances will clarify further the potential of 19NT-HPP.
You shouldn't have to quote that study JB, if BB had payed attention he would have seen that the authors of the study he quoted made the same statement in reference to the same study :
quote:
It should be noted that the same dose of 19NT-HPP given without GnRH analogues consistently suppressed gonadotrophins (Behre et al., 1992).
Secondly there are a few things not taken into account by the authors here, such as the possibility of upregulation of GnRH receptors as well as a few dozen targets downstream in the HPTA as the result of use of a GnRH agonist. If everything is upregulated, its not unlikely to expect an increase under low dose phenylprop.
Lastly on a personal azoospermia is not synonymous with supression. Azoospermia is one area of supression. But simply the return of normal testosterone concentration is a first goal, and under those conditions azoospermia can still be an issue, even with normal HPTA. Vice versa, reversing azoospermia does not indicate a significantly recovered testosterone level, that is acceptable for a healthy male bodybuilder.
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.
I agree with you two.
To be more clear, I do not want to say that nandrolone is not suppressive, of course it is. I just want to show that nandrolone is not necessary as suppressive as some guys think and to put in light that aromatisation could be an important key (but not the sole of course) in the HPTA suppression processus.
Vice versa, reversing azoospermia does not indicate a significantly recovered testosterone level, that is acceptable for a healthy male bodybuilder.
In the present study we have both a significant increase of gonadotrophins and endogenous T and a spermatogenesis recovery.
I agree with you two.
To be more clear, I do not want to say that nandrolone is not suppressive, of course it is. I just want to show that nandrolone is not necessary as suppressive as some guys think and to put in light that aromatisation could be an important key (but not the sole of course) in the HPTA suppression processus.
Well, actually what we were pointing out is that this says very little about comparative ability to supress, considering we are talking low dose after an abnormal condition, like GnRH blocking, that could be leading to all manners of upregulation downstream in the HPTA and not compared to any other steroid.
The blood results of a several million athletes will show you beyond a shadow of a doubt that nandrolone is considerably more supressive than all of the other major 7 steroids that are commonly abused : testosterone,Stanozolol, boldenone, methenolone, oxandrolone, oxymetholone, methandrostenolone. In equipotent doses.
So your argument is very relative. Is nandrolone very supressive ? That depends on where you put the line for very supressive. But when you ask is nandrolone very supressive compared to other drugs that are commonly used, the answer is a very definite yes.
As i also pointed out in the other thread, nandrolone is 60% as estrogenic as estradiol itself, albeit through the androgen receptor. So stating that lack of aromatisation is the source of less supression wouldn't hold up anyway.
quote:
In the present study we have both a significant increase of gonadotrophins and endogenous T and a spermatogenesis recovery.
True, after use of a GnRH antagonist, which will lead to rebound from the top down of all steroids in the HPTA, the sum of which is responsible for normospermia.
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.
Well, actually what we were pointing out is that this says very little about comparative ability to supress ...
My last answer has to be read in the context of the whole thread and the other things I have quoted before.
quote:
The blood results of a several million athletes will show you beyond a shadow of a doubt that nandrolone is considerably more supressive than all of the other major 7 steroids that are commonly abused ...
I have never seen anyone. Actually to work with a scientific approach in this subject we have only the litterature about male contraception, that's mean administration of androgens (with sometimes the addition of other products) in normal healthy men. I think it's informative of the potential of the different AAS in terms of HPTA and endogenous T production suppression.
By the way, at the doses used by bodybuilding's athletes, all products can achieve strong HPTA and endogenous T production suppression, so it's difficult to compare and maybe irrelevant.
quote:
So your argument is very relative.
Yes, it is.
quote:
Is nandrolone very supressive ? That depends on where you put the line for very supressive. But when you ask is nandrolone very supressive compared to other drugs that are commonly used, the answer is a very definite yes.
My idea was to compare nandrolone to testosterone. Because 19-NT is a more potent anabolic agent than the androgen of reference, you will need lower doses to achieve the same goal in terms of muscle gains and athletic performances. I think with comparable (maybe be with slighty more or less) HPTA and endogenous T production suppression.
I have wanted to open the debate, not to claim that nandrolone is safe in regard of HPTA suppression, of course it is not (but no AAS is).
quote:
As i also pointed out in the other thread, nandrolone is 60% as estrogenic as estradiol itself, albeit through the androgen receptor. So stating that lack of aromatisation is the source of less supression wouldn't hold up anyway.
I have read your article and the references you have quoted and I think we must be very careful with this sort of very advanced researches.
Actually we have no proof that 19-NT can compensate the lack of aromatisation by an estrogenic AR mediated effect. That's not because 19 NT is able to induce estrogenic effect via the AR that it can achieve all the estrogenic effects like a real estrogen via the ER. We know that aromatisation is the first step for HPTA suppression but non-aromatisable androgens are able to regulate the HPTA via their androgenic receptors (as a second step and not necessary via an estrogenic AR mediated answer).
And I disagree to say that nandrolone is 60% as estrogenic as estradiol in regard of the references you have quoted. You have made this statement based on the result of a study which has retain one parameter to measure estrogenic effect. That does not mean that nandrolone is as estrogenic in the rest of the spectrum of effects. Nandrolone is an androgen and has been used on women in the treatment of hormonal dependent cancers.
Just to say that nandrolone is 60% as estrogenic as estradiol (without other precisions) mean that nandrolone is just a weaker estrogen and that we could achieve all the same effects whith higher doses, and that's not the case.
To return to nandrolone and T comparaison, some studies have also demonstrated estrogenic effects from T (itself without aromatisation) and DHT mediated by the ER or the AR (Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays. Markiewicz L, Gurpide E.)
I just want to argue, not to say that the truth comes from my mouth.
I have never seen anyone. Actually to work with a scientific approach in this subject we have only the litterature about male contraception, that's mean administration of androgens (with sometimes the addition of other products) in normal healthy men. I think it's informative of the potential of the different AAS in terms of HPTA and endogenous T production suppression.By the way, at the doses used by bodybuilding's athletes, all products can achieve strong HPTA and endogenous T production suppression, so it's difficult to compare and maybe irrelevant.
You make a good point, I'm speaking entirely from experience and have found no comparative data in sufficient dose to make a statistically conclusive argument that I can carry forth as fact. However in my experience, which of course is just my experience, results from athletes using nandrolone, are always worse than those on equipotent doses of other drugs. Considerably worse.
quote:
My idea was to compare nandrolone to testosterone. Because 19-NT is a more potent anabolic agent than the androgen of reference, you will need lower doses to achieve the same goal in terms of muscle gains and athletic performances. I think with comparable (maybe be with slighty more or less) HPTA and endogenous T production suppression.
I have wanted to open the debate, not to claim that nandrolone is safe in regard of HPTA suppression, of course it is not (but no AAS is).
Actually that is an argument you can't make on any sound basis. The relative anabolic potency is dependent on factors that simply haven't been determined yet, and as any athlete will tell you, mg for mg, testosterone yields more results than nandrolone. Those with blood results will also tell you that it is more supressive at an equipotent dose.
I haven't seen anyone gain on 750 mg of deca as they did on 750 mg of Testosterone Enanthate for instance.
I do like this discussion though, it does point out that this is one area where we still base ourselves mostly on the results of one or more individuals and not a controlled double-blind group. Hence some of the statements in this regard will be somewhat skewed. I don't think its the case for nandrolone though, its been around long enough, and widely used, as is testosterone, the results I have seen alone would form an acceptable subject group. But the argument may hold for a great deal of other steroids that we misinterpret their ability to supress.
After all, I know I for instance base myself on three key measurements to make that call, but the third is two weeks after the end of PCT, when for most cycles recovery is complete, and indistinguishable.
quote:
I have read your article and the references you have quoted and I think we must be very careful with this sort of very advanced researches.
Actually we have no proof that 19-NT can compensate the lack of aromatisation by an estrogenic AR mediated effect. That's not because 19 NT is able to induce estrogenic effect via the AR that it can achieve all the estrogenic effects like a real estrogen via the ER. We know that aromatisation is the first step for HPTA suppression but non-aromatisable androgens are able to regulate the HPTA via their androgenic receptors (as a second step and not necessary via an estrogenic AR mediated answer).
Its not that advanced, this is actually my field of research, molecular biology. Nandrolone does indeed induce, like any AR, negative feedback via concensus ARE's as well of course, however its increased supression (which I have to stand by in light of the evidence I have seen) could be the result of the ERE stimulation. its more likely than its aromatization or progestagenic activity, since the studies I posted there indicated that inhibition of PR or aromatase had no effect on estrogenic potency.
At the same time your point is very valid, the degree of estrogenic activity does not linearly correlate with the increase in supression. If that was the case, nandrolone would be even more supressive. Likely, as you profer, the AR-N only stimulates a few of the ERE's involved in HPTA downregulation, or more likely, is incapable of stimulating the ERE to the same extent as the ER would.
quote:
And I disagree to say that nandrolone is 60% as estrogenic as estradiol in regard of the references you have quoted. You have made this statement based on the result of a study which has retain one parameter to measure estrogenic effect. That does not mean that nandrolone is as estrogenic in the rest of the spectrum of effects. Nandrolone is an androgen and has been used on women in the treatment of hormonal dependent cancers.
Just to say that nandrolone is 60% as estrogenic as estradiol (without other precisions) mean that nandrolone is just a weaker estrogen and that we could achieve all the same effects whith higher doses, and that's not the case.
Actually it may be, don't forget that nandrolone is a by-product of aromatization as well. Likely it serves that very purpose. Its effects on osteoporosis and such would indicate likewise. And yes nandrolone has been tested (but is not clinically used) in breast cancer, but so was testosterone, with even better results, suggesting this is an entirely AR mediated effect. this was discussed in the masteron thread as well.
quote:
To return to nandrolone and T comparaison, some studies have also demonstrated estrogenic effects from T (itself without aromatisation) and DHT mediated by the ER or the AR (Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays. Markiewicz L, Gurpide E.)
Well if you go back to the thread about estrogen independent estrogenic effects you will find that I discussed this as well, and the culprit is not T or DHT, but rather a metabolite called 3-beta-androstanediol. Testosterone loses its estrogenic effect when used in conjunction with a 5AR blocker ...
quote:
I just want to argue, not to say that the truth comes from my mouth.
Well we are arguing the point. Hopefully the truth will come forth from the argument. I just wanted to point out there are some holes in your argument.
The discussion in itself I applaud, just don't like the conclusions you make about nandrolone not being so supressive without concrete proof, as I have seen too many blood results that say otherwise, and I wouldn't want anyone to get in trouble because they thought nandrolone was no more supressive than testosterone.
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.
In all the litterature I have read, nandrolone is said to be a more efficient myotrophic agent. I can quote but if you said that from your own experiences it is not, it will be difficult to argue.
To say, that 19-nor is a by-product of aromatisation does not mean that it's an estrogen, when we speak about steroids, we speak about a cycle, they are all by-products (and often but not always reversible) of the others. And natural production of nandrolone metabolites in humans is anecdotal. To classify steroids we look at their main receptor target. Nandrolone acts mainly by the androgen receptors and generate androgenic answers. The fact, that it is a by-product of aromatisation as nothing to do with its ability to promote estrogenic AR-mediated effects, DHT (or its metabolites) can too and maybe other androgens.
About the effects of androgens in the treatment of osteoporosis, I have a study with good results with the androgen Oral-Turinanol (for which estrogenic and progestational activity has been excluded in experiments), these effects are certainly both AR (and only AR in the case of OT) and ER via aromatisation mediated.
It's a little funny to worry about nandrolone's suppressive effect in regard of the doses commonly used by bodybuilding athletes and competitors. I mean, bodybuilders usually use big amount of T (often in conjonction with other AAS), they certainly achieve strong inhibition of their HPTA and their endogenous T production, so by the way if they use T or nandrolone. Now to speak about PCT, which is more interesting, in regard of the studies I have quoted, there is no reason to think that nandrolone is worst than T (of course not on a mg for mg basis). another thing has to be taken into account : nandrolone is generally used with the decanoate ester, that's mean slow release and long duration, it has to be taken into account too, but it's another thing that to strictly compare T and nandrolone (parent form).
I am trying to piece together what Big Cat's summary is on Nandro.
Big Cat, could you give us the "bullet points" on this med?
Also when, if ever would you rec this med for BB purposes.
Thanks
Do not mistaken, I have a lot of respect for BC and his work. It's just a debate without any animosity. We confront our point of view, that's nothing to do with the respect you can have to someone. Of course, BC is a great contributor on this board and in the ergogenic aids field.
By the past, I have discussed and sometimes be in disagreement with Nandi, but it has never question the profound respect I have for his person.
Black B,
I hope my post did not trigger your response. I am not taking sides nor do I find any exchange disrespectful. I find this thread very interesting. I have to dig out my old textbooks to keep up though. LOL Much more entertaining/educational than the HRT forum.
i agree this is a most useful thread, keep going here. I think the distinction here is between bodybuilding doses and say hrt doses.
jb
or at least an HPTA that WILL recover--regardless of dose.
Not sure I will run Nandro again though. Lets see, It has been called a progestin. It is estrogenic via aromatase and through the AR. It bolster prolactin, the parent compound is more androgenic then its metabolites(?? least the bond between the AR and DHN is weaker) Whats so good about it? LOL
[B]In all the litterature I have read, nandrolone is said to be a more efficient myotrophic agent. I can quote but if you said that from your own experiences it is not, it will be difficult to argue.
How can you in good conscience suggest that nandrolone is better for muscle building than testosterone ?
quote:
To say, that 19-nor is a by-product of aromatisation does not mean that it's an estrogen, when we speak about steroids, we speak about a cycle, they are all by-products (and often but not always reversible) of the others. And natural production of nandrolone metabolites in humans is anecdotal. To classify steroids we look at their main receptor target. Nandrolone acts mainly by the androgen receptors and generate androgenic answers. The fact, that it is a by-product of aromatisation as nothing to do with its ability to promote estrogenic AR-mediated effects, DHT (or its metabolites) can too and maybe other androgens.
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.
quote:
About the effects of androgens in the treatment of osteoporosis, I have a study with good results with the androgen Oral-Turinanol (for which estrogenic and progestational activity has been excluded in experiments), these effects are certainly both AR (and only AR in the case of OT) and ER via aromatisation mediated.
And did the test also exclude AR activation of ERE's? that seems doubtful ...
quote:
It's a little funny to worry about nandrolone's suppressive effect in regard of the doses commonly used by bodybuilding athletes and competitors. I mean, bodybuilders usually use big amount of T (often in conjonction with other AAS), they certainly achieve strong inhibition of their HPTA and their endogenous T production, so by the way if they use T or nandrolone. Now to speak about PCT, which is more interesting, in regard of the studies I have quoted, there is no reason to think that nandrolone is worst than T (of course not on a mg for mg basis). another thing has to be taken into account : nandrolone is generally used with the decanoate ester, that's mean slow release and long duration, it has to be taken into account too, but it's another thing that to strictly compare T and nandrolone (parent form).
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.
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.
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.
or at least an HPTA that WILL recover--regardless of dose.
Not sure I will run Nandro again though. Lets see, It has been called a progestin. It is estrogenic via aromatase and through the AR. It bolster prolactin, the parent compound is more androgenic then its metabolites(?? least the bond between the AR and DHN is weaker) Whats so good about it? LOL
Yes, regardless of this debate, for bodybuilding purposes nandrolone is not really the best drug of choice. Especially if you consider its main point of attraction is its comparatively low androgenicity in androgenic target tissues, but that the occurence of androgenic problems (aside from acne) in healthy young males is extremely low in commonly used bodybuilding doses of common bodybuilding steroids.
That does not detract the merit of low dose nandrolone for therapeutic single cycle purposes in the treatment of AIDS, myastenia gravis, other muscular disorders, dystrophy following surgery or trauma or even osteoporosis, its character lends it the possibility to even treat women and older men with low doses.
But as a bodybuilding drug I find nandrolone to be a very crude drugs with too many problems that cannot easily be treated.
I hope to publish the nandrolone profile from the book soon now, it totals ten pages and should explain things more clearly and in more detail than a web-board debate allows.Its one of the few profiles that nandi got to read before his passing, and the only one he ok'ed the final draft for, so its indicative of the level of research and writing I'm ambiating for the rest of the book as well.
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.