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You cannot speak in generalities about 19-nortestosterone analogues like this. They're all markedly different in their HPG axis suppression. For one: only the longest-acting esters would suppress a healthy user for 5 months. Then, nandrolone is less suppressive than testosterone. Testosterone is actually quite suppressive (based on contraceptive efficacy) due to aromatization at a high rate to estradiol (negatively inhibits HPG axis functioning). Some 19-nortestosterone analogues are more suppressive and some are less suppressive. There's data on MENT (although it's perhaps more accurately considered a progestin) that shows it is quite suppressive. There's no data on tren in this regard, but we can surmise that due to its AR potency, its structure binding to ER, PR, its likely acting at KNDy dendrons to affect hypothalamic function, and what we've collectively reported anecdotally it is particularly suppressive as well.Is It true that the hormone 19 nor in deca n tren, will keep hpta suppressed for up to 5 months and there's no point on doin pct till then?
Use steroid plotter to determine when the ester clears roughly, then start your PCT meds like a SERM at least the week before the ester clears for all compounds. Do note, hCG+hMG on cycle is the optimal method to maintain HPG axis functioning rather than trying to kickstart things, because doing the latter (just using SERMS post cycle) just artificially boosts pituitary secretion of LH transiently while also negatively inhibiting hypothalamic-pituitary output... so you'll feel better from that, but are just masking and contributing further to keeping the systems offline. Maintaining testes function with hCG on cycle is the barest minimum and then use a SERM towards the end of your cycle for a while (e.g. 3-6 weeks) if you so choose, though I don't think it's worthwhile as it's really just a band-aid that contributes towards prolonged suppression.Thanks for the reply info, So how long would wait to do PCT after deca/tren/test cycle
Ok thanks alot I really appreciate the help.... What is hMG?Use steroid plotter to determine when the ester clears roughly, then start your PCT meds like a SERM at least the week before the ester clears for all compounds. Do note, hCG+hMG on cycle is the optimal method to maintain HPG axis functioning rather than trying to kickstart things, because doing the latter (just using SERMS post cycle) just artificially boosts pituitary secretion of LH transiently while also negatively inhibiting hypothalamic-pituitary output... so you'll feel better from that, but are just masking and contributing further to keeping the systems offline. Maintaining testes function with hCG on cycle is the barest minimum and then use a SERM towards the end of your cycle for a while (e.g. 3-6 weeks) if you so choose, though I don't think it's worthwhile as it's really just a band-aid that contributes towards prolonged suppression.
It's a combination drug that stimulates FSH & LH (as opposed to hCG only stimulating the latter). Again, it's optimal to use it, but hCG works better than nothing.Ok thanks alot I really appreciate the help.... What is hMG?
I don't wanna spam you with a long video, but a few youtubers (lol) said lack of progesterone suppresses t3 production. Meaning take TRT without HCG and you're low in t3.Use steroid plotter to determine when the ester clears roughly, then start your PCT meds like a SERM at least the week before the ester clears for all compounds. Do note, hCG+hMG on cycle is the optimal method to maintain HPG axis functioning rather than trying to kickstart things, because doing the latter (just using SERMS post cycle) just artificially boosts pituitary secretion of LH transiently while also negatively inhibiting hypothalamic-pituitary output... so you'll feel better from that, but are just masking and contributing further to keeping the systems offline. Maintaining testes function with hCG on cycle is the barest minimum and then use a SERM towards the end of your cycle for a while (e.g. 3-6 weeks) if you so choose, though I don't think it's worthwhile as it's really just a band-aid that contributes towards prolonged suppression.
Thank you for not spamming me with the video.I don't wanna spam you with a long video, but a few youtubers (lol) said lack of progesterone suppresses t3 production. Meaning take TRT without HCG and you're low in t3.
Meaning you need HCG to get your natty t3/t4 levels. Do you think that's true?
So decatest is kicked off the mod team due to power tripping banning people who speak against his research on hgh EOD being better than ED, 19-nors being highly suppressive, 19-nors being cardio and neurotoxic and MENT being a miracle drug. The subreddit is working on changing the views on MENT. He was also caught working with a MENT vendor.You cannot speak in generalities about 19-nortestosterone analogues like this. They're all markedly different in their HPG axis suppression. For one: only the longest-acting esters would suppress a healthy user for 5 months. Then, nandrolone is less suppressive than testosterone. Testosterone is actually quite suppressive (based on contraceptive efficacy) due to aromatization at a high rate to estradiol (negatively inhibits HPG axis functioning). Some 19-nortestosterone analogues are more suppressive and some are less suppressive. There's data on MENT (although it's perhaps more accurately considered a progestin) that shows it is quite suppressive. There's no data on tren in this regard, but we can surmise that due to its AR potency, its structure binding to ER, PR, its likely acting at KNDy dendrons to affect hypothalamic function, and what we've collectively reported anecdotally it is particularly suppressive as well.
Deca < Test in suppression (once the ester is cleared)
Tren probably >= Test in suppression, though I lean towards >
This study didn't even look at HPG axis suppression in their testosterone group, but only at nandrolone. It showed that at the 6 mo followup, FSH & LH had increased to 3.31 IU/L & 2.3 IU/L.So decatest is kicked off the mod team due to power tripping banning people who speak against his research on hgh EOD being better than ED, 19-nors being highly suppressive, 19-nors being cardio and neurotoxic and MENT being a miracle drug. The subreddit is working on changing the views on MENT. He was also caught working with a MENT vendor.
But it will take some time to change these views on MENT and 19-nors. Reddit is a giant hivemind after all. And because threads are forbidden there, it will take a very long time for the daily discussion threads to catch on.
The main argument for 19-nors being highly suppressive is this study. Which I don't think he has read. Because he only cites what's viewable without paying.
Long term perturbation of endocrine parameters and cholesterol metabolism after discontinued abuse of anabolic androgenic steroids - PubMed
Some individuals had a sustained suppression of LH and FSH for a period of 1 year whereas the cholesterol profile was normalized within 6 month. The long term consequences of these findings remain to be established.pubmed.ncbi.nlm.nih.gov
What's your take on this?
Yeah, testosterone vs. nandrolone, same ester weight, testosterone is more suppressive than nandrolone. But the principal factor in duration of suppression is the ester (it has to clear; enanthate/cypionate clear faster than decanoate; whereas NPP is less chronically suppressive than testosterone enanthate/cypionate). Second, are mechanisms like aromatization to estrogens (T > nand) as estrogens negatively feed back at the pituitary (more so than androgens; but both contribute). T aromatizes ~5x as much as nandrolone. There are other mechanisms including KNDy dendron pulsatility that progestins tend to alter, but as we can see with testosterone, this feature doesn't overcome the suppression of good old T for male birth control.I'd love to know because despite being kicked off the mod team just a few days ago, he's still browsing the subreddit and spreading this info.
I've tried to get the current mods to look at these and edit the wiki. But as long as that other study doesn't have any good counter arguments, it's hard to do. And no, we don't have any PeterBonds there that can look at this.
Detection of anabolic androgenic steroid abuse in doping control using mammalian reporter gene bioassays - PubMed
Anabolic androgenic steroids (AAS) are a class of steroid hormones related to the male hormone testosterone. They are frequently detected as drugs in sport doping control. Being similar to or derived from natural male hormones, AAS share the activation of the androgen receptor (AR) as common...pubmed.ncbi.nlm.nih.govSuppression of spermatogenesis to azoospermia by combined administration of GnRH antagonist and 19-nortestosterone cannot be maintained by this non-aromatizable androgen alone - PubMed
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.pubmed.ncbi.nlm.nih.gov
Thank you very much. Great read. You should mod the subreddit lol.This study didn't even look at HPG axis suppression in their testosterone group, but only at nandrolone. It showed that at the 6 mo followup, FSH & LH had increased to 3.31 IU/L & 2.3 IU/L.
Considerations:
- Clearance time for most nandrolone products is typically the decanoate (long) ester which clears more slowly than the common enanthate or cypionate esters for testosterone.
- 7/21 (1/3) of their nandrolone group were using test+nandrolone
When we look at HPG axis suppression (spermatogenesis) we see that nandrolone alone fails to suppress spermatogenesis, whereas T alone is successful in suppressing spermatogenesis:
Swerdloff, R. S., Bagatell, C. J., Wang, C., Anawalt, B. D., Berman, N., Steiner, B., & Bremner, W. J. (1998). Suppression of Spermatogenesis in Man Induced by Nal-Glu Gonadotropin Releasing Hormone Antagonist and Testosterone Enanthate (TE) Is Maintained by TE Alone. The Journal of Clinical Endocrinology & Metabolism, 83(10), 3527–3533. doi:10.1210/jcem.83.10.5184
versus
Behre, H. M., Kliesch, S., Lemcke, B., von Eckardstein, S., & Nieschlag, E. (2001). Suppression of spermatogenesis to azoospermia by combined administration of GnRH antagonist and 19-nortestosterone cannot be maintained by this non-aromatizable androgen alone. Human Reproduction, 16(12), 2570–2577. doi:10.1093/humrep/16.12.2570
The nature of acute (as opposed to chronic) suppression between nandrolone & testosterone is similar when looking at pharmacodynamics:
Nandrolone phenylpropionate, decanoate
- Testosterone suppression: complete suppression between 5-10 days with a single 100mg bolus
- "Plasma testosterone concentrations were most rapidly and completely suppressed within the first week after injections of the phenylpropionate ester, but this suppression was sustained for the shortest time. The duration of suppression was significantly longest after the gluteal 1-ml injection. Plasma testosterone concentrations returned to base line by day 13 after the phenylpropionate ester but required >20 days to return to base-line levels after the decanoate ester." [27]
- FSH suppression occurred rapidly (day 3 or 4) but returned to base-line practically immediately after phenylpropionate (IM gluteal) and after about a week with decanoate (Table 6, Inhibin, p. 100) [27]
[27] Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ. Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther. 1997 Apr;281(1):93-102. PMID: 9103484.
Testosterone enanthate; cypionate
See [22] Gårevik N, Rane A, Björkhem-Bergman L, Ekström L. Effects of different doses of testosterone on gonadotropins, 25-hydroxyvitamin D3, and blood lipids in healthy men. Subst Abuse Rehabil. 2014;5:121-127. Published 2014 Dec 10. doi:10.2147/SAR.S71285
From memory, Testosterone Enanthate 500mg is almost immediately (w/i 4 days) suppressive and almost totally by 14 days of LSH, FSH. 250mg did not fare much better. 150mg was suppressive, but didn't alter lipids.
- LH suppression was mostly reversed by week 6 post-cycle with 250mg Test Cyp per week versus week 10 post-cycle in 500mg group.
- Spermatogenesis suppression (sperm count) was substantial: by the end of a 14 week cycle, 250mg and 500mg groups were suppressed at about 48% for 250g at week 28(!) versus 67% for 500mg. By week 40, sperm counts almost normal in 250mg group but still lower than baseline
- The endogenous T secretion rate returned to baseline at approx week 23 in all groups
Yeah, testosterone vs. nandrolone, same ester weight, testosterone is more suppressive than nandrolone. But the principal factor in duration of suppression is the ester (it has to clear; enanthate/cypionate clear faster than decanoate; whereas NPP is less chronically suppressive than testosterone enanthate/cypionate). Second, are mechanisms like aromatization to estrogens (T > nand) as estrogens negatively feed back at the pituitary (more so than androgens; but both contribute). T aromatizes ~5x as much as nandrolone. There are other mechanisms including KNDy dendron pulsatility that progestins tend to alter, but as we can see with testosterone, this feature doesn't overcome the suppression of good old T for male birth control.
I suspend judgment on the precise nature and degree of tren suppression in humans due to lack of data, though from personal experience and some reasonable supposition, I believe that as it is such a potent androgen AND potent progestin (it's a triene, but acts analogously [but more potently] to progesterone at the hypothalamus in inhibiting KNDy dendron pulsatility and slowing the rate of GnRH pulses) that it is highly suppressive. It's just impossible to determine with real precision how markedly it suppresses HPG axis functioning other than by such supposition. With compounds that have been investigated for human contraception like nandrolone, testosterone, and MENT, we don't have to suppose, we can look at the data.Thank you very much. Great read. You should mod the subreddit lol.
What about suppression from tren?
17α-Trenbolone, 17β-Trenbolone and Trendione. Each of these compounds are highly suppressive of the HPTA axis. Each are able to convert into one another, which substantially prolongs their elimination time: up to eighteen months post-cessation.
Thanks brother. You are a wealth of information.I suspend judgment on the precise nature and degree of tren suppression in humans due to lack of data, though from personal experience and some reasonable supposition, I believe that as it is such a potent androgen AND potent progestin (it's a triene, but acts analogously [but more potently] to progesterone at the hypothalamus in inhibiting KNDy dendron pulsatility and slowing the rate of GnRH pulses) that it is highly suppressive. It's just impossible to determine with real precision how markedly it suppresses HPG axis functioning other than by such supposition. With compounds that have been investigated for human contraception like nandrolone, testosterone, and MENT, we don't have to suppose, we can look at the data.
What do you mean by "versus"? The word to me sounds like the two studies oppose each other. But when reading them it seems to me they are concluding the same thing when discussing suppression from nandrolone?This study didn't even look at HPG axis suppression in their testosterone group, but only at nandrolone. It showed that at the 6 mo followup, FSH & LH had increased to 3.31 IU/L & 2.3 IU/L.
Considerations:
- Clearance time for most nandrolone products is typically the decanoate (long) ester which clears more slowly than the common enanthate or cypionate esters for testosterone.
- 7/21 (1/3) of their nandrolone group were using test+nandrolone
When we look at HPG axis suppression (spermatogenesis) we see that nandrolone alone fails to suppress spermatogenesis, whereas T alone is successful in suppressing spermatogenesis:
Swerdloff, R. S., Bagatell, C. J., Wang, C., Anawalt, B. D., Berman, N., Steiner, B., & Bremner, W. J. (1998). Suppression of Spermatogenesis in Man Induced by Nal-Glu Gonadotropin Releasing Hormone Antagonist and Testosterone Enanthate (TE) Is Maintained by TE Alone. The Journal of Clinical Endocrinology & Metabolism, 83(10), 3527–3533. doi:10.1210/jcem.83.10.5184
versus
Behre, H. M., Kliesch, S., Lemcke, B., von Eckardstein, S., & Nieschlag, E. (2001). Suppression of spermatogenesis to azoospermia by combined administration of GnRH antagonist and 19-nortestosterone cannot be maintained by this non-aromatizable androgen alone. Human Reproduction, 16(12), 2570–2577. doi:10.1093/humrep/16.12.2570
The nature of acute (as opposed to chronic) suppression between nandrolone & testosterone is similar when looking at pharmacodynamics:
Nandrolone phenylpropionate, decanoate
- Testosterone suppression: complete suppression between 5-10 days with a single 100mg bolus
- "Plasma testosterone concentrations were most rapidly and completely suppressed within the first week after injections of the phenylpropionate ester, but this suppression was sustained for the shortest time. The duration of suppression was significantly longest after the gluteal 1-ml injection. Plasma testosterone concentrations returned to base line by day 13 after the phenylpropionate ester but required >20 days to return to base-line levels after the decanoate ester." [27]
- FSH suppression occurred rapidly (day 3 or 4) but returned to base-line practically immediately after phenylpropionate (IM gluteal) and after about a week with decanoate (Table 6, Inhibin, p. 100) [27]
[27] Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ. Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther. 1997 Apr;281(1):93-102. PMID: 9103484.
Testosterone enanthate; cypionate
See [22] Gårevik N, Rane A, Björkhem-Bergman L, Ekström L. Effects of different doses of testosterone on gonadotropins, 25-hydroxyvitamin D3, and blood lipids in healthy men. Subst Abuse Rehabil. 2014;5:121-127. Published 2014 Dec 10. doi:10.2147/SAR.S71285
From memory, Testosterone Enanthate 500mg is almost immediately (w/i 4 days) suppressive and almost totally by 14 days of LSH, FSH. 250mg did not fare much better. 150mg was suppressive, but didn't alter lipids.
- LH suppression was mostly reversed by week 6 post-cycle with 250mg Test Cyp per week versus week 10 post-cycle in 500mg group.
- Spermatogenesis suppression (sperm count) was substantial: by the end of a 14 week cycle, 250mg and 500mg groups were suppressed at about 48% for 250g at week 28(!) versus 67% for 500mg. By week 40, sperm counts almost normal in 250mg group but still lower than baseline
- The endogenous T secretion rate returned to baseline at approx week 23 in all groups
Yeah, testosterone vs. nandrolone, same ester weight, testosterone is more suppressive than nandrolone. But the principal factor in duration of suppression is the ester (it has to clear; enanthate/cypionate clear faster than decanoate; whereas NPP is less chronically suppressive than testosterone enanthate/cypionate). Second, are mechanisms like aromatization to estrogens (T > nand) as estrogens negatively feed back at the pituitary (more so than androgens; but both contribute). T aromatizes ~5x as much as nandrolone. There are other mechanisms including KNDy dendron pulsatility that progestins tend to alter, but as we can see with testosterone, this feature doesn't overcome the suppression of good old T for male birth control.
Nevermind, I get it now.What do you mean by "versus"? The word to me sounds like the two studies oppose each other. But when reading them it seems to me they are concluding the same thing when discussing suppression from nandrolone?
Great postings professor!This study didn't even look at HPG axis suppression in their testosterone group, but only at nandrolone. It showed that at the 6 mo followup, FSH & LH had increased to 3.31 IU/L & 2.3 IU/L.
Considerations:
- Clearance time for most nandrolone products is typically the decanoate (long) ester which clears more slowly than the common enanthate or cypionate esters for testosterone.
- 7/21 (1/3) of their nandrolone group were using test+nandrolone
When we look at HPG axis suppression (spermatogenesis) we see that nandrolone alone fails to suppress spermatogenesis, whereas T alone is successful in suppressing spermatogenesis:
Swerdloff, R. S., Bagatell, C. J., Wang, C., Anawalt, B. D., Berman, N., Steiner, B., & Bremner, W. J. (1998). Suppression of Spermatogenesis in Man Induced by Nal-Glu Gonadotropin Releasing Hormone Antagonist and Testosterone Enanthate (TE) Is Maintained by TE Alone. The Journal of Clinical Endocrinology & Metabolism, 83(10), 3527–3533. doi:10.1210/jcem.83.10.5184
versus
Behre, H. M., Kliesch, S., Lemcke, B., von Eckardstein, S., & Nieschlag, E. (2001). Suppression of spermatogenesis to azoospermia by combined administration of GnRH antagonist and 19-nortestosterone cannot be maintained by this non-aromatizable androgen alone. Human Reproduction, 16(12), 2570–2577. doi:10.1093/humrep/16.12.2570
The nature of acute (as opposed to chronic) suppression between nandrolone & testosterone is similar when looking at pharmacodynamics:
Nandrolone phenylpropionate, decanoate
- Testosterone suppression: complete suppression between 5-10 days with a single 100mg bolus
- "Plasma testosterone concentrations were most rapidly and completely suppressed within the first week after injections of the phenylpropionate ester, but this suppression was sustained for the shortest time. The duration of suppression was significantly longest after the gluteal 1-ml injection. Plasma testosterone concentrations returned to base line by day 13 after the phenylpropionate ester but required >20 days to return to base-line levels after the decanoate ester." [27]
- FSH suppression occurred rapidly (day 3 or 4) but returned to base-line practically immediately after phenylpropionate (IM gluteal) and after about a week with decanoate (Table 6, Inhibin, p. 100) [27]
[27] Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ. Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther. 1997 Apr;281(1):93-102. PMID: 9103484.
Testosterone enanthate; cypionate
See [22] Gårevik N, Rane A, Björkhem-Bergman L, Ekström L. Effects of different doses of testosterone on gonadotropins, 25-hydroxyvitamin D3, and blood lipids in healthy men. Subst Abuse Rehabil. 2014;5:121-127. Published 2014 Dec 10. doi:10.2147/SAR.S71285
From memory, Testosterone Enanthate 500mg is almost immediately (w/i 4 days) suppressive and almost totally by 14 days of LSH, FSH. 250mg did not fare much better. 150mg was suppressive, but didn't alter lipids.
- LH suppression was mostly reversed by week 6 post-cycle with 250mg Test Cyp per week versus week 10 post-cycle in 500mg group.
- Spermatogenesis suppression (sperm count) was substantial: by the end of a 14 week cycle, 250mg and 500mg groups were suppressed at about 48% for 250g at week 28(!) versus 67% for 500mg. By week 40, sperm counts almost normal in 250mg group but still lower than baseline
- The endogenous T secretion rate returned to baseline at approx week 23 in all groups
Yeah, testosterone vs. nandrolone, same ester weight, testosterone is more suppressive than nandrolone. But the principal factor in duration of suppression is the ester (it has to clear; enanthate/cypionate clear faster than decanoate; whereas NPP is less chronically suppressive than testosterone enanthate/cypionate). Second, are mechanisms like aromatization to estrogens (T > nand) as estrogens negatively feed back at the pituitary (more so than androgens; but both contribute). T aromatizes ~5x as much as nandrolone. There are other mechanisms including KNDy dendron pulsatility that progestins tend to alter, but as we can see with testosterone, this feature doesn't overcome the suppression of good old T for male birth control.