TREST/MENT without a test base?

[Type-IIx]

So many scientists lately reinventing wheel lol...

Just stick to what works.

There is not yet a perfectly suppressive male contraceptive drug.

Testosterone + a progestin like etonogestrel is still the best solution, but some men remain merely oligozoospermic rather than azoospermic (completely infertile). MENT had potential due to its potent suppressive effects and dissociated muscle anabolism from suppression.

That is to say, it's considered a good thing for contraceptive drugs to maximally suppress spermatogenesis at a dose below that which stimulates muscle growth because the drug has reduced abuse potential (by athletes, bodybuilders).

 

[Zeus45]

@Zeus45 I read the study:
Anderson, R. A., Martin, C. W., Kung, A. W. C., Everington, D., Pun, T. C., Tan, K. C. B., … Baird, D. T. (1999). 7α-Methyl-19-Nortestosterone Maintains Sexual Behavior and Mood in Hypogonadal Men1. The Journal of Clinical Endocrinology & Metabolism, 84(10), 3556–3562. doi:10.1210/jcem.84.10.6028

It's well designed. It supports your point. It provides evidence that a 0.46 mg/d dose of MENT may optimally support sexual function (this is ~65%> the dose used in the trial that I cited where sexual function was suppressed).

It fails to demonstrate that MENT can supplant the function of 5α-reductase to support sexual function or that MENT supplants DHT's role, however.

This is because the dose trialled here does not abolish basal T secretion. Though the wash-out phase assured a hypogonadal state in all subjects (excellent), the MENT treatment arm subsequent to TE treatment saw subjects remain eugonadal (due to nadir T being maintained > 9 nmol/L), and the researchers acknowledge a positive mood effect due to carryover from >eugonadal nadir T concentrations.

Throughout all treatment phases, this low MENT dose (much lower than that used by bodybuilders/for muscle anabolism) fails to abolish endogenous T secretion.

This (well-designed) trial shows that MENT's androgenic effects and maintenance of sexual function is additive to the effects of DHT, that are amplified in 5α-reductase rich tissues by even low T secretion, and especially so in the MENT treatment arm subsequent to TE (where a carryover effect of >eugonadal nadir T concentrations have an acknowledged positive effect on mood).

It is my view that MENT doses used in practice by bodybuilders will not maintain sexual function without adjuvant use of androgen that provides for 5α-reductase function (or DHT, e.g., Andractim patch slapped on the testes), because these doses abolish endogenous T secretion.

DHT is the most potent natural male sex hormone, much more androgenic than Testosterone. I am aware DHT has awesome effects on Libido and well being, I take proviron everyday and love it.

But just because MENT does not Convert to DHT (neither do a lot of powerful androgens) does not mean Trestolone can't support sexual functioning. Like i said before compounds like MENT do not need to 5AR to exert its Highly Androgenic Effects.

 

[Type-IIx]

DHT is the most potent natural male sex hormone, much more androgenic than Testosterone. I am aware DHT has awesome effects on Libido and well being, I take proviron everyday and love it.

But just because MENT does not Convert to DHT (neither do a lot of powerful androgens) does not mean Trestolone can't support sexual functioning. Like i said before compounds like MENT do not need to 5AR to exert its Highly Androgenic Effects.

You're repeating yourself tautologically without providing any additional evidence to bolster your claim. Your claim is valid, but I present contrary evidence from the study itself - the fact that endogenous T secretion was never abolished and nadir T concentrations were >eugonadal in the TE then MENT arm, enhancing mood. MENT acetate dose as used in practice for anabolism will necessarily be substantially > 0.46 mg/d (due to dissociation between suppression of spermatogenesis & anabolism inherent to its clinical application). Even the researchers here are less than confident in putting forward this indirect evidence (that may be used to formulate a subsequent testable hypothesis):

"MENT can be converted by aromatase to an active estrogen, 7α-methyl estradiol (34), but it is resistant to 5α-reductase (6). The effects of MENT may thus in part reflect those functions of testosterone that are mediated by estrogen receptors, but to a lesser degree those functions that involve amplification by 5α-reductase. The metabolism of testosterone is important in mediating its effects in several physiological systems, including aromatization in the control of gonadotropin secretion (35) and 5α-reduction in the prostate (36). 5α-Reductase is also present in the human brain (37); however, the isoform present in cerebral cortical tissue is type I rather than type II, which predominates in reproductive tract tissues (38 - 40). Although it is clear that testosterone is necessary for normal sexual function (41), the role of aromatization or 5α-reduction in humans is uncertain (42 - 44). In castrate male rodents, MENT fully restores sexual behavior (45, 46), but does not restore aggressive behavior, in contrast to testosterone, which restored both (13). Effects on libido and potency were reported by only small numbers of men during administration of the 5α-reductase inhibitor finasteride for treatment of benign prostatic hyperplasia (47); however, that drug has selectivity for the type II isoform not detected in human cerebral cortex (39, 40). The demonstration here of the effectiveness of MENT in restoring sexual function and mood in hypogonadal men provides indirect evidence that 5α-reduction is not required for mediation of the influence of testosterone on these behaviors in men."

 

[Zeus45]

You're repeating yourself tautologically without providing any additional evidence to bolster your claim. Your claim is valid, but I present contrary evidence from the study itself - the fact that endogenous T secretion was never abolished and nadir T concentrations were >eugonadal in the TE then MENT arm, enhancing mood. MENT acetate dose as used in practice for anabolism will necessarily be substantially > 0.46 mg/d (due to dissociation between suppression of spermatogenesis & anabolism inherent to its clinical application). Even the researchers here are less than confident in putting forward this indirect evidence (that may be used to formulate a subsequent testable hypothesis):

"MENT can be converted by aromatase to an active estrogen, 7α-methyl estradiol (34), but it is resistant to 5α-reductase (6). The effects of MENT may thus in part reflect those functions of testosterone that are mediated by estrogen receptors, but to a lesser degree those functions that involve amplification by 5α-reductase. The metabolism of testosterone is important in mediating its effects in several physiological systems, including aromatization in the control of gonadotropin secretion (35) and 5α-reduction in the prostate (36). 5α-Reductase is also present in the human brain (37); however, the isoform present in cerebral cortical tissue is type I rather than type II, which predominates in reproductive tract tissues (38 - 40). Although it is clear that testosterone is necessary for normal sexual function (41), the role of aromatization or 5α-reduction in humans is uncertain (42 - 44). In castrate male rodents, MENT fully restores sexual behavior (45, 46), but does not restore aggressive behavior, in contrast to testosterone, which restored both (13). Effects on libido and potency were reported by only small numbers of men during administration of the 5α-reductase inhibitor finasteride for treatment of benign prostatic hyperplasia (47); however, that drug has selectivity for the type II isoform not detected in human cerebral cortex (39, 40). The demonstration here of the effectiveness of MENT in restoring sexual function and mood in hypogonadal men provides indirect evidence that 5α-reduction is not required for mediation of the influence of testosterone on these behaviors in men."

My claim from the start has been Trestolone can replace testosterone as a form of androgen replacement therapy.

 

[theotherguy]

My claim from the start has been Trestolone can replace testosterone as a form of androgen replacement therapy.

I’ll ask again, what do you do to replace DHT when using MENT only? You seem to be ignoring my question over and over, it’s starting to seem intentional because you don’t have an answer

 

[Zeus45]

I’ll ask again, what do you do to replace DHT when using MENT only? You seem to be ignoring my question over and over, it’s starting to seem intentional because you don’t have an answer

Have you read the study? MENT replaces Testosterone AND its metabolite DHT. DHT is not nearly as Androgenic as MENT. Trestolone is a more potent androgen. What isnt clicking?

Thus, in monkeys, MENT is 10 times more potent than testosterone with regard to the clinically desirable end points of gonadotropin suppression and anabolism, but only twice as potent at stimulating prostate growth.

 

[Rido]

Have you read the study? MENT replaces Testosterone AND its metabolite DHT. DHT is not nearly as Androgenic as MENT. Trestolone is a more potent androgen. What isnt clicking?

Thus, in monkeys, MENT is 10 times more potent than testosterone with regard to the clinically desirable end points of gonadotropin suppression and anabolism, but only twice as potent at stimulating prostate growth.

Am I having a stroke? What study is talking about monkey's? Also is there a study that would show that it would have them with a full shutdown?

What study did you link?

 

[Zeus45]

Am I having a stroke? What study is talking about monkey's? Also is there a study that would show that it would have them with a full shutdown?

What study did you link?

7alpha-Methyl-19-nortestosterone (MENT) is a potent synthetic androgen that cannot be converted to dihydrotestosterone. In this study we determined the relative androgenic, antigonadotropic, and anabolic potencies of testosterone vs. MENT in the nonhuman primate M. fascicularis. In castrated monkeys, dose-response relationships were generated for the effects of testosterone and MENT on gonadotropin levels, prostate growth, body weight, and lipid metabolism. In a pilot study, four monkeys were castrated, and magnetic resonance imaging (MRI) was used to document a 50% loss of prostate volume within 8 weeks, verifying that MRI is a reliable means to measure prostate size in this species. Two additional groups of six monkeys each were then castrated and serially administered four graded dosages of testosterone or MENT via osmotic minipumps over 20 weeks. Complete suppression of LH was achieved with a minimum of 0.3 mg/day MENT, compared to 3.0 mg/day testosterone. MENT supported body weight 10 times more potently than did testosterone. Baseline prostate volumes were maintained with 0.1-0.2 mg/day MENT vs. 0.3 mg/day testosterone. Thus, in monkeys, MENT is 10 times more potent than testosterone with regard to the clinically desirable end points of gonadotropin suppression and anabolism, but only twice as potent at stimulating prostate growth. These results suggest that MENT may have a wider therapeutic index than testosterone for human androgen replacement and male contraception.

 

[Zeus45]

Am I having a stroke? What study is talking about monkey's? Also is there a study that would show that it would have them with a full shutdown?

What study did you link?

Another study about MENT as a treatment for hypogonadism

Pharmacokinetics of 7 alpha-methyl-19-nortestosterone (MENT) delivery using subdermal implants in healthy men - PubMed

We studied the pharmacokinetics of 7 alpha-methyl-19-nortestosterone (MENT), a potent synthetic androgen, administered by subdermal implants. The implants contained 112 +/- 4 mg of MENT acetate in a polyethylene vinyl acetate copolymer. MENT acetate released from the implants is rapidly...

pubmed.ncbi.nlm.nih.gov

"The study suggests that MENT acetate implants are a promising method for long-term androgen administration in hypogonadism and male contraception."

Comparison of 7α-methyl-19-nortestosterone effectiveness alone or combined with progestins on androgen receptor mediated-transactivation - PubMed

7α-methyl-19-nortestosterone (MENT) is an androgen with potent gonadotropin inhibitory activity and prostate-sparing effects. These attributes give MENT advantages over testosterone as a male contraceptive, but, as in the case of testosterone, a partial dose-dependent suppression of...

pubmed.ncbi.nlm.nih.gov

As expected, MENT induced gene transactivation through either the progesterone receptor (PGR) or the AR. MENT was as efficient as progesterone in activating PGR-mediated reporter gene expression, but it was ten times more potent than testosterone and dihydrotestoterone in activating of AR-driven gene expression.

^ study showing MENT being 10x more potent than DHT.

 

[Rido]

A 4 week study? Come on man. It may suggest it may be a good replacement for TRT. But there is no hard long term evidence it would be.

 

[theotherguy]

Have you read the study? MENT replaces Testosterone AND its metabolite DHT. DHT is not nearly as Androgenic as MENT. Trestolone is a more potent androgen. What isnt clicking?

Thus, in monkeys, MENT is 10 times more potent than testosterone with regard to the clinically desirable end points of gonadotropin suppression and anabolism, but only twice as potent at stimulating prostate growth.

Did I read the study you posted that had MENT and test combined? How does that prove that MENT replaces DHT?

EDIT: to be clear, I’m not saying you’re wrong, but so far there is no evidence that shows what you’re saying is correct.

 

[Zeus45]

Did I read the study you posted that had MENT and test combined? How does that prove that MENT replaces DHT?

EDIT: to be clear, I’m not saying you’re wrong, but so far there is no evidence that shows what you’re saying is correct.

No evidence? "ten times more potent than testosterone and dihydrotestoterone in activating of AR-driven gene expression."

Is that not evidence for Trestolone being a more potent androgen than DHT? The entire point of MENT is to replace testosterone INCLUDING DHT.

 

[Rido]

No evidence? "ten times more potent than testosterone and dihydrotestoterone in activating of AR-driven gene expression."

Is that not evidence for Trestolone being a more potent androgen than DHT? The entire point of MENT is to replace testosterone INCLUDING DHT.

no one is saying it is not a potent androgen. DHT does serve other functions. Jesus Christ.



you are also quoting studies that are not long enough to establish it is a TRT replacement. There was nothing done on a substantial period of time.

How long until you have a full HPTA shutdown? 6 weeks?

 

[Zeus45]

no one is saying it is not a potent androgen. it serves other functions. Jesus Christ.

Serves other functions... that can be replaced by Trestolone.

7alpha-methyl-19-nortestosterone, a synthetic androgen with high potency: structure-activity comparisons with other androgens - PubMed

MENT was found to be the most potent followed by DHT, 19-NT, T, and CNNT.

 

[Rido]

Serves other functions... that can be replaced by Trestolone.
Steroid Forum
7alpha-methyl-19-nortestosterone, a synthetic androgen with high potency: structure-activity comparisons with other androgens - PubMed

MENT was found to be the most potent followed by DHT, 19-NT, T, and CNNT.

whatever dude

 

[Type-IIx]

Serves other functions... that can be replaced by Trestolone.

7alpha-methyl-19-nortestosterone, a synthetic androgen with high potency: structure-activity comparisons with other androgens - PubMed

MENT was found to be the most potent followed by DHT, 19-NT, T, and CNNT.

Rather than demonstrating that AAS can both exert androgenic effects in all androgen-sensitive tissues, and that their relative effects in any tissue depend upon their relative concentrations and potency, this data rather supports a model wherein testosterone's conversion to DHT is not obligatory, but amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone.
Bhasin S, Travison TG, Storer TW, Lakshman K, Kaushik M, Mazer NA, Ngyuen AH, Davda MN, Jara H, Aakil A, Anderson S, Knapp PE, Hanka S, Mohammed N, Daou P, Miciek R, Ulloor J, Zhang A, Brooks B, Orwoll K, Hede-Brierley L, Eder R, Elmi A, Bhasin G, Collins L, Singh R, Basaria S. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012 Mar 7;307(9):931-9. doi: 10.1001/jama.2012.227.

Without 5α-reductase function, MENT will never satisfactorily replace T when doses used abolish endogenous T (as will always happen in practical use for anabolic effects, because nobody cares whether MENT can suffice as a male contraceptive/androgen replacement at very low doses).

This is because MENT cannot exert androgenic effects in all androgen-sensitive tissues, and because its relative effects in androgen-sensitive human male sex & nervous tissue (expressing 5α-reductase) does not depend upon its systemic concentrations and potency. Rather, because it does not have any 5α-reductase function, it cannot (without at least basal T secretion) confer sexual function.

 

[theotherguy]

No evidence? "ten times more potent than testosterone and dihydrotestoterone in activating of AR-driven gene expression."

Is that not evidence for Trestolone being a more potent androgen than DHT? The entire point of MENT is to replace testosterone INCLUDING DHT.

Rather than demonstrating that AAS can both exert androgenic effects in all androgen-sensitive tissues, and that their relative effects in any tissue depend upon their relative concentrations and potency, this data rather supports a model wherein testosterone's conversion to DHT is not obligatory, but amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone.
Bhasin S, Travison TG, Storer TW, Lakshman K, Kaushik M, Mazer NA, Ngyuen AH, Davda MN, Jara H, Aakil A, Anderson S, Knapp PE, Hanka S, Mohammed N, Daou P, Miciek R, Ulloor J, Zhang A, Brooks B, Orwoll K, Hede-Brierley L, Eder R, Elmi A, Bhasin G, Collins L, Singh R, Basaria S. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012 Mar 7;307(9):931-9. doi: 10.1001/jama.2012.227.

Without 5α-reductase function, MENT will never satisfactorily replace T when doses used abolish endogenous T (as will always happen in practical use for anabolic effects, because nobody cares whether MENT can suffice as a male contraceptive/androgen replacement at very low doses).

This is because MENT cannot exert androgenic effects in all androgen-sensitive tissues, and because its relative effects in androgen-sensitive human male sex & nervous tissue (expressing 5α-reductase) does not depend upon its systemic concentrations and potency. Rather, because it does not have any 5α-reductase function, it cannot (without at least basal T secretion) confer sexual function.

@Type-IIx is too smart for his own good sometimes lol. I think I can say this in a simpler way and hopefully he’ll correct me if I’m inaccurate, or has a better analogy.

Hormones (among many other things) are like keys and the receptors are like keyholes. The key has to fit the lock in order to activate it. Some keys work on multiple locks and some locks can take multiple keys, but there is no universal key.

MENT can replace SOME functions of test and DHT but not ALL functions. Just because it is a powerful androgen does not make it a master key for all tissues requiring DHT or test.

So yes, you still have no evidence that MENT only is sufficient long term.

I appreciate a good, constructive debate that leads to answers and resolution, and frankly, I appreciate your thought process, but it’s still missing the key function of DHT

 

[Zeus45]

Rather than demonstrating that AAS can both exert androgenic effects in all androgen-sensitive tissues, and that their relative effects in any tissue depend upon their relative concentrations and potency, this data rather supports a model wherein testosterone's conversion to DHT is not obligatory, but amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone.
Bhasin S, Travison TG, Storer TW, Lakshman K, Kaushik M, Mazer NA, Ngyuen AH, Davda MN, Jara H, Aakil A, Anderson S, Knapp PE, Hanka S, Mohammed N, Daou P, Miciek R, Ulloor J, Zhang A, Brooks B, Orwoll K, Hede-Brierley L, Eder R, Elmi A, Bhasin G, Collins L, Singh R, Basaria S. Effect of testosterone supplementation with and without a dual 5α-reductase inhibitor on fat-free mass in men with suppressed testosterone production: a randomized controlled trial. JAMA. 2012 Mar 7;307(9):931-9. doi: 10.1001/jama.2012.227.

Without 5α-reductase function, MENT will never satisfactorily replace T when doses used abolish endogenous T (as will always happen in practical use for anabolic effects, because nobody cares whether MENT can suffice as a male contraceptive/androgen replacement at very low doses).

This is because MENT cannot exert androgenic effects in all androgen-sensitive tissues, and because its relative effects in androgen-sensitive human male sex & nervous tissue (expressing 5α-reductase) does not depend upon its systemic concentrations and potency. Rather, because it does not have any 5α-reductase function, it cannot (without at least basal T secretion) confer sexual function.

Then explain people running Nandrolone only cylces claiming to be functioning sexually? Based on your logic using any other androgen without T will lead to sexual dysfunction? What about all the Dbol that was perscribed for HRT?

Why don't you try Trestolone and get back to me, instead of speaking on something you never tried. Plenty of people have reported MENT working well without T.

 

[Type-IIx]

Then explain people running Nandrolone only cylces claiming to be functioning sexually? Based on your logic using any other androgen without T will lead to sexual dysfunction? What about all the Dbol that was perscribed for HRT?

Why don't you try Trestolone and get back to me, instead of speaking on something you never tried. Plenty of people have reported MENT working well without T.

No, based on my logic (and in accordance with clinical & practical use, including experience of bodybuilders) besides testosterone, fluoxymesterone (Halo), methandienone (Dianabol; 10 mg daily provides ~replacement T sexual functioning), and hell, even nandrolone (Deca/NPP is 5α-reduced to DHN, a weakened androgen, but that can still provide 5α-reductase function at appropriate doses), all function as 5α-reducible (or 5α/5β-reducible) androgens approprate to support sexual function. Halo in particular is used specifically for this therapeutically, it is used not only for hypogonadism but also in delayed or disrupted puberty.

I have yet to see an unbiased source report MENT adequately supported sexual function (anyone besides /r/steroids mods & you, actually) with solo use at anabolic (e.g., bodybuilding) doses. I have seen ample evidence of the opposite.

 

[Type-IIx]

No, based on my logic (and in accordance with clinical & practical use, including experience of bodybuilders) besides testosterone, fluoxymesterone (Halo), methandienone (Dianabol; 10 mg daily provides ~replacement T sexual functioning), and hell, even nandrolone (Deca/NPP is 5α-reduced to DHN, a weakened androgen, but that can still provide 5α-reductase function at appropriate doses), all function as 5α-reducible (or 5α/5β-reducible) androgens approprate to support sexual function. Halo in particular is used specifically for this therapeutically, it is used not only for hypogonadism but also in delayed or disrupted puberty.

I have yet to see an unbiased source report MENT adequately supported sexual function (anyone besides /r/steroids mods & you, actually) with solo use at anabolic (e.g., bodybuilding) doses. I have seen ample evidence of the opposite.

P.S., @Zeus45 - are you aware of why nandrolone (Deca/NPP) is the drug of choice rather than testosterone for men with HIV wasting?

It's because it kills libido and sexual function at anabolic doses sufficient to prevent catabolism (lower than bodybuilding doses). It's to prevent spread of disease.