Normally, an inadequate testosterone level causes undesirable effects such as fatigue, loss of skeletal muscle mass, reduced libido, and weight gain. However, the androgenic and anabolic properties of trestolone largely ameliorate this problem— essentially, trestolone replaces testosterone's role as the primary male hormone in the body.
MESO-Rx
Anabolic Steroids
TREST/MENT without a test base?
- Thread starter Jpmerr2021
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Normally, an inadequate testosterone level causes undesirable effects such as fatigue, loss of skeletal muscle mass, reduced libido, and weight gain. However, the androgenic and anabolic properties of trestolone largely ameliorate this problem— essentially, trestolone replaces testosterone's role as the primary male hormone in the body.
Rido
Subscriber
So have you had trestelone replacement therapy? Where are you coming up with this information? Have you conducted a study where they gave people adequate amount of trestelone?
In a 1992 study in rats investigating the pharmacology of MENT, researchers found the anabolic potency of MENT to be 10× greater than Testosterone, while also being 12× more suppressive to the HTPA. The average male produces 4-7mg of testosterone daily to keep muscle mass and sexual function, so 400-700mcg of MENT daily (10× less) is sufficient to produce the same results. A clinical contraceptive study employed doses of one, two and four patches that released 400mcg per day each, for an effective daily dose of 400mcg, 800mcg, and 1600mcg (1.6mg). Clinical studies ranging from 400-700mcg on up to 1-2mg found a close approximation to TRT dose. Given the lack of side effects or negative impact on bloodwork, some bodybuilders have opted to follow an “enhanced” cruise protocol of 5-10mg/day—technically a blast and not a true cruise at all, yet yielding enhanced strength and recovery with minimal impact on measurable markers.
more on trestolone vs TRT
The synthetic steroid 7alpha-methyl-19-nortestosterone (MENT) is a potent androgen that is resistant to 5alpha-reductase. It thus has decreased activity at the prostate and may have advantages over testosterone-based regimens in long term treatment or as part of a male contraceptive. Administration to eugonadal men results in suppression of gonadotropins, but its ability to support androgen-dependent behavior has not been investigated. For sustained release administration, MENT acetate was used, because its diffusion characteristics were more suitable for use in implants. However, upon release the acetate is rapidly hydrolyzed, and MENT is the biologically active moiety in circulation. We studied the effects of MENT on sexual interest and activity, spontaneous erection, and mood states in comparison with testosterone enanthate (TE) in 20 Caucasian and Chinese hypogonadal men recruited in Edinburgh and Hong Kong (n = 10 in each center). Outcomes were measured using a combination of daily diaries, semistructured interviews, and questionnaires. Nocturnal penile tumescence (NPT) was also recorded in the Edinburgh group. After withdrawal of androgen replacement treatment (wash-out phase) for a minimum of 6 weeks, subjects were randomized to two groups in a cross-over design. Drug treatment regimens were of 6-week duration and consisted of two implants, each containing 115 mg MENT acetate, inserted s.c. into the upper arm and removed after 6 weeks and two injections of TE (200 mg, i.m.) 3 weeks apart. MENT treatment resulted in stable plasma MENT concentrations of 1.4 +/- 0.1 nmol/L after 3 weeks and 1.3 +/- 0.1 nmol/L after 6 weeks (mean +/- SEM; all men). Nadir testosterone concentrations were 3.6 +/- 0.6 nmol/L at the end of the wash-out phase and 9.4 +/- 0.6 nmol/L 3 weeks after each injection. There were no differences in hormone concentrations between centers. There were no adverse toxicological effects. There were only minor differences between the two treatments. Both MENT and TE treatment resulted in significant increases in sexual interest and activity, spontaneous erection (both by self-report and NPT measurement), and increases in positive moods, with decreases in negative moods in the Edinburgh group. In the Hong Kong group, both treatments increased waking erection, with a trend toward increased sexual interest and activity. Mood states appeared to be less affected during the wash-out phase than in Edinburgh men and showed no significant response to either treatment. These results demonstrate that MENT has similar effects on sexual activity and mood states as testosterone in hypogonadal men. As NPT is a physiological androgen-dependant outcome, these data provide further evidence for the androgenicity of MENT. The lack of detected effect of either androgen in Hong Kong men other than on waking erection illustrates the importance of the cultural context of symptomatology and its measurement. The appropriate dose of MENT remains to be determined, but these results support its development as a potential androgen replacement therapy.
The synthetic steroid 7alpha-methyl-19-nortestosterone (MENT) is a potent androgen that is resistant to 5alpha-reductase. It thus has decreased activity at the prostate and may have advantages over testosterone-based regimens in long term treatment or as part of a male contraceptive. Administration to eugonadal men results in suppression of gonadotropins, but its ability to support androgen-dependent behavior has not been investigated. For sustained release administration, MENT acetate was used, because its diffusion characteristics were more suitable for use in implants. However, upon release the acetate is rapidly hydrolyzed, and MENT is the biologically active moiety in circulation. We studied the effects of MENT on sexual interest and activity, spontaneous erection, and mood states in comparison with testosterone enanthate (TE) in 20 Caucasian and Chinese hypogonadal men recruited in Edinburgh and Hong Kong (n = 10 in each center). Outcomes were measured using a combination of daily diaries, semistructured interviews, and questionnaires. Nocturnal penile tumescence (NPT) was also recorded in the Edinburgh group. After withdrawal of androgen replacement treatment (wash-out phase) for a minimum of 6 weeks, subjects were randomized to two groups in a cross-over design. Drug treatment regimens were of 6-week duration and consisted of two implants, each containing 115 mg MENT acetate, inserted s.c. into the upper arm and removed after 6 weeks and two injections of TE (200 mg, i.m.) 3 weeks apart. MENT treatment resulted in stable plasma MENT concentrations of 1.4 +/- 0.1 nmol/L after 3 weeks and 1.3 +/- 0.1 nmol/L after 6 weeks (mean +/- SEM; all men). Nadir testosterone concentrations were 3.6 +/- 0.6 nmol/L at the end of the wash-out phase and 9.4 +/- 0.6 nmol/L 3 weeks after each injection. There were no differences in hormone concentrations between centers. There were no adverse toxicological effects. There were only minor differences between the two treatments. Both MENT and TE treatment resulted in significant increases in sexual interest and activity, spontaneous erection (both by self-report and NPT measurement), and increases in positive moods, with decreases in negative moods in the Edinburgh group. In the Hong Kong group, both treatments increased waking erection, with a trend toward increased sexual interest and activity. Mood states appeared to be less affected during the wash-out phase than in Edinburgh men and showed no significant response to either treatment. These results demonstrate that MENT has similar effects on sexual activity and mood states as testosterone in hypogonadal men. As NPT is a physiological androgen-dependant outcome, these data provide further evidence for the androgenicity of MENT. The lack of detected effect of either androgen in Hong Kong men other than on waking erection illustrates the importance of the cultural context of symptomatology and its measurement. The appropriate dose of MENT remains to be determined, but these results support its development as a potential androgen replacement therapy.
Rido
Subscriber
Cool you linked the abstract. Seems like you have it all figured out.
You think a 20 subject, 6 week study is good enough to determine if it's good as a TRT?
Type-IIx
Member
I'd like to read this study, if you could please share the citation.
Rido
Subscriber
7α-Methyl-19-Nortestosterone Maintains Sexual Behavior and Mood in Hypogonadal Men*
Abstract. The synthetic steroid 7α-methyl-19-nortestosterone (MENT) is a potent androgen that is resistant to 5α-reductase. It thus has decreased activity
academic.oup.com
I don't like care for the layout
lukiss96
Member
It seems so strange that some people are very hesistant to use Testosterone, but even if they can't handle the usual 500mg or so, they can use it in lower amounts like say 250mg/week. Also if they are really poor responders and prone to every side effect then 150mg as a generous dose of TRT should work. Add in something on top of your preference and you have got a decent cycle. By the way 200-300mg/week is a moderate amount that I find doesn't cause too much water retention/bloat.
theotherguy
Member
What am I missing here? Didn't @Zeus45 say that test isn't needed with trest? This study he quoted and you posted has subjects using both combined...7α-Methyl-19-Nortestosterone Maintains Sexual Behavior and Mood in Hypogonadal Men*
Abstract. The synthetic steroid 7α-methyl-19-nortestosterone (MENT) is a potent androgen that is resistant to 5α-reductase. It thus has decreased activity
I don't like care for the layout
Rido
Subscriber
I was a little confused about his argument too...
I dont know if he actually read the study.
even then, we know TE administrations of 3 weeks apart(shit even 2 weeks) is not ideal for hypogonadal symptom management.
I think he is just spouting off nonsense and linking to abstracts of the studies. This is one of the issues with so many people trying to interpret data and they do not know how to search for weaknesses of the study.
Last edited:
theotherguy
Member
My main argument against MENT only was about needing DHT, maybe those running the study realized the same thing? I’m not really sure as it doesn’t really seem to go into “why” test was also used (or I didn’t read deep enough into it).
Do hypogonadal symptoms arise from lack of test or DHT? Or both? I’m not knowledgeable enough to be able to determine all of this, but it does seem telling that the researchers used both
Both MENT and TE treatment resulted in significant increases in sexual interest and activity, spontaneous erection (both by self-report and NPT measurement), and increases in positive moods, with decreases in negative moods in the Edinburgh group. In the Hong Kong group, both treatments increased waking erection, with a trend toward increased sexual interest and activity. Mood states appeared to be less affected during the wash-out phase than in Edinburgh men and showed no significant response to either treatment. These results demonstrate that MENT has similar effects on sexual activity and mood states as testosterone in hypogonadal men.
Have you used Trestolone? It's a very. potent androgen. Much more androgenic than testosterone.
lukiss96
Member
So many scientists lately reinventing wheel lol...
Just stick to what works.
Just stick to what works.
In conclusion, these results demonstrate that MENT is able to provide physiological and behavioral androgen replacement in hypogonadal men. MENT was demonstrated to have effects on two groups of hypogonadal men from different ethnic backgrounds, confirming the validity of the data. There were only minor differences between the responses to MENT and to conventional testosterone replacement therapy using a range of outcome measures, but the appropriate dose for this or other clinical indications remains to be established. MENT may therefore provide effective replacement therapy with a degree of selectivity at different androgen-responsive sites.
theotherguy
Member
What are the long term effects of low/no DHT?
Rido
Subscriber
You are saying that trestelone replaces testosterone. There is nothing you linked that supports your statement.
Rido
Subscriber
Meant the argument from Zeus.
Yea I have no idea. The study layout and groups seem whack.
There are things more androgenic and anabolic than test right? But can't serve as a replacement...
theotherguy
Member
O no, I was with you 100%, I just didn't articulate what I was saying very clearly. We are on the same page
MysqlMan
Member
I've always read you don't need a test base with MENT.
I've run it before without and it actually improved my sex life (at 60+ years old).
I usuall;y nmeed Viagra, but not with MENT.
Type-IIx
Member
@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.
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.
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