MENT solo in lieu of TRT

[bigdaddyandfriends]

New member here, first post.

About a month ago, I began using it solo in lieu of TRT. It has advantages over testosterone - basically for a dose similarly androgenic to test, it is about 3x as anabolic. It converts via multiple pathways into estrogen, via aromatase as well as through an estrone intermediary, but is not subject to 5a-reductase so cannot convert to DHT. It also does not raise hematocrit and is more selective than test, at least at lower dosages, so is less likely to cause hair loss and BPH. It's also an ideal compound to 'blast and cruise' on... cruise <5mg/day, increasing up to 50mg/day for a blast.

The 7a-methylestradiol activates ER similarly to regular estradiol, but it is eliminated from the body more slowly so can accumulate resulting in estrogenic effects. So AI and/or SERM can be useful - particularly at higher dosages, in those also using test, or those with genetically high aromatase activity. It also activates progesterone receptors and therefore should be expected to increase prolactin in a dose-dependent manner; at all but high dosages, this is probably insignificant although I am taking Inhibit-P/P5P; at very high dosages, something stronger i.e. cabergoline or praxiprexole might be needed for some.

I'm currently injecting 20mg/day subQ (completely painless) in divided doses for a mini-blast. My adjuncts are Raloxifene 30mg/day for gyno prophylaxis, since 7a-methylestradiol cannot be measured via blood, and Aromasin 12.5mg EOD. I have neither excess water retention or elevation of BP, nor have I had any low E2 symptoms. My joints feel great and libido is improving. Over the past few weeks I have noticed a significant increase in muscle mass (+1 inch on my arms) and strength, with my weight remaining stable @ 200lbs... so it is working well, as intended, for body recomposition purposes.

Btw I'm a 54 year old physician (MD/radiologist) and have done extensive research on this compound.

 

[JackSkel]

How do you get by with zero DHT?

How is it determined to be 3x more anabolic?

 

[TexasT]

New member here, first post.

About a month ago, I began using it solo in lieu of TRT. It has advantages over testosterone - basically for a dose similarly androgenic to test, it is about 3x as anabolic. It converts via multiple pathways into estrogen, via aromatase as well as through an estrone intermediary, but is not subject to 5a-reductase so cannot convert to DHT. It also does not raise hematocrit and is more selective than test, at least at lower dosages, so is less likely to cause hair loss and BPH. It's also an ideal compound to 'blast and cruise' on... cruise <5mg/day, increasing up to 50mg/day for a blast.

The 7a-methylestradiol activates ER similarly to regular estradiol, but it is eliminated from the body more slowly so can accumulate resulting in estrogenic effects. So AI and/or SERM can be useful - particularly at higher dosages, in those also using test, or those with genetically high aromatase activity. It also activates progesterone receptors and therefore should be expected to increase prolactin in a dose-dependent manner; at all but high dosages, this is probably insignificant although I am taking Inhibit-P/P5P; at very high dosages, something stronger i.e. cabergoline or praxiprexole might be needed for some.

I'm currently injecting 20mg/day subQ (completely painless) in divided doses for a mini-blast. My adjuncts are Raloxifene 30mg/day for gyno prophylaxis, since 7a-methylestradiol cannot be measured via blood, and Aromasin 12.5mg EOD. I have neither excess water retention or elevation of BP, nor have I had any low E2 symptoms. My joints feel great and libido is improving. Over the past few weeks I have noticed a significant increase in muscle mass (+1 inch on my arms) and strength, with my weight remaining stable @ 200lbs... so it is working well, as intended, for body recomposition purposes.

Btw I'm a 54 year old physician (MD/radiologist) and have done extensive research on this compound.

Sounds like you’re running legit
MENT. Mind telling us the source so the members can bring them some new business? Thanks so much.

 

[revono]

New member here, first post.

About a month ago, I began using it solo in lieu of TRT. It has advantages over testosterone - basically for a dose similarly androgenic to test, it is about 3x as anabolic. It converts via multiple pathways into estrogen, via aromatase as well as through an estrone intermediary, but is not subject to 5a-reductase so cannot convert to DHT. It also does not raise hematocrit and is more selective than test, at least at lower dosages, so is less likely to cause hair loss and BPH. It's also an ideal compound to 'blast and cruise' on... cruise <5mg/day, increasing up to 50mg/day for a blast.

The 7a-methylestradiol activates ER similarly to regular estradiol, but it is eliminated from the body more slowly so can accumulate resulting in estrogenic effects. So AI and/or SERM can be useful - particularly at higher dosages, in those also using test, or those with genetically high aromatase activity. It also activates progesterone receptors and therefore should be expected to increase prolactin in a dose-dependent manner; at all but high dosages, this is probably insignificant although I am taking Inhibit-P/P5P; at very high dosages, something stronger i.e. cabergoline or praxiprexole might be needed for some.

I'm currently injecting 20mg/day subQ (completely painless) in divided doses for a mini-blast. My adjuncts are Raloxifene 30mg/day for gyno prophylaxis, since 7a-methylestradiol cannot be measured via blood, and Aromasin 12.5mg EOD. I have neither excess water retention or elevation of BP, nor have I had any low E2 symptoms. My joints feel great and libido is improving. Over the past few weeks I have noticed a significant increase in muscle mass (+1 inch on my arms) and strength, with my weight remaining stable @ 200lbs... so it is working well, as intended, for body recomposition purposes.

Btw I'm a 54 year old physician (MD/radiologist) and have done extensive research on this compound.

You have protected yourself from DHT, but what about Pitt's theory?

 

[Type-IIx]

Interesting. I'll refer back to this as a case where solo MENT ostensibly served as an adequate testosterone replacement then. I've been skeptical of this use given the lack of robustness of the data in supporting basal sexual function in men.

 

[JackSkel]

Interesting. I'll refer back to this as a case where solo MENT ostensibly served as an adequate testosterone replacement then. I've been skeptical of this use given the lack of robustness of the data in supporting basal sexual function in men.

I wouldn’t. It’s just one guy’s experience. A male needs at least a little DHT, there’s no bypassing that.

And 1-inch added to arms “in several weeks”. No difference in the scale.

Ment must be the magic formula.

 

[AbstractMind]

I wouldn’t. It’s just one guy’s experience. A male needs at least a little DHT, there’s no bypassing that.

That’s what I’m thinking too. If it hasn’t effect him yet, it will eventually

 

[Type-IIx]

I wouldn’t. It’s just one guy’s experience. A male needs at least a little DHT, there’s no bypassing that.

And 1-inch added to arms “in several weeks”. No difference in the scale.

Ment must be the magic formula.

That’s what I’m thinking too. If it hasn’t effect him yet, it will eventually

Believe me, I still regard the following as contrary evidence of greater weight:

2 of 13 (15%) MENT subjects withdrew after 8 weeks of treatment due to low libido & erectile dysfunction...Adverse events included reduced libido & erectile function in 4 *additional* subjects in the MENT group who completed treatment (6/13, or 46%) [these adverse effects were not reported by any subject in the testosterone group]...Due to the incidence of reports of low libido and early withdrawal in the MENT group, it was decided in consultation with the study Data Monitoring and Safety Committe to shorten the MENT treatment period to 24 weeks whereas men in the testosterone group completed 48 weeks of treatment. Walton, M. J., Kumar, N., Baird, D. T., Ludlow, H., & Anderson, R. A. (2007). 7 -Methyl-19-Nortestosterone (MENT) vs Testosterone in Combination With Etonogestrel Implants for Spermatogenic Suppression in Healthy Men. Journal of Andrology, 28(5), 679–688. doi:10.2164/jandrol.107.002683.

There are a few questionable statements contained in his post. I just don't want to disregard outright a quasi-case report like this based on such minor criticisms.

 

[JackSkel]

Believe me, I still regard the following as contrary evidence of greater weight:

2 of 13 (15%) MENT subjects withdrew after 8 weeks of treatment due to low libido & erectile dysfunction...Adverse events included reduced libido & erectile function in 4 *additional* subjects in the MENT group who completed treatment (6/13, or 46%) [these adverse effects were not reported by any subject in the testosterone group]...Due to the incidence of reports of low libido and early withdrawal in the MENT group, it was decided in consultation with the study Data Monitoring and Safety Committe to shorten the MENT treatment period to 24 weeks whereas men in the testosterone group completed 48 weeks of treatment. Walton, M. J., Kumar, N., Baird, D. T., Ludlow, H., & Anderson, R. A. (2007). 7 -Methyl-19-Nortestosterone (MENT) vs Testosterone in Combination With Etonogestrel Implants for Spermatogenic Suppression in Healthy Men. Journal of Andrology, 28(5), 679–688. doi:10.2164/jandrol.107.002683.

There are a few questionable statements contained in his post. I just don't want to disregard outright a quasi-case report like this based on such minor criticisms.

I may be being cynical but I strongly doubt that he’ll ever post again.

His post had a “commercial feel” to it and seemed to coincide with another post about ment.

 

[freakyjacked29]

Radiologist interesting would you ever have a look at mri scans if anyone showed you them ?

as many orthopaedic surgeons can’t read a mri correctly.

 

[bigdaddyandfriends]

I’m not sure DHT is truly necessary in conjunction with Trestolone, which is a a more potent androgen than even DHT. Remember DHT is just another ligand for the same androgen receptor, albeit a more potent one than testosterone.

That said, Epiandrosterone (oral) could certainly be used as a “DHT base” as it’s a prohormone converted in vivo to DHT. I have some on hand but have needed to use it yet. This method does reduce tissue specificity, however, which I suppose is good for the hairline, skin/acne, and prostate; but less good for the Johnson. I say this because normally DHT is formed from testosterone within tissues with high 5-aR expression ie skin and reproductive organs.

And yes I can read MRIs!

 

[bigdaddyandfriends]

I may be being cynical but I strongly doubt that he’ll ever post again.

His post had a “commercial feel” to it and seemed to coincide with another post about ment.

No I absolutely don’t sell anything. Just found MENT to be a very interesting compound once I began researching PEDs (which needless to say are not part of a med school pharmacology class).

If there was another post, it was coincidental.

 

[bigdaddyandfriends]

Believe me, I still regard the following as contrary evidence of greater weight:

2 of 13 (15%) MENT subjects withdrew after 8 weeks of treatment due to low libido & erectile dysfunction...Adverse events included reduced libido & erectile function in 4 *additional* subjects in the MENT group who completed treatment (6/13, or 46%) [these adverse effects were not reported by any subject in the testosterone group]...Due to the incidence of reports of low libido and early withdrawal in the MENT group, it was decided in consultation with the study Data Monitoring and Safety Committe to shorten the MENT treatment period to 24 weeks whereas men in the testosterone group completed 48 weeks of treatment. Walton, M. J., Kumar, N., Baird, D. T., Ludlow, H., & Anderson, R. A. (2007). 7 -Methyl-19-Nortestosterone (MENT) vs Testosterone in Combination With Etonogestrel Implants for Spermatogenic Suppression in Healthy Men. Journal of Andrology, 28(5), 679–688. doi:10.2164/jandrol.107.002683.

There are a few questionable statements contained in his post. I just don't want to disregard outright a quasi-case report like this based on such minor criticisms.

I've reviewed that, and pretty much all other articles on PubMed as well as reading Llewelyn's Anabolics and anecdotal reports on various forums, watching videos from knowledgable YT'ers for instance Drs. O'Connor (AnabolicDoc) & Nicholas Downey. I've also listened to bodybuilder YT's (ie Kai, Formula Sec INITIATED) experiences with it at significantly higher doses exceeding 350mg/week.

Keep in mind that in the report you cited, extremely low dosages were used i.e. 0.4-0.8mg/day, and as implanted pellets rather than daily injections; at that amount I don't believe trestolone would provide enough 7a-methylestradiol to maintain libido and other functions, and maybe not enough androgenic effect to compensate for absent DHT. A more realistic "TRT" dose, I believe, is 2-5mg/day. Remember it is generally considered to be 10x as potent as testosterone, so 2mg/day equates to ~140mg/week test. After my mini-blast is completed, I will taper the dose down into that range, until I feel like it is insufficient than raise it slightly for potential long term use. My first week was at 5mg/day and I felt good on it, although I clearly had residual testosterone/DHT/estrogen in my system at that point.

As of yesterday, I increased to 24mg/day Trest Ace which is the maximum dose I'm willing to take at my age. I can elaborate on my personal experience with estrogenic effects of trestolone, if anyone is interested; they seem very easy to control, at least in the absence of additional testosterone.

 

[Country Club Hero]

I did this experiment a few months ago after researching. But I was only using between 2-5mg daily of Trest Acetate. I felt great on it but it turned on the oil glands in my skin like I was a 15 year old, greasy teenager.

That was pretty much the only negative I encountered after almost 2 months. But it was just too much for me to stick with.

 

[Iron_Yuppie]

A male needs at least a little DHT, there’s no bypassing that.

I used it solo at a very low dose for almost eight months as trt and never once missed DHT. It seems to be androgenic enough that the lack of conversion to DHT is merely an afterthought.

 

[bigdaddyandfriends]

I did this experiment a few months ago after researching. But I was only using between 2-5mg daily of Trest Acetate. I felt great on it but it turned on the oil glands in my skin like I was a 15 year old, greasy teenager.

That was pretty much the only negative I encountered after almost 2 months. But it was just too much for me to stick with.

I have noticed my skin being a bit more oily too, particularly as I've ramped up the dosage to 24mg/day. But it's kind of dry normally and have not had any acne issues, so just monitoring it for now.

 

[demon]

M

I have noticed my skin being a bit more oily too, particularly as I've ramped up the dosage to 24mg/day. But it's kind of dry normally and have not had any acne issues, so just monitoring it for now.

very interesting. Please keep us update on your progress. Being older, I’ve been reading as much as I can about trest as well!

 

[Type-IIx]

I've reviewed that, and pretty much all other articles on PubMed as well as reading Llewelyn's Anabolics and anecdotal reports on various forums, watching videos from knowledgable YT'ers for instance Drs. O'Connor (AnabolicDoc) & Nicholas Downey. I've also listened to bodybuilder YT's (ie Kai, Formula Sec INITIATED) experiences with it at significantly higher doses exceeding 350mg/week.

Not familiar with the YTers, but I appreciate that you've been scouring everything on the topic on PubMed, as have I.

Keep in mind that in the report you cited, extremely low dosages were used i.e. 0.4-0.8mg/day, and as implanted pellets rather than daily injections; at that amount I don't believe trestolone would provide enough 7a-methylestradiol to maintain libido and other functions, and maybe not enough androgenic effect to compensate for absent DHT.

I've had this thought myself plenty. It's why I remember without even looking back at your OP that you've been using 20 mg/d s.c. Important.

A more realistic "TRT" dose, I believe, is 2-5mg/day. Remember it is generally considered to be 10x as potent as testosterone, so 2mg/day equates to ~140mg/week test.

Maybe, have you read my MENT profile? See: MENT Profile. Therein, I share (first portion) a detailed Q&A with a guy that I trust, as well as put the reader on notice that I do hold some preconceptions with respect to MENT, with respect to its utility for those that cycle off and that admittedly too includes a tendency towards assuming, at best, that its androgenicity sufficient for replacement in man is unknown. While I believe that I am capable of setting aside my preconceptions & assumptions readily when new data presents (at least I think I am more capable than most at this), I'm human.

I've since added some data, I think some nuclear retention data comparing it to some trienes and the like.

After my mini-blast is completed, I will taper the dose down into that range, until I feel like it is insufficient than raise it slightly for potential long term use. My first week was at 5mg/day and I felt good on it,

I'd really be fascinated to see what you report after 24 weeks at 5 mg/d if that's something you can do - or at least after conclusion of something like 16 weeks. You can probably see why (if we use the Walton, et al. as reference, 24 weeks was what they shortened the MENT treatment group to whereas the TE group continued for 48).

although I clearly had residual testosterone/DHT/estrogen in my system at that point.

Right, this is a problem that's seen with many studies - the s.c. testosterone studies showing its adequacy with nonspecialized formulations like Xyosted come to mind - that did not have any washout, but crossover designs A/B where the s.c. arm followed the i.m. arm. We have to apply an appropriate degree of parsimony; some might even fairly argue to disregard the findings outright.

As of yesterday, I increased to 24mg/day Trest Ace which is the maximum dose I'm willing to take at my age. I can elaborate on my personal experience with estrogenic effects of trestolone, if anyone is interested; they seem very easy to control, at least in the absence of additional testosterone.

Sure, I am interested in your dosing and frequency of, was it exemestane and a SERM?

 

[Country Club Hero]

I have noticed my skin being a bit more oily too, particularly as I've ramped up the dosage to 24mg/day. But it's kind of dry normally and have not had any acne issues, so just monitoring it for now.

Yeah it’s a nightmare for someone with already oily skin.

 

[bigdaddyandfriends]

Not familiar with the YTers, but I appreciate that you've been scouring everything on the topic on PubMed, as have I.

I've had this thought myself plenty. It's why I remember without even looking back at your OP that you've been using 20 mg/d s.c. Important.

Maybe, have you read my MENT profile? See: MENT Profile. Therein, I share (first portion) a detailed Q&A with a guy that I trust, as well as put the reader on notice that I do hold some preconceptions with respect to MENT, with respect to its utility for those that cycle off and that admittedly too includes a tendency towards assuming, at best, that its androgenicity sufficient for replacement in man is unknown. While I believe that I am capable of setting aside my preconceptions & assumptions readily when new data presents (at least I think I am more capable than most at this), I'm human.

I've since added some data, I think some nuclear retention data comparing it to some trienes and the like.

I'd really be fascinated to see what you report after 24 weeks at 5 mg/d if that's something you can do - or at least after conclusion of something like 16 weeks. You can probably see why (if we use the Walton, et al. as reference, 24 weeks was what they shortened the MENT treatment group to whereas the TE group continued for 48).

Right, this is a problem that's seen with many studies - the s.c. testosterone studies showing its adequacy with nonspecialized formulations like Xyosted come to mind - that did not have any washout, but crossover designs A/B where the s.c. arm followed the i.m. arm. We have to apply an appropriate degree of parsimony; some might even fairly argue to disregard the findings outright.

Sure, I am interested in your dosing and frequency of, was it exemestane and a SERM?

I have read your post and there is a wealth of information in it! You've clearly done your research. Thank you.

I've been pretty aggressive with AI/SERM use after the first week @ 5mg/day, which was both a trial and antidote for crashed E2 (after adding YK11 to a RAD140/enclo cycle). I guess it is working, since I have zero gyno, blood pressure is stable/normal, and I have not accumulated excess water weight. I should mention that my baseline blood pressure is high, and I take Edarbi/azilsartin plus Carditone (basically reserpine) to keep it on the lower side. This is my estrogen control regimen:

SERM: Raloxifene 30mg/day, once a day as half life is long
AI: Aromasin, currently running 20mg/day in divided doses
Supplements: I3C (400mg / SNS Inhibit-E) + DIM (300mg/day)

With trestolone ace I've continued the YK11, which is a very interesting compound. While it's considered and sold as a SARM, it has a 19-nor structure and is a partial rather than full agonist of the AR. At least as an injectable, its effect seems more akin to a DHT-derived AAS - very dry and with an anti-estrogen effect. I had minimal signs of suppression with my prior attempted RAD140+enclo SARM/SERM cycle, but crashed my E2 almost immediately after adding 10mg/day of YK11. I would prefer to use something like Primobolan instead, being much better researched, but don't have a source, unfortunately.

I'm currently injecting 12.5mg trest ace + 5mg YK11 twice daily. Injections are painless/subQ so higher frequency and subQ absorption is slower than IM, so I felt this should minimize spikes in aromatizable androgen.

Also I'm almost certainly 100% suppressed at this point, the 'boys' went from big on enclo to raisins now, so there is likely nearly zero testosterone in my body, save for whatever my adrenals make. I think the E2 issues many experience with this compound are greatly exacerbated by concurrent use of testosterone and/or other AAS that aromatize.

I anticipate eliminating the estrogen control once I reduce my dose to < 5mg/day as "TRT". I'll see how that goes for a few months, check bloods, then can blast again for 8-12 weeks, if I want to - which I likely will!

I do wish there was a blood test for 7a-methylestradiol, it would make management much more straightforward. Without it, just need to make on the fly adjustments based on judgment and symptoms.

Note: I also think trestolone may convert directly into estrone, probably in the liver, which can then metabolize into estradiol... I'm still trying to figure that pathway out.