MENT, gyno, dialing in E2 with estradiol... or something better?

[Type-IIx]

MENT AND ITS AROMATIC PRODUCT THAT IS STRONGER THAN E2 (BY A LOT)
by Type-IIx

An influential poster, possible the admin/wiki author on a related subreddit seems to be deliberately misrepresenting MENT and just generally putting out a deluge of incredibly wrong information in a highly confident manner. That’s not THAT bad, but it seems that wiki is read by a majority of the guys here.

I’m seeing guys taking estradiol pills to dial in E2, I’m seeing guys that think MENT is barely suppressive because of research where pellets were defective or broke and IV injections into monkeys.

Without actually posting his flagrant misrepresentations, I want to use the paper this decatest claimed as support (which I had to dig a bit to find), although it’s being cited as “research” (in actuality an imgur link to a deceptive Table from this study).

So, let’s look a bit at MENT! It’s not a bad compound at all, provided that it is understood. The problem is that it is being claimed, with a great deal of intentional misrepresentation I believe, that it doesn’t cause gyno or estrogenic effects. And it definitely does.



MENT's aromatic product (7α-methylestradiol; 7α-ME) is 4x(!) as potent (technically "efficacious," its being a bad thing here) in ER-containing cells [1]. Efficacy is determined by measuring the effect, e.g., growth (here, in breast cancer cells). The EC₅₀ (EC50) is determined by the concentrations at which the ligand triggers growth. This may be confirmed by measurements of cell cycle progression (i.e., the S-phase entry during the cell cycle).

The binding affinity (IC₅₀) of MENT's aromatic product (7α-methylestradiol) is 102% that of estradiol[1], which is noteworthy as E2 is typically used as the reference compound for ER binding given its particularly high efficacy, potency, and affinity for the ERα receptor, in the literature.

Given the findings of Attardi et al, in comparing the rate of aromatization between MENT and nandrolone, that "At 180 min, about 23% of MENT was converted to 7α-ME and about 13% of 19-NT to E2," knowing that nandrolone [19-NT] aromatizes at 20% the rate of Test [2], we can deduce that MENT aromatizes at roughly 35% the rate of Test... to 7α-ME (an aromatic product with four-fold E2's “potency” for causing growth in breast cancer cells). Simple multiplication of the rate of aromatization (35%) * EC50(7α-methylestradiol) * RBA(7α-methylestradiol) ≈

MENT has a roughly 40% greater growth potential in ER-containing cells than T.

This would certainly seem to support the anecdotes that MENT is quite a potent gynecomastic agent.

PRACTICAL

With consideration of the real world, if the MENT dosage is ~70% the Test dosage, it's on par with the estrogenicity of T, and given the aromatization of MENT to 7α-ME rather than E2, this consequence is unlikely to be reflected in bloodwork results. By way of comparison: 35mg daily of MENT E ≈ as estrogenic as 350mg of Test E weekly.

And MENT does also has progestational activity to take into consideration.

DIALING IN E2 WITH PRECISION

Since it is the androgen-to-estrogen ratio that primarily determines the severity/experience of gyno [3][4], it makes a lot of sense to “dial in” E2 with an androgen rather than a female hormone.

Here, I provide the "Type-IIx continuum of aromatization":

Ment (140% aromatization of Test) > Test > Adrol > Dbol >> Deca (20% of Test)

Back in the day, it was common for guys to pop a Dbol to keep their E2 up on deca/dbol cycles. Guys used to cycle off and on, because they could, because they weren’t acutely nor chronically suppressed (once the decanoate ester cleared, after 4.5 half lives or so), believe it or not, with these compounds. That’s right, "19-nors" are not particularly suppressive as a class. Quite the opposite. But MENT kind of is, because of its aromatic product.

REFERENCES
[1] Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR. Dimethandrolone (7alpha,11beta-dimethyl-19-nortestosterone) and 11beta-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase. J Steroid Biochem Mol Biol. 2008;110(3-5):214-222.
[2] Ryan, Kenneth J. “Biological aromatization of steroids.” Journal of Biological Chemistry 234.2 (1959): 268-272.
[3] Bond, Peter. Book on Steroids. (2020). PeterBond.org.
[4] Vanderschueren D, Vandenput L, Boonen S, Lindberg MK, Bouillon R, Ohlsson C. Androgens and bone. Endocr Rev. 2004 Jun;25(3):389-425. doi: 10.1210/er.2003-0003. PMID: 15180950.

 

[PeterBond]

Since it is the androgen-to-estrogen ratio that primarily determines the severity/experience of gyno [3][4],

Do note that I write the following with regard to high dosages:

A decreased androgen to estrogen ratio is therefore unlikely with the usage of testosterone in high dosages. If, therefore, someone develops gynecomastia on such a cycle, it seems only reasonable to assume it’s the absolute excess of estrogen.

Keep in mind that you also need to consider the rate of breakdown of the produced 7a-methylestradiol, as well as the estrogenic potency of the resulting metabolites. (The rate of 7a-methylestradiol formation wasn't determined in a breast cell, so further metabolism wasn't taken into account.)

 

[Type-IIx]

Do note that I write the following with regard to high dosages:


Keep in mind that you also need to consider the rate of breakdown of the produced 7a-methylestradiol, as well as the estrogenic potency of the resulting metabolites. (The rate of 7a-methylestradiol formation wasn't determined in a breast cell, so further metabolism wasn't taken into account.)

You're right of course. Is enough known about its metabolic pathway to meaningfully characterize 7alpha-methylestradiol versus E2? I feel it's important that people know an AI is an effective deterrent, that MENT is highly estrogenic, the relative aromatization potencies of these compounds (I believe it's fair to say) fall into a continuum with: MENT > Test > Adrol > Dbol >> Deca, and that the E2 sensitive LC/MS bloodwork will not reflect MENT's estrogenic potency. This [link] is the sort of thing that's being said by that apparent wiki author/admin.

 

[sakuraba126]

MENT AND ITS AROMATIC PRODUCT THAT IS STRONGER THAN E2 (BY A LOT)
by Type-IIx

An influential poster, possible the admin/wiki author on a related subreddit seems to be deliberately misrepresenting MENT and just generally putting out a deluge of incredibly wrong information in a highly confident manner. That’s not THAT bad, but it seems that wiki is read by a majority of the guys here.

I’m seeing guys taking estradiol pills to dial in E2, I’m seeing guys that think MENT is barely suppressive because of research where pellets were defective or broke and IV injections into monkeys.

Without actually posting his flagrant misrepresentations, I want to use the paper this decatest claimed as support (which I had to dig a bit to find), although it’s being cited as “research” (in actuality an imgur link to a deceptive Table from this study).

So, let’s look a bit at MENT! It’s not a bad compound at all, provided that it is understood. The problem is that it is being claimed, with a great deal of intentional misrepresentation I believe, that it doesn’t cause gyno or estrogenic effects. And it definitely does.

View attachment 155294

MENT's aromatic product (7α-methylestradiol; 7α-ME) is 4x(!) as potent (technically "efficacious," its being a bad thing here) in ER-containing cells [1]. Efficacy is determined by measuring the effect, e.g., growth (here, in breast cancer cells). The EC₅₀ (EC50) is determined by the concentrations at which the ligand triggers growth. This may be confirmed by measurements of cell cycle progression (i.e., the S-phase entry during the cell cycle).

The binding affinity (IC₅₀) of MENT's aromatic product (7α-methylestradiol) is 102% that of estradiol[1], which is noteworthy as E2 is typically used as the reference compound for ER binding given its particularly high efficacy, potency, and affinity for the ERα receptor, in the literature.

Given the findings of Attardi et al, in comparing the rate of aromatization between MENT and nandrolone, that "At 180 min, about 23% of MENT was converted to 7α-ME and about 13% of 19-NT to E2," knowing that nandrolone [19-NT] aromatizes at 20% the rate of Test [2], we can deduce that MENT aromatizes at roughly 35% the rate of Test... to 7α-ME (an aromatic product with four-fold E2's “potency” for causing growth in breast cancer cells). Simple multiplication of the rate of aromatization (35%) * EC50(7α-methylestradiol) * RBA(7α-methylestradiol) ≈

MENT has a roughly 40% greater growth potential in ER-containing cells than T.

This would certainly seem to support the anecdotes that MENT is quite a potent gynecomastic agent.

PRACTICAL

With consideration of the real world, if the MENT dosage is ~70% the Test dosage, it's on par with the estrogenicity of T, and given the aromatization of MENT to 7α-ME rather than E2, this consequence is unlikely to be reflected in bloodwork results. By way of comparison: 35mg daily of MENT E ≈ as estrogenic as 350mg of Test E weekly.

And MENT does also has progestational activity to take into consideration.

DIALING IN E2 WITH PRECISION

Since it is the androgen-to-estrogen ratio that primarily determines the severity/experience of gyno [3][4], it makes a lot of sense to “dial in” E2 with an androgen rather than a female hormone.

Here, I provide the "Type-IIx continuum of aromatization":

Ment (140% aromatization of Test) > Test > Adrol > Dbol >> Deca (20% of Test)

Back in the day, it was common for guys to pop a Dbol to keep their E2 up on deca/dbol cycles. Guys used to cycle off and on, because they could, because they weren’t acutely nor chronically suppressed (once the decanoate ester cleared, after 4.5 half lives or so), believe it or not, with these compounds. That’s right, "19-nors" are not particularly suppressive as a class. Quite the opposite. But MENT kind of is, because of its aromatic product.

REFERENCES
[1] Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR. Dimethandrolone (7alpha,11beta-dimethyl-19-nortestosterone) and 11beta-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase. J Steroid Biochem Mol Biol. 2008;110(3-5):214-222.
[2] Ryan, Kenneth J. “Biological aromatization of steroids.” Journal of Biological Chemistry 234.2 (1959): 268-272.
[3] Bond, Peter. Book on Steroids. (2020). PeterBond.org.
[4] Vanderschueren D, Vandenput L, Boonen S, Lindberg MK, Bouillon R, Ohlsson C. Androgens and bone. Endocr Rev. 2004 Jun;25(3):389-425. doi: 10.1210/er.2003-0003. PMID: 15180950.

Could we perform a similar, rough calculation for dbol? Missing some variables... I don't understand where the 70% ment:test dosage comes from.
If memory serves, dbol aromatizes at roughly 50% the rate of test, but also to 7a(Me)estro...4x efficacy.
Original replacement dose of dbol was like 5 mg qd, 35 mg per week? Compared to true trt test at like 100 mg a week - so dosing is roughly 1/3 test? Think oral bioavailability is already accounted for there, so leaving that out.
50%(aromatization) , 4x (ch3-estro efficacy) , 3x (dosage) ....?
Fuck it . I'm out

 

[TRENdy07]

You're right of course. Is enough known about its metabolic pathway to meaningfully characterize 7alpha-methylestradiol versus E2? I feel it's important that people know an AI is an effective deterrent, that MENT is highly estrogenic, the relative aromatization potencies of these compounds (I believe it's fair to say) fall into a continuum with: MENT > Test > Adrol > Dbol >> Deca, and that the E2 sensitive LC/MS bloodwork will not reflect MENT's estrogenic potency. This [link] is the sort of thing that's being said by that apparent wiki author/admin.

So e2 can’t be measured by blood work while using ment?

 

[cmK9s33]

So e2 can’t be measured by blood work while using ment?

The 7a-ME-E2 is likely sufficiently different to escape being detected on a typical blood panel.

 

[99powerstroke]

Doesn’t MENT affect your prolactin?

 

[Type-IIx]

Could we perform a similar, rough calculation for dbol? Missing some variables... I don't understand where the 70% ment:test dosage comes from.
If memory serves, dbol aromatizes at roughly 50% the rate of test, but also to 7a(Me)estro...4x efficacy.
Original replacement dose of dbol was like 5 mg qd, 35 mg per week? Compared to true trt test at like 100 mg a week - so dosing is roughly 1/3 test? Think oral bioavailability is already accounted for there, so leaving that out.
50%(aromatization) , 4x (ch3-estro efficacy) , 3x (dosage) ....?
Fuck it . I'm out

It's possible but I'm not motivated to do it right now. Maybe forthcoming, but at present I don't have the two German language papers required (though I can likely acquire them) and I am disinclined to try to trudge through a language I cannot read and attempt to discern its meaning, assuming the chemistry notation is comprehensible, for no benefit. By the way, I doubt anyone has done this work at least within the last decade, and that a lot of the (if your memory in fact serves you correctly) oft repeated rates of aromatization with respect to 17a-methylestradiol from Dbol are simply made up like 90% of these factoids.

 

[TRENdy07]

The 7a-ME-E2 is likely sufficiently different to escape being detected on a typical blood panel.

So if this is the case, should you still aim to have normal e2 numbers while blasting primo? My plan was to keep test trt while blasting 25mg ment/day and 800 primo but would it be better to keep the test in abs just use nolva for gyno control?

 

[Type-IIx]

Doesn’t MENT affect your prolactin?

Elevated prolactin as a result of aromatizing androgens is best addressed with an AI, since estrogens (aromatic products) may cause hyperprolactinemia. The primary function by which prolactin causes secondary hypogonadism is by suppression of LH and FSH.

Androgens generally lower prolactin whereas estrogens (including the very potent aromatic product of MENT) can increase it.

 

[EatClen/TrenHard]

Elevated prolactin as a result of aromatizing androgens is best addressed with an AI, since estrogens (aromatic products) may cause hyperprolactinemia. The primary function by which prolactin causes secondary hypogonadism is by suppression of LH and FSH.

Androgens generally lower prolactin whereas estrogens (including the very potent aromatic product of MENT) can increase it.

do you think Nolvadex is a better SERM to use than an AI like aromasin/Arimidex to prevent gyno on MENT?

This is something Ironman would say, but to for a meathead to figure out how much Trest estrogenizes, how many mg of aromasin do I need a week on 500mg MENT compared to 500mg Test (25mg/week split into two). That's the real question here.
How many mg of

 

[Type-IIx]

do you think Nolvadex is a better SERM to use than an AI like aromasin/Arimidex to prevent gyno on MENT?

This is something Ironman would say, but to for a meathead to figure out how much Trest estrogenizes, how many mg of aromasin do I need a week on 500mg MENT compared to 500mg Test (25mg/week split into two). That's the real question here.
How many mg of

Theoretically, assuming dose-response is linear at this point (before increasing at a decreasing rate, inflection point in dose-response) you'd start with 35 mg weekly. I'd probably just round up to an even 50mg weekly and think that'll be just fine.

The truth, though, is that we don't know the difference in efficacy between Nolva & Aromasin with the resultant 7α-methylestradiol concentrations. I tend to prefer Aromasin to Nolva in terms of tolerability & I prefer keeping E2 levels within sane levels, but unfortunately, 7α-methylestradiol likely isn't detected by E2 ultrasensitive tests.

 

[EatClen/TrenHard]

Theoretically, assuming dose-response is linear at this point (before increasing at a decreasing rate, inflection point in dose-response) you'd start with 35 mg weekly. I'd probably just round up to an even 50mg weekly and think that'll be just fine.

The truth, though, is that we don't know the difference in efficacy between Nolva & Aromasin with the resultant 7α-methylestradiol concentrations. I tend to prefer Aromasin to Nolva in terms of tolerability & I prefer keeping E2 levels within sane levels, but unfortunately, 7α-methylestradiol likely isn't detected by E2 ultrasensitive tests.

Aromasin/Adex kill estro on-sight and can't kill 7a-methylestradiol. Since Nolva stops at the receptor, do you think it can stop 7a-methlestradiol?

And why don't we just use Nolvadex as a SERM because it stops Estrogen at the relevant receptor and still allows estrogen to flow freely for other bodily functions?

Does Letrozole stop 7a-methylestradiol? Is there anything that can be done about Methyl-estradiol?

Also does MENT raise prolactin? It's a 19-NOR

 

[Type-IIx]

Aromasin/Adex kill estro on-sight and can't kill 7a-methylestradiol. Since Nolva stops at the receptor, do you think it can stop 7a-methlestradiol?

And why don't we just use Nolvadex as a SERM because it stops Estrogen at the relevant receptor and still allows estrogen to flow freely for other bodily functions?

Does Letrozole stop 7a-methylestradiol? Is there anything that can be done about Methyl-estradiol?

Also does MENT raise prolactin? It's a 19-NOR

Aromasin/Adex decreases the activity of Aromatase, and MENT aromatizes to 7α-methylestradiol. SERMs act as ER antagonists in a cell-dependent fashion. I don't know about the efficacy of one compound versus any other in terms of mitigating the potency of 7α-methylestradiol (nobody does, that's the problem).

MENT itself serves to lowers prolactin, as do all androgens. MENT, as a progestin has direct activity at the PR; and its aromatic product, 7α-methylestradiol, can serve to increase serum prolactin theoretically.

I view MENT as a messy compound all around.

 

[Para_33]

MENT AND ITS AROMATIC PRODUCT THAT IS STRONGER THAN E2 (BY A LOT)
by Type-IIx

An influential poster, possible the admin/wiki author on a related subreddit seems to be deliberately misrepresenting MENT and just generally putting out a deluge of incredibly wrong information in a highly confident manner. That’s not THAT bad, but it seems that wiki is read by a majority of the guys here.

I’m seeing guys taking estradiol pills to dial in E2, I’m seeing guys that think MENT is barely suppressive because of research where pellets were defective or broke and IV injections into monkeys.

Without actually posting his flagrant misrepresentations, I want to use the paper this decatest claimed as support (which I had to dig a bit to find), although it’s being cited as “research” (in actuality an imgur link to a deceptive Table from this study).

So, let’s look a bit at MENT! It’s not a bad compound at all, provided that it is understood. The problem is that it is being claimed, with a great deal of intentional misrepresentation I believe, that it doesn’t cause gyno or estrogenic effects. And it definitely does.

View attachment 155294

MENT's aromatic product (7α-methylestradiol; 7α-ME) is 4x(!) as potent (technically "efficacious," its being a bad thing here) in ER-containing cells [1]. Efficacy is determined by measuring the effect, e.g., growth (here, in breast cancer cells). The EC₅₀ (EC50) is determined by the concentrations at which the ligand triggers growth. This may be confirmed by measurements of cell cycle progression (i.e., the S-phase entry during the cell cycle).

The binding affinity (IC₅₀) of MENT's aromatic product (7α-methylestradiol) is 102% that of estradiol[1], which is noteworthy as E2 is typically used as the reference compound for ER binding given its particularly high efficacy, potency, and affinity for the ERα receptor, in the literature.

Given the findings of Attardi et al, in comparing the rate of aromatization between MENT and nandrolone, that "At 180 min, about 23% of MENT was converted to 7α-ME and about 13% of 19-NT to E2," knowing that nandrolone [19-NT] aromatizes at 20% the rate of Test [2], we can deduce that MENT aromatizes at roughly 35% the rate of Test... to 7α-ME (an aromatic product with four-fold E2's “potency” for causing growth in breast cancer cells). Simple multiplication of the rate of aromatization (35%) * EC50(7α-methylestradiol) * RBA(7α-methylestradiol) ≈

MENT has a roughly 40% greater growth potential in ER-containing cells than T.

This would certainly seem to support the anecdotes that MENT is quite a potent gynecomastic agent.

PRACTICAL

With consideration of the real world, if the MENT dosage is ~70% the Test dosage, it's on par with the estrogenicity of T, and given the aromatization of MENT to 7α-ME rather than E2, this consequence is unlikely to be reflected in bloodwork results. By way of comparison: 35mg daily of MENT E ≈ as estrogenic as 350mg of Test E weekly.

And MENT does also has progestational activity to take into consideration.

DIALING IN E2 WITH PRECISION

Since it is the androgen-to-estrogen ratio that primarily determines the severity/experience of gyno [3][4], it makes a lot of sense to “dial in” E2 with an androgen rather than a female hormone.

Here, I provide the "Type-IIx continuum of aromatization":

Ment (140% aromatization of Test) > Test > Adrol > Dbol >> Deca (20% of Test)

Back in the day, it was common for guys to pop a Dbol to keep their E2 up on deca/dbol cycles. Guys used to cycle off and on, because they could, because they weren’t acutely nor chronically suppressed (once the decanoate ester cleared, after 4.5 half lives or so), believe it or not, with these compounds. That’s right, "19-nors" are not particularly suppressive as a class. Quite the opposite. But MENT kind of is, because of its aromatic product.

REFERENCES
[1] Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR. Dimethandrolone (7alpha,11beta-dimethyl-19-nortestosterone) and 11beta-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase. J Steroid Biochem Mol Biol. 2008;110(3-5):214-222.
[2] Ryan, Kenneth J. “Biological aromatization of steroids.” Journal of Biological Chemistry 234.2 (1959): 268-272.
[3] Bond, Peter. Book on Steroids. (2020). PeterBond.org.
[4] Vanderschueren D, Vandenput L, Boonen S, Lindberg MK, Bouillon R, Ohlsson C. Androgens and bone. Endocr Rev. 2004 Jun;25(3):389-425. doi: 10.1210/er.2003-0003. PMID: 15180950.

Anecdotal-For what it’s worth, I didn’t experience any ball shrinkage until I upped my nandrolone to high doses. Id assume that’s some method of determining how shut down you are. And I hear all the time about guys needing to bridge with testosterone for upward of a year and then pct and do fine. Anecdotally hcg even becomes less affective with nandrolone for myself included. I suspect ethinyl estradiol is much more powerful than methylestradiol. Which is why that’s used in BC- most often combined with a progestin. Like nandrolone only it’s levonorgestrel most commonly in BC.

This is with hcg too that testicular atrophy occurs. Progestins work through additional mechanisms entirely. I think through inhibin b directly in the gonads unlike estradiol.

I do the ball dip displacement test. To measure volume. I went from 60cc down to 40s as soon as I added nandrolone in. Was using high doses of testosterone and has high estradiol before.

Anecdotal- injectable EV hasn’t made em any smaller and the size I’ve regained by going to 500iu hcg eod, hasn’t been lost since keeping my e2 at 65-100pg/ml where I feel better and my strength has gone up. I even broke through a plateau around this time.

I understand that aromatase is contained in other tissues, and serum level isn’t indicative of the actual aromatase activity going on through aromatized test. But I feel better like this.

Also, I used ment A at 150mg per week, wasn’t using e2 exogenous at this time. Didn’t feel any benefit or negative from the Methyl e2,which honestly makes sense for me. but I was on it for too short of a time. It was a bit stupid because I only used it for 2 weeks for the methylestradiol to see how it made me feel.