MENT Profile

Type-IIx

Well-known Member
A Profile of MENT (Trestolone)
Author: Type-IIx

Personally, I believe MENT is a particularly suppressive compound comparable to testosterone+etonogestrel in its HPG axis suppression. It may provoke a significant rise in systolic blood pressure versus replacement T dosages [1]. However, I know it is gaining popularity quickly despite a paucity of evidence on tolerability, recovery of HPG axis function post-cycle, so as to make it difficult to make appropriate risk-balancing considerations. My personal belief is that you may want to steer clear of MENT, at least until more data is available, if you intend to cycle off (i.e., you do not intend to BnC forever).

Putting my personal view aside, here's my findings on MENT with literature and the detailed anecdotes of a veteran that I respect a great deal for his experience with AAS generally, and MENT in particular:

Trestolone; Methylnortestosterone; 7 alpha-methyl-19-nortestosterone
Non-5α-reducible; particularly estrogenic (aromatizes to 7α-ME), progestid

Ref. p. 347 (330) of Llewellyn
[Conservative] Dose: Under 10 mg daily - with an acetate ester, typically 10-20 mg e2-3d

Regarding potency, consider that cheque drops (mibolerone) is the 17α-methylated form of MENT.

7α-methylation
7α-methylation serves to increase the anabolic potency of MENT by:
- ↑AR affinity [2]
- ↓reduction of the delta-4 (Δ⁴) bond ∴ delta-5(10) isomers are the major excreted metabolites (hindering metabolic inactivation) [3]
- ↓affinity for SHBG binding [4]

Aromatization

MENT-aromatic-product-efficacy-gt4x-T-E2.png
MENT's aromatic product (7α-methylestradiol; 7α-ME) is more than 4x(!) as potent ("efficacious," a bad thing here) in ER-containing cells [5]. 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 [5] which is typically used as the reference compound for ER binding given its noteworthy 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 aromatizes at 20% the rate of T [6], we can deduce that MENT aromatizes at roughly 35% the rate of T... to 7α-ME (an aromatic product with four-fold E2's potency, i.e., for causing growth in breast cancer cells). Simple multiplication of the rate of aromatization (35%) * EC50(7α-methylestradiol) * RBA(7α-methylestradiol) ≈ a 40% greater growth potential in ER-containing cells than T.
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 (Peter Bond, Oct 20 2021)

This would seem to support the anecdotes that MENT is quite a potent gynecomastic agent. With consideration of practical use, if the MENT dosage is ~70% the Test dosage it's on par with the estrogenicity of T, and given the aromatization to 7α-ME rather than E2, this consequence is unlikely to be reflected in bloodwork results. By way of comparison, e.g.: 35mg daily of MENT E ≈ as estrogenic as 350mg of Test E weekly (sans data on metabolism).

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

SHBG
Despite MENT's lack of affinity for SHBG:
...clear decreases in SHBG concentrations...mean serum SHBG concentration of all 24 subjects decreased from 31 ± 2.2 (baseline) to 26 ± 2.1 nmol/l (two days after the last injection). This decrease in SHBG concentrations after the i.m. injections was significant...
[7]

The dose-response relationship was not established between MENT and SHBG.

Another study [8] confirmed the SHBG reduction from MENT:
SHBG concentrations decreased significantly in the groups that used two and four implants (P=0.043 and 0.001, respectively) (Figure 2)

[4] shows MENT a weak SHBG ligand (virtually no binding to SHBG after acute administration)

Joints
Nothing quite provides the joint relief of nandrolone, however said joint relief can be achieved with just 150-200mgs ran along side any cycle. NPP being preferable for more mg per mg of actual compound but still. Do I note a subtle different in my knees when running just trestolone versus my baseline? Yeah but one tenth that of incorporating 200mgs of deca/npp.

However in the past running 100mg every day of ment ace, was comparable to 200-250mg of npp per day regarding performance metrics and lean tissue growth. Actually probably more likened to 150-200mg NPP ED run alongside Anadrol. You lack the aggression of tren, so you don’t have that “not heavy enough” attitude, but the weights you were moving will move a lot faster, and for more reps. You’re not going to tire out very quickly at all.

Ideally for your first ment cycle if you have joint issues, so long as you don’t have issues running 19nors, I would run 4 weeks at 25mg/day or 50mg/eod of ment, and at 3-4 weeks once you’ve seen how you’re going to react to ment add in 25mg/day or 50mg EOD of npp. Understand that both of these compound will compete at the receptor and testosterone will just be left to convert to estradiol or DHT. When running something like trestolone I find it but to run 100-150mg (TRT dose) of test along side but not more. If you have issues with 19 Nors, this drug will not be pleasant. This is the only drug that at high doses made me lactate and require prami.

Dosage
25mg per day or 50mg EOD to start. Twice weekly even for Trest E is too infrequent.

This dosage speculation [from Llewellyn] is largely based on the fact that a therapeutic replacement dose was less than 1mg per day, however in practice it really doesn't translate well. No, 1mg per day of testolone acetate is not going to replace a 100-200mg TRT dosage in the grand scheme of things. One of the primary factors in it being dropped was that at such a dosage there was insufficient estradiol conversion and activity at such dosages. While it is very anabolic, in terms of taking to improve performance metrics a higher dose is needed. Goals as well as experience and tolerability of a compound for you the individual come into play. Also keep in mind that just because at X dose its 10 fold stronger than testosterone, doesn't mean that at higher dosages that scales evenly. I would say 3:1 to 5:1 depending on how you respond once your in the 200-400mg range, not 10:1. The beauty of ment for me would be the mineral retention, and insanely rapid glycogen replenishment (diet supporting of course). I will tell you that running 700mg/week in the past that it was not equal to running 7 grams of test (10:1), nor 3500mg of test (5:1), but more like 2.5-3 grams at most.

Side-Effects
blood pressure
Ment is very powerful, and can have insane sides if you don't keep your levels relatively stable. Also your diet is of the utmost importance.
Important considerations: OFFSEASON/OFFCYCLE blood pressure & resting heart rate

Treat this like doing your first tren cycle. Once you find out how you tolerate the drug you can experiment with your dosing frequency, but not before then.

And no I am not trying to scare anyone. It can be an extremely well tolerated and effective drug if run properly. As with everything though, this comes down to the user and all outside factors. The harsher the compound, the more this comes into effect.

core temperature
Any form of trestolone will increase your body temp. You will note this within 1-3 weeks of starting. Night sweats are to be expected.

libido, erectile function
Very high but not like the tren androgen "rapey" mood. Far more pleasant and controllable. I haven't had ED while on any 19nor so I can't speak on that. That being said, just like any 19nor if your prolactin levels get too high you're going to have issues coming to climax. Keeping estrogen at your happy level whatever that is, and your prolactin in check will alleviate this.

appetite
definitely increased but again I wouldn't say I'm going hypoglycemic like I do on tren. Just wanting more food in general.

liver
While I will need to censor some things in my lab work to post if I decide, I did find some of my older labs from a ment cycle to answer this question. My baseline AST/ALTs are in the low to mid teens generally. On cycle, they rose to 32 and 38 respectively.

blood pressure
This is a big one. My offseason/offcycle BP is generally 110 over 60 or lower. This morning it was 118 over 76. Previous experiences for me with ment I will say it would get higher than I like but not dangerously so. Mind you I do have a lot of ancillary supplements that I take religiously, but on ment my resting BP with never goes over 130/90, ever. That said, there is a noted increase that people definitely need to pay attention to. If you drink, if you eat like shit, or just are genetically predisposed, this drug will seriously mess with your BP. No different than a high dose anadrol cycle.

pumps
I hate them, some love them. You're going to have very full muscles and naturally very strong pumps. This is a pro for some, and really the only major con of AAS for me. This mornings run sucked, I will be wearing compression wear to minimize calf pumps from now on.

digestive (nausea/acid reflux)
While tren and nandrolone give me acid reflux to some extent, I honestly have never had severe issues there while on trestolone. Everyone is different here but I know a few people that can not run nandrolone or tren due to that issue.

PR binding
Regarding its progestational activity, its actually not that different than its ability to bind to the androgen receptor. Is is a very strong progestin. Much more so than tren, or nandrolone. More comparable to medroxyprogesterone acetate. Given its affinity to the receptor site, mifepristone really isnt strong enough to inhibit the effects completely. Noting this, yes it is absolutely essential to have either caber or prami on hand if you're sensitive to progesterone related side effects, well more specifically prolactin.

Remember this was in research as a form of MALE BIRTH CONTROL. Its harsh progestational nature was and is a priority to have this effect. This is why I liken its activity as similar to medroxyprogesterone which is 10-15x the progestin in comparison to progesterone. An anti-progestin that is designed to knock off natural progesterone isn't going to be able to compete with a lot of the modern synthetics. Much in the sense that you could take halotestin and bicalutamide (anti androgen) together and still have androgenic rage...

_______________________________________
References:
[1] 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
[2] Fragkaki, A. G., Angelis, Y. S., Koupparis, M., Tsantili-Kakoulidou, A., Kokotos, G., & Georgakopoulos, C. (2009). Structural characteristics of anabolic androgenic steroids contributing to binding to the androgen receptor and to their anabolic and androgenic activities. Steroids, 74(2), 172–197. doi:10.1016/j.steroids.2008.10.016
[3] Recent advances in doping analysis (12)... Koln (2004): 261 - 268
[4] Kumar, N., Suvisaari, J., Tsong, Y., Aguillaume, C., Wayne, C. et al. (1997). Pharmacokinetics of 7alpha-methyl-19-nortestosterone in men and cynmolgus monkeys. Journal of Andrology, 18(4), 352-358.
[5] 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. doi:10.1016/j.jsbmb.2007.11.009
[6] Ryan, Kenneth J. “Biological aromatization of steroids.” Journal of Biological Chemistry 234.2 (1959): 268-272.
[7] Suvisaari, J., Sundaram, K., Noe, G., Kumar, N., Aguillaume, C., Tsong, Y. Y., … Bardin, C. W. (1997). Pharmacokinetics and pharmacodynamics of 7alpha-methyl-19- nortestosterone after intramuscular administration in healthy men. Human Reproduction, 12(5), 967–973. doi:10.1093/humrep/12.5.967
[8] Noé, G., Suvisaari, J., Martin, C., Moo-Young, A. J., Sundaram, K., Saleh, S. I., … Lähteenmäki, P. (1999). Gonadotrophin and testosterone suppression by 7α-methyl-19-nortestosterone acetate administered by subdermal implant to healthy men. Human Reproduction, 14(9), 2200–2206. doi:10.1093/humrep/14.9.2200
 
ADDENDUM

The anecdotal reports on prami/caber and prolactin are not my writing, nor the PR binding section.

In my view, the only relationship that exists between 19-nortestosterone derivatives and prolactin is that of androgens and prolactin generally: they generally suppress prolactin. With Deca & MENT, since they aromatize, the aromatic products (estradiol or 17alpha-methylestradiol) can increase prolactin secretion (also, certain medications, a prolactin-secreting tumor). Prolactin, if it IS a problem for someone, seems totally dissociated from progestids or progesterone. But, if it is a problem arising from aromatic products, it would indicate for the use of an AI.

Data on the direct PR binding of MENT (as well as its binding to ERalpha, ERbeta, and the AR) can be found in:

Houtman, C. J., Sterk, S. S., van de Heijning, M. P. M., Brouwer, A., Stephany, R. W., van der Burg, B., & Sonneveld, E. (2009). Detection of anabolic androgenic steroid abuse in doping control using mammalian reporter gene bioassays. Analytica Chimica Acta, 637(1-2), 247–258. doi:10.1016/j.aca.2008.09.037
 
@Type-IIx , do you have any data /anecdotes /advice regarding DHB's (anti?) estrogenic effects.
I've seen claims it acts as an AI like its relatives, Eq and primo. Obviously doesn't aromatize directly, but read a report that it raised e2, theoretically due to having a higher AR binding affinity than test, resulting in more free test for the aromatase enzyme.
In your opinion, would it be worth stacking with mast, proviron or winstrol or would that be redundant?
 
A piece of advice for all you SARM users is just taking a look at Tony Huge and his organ failure. All I have to say been using gear for 30 years on-off and have no issues like that... You Sarm clowns think that it's safer and I have to say after 5 years of following SARMS and the damage it has done I rather do crack than use sarms. Just my 2 cents.

Tony Huge’s echocardiogram reveals mitral valve prolapse​

Test results revealed Tony Huge’s CPK and CK-MB levels multiple times higher than the normal range. A thorough investigation by doctors revealed that Rosuvastatin could be the culprit for elevated CPK and CK-MB levels. Tony Huge added:

“(The doctor’s) like Rosuvastatin has a ton of side effects. I’m like but the side effects I’m having are with my heart and Rosuvastatin is a statin that is supposed to be for the heart. That’s supposed to fix my lipid panel, fix my cholesterol so that I don’t have heart issues.”
The doctor advised Tony Huge to completely stop using Rosuvostatin immediately to see the difference. She also encouraged him to get an echocardiogram to see how the heart is performing. The results showed mitral valve prolapse with an ejection fraction of 59 percent.

“At 59 percent with mitral valve prolapse, they say you are a candidate for surgery. They can go in and repair the valve,” Tony Huge stated.
 
@Type-IIx , do you have any data /anecdotes /advice regarding DHB's (anti?) estrogenic effects.
I've seen claims it acts as an AI like its relatives, Eq and primo. Obviously doesn't aromatize directly, but read a report that it raised e2, theoretically due to having a higher AR binding affinity than test, resulting in more free test for the aromatase enzyme.
In your opinion, would it be worth stacking with mast, proviron or winstrol or would that be redundant?
Well, 1-Testo is not a cousin of EQ/boldenone despite its being mislabeled as "DHB." It is of the same class as Primo. With all of these claims of potent androgens acting as AIs despite lack of commonality, the most parsimonious hypothesis is that an increased androgen/estrogen ratio is the likeliest explanation, with the presence of a secondary 17β-hydroxy group in a non-aromatizing androgen leading in some individuals, dependent on metabolism, to symptoms of low estrogens (due mostly to net androgenic potency).

The report of 1-Testo raising E2 is, if anything, a misattribution of increased E2 to 1-Testo. There is no mechanism by which 1-Testo would increase E2. Further, it does not follow that 1-Testo's supposed higher binding affinity (if even true that its "affinity" is higher than T's, I doubt this has been measured, and certainly not in man) would result in more free test for aromatase thereby increasing E2. Basically, this is all bullshit.

Stacking 1-Testo with Mast, Proviron, or Winstrol? Why, because someone reported that it increases E2 and these might somehow synergize well with 1-Testo as a result? I don't follow at all.
 
I actually aromatize very, little, struggle with low e2 using even 3:2 ratios of test to eq, primo. Confirmed by bloodwork.
I do however, tend to favor dht derivatives for the neural, athletic and cosmetic benefits. Hence my query - does dhb have similar, androgenic benefits or is it as "purely anabolic" as some claim?
I'm hoping dhb is essentially e2 neutral so I can limit test to high trt levels, and asked about mast, winstrol as I love most dht family steroids... Cosmetic effects, neural benefits that are great for bjj/mma, and just general well being (for me). I'm wary of having too high a dht:e2 ratio and suffering low estrogen symptoms, negating any athletic benefit.
Or just wary of adding unnecessary compounds to my cycle- does dhb do everything mast or winstrol etc do, or would stacking them result in a1+1=3 synergy.
 
I actually aromatize very, little, struggle with low e2 using even 3:2 ratios of test to eq, primo. Confirmed by bloodwork.
I do however, tend to favor dht derivatives for the neural, athletic and cosmetic benefits. Hence my query - does dhb have similar, androgenic benefits or is it as "purely anabolic" as some claim?
I'm hoping dhb is essentially e2 neutral so I can limit test to high trt levels, and asked about mast, winstrol as I love most dht family steroids... Cosmetic effects, neural benefits that are great for bjj/mma, and just general well being (for me). I'm wary of having too high a dht:e2 ratio and suffering low estrogen symptoms, negating any athletic benefit.
Or just wary of adding unnecessary compounds to my cycle- does dhb do everything mast or winstrol etc do, or would stacking them result in a1+1=3 synergy.
Bro, my apologies, but there's just so much to unpack in this post. From the "DHT derivative" misnomer, to how precisely you define androgenic, to common "ratio" broscience. I feel like we might be speaking different languages altogether. But to answer your question, no, these compounds (Mast, Winstrol, and 1-Testo) do not offer by way of their unique properties any synergistic (greater than additive) action. I really like that you're a BJJ/MMA guy though! Based on that fact I can infer your likeliest view of androgenic properties, but there are a lot of assumptions made in your post that we'd have to disentangle before we got anywhere.

What I think 1-Testo offers to a combat athlete is either complete unusability due to unbearable PIP (worst case) or (best case) a similar compound to stenbolone.
 
It is DHB. It's just that DHB is a very poor name for it given its complete and utter lack of connection to boldenone whatsoever.
I was under the impression Boldenone (at a very low rate) converted to DHB (its metabolite) through 5a reductase enzymes.
 
Lot of bad info on YouTube.

EQ has no meaningful 5α-reduced metabolites... (5 alpha-androst-1-ene-3,17-dione in miniscule amounts) See Metabolism of boldenone in man: gas chromatographic/mass spectrometric identification of urinary excreted metabolites and determination of excretion rates - PubMed

Also, actual names for 1-Testo include the following: 1-Testosterone
Just because there's no detectable 1-testo/dhb in urine, does that unequivocally mean it isn't produced by 5-ar reduction of boldenone? Genuinely asking, this is not my academic area. Couldn't it be produced (in small amounts) and further metabolized or just used entirely and not excreted.
Wikipedia, says 1-testo is produced by 5-ar reduction of boldenone- is that just based on looking at the structures, extrapolating that the pi bond in A ring of eq is reduced in the same way test is reduced to dht? Not based on knowledge of what actually happens in the body / how the compound is synthesized artificially? If you took EQ raws, 5 AR reductase enzyme and biocompatible conditions/catalysts, would you end up with with dhb?
 
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Bro, my apologies, but there's just so much to unpack in this post. From the "DHT derivative" misnomer, to how precisely you define androgenic, to common "ratio" broscience. I feel like we might be speaking different languages altogether. But to answer your question, no, these compounds (Mast, Winstrol, and 1-Testo) do not offer by way of their unique properties any synergistic (greater than additive) action. I really like that you're a BJJ/MMA guy though! Based on that fact I can infer your likeliest view of androgenic properties, but there are a lot of assumptions made in your post that we'd have to disentangle before we got anywhere.

What I think 1-Testo offers to a combat athlete is either complete unusability due to unbearable PIP (worst case) or (best case) a similar compound to stenbolone.
And admittedly getting alot of my info on androgenic, athletic, neural benefits of dht () from podcasts, forums.. Aka broscience.
Better than nothing but if you can recommend any real studies, sources I'd appreciate it.
I'm sure I have entangled many concepts and made faulty correlations regarding DHT/androgenicity, it's role in evolution/fetal brain development and role for a combat athlete (hobbyist). Can you point me in the right direction to correct them, optimize my aas use?
 

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