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Male Contraception with MENT

Good day,

wanted to discuss a topic I’ve read about a bit and get your guys opinion on it. First thing is MENT in bodybuilding and then secondly male hormonal contraception.

MENT was originally developed as a contraceptive for men. As some guys (per example @unreal24278 ) stated before it is of great risk to use it.

The daily news writes:

“ However, this is where Ment differs; in fact, Trestolone is the only steroid in the market today that is capable of enabling a man to have normal physiology in the absence of testosterone, including sustaining an erection.”


“ For bodybuilders who want to build strength and lean muscle mass while simultaneously reducing excess body fat, Trestolone is the best steroid”

What do you think about the effects? @mnben87 @readalot @iron_yuppie

From what I read I’m more than skeptical that it’s as hunky dory as they say in bodybuilding as well as in male contraception.

And now to T based stuff: they are injecting testosterone undecanoate every 12 weeks for contraception. Who TF would do that if they’d read any experience on this and why would BigPharma do it every 12 weeks whilst knowing kinetics? Ridiculous.

Also, people do impregnate their woman when they are on cycle so I don’t know how reliable a testosterone based contraception would be.

I don’t see a male hormonal contraceptive method on the horizon and I don’t think it’s the way to go.

If you’re referring to the design protocols employed with testosterone undecanoate I’d tend to agree, the dosage protocol clinically employed isn’t optimal.

I’ve seen clinical trials wherein injections e6-8 weeks produced solid results (testosterone concentrations within the upper range of normality). But given the half life of test-u (regardless of carrier oil which can slightly alter HL) you’re still inducing a hormonal rollercoaster with shots e12-14 weeks. Test U was released with the intent being to allow infrequent shots of which would reliably release a stable, therapeutic dose of testosterone. This would work in theory if the shots weren’t spaced out so far apart (2-3 half lives elapse prior to getting the next shot).

Initially they do front load test U (at least in Australia they do). It’s 2-3 shots every 6 weeks followed by a shot every 12 weeks. It’s expensive and adverse injection site reactions are well documented/more pronounced with test U (pulmonary oil microembolism in particular leading to temporary dyspnea or syncope). I had the option to use test U at one point but decided against it due to cost alone.

Coincidentally I mentioned MENT earlier today. As with all designer drugs, I believe risk outweighs the reward as we don’t fully understand the pharmacokinetics/pharmacodynamics associated with these substances. If one is to experiment with designer substances, they should go about doing so with extreme caution. With something like trestolone (7 alpha methyl 19 nortestosterone) the substance at hand is so just so exceedingly powerful… I can’t foresee a scenario wherein the reward would outweigh the risk.

I think you should inject at least every 10 days even with undecanoate having a half life of let’s say 3 weeks. Otherwise the levels won’t be stable at all.
Then there’s the problem that you must inject a testosterone dose lasting for 6-12 weeks, that’s an absurd amount of Test.
I think every 10 days would be doable for most people and would generate stable levels. You could do it at home and testosterone U is not that expensive.

I don’t understand why a big company would waste money on a study with injections every 12 weeks. And who would green light it? It’s nearly clear from the get go that people would complain about depression and other side effects.

Compliance rates. The avg joe on TRT isn’t looking for protocal optimisation. All that matters is that they feel better when compared to baseline. With that in mind, just about any protocal (aside from e3-4wk test E) should beat baseline.

Most people don’t like needles and/or don’t want to stick themselves weekly. The companies that designed reandron/aveed were probably looking for a product that reliably produced serum TT above say… 350ng/dl + infrequent shots to increase patient compliance.

Also reandron is more expensive than primoteston here. I’m currently very happy with primoteston (test E) @100mg/wk. Only costs me 30-35$ for 7.5 weeks worth.

Gives me more money to cover gas and strange foods that I like such as avocados, cooked barley, uncooked cloves of raw garlic and sardines… AnD mAlVa PuDdInG

Look at the clinical trials involving oral dimethandrolone undecanoate for male contraception. I believe the prospect of MENT being used for male contraception was ditched years ago.

Trials also exist using nandrolone decanoate, testosterone enanthate (200-250mg/wk) and testosterone + progestognenic agents. If a male birth control pill/patch/injection is ever marketed I’d be willing to bet 20$ that it’s non-hormonal in nature.

I saw some trials and I don’t think there will be something coming out of it.

Dimethandrolone looks promising. No aromatization, no reduction through 5a-reductase. But exactly there lies the problem again if it’s applied systemically. Is the plan to substitute estrogen and DHT with it and that individually? Too complex, too expensive.
I read something about it being applied topically, but I don’t know how that would work.

There’s more ways to target sperm without having hormonal sides. So I don’t think this will be a winning strategy. They even tried GnRH superagonists. Treat young men like cancer patients, that’s the pitch?

Seriously I’d rather take androgel, the only problem there is varying plasma levels which can easily be fixed from day to day.

This is what I have heard.

The issue with MENT is E2 IMO. I haven’t taken it, I haven’t seen others blood work, so I can’t quantify how much it converts to E2 (would love if someone had a good solid mg to mg comparison to testosterone for example), but I have heard others say they pop adex like candy on it to keep E2 at bay while taking it. I have heard 2 mg of adex a day while cycling it! IMO, if I need high amounts adex, then I would just find a different compound. Adex has lots of negatives that outweigh the MENT positives. Just my $0.02 on this compound.

Thanks for bringing this topic up.

Good review:

We did not observe a significant decrease in sperm concentrations despite marked suppression of T and gonadotropin production with DMAU administration. However, this was not unexpected given the length of treatment of 28 days, the 72 days required for the completion of spermatogenesis in men, and that maximal suppression of T production was not observed until day 7 of treatment. Interestingly, 4 of 59 men in the treatment groups did achieve sperm concentrations of <5 million/mL at 28 days, whereas none did in the placebo group. The effectiveness of DMAU in suppression of spermatogenesis is currently being studied in a longer-term study. In studies of injectable androgen plus progestin combinations ([33](javascript:;)), sperm concentrations begin to fall after 4 weeks of treatment, but require at least 6 to 8 weeks to demonstrate marked suppression of spermatogenesis to levels compatible with contraceptive efficacy.

Look at reference 33:

You’d have to be a riverboat gambler to try and time fertility using a hormonal contraceptive method with a male. If you superimpose a women’s fertility using the pill the onset of action (~99% effectiveness) is ~ 10x faster and works within a week if you do it correctly.

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@unreal24278 has covered this in detail. Beautiful summaries. The quote you shared says it all. Most on here don’t want all the details so I am avoiding it for the most part now. It all you want is muscle and ripped look I am sure with the right protocol it would be quite helpful. Google Munzer or Hans Hopstaken. The part that doesn’t get daylighted for the young guys (not nearly enough) is the even remote chance of CHF/XXX/YYY at 40, 45 even 55 should rightly scare you.

Hardcore bodybuilding really is a death cult and we should be transparent about that. When people look at the cover of BodyOpus, how many really appreciate what happened to this very nice person?


Some are more comfortable with gambling than others.

Also I think the allure of getting the most gain with the least side effects is this really attractive goal for some or they discount the real potential dangers. Odds are if you are looking for that added chemical edge to improve your physique then you probably aren’t someone who has the genetics to respond favorably to the AAS anyway (high positive to negative side effect ratio vs the opposite). Wouldn’t it be nice to do genetic fingerprinting and let folks know they aren’t going to respond like Kevin Levrone to a 3 month protocol?

In the case of MENT, no one should consider it unless their time horizon for life is less than 5 years (I have to say this using a 99% confidence level). No I am not talking about you Mr. Ozzy Ozzbourne genetics guy. But you don’t know if you have those genetics till you test your LD50.

It’s like investing, everyone says their risk tolerance is through the roof until the bottom drops out and they learn their real tolerance. In theory, discussing all this stuff is fun and intellectually stimulating, etc. In reality, it always end in tears unless you are a very disciplined person, know exactly what to look for, genetic elite, and maybe some luck.

I believe the “death cult” mentality reared its ugly head around the early/mid 1970s. I don’t believe the avg AAS cycle was really 100mg primo/wk +10mg dbol/day. Given the conflicting reports from people like Arnold, Pete Gyrmkowski, Mike Mentzer etc I somewhat believe many toned down the notion of abuse to preserve legacy.

It’s been said that Arnold was juicing at FIFTEEN… Let alone during the “golden age” of bodybuilding.

I believe the chance is higher than “remote”. If you’re a kid consistently blasting grams of gear, there’s probably a decent chance you’ll end up with CHF 15-20 years down the line. Numerous mechanisms can be explained within relation to how AAS wreck havok upon the cardiovascular system when abused. One can mitigate some of these risks, but in the end it’s probably impossible to neuter/mediate pure cardiomyocyte hypertrophy mediated via androgen receptor binding

To be fair I think he died due to complications associated with polycystic kidney diseaae

I completely agree with you. That’s why I said:

The part that doesn’t get daylighted for the young guys (not nearly enough) is the even remote chance of CHF/XXX/YYY at 40, 45 even 55 should rightly scare you.

Stress would be on the word “even”. As if even if it is a remote chance…

I’m talking about the guy on the cover, not Duchaine who had PKD. Hans Hopstaken had kidney disease?

From an internet source I can’t link to here:

According to friends, Hans was taken to the hospital about six weeks ago due to congestive heart problems. Both of his parents passed away from heart problems. He was in the hospital for a while, and was recovering, and was released. Last Saturday, Hans developed a cold, which then turned into pnuemonia. On Thursday evening, he has not doing well, his blood pressure even going as low as 40 over 10, and the doctors had to revive him. Friday, April 12, around 2pm, Hans was in a coma, and passed away.

Reading this stuff makes me sad.


There was a small but significant elevation of systolic blood pressure in the MENT group with no change in the testosterone group. A similar finding was reported in a previous study investigating MENT alone (von Eckardstein et al, 2003). Systolic blood pressure may reflect arterial stiffness and is increasingly recognized to be a strong cardiovascular risk factor (Oliver and Webb, 2003). Arterial stiffness is inversely related to testosterone concentrations in older men (Hougaku et al, 2006) and was increased by induced hypogonadism in men with prostate cancer (Smith et al, 2001). During MENT administration both testosterone and estradiol concentrations are low. Recent data suggest that endogenous estradiol may be vasculoprotective (Arnlov et al, 2006). Although MENT is aromatized to an active estrogen (LaMorte et al, 1994), the low serum concentrations both of MENT and therefore of potential active metabolites may contribute to increased arterial stiffness and a rise in systolic blood pressure, which therefore might actually be less affected by administration of a higher, more effective dose.

Anyone see a potential huge flaw in discussion above?

Study Design and Medication

The study was a randomized, open‐label trial investigating MENT implants or testosterone in combination with etonogestrel implants, with both groups scheduled for treatment for 48 weeks. Following 2 screening visits, subjects were randomized using a computer‐generated list and numbered sealed envelopes. Subjects in the MENT group were administered 2 implants each containing 135 mg of MENT acetate formulated as in previous studies to release about 400 μg of MENT Ac per implant per day (Anderson et al, 2003; von Eckardstein et al, 2003) subcutaneously with local anesthesia into the medial aspect of 1 arm, and 2 etonogestrel implants 4 cm long, each containing 68 mg of etonogestrel (Implanon; N.V. Organon, Oss, The Netherlands) into the other upper arm. The testosterone group was administered 600‐mg testosterone pellets (3 × 200 mg, N.V. Organon) subcutaneously into the anterior abdominal wall, repeated at weeks 12, 24, and 36, with 2 etonogestrel implants at first administration of testosterone. The etonogestrel and MENT implants were removed at the end of the treatment period, at which time the subjects entered the recovery phase.

Well they say a smaller dose increased systolic BP, and arterial stiffness, in their trial, but suggest upping the MENT to lower BP and Arterial stiffness. They are using a testosterone study not a MENT study to justify this claim. It is taking a leap of faith with that one.

Not sure if that is what you are getting at. The article is discussion is kinda a cluster fuck.

bingo, Trestolone converts to https://en.wikipedia.org/wiki/7α-Methylestradiol

Estradiol also lowers blood pressure in several animal models of hypertensive, including SHR [63], stroke prone SHR (SHRSP; [64]), rats with deoxycortisterone acetate-salt induced hypertension [65], Dahl salt-sensitive rats [66] and rats with pulmonary hypertension [67,68]. In contrast, ovariectomy does not affect the development of hypertension in SHRs [6], suggesting that the effects of estradiol on blood pressure in rats are pharmacological rather than physiological. Unlike the natural estrogen estradiol, the synthetic estrogen ethinyl estradiol increases blood pressure [55], suggesting that the effects of natural and synthetic estrogens differ markedly and may influence distinct mechanisms involved in the regulation of blood pressure. For example, even though contraceptive estrogens are administered at a lower dose (30–200 μg) than estrogens (0.625–2 mg) used for hormone replacement therapy, contraceptive estrogens increase blood pressure [55].

Kind of important which estrogen that trestolone is aromatized to.


I was under the impression that it converted to estradiol (E2), learned something new today.

Your post above is spot on in terms of sides, you would still get all the potential negative “estrogen bodybuilding” sides, just wouldn’t get the vasoprotective positive sides that you would get estradiol (aromatase product of test). I am not aware of study showing direct measurement of 7α-Methylestradiol effect of blood pressure or titration of it vs E2.



Trestolone is on my list for experimentation. Some guys call in gyno in a bottle, but interestingly those who run it with very small amounts of testosterone (like 100mg or less per week) don’t seem to have to fight off the monstrous e2 conversion. A nandrolone derivative that doesn’t have the brutal mental side effects usually associated with that class of drugs? Yeah, sign me up.

Edit for clarity: when I say experiment I don’t mean “I’ll take this for six months and see what happens”. I’m talking like a four week trial where I see what it can do, how it makes me feel, and whether or not it’s actually worth fooling around with. Reality is at my age it makes more sense to do one nice primo blast a year and just keep making slow, steady gains without the risks associated with all the other shit out there. But I also like to tinker, soooo…

The aromatase reactions are very complex.
I’ll try to give a quick overview. The aromatase enzyme acts on Ring A of the steroid structure. It demethylates the 19 position. Which chemical mechanism it uses defines which product will be received. Important is, that the action is always on Ring A (not always on the methyl group). This means that other substituents won’t be affected.

At first I thought that the enzyme just dihydroxylates the 19 methyl group and then eliminates it but it can also produce a carboxylic acid group at the 19 methyl group and eliminate that through unknown mechanisms. These are the reactions on the left. The reaction on the right is the normal elimination and production of E2.

The implications hereof are very interesting, as you can see in the next study:

From: https://onlinelibrary.wiley.com/doi/full/10.1002/dta.2192

That means Nandrolon is a natural metabolite of testosterone and androstenedione.

Now, the aromatase needs the 19 methyl group to do its job so aromatization of 19-nor-compounds can’t happen through this mechanism. MENT, nandrolone and others don’t get aromatized through the Aromatase. How then?
Fat tissue, ovaries and so on contain aromatase but the adult human liver doesn’t. Studies on the first pass effect showed that 19-Nors get aromatized by passing the liver:

“ Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes.”

For that the only thing that would have to happen would be a hydroxylation in Ring a which is the normal function of many CYP enzymes.

That means that aromatization of MENT and others can’t be stopped through AIs. (Don’t know if there exists proof of concept, would be nice)

But I read a study where they took aromatase and gave it MENT and there was aromatization. It was in vitro and there could be things that have gone wrong but maybe it works and the Aromatase is even more complex.

So different compounds get aromatized into different estrogens. E2 is one thing that can come out if certain chemical requirements are met. But in a lot of cases another estrogen with unknown effects forms in the body.

Edit: Just found a study that supports this.


I had some time to skim through the studies and one thing that struck me was this sentence in the discussion of https://academic.oup.com/humrep/article/20/6/1733/748875

In recovery rates, the differences between centres appeared to be fully accounted for by the geographical factor whereas for suppression rates there remained significant variations between the six predominantly Chinese and between the 10 non-Chinese centres.

I don’t know about you guys but the last thing I’d do is take a steroid in a low dose for birth control and then come off with low T. Some guys will probably have to PCT after that, but that shouldn’t shock anybody on here.