Trestolone as PH or DS "Base"

Spaniard

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Trestolone as a PH or DS “Base”​

There has been an increasing amount of “base” threads lately so I’m going to copy and paste a few snippets from one of my blog articles.

Trestolone is a new compound currently being used in trials for various purposes by pharmaceutical companies. The possible uses for this compound reside in the fields of hormone replacement therapy and a possible male contraceptive (I’ve waited long enough for one of these lol). The excitement surrounding this compound is its abilities to fulfill the mechanisms that testosterone does.

To understand the implications of this we will take a quick look at testosterone and a few of the processes it is involved in. Testosterone is a precursor to the hormones DHT (dihydrotestosterone) – the primary androgen - and estrogen. DHT and estrogen are synthesized via testosterone reduction by specific enzymes. The enzymes for these reactions are 5AR (5-alpha reductase) and estrogen synthetase (aromatase). Both of these hormones must be biosynthesized to maintain homeostasis (normal bodily balance/operation). Testosterone is reduced quite significantly in the body via conversion to other hormones and being bound up substantially by SHBG (sex hormone-binding globulin).

ENTER TRESTOLONE

Trestolone from what we have seen in the studies fulfills these roles with great efficiency, either by direct conversion to a potent estrogen (7-alpha-methyl-estradiol) via aromatase or by the high androgenic nature of the hormone, making up for the absence of DHT conversion. 7-alpha-methyl-estradiol, has much greater binding affinity for the ER (estrogen receptor) making it a more potent estrogen than estradiol itself. This does indicate the need for an aromatase inhibitor ran concurrently to minimize high estrogen side effects. Remember though guys we want to control estrogen not crush it.

Trestolone unlike testosterone does not bind to 5AR, which limits the conversion to DHT. DHT again is important due to its androgenic effects. From early anecdotal feedback (the logs), we have seen that even with the absence of DHT conversion the high androgenic nature of Trestolone seems to make up for the lack of this conversion. Trestolone also holds no affinity for SHBG, which allows for high levels of the circulating hormone to be bound to the receptor instead of SHBG. The high affinity for the AR (androgen receptor) is likely the pathway that makes up for its lack of DHT conversion. I have seen it posted that DHT is more androgenic than Trestolone however, where Trestolone may lack an androgenic ratio comparable to that of DHT it seems to make up for by not binding to SHBG. DHT like testosterone does bind strongly to SHBG whereas Trestolone does not.

Now the translation into why Trestolone is the best choice for an on cycle “base”. As we all well know or may not know. When consuming an exogenous hormone source our own natural testosterone production (testosterone biosynthesis) is downregulated. Once suppression occurs, what we are left with is the hormone in which we have introduced to our system. Some of these hormones can have side effects such as loss of libido, fatigue, mood decreases etc. What some are not aware of is that these side effects can sometimes be directly attributed to the fact that downregulation has occurred giving you little to no endogenous testosterone.

With the absence of testosterone, is the absence of the previously mentioned testosterone metabolites – DHT and estrogen. When all of these hormones, including testosterone, are downregulated, you will feel the effects of suppression, which can directly affect mood, libido, energy, and so forth. To correct this problem many people resort to using exogenous testosterone (out of body). The problem with this is you are either toeing the line of legality, straight up breaking the law or using prohormones that have low conversion rates to testosterone such as 4 DHEA etc. Other possible bases that people use are prohormones to stanolone (DHT), DHEA products, and the like. These options have been used with success for quite some time. That is until now.

Trestolone as seen in the studies and anecdotal feedback can indeed be used as a viable and potent option for a base alternative. The reason for this is the ability to fulfill the mechanisms outlined in this article. It can convert to estrogen, albeit a more potent estrogen but estrogen none the less. What this does for you is keeps your body in a homeostatic (normal operating) state. You still have adequate estrogen levels keeping your mood, libido, erection function and quality up etc. Due to the androgenic nature and lack of SHBG affinity of Trestolone you also get the androgenic benefits that you would with DHT conversion, which can also effect libido, mood, aggression, energy etc.

Any other questions post them up or to add input post it up.

Good luck
-V
 
Spaniard

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This in no way discredits Trestolone as a standalone compound. It is highly recommended as both base and solo for the reasons discussed
 
Abadjiev

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Awesome post.

This is some of the exact info I've been looking for in regards to the trest.

Thanks, Spaniard.
 
justeat

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Excellent!
 
dallasboy22

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One question , will trest be hard on the hairline like DHT compounds?
 
g0hardorgohom

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One question , will trest be hard on the hairline like DHT compounds?
From my personal experience, no.I always need to wash my hair with ketoconazol shampoo when I'm using DHT derived compounds but that's not the case with trestolone.
 
Abadjiev

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What does a solid cycle length for Tr3st as a standalone look like? Max length for it as a base alongside other compounds?
 
g0hardorgohom

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What does a solid cycle length for Tr3st as a standalone look like? Max length for it as a base alongside other compounds?
Getting bloods done is the only way to know for sure. IMO there shouldn't be "max length" even for methyls but 6 weeks for methylated compounds is a good general recommendation because most of us do not get bloods done.

8 weeks of TR3ST should be good.
 
Spaniard

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One question , will trest be hard on the hairline like DHT compounds?
It shouldn't be but there is always the chance you may respond to a hormone differently than others. There are 5AR enzymes in the scalp. As previously stated, Trestolone has no affinity for 5AR, which means it will not bind at the 5AR enzymes in the scalp. Meaning that Trestolone should be relatively easy on the hair line.

What does a solid cycle length for Tr3st as a standalone look like? Max length for it as a base alongside other compounds?
If you were to run Trestolone solo I would opt for a TD Trestolone preparation and oral Trestolone. This should give you the best bang for your buck. The TD will provide a slow release of the hormone while it permeates through the layers of the skin. The oral will give you that immediate bolus dose that most utilize for preworkout.

In regards to cycle length that would more than likely be user dependent. Just know that orally there is more hepatic concern than originally thought and it is 12x as suppressive as testosterone. I would say that 8 weeks would be a good strategy although more experienced/advanced users have gone as long as 12 weeks. These users had labs drawn some came back with negative markers some had zero impact. Again, this is user dependent. Labs on longer cycles are always advisable in my opinion.

you can run it as long as you want, it's not a methyl. you could cruise on it theoretically. shutdown is hard tho, so i wouldn't recommend using it too long.
I wouldn't "cruise" on oral. TD or another preparation would be your best bet for a "cruise". Trestolone has shown to be hepatotoxic. Granted not to the degree of a 17a methylated hormone but hepatotoxic none the less.
 
Spaniard

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There was a guy that ran 100mg of IM trest for 8 weeks and his liver enzymes were pretty well elevated.
Exactly why I'm trying to minimize the spread of Trestolone not being hepatotoxic. Like all other PO compounds it has the risk of being hepatotoxic. Even in IM preparations.

Now in the case you're talking about specifically many factors could be at play there but it's important to note feedback like that
 
Spaniard

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Yeah I followed along also. The main reason he dropped was due to the short half life of the acetate ester and he got tired of the frequent pinning. It also became cost prohibitive with frequent pinnings etc. The liver enzymes were secondary and the reason he had decided not to get back on

There were a few others that had done similar research that didn't have the same outcome
 
g0hardorgohom

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Do you guys have a transdermal version of tr3st?
Yeah. DermaTREST. Nutriverse is having a presale right now - use discount code TRANSDERMAL15 to get 15% off!
 

Stierenek213

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It shouldn't be but there is always the chance you may respond to a hormone differently than others. There are 5AR enzymes in the scalp. As previously stated, Trestolone has no affinity for 5AR, which means it will not bind at the 5AR enzymes in the scalp. Meaning that Trestolone should be relatively easy on the hair line.




If you were to run Trestolone solo I would opt for a TD Trestolone preparation and oral Trestolone. This should give you the best bang for your buck. The TD will provide a slow release of the hormone while it permeates through the layers of the skin. The oral will give you that immediate bolus dose that most utilize for preworkout.

In regards to cycle length that would more than likely be user dependent. Just know that orally there is more hepatic concern than originally thought and it is 12x as suppressive as testosterone. I would say that 8 weeks would be a good strategy although more experienced/advanced users have gone as long as 12 weeks. These users had labs drawn some came back with negative markers some had zero impact. Again, this is user dependent. Labs on longer cycles are always advisable in my opinion.



I wouldn't "cruise" on oral. TD or another preparation would be your best bet for a "cruise". Trestolone has shown to be hepatotoxic. Granted not to the degree of a 17a methylated hormone but hepatotoxic none the less.
Not sure if I read this correct, so Tr3st is really 12 times as suppresive as testosterone? Is that applicable for only the oral tr3st or as well for the td?
 
Spaniard

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Not sure if I read this correct, so Tr3st is really 12 times as suppresive as testosterone? Is that applicable for only the oral tr3st or as well for the td?
You read that correctly. Trestolone no matter the product it is in is 12 times more suppressive than Test. This is the reason it is being looked into for male contraception. Low doses, shut you down hard and fast, while being able to maintain quality of life.
 
justeat

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Is there any idea of what the half life is for TD? I'm starting DermaTREST at 50mg ed... Thinking of using a liquid dropper to measure out 25mg and dosing twice a day. Wake up and post workout (6pm). This would be accompanied by 25mg orally pwo at around 4pm.

I assumed to give it about 6-8 hours of active absorption, but then again I have no real basis to assert that. If there isn't much info out there yet I'll try different dosing schedules (1 week each) and report back...
 
g0hardorgohom

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Is there any idea of what the half life is for TD? I'm starting DermaTREST at 50mg ed... Thinking of using a liquid dropper to measure out 25mg and dosing twice a day. Wake up and post workout (6pm). This would be accompanied by 25mg orally pwo at around 4pm.

I assumed to give it about 6-8 hours of active absorption, but then again I have no real basis to assert that. If there isn't much info out there yet I'll try different dosing schedules (1 week each) and report back...
Half-life of trestolone base in it is of course the same than half-life of oral version. But the thing is, it absorbs through the skin over 8-12ish hours so short half-life doesn't really matter.
 

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I'm heading into week 7 running 100mg trest td Daily (50mg after my morning shower, 50 mg after my post w/o shower) with 100mg formestane td daily (same schedule as the trest). Stacked with 30 mg of Epi oral and 125mg arimistane daily. Just added the Epi and a-stane a week ago. I've been taking a DHEA sup (Sterone D3- 2 caps AM, 2 caps PM) from jump. My plan is to run the trest for 12 weeks. Does this look like overkill?
 

uubiduu

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I'm heading into week 7 running 100mg trest td Daily (50mg after my morning shower, 50 mg after my post w/o shower) with 100mg formestane td daily (same schedule as the trest). Stacked with 30 mg of Epi oral and 125mg arimistane daily. Just added the Epi and a-stane a week ago. I've been taking a DHEA sup (Sterone D3- 2 caps AM, 2 caps PM) from jump. My plan is to run the trest for 12 weeks. Does this look like overkill?
Test cycles are also 12 or More Weeks so why not
 

Guinnessmike

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Thanks. This is my first run with trest. I researched as much as I could find before I started, but had trouble finding definitive cycle length info.
 

whatsnatty

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For my next cycle I'm looking at running an 8 week base of either 4 andro or trest. Im going to run alpha 1 and msten with it looking for a strong wet bulk.
Week 1-8: 4 andro or Trest (8 weeks)
Week 2-8: Msten ( 6 weeks)
Week 4-8: Alpha 1 (4 weeks)

What do you guys think? Any suggestions on whether to run 4 andro as a base or trest? What's the difference between the two that makes one better than another in terms of a base for this cycle? Of course, I have my PCT and support agents as well. Let me know guys!
 
g0hardorgohom

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Trestolone (I prefer DermaTREST) blows 4-DHEA out the water. It's simply just so much more potent.

I would pick either M-Sten or Alpha 1, not use both. Actually I'd prefer DMZ over those two but that's just me.
 

whatsnatty

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I appreciate the response. How long can I run trest as a test base for? & I decided to go with alpha 1 for the wet bulk. On cycle plus ai? Wicked PCT + Ostarine + reduce + tudca for post
 

whatsnatty

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I appreciate the response. How long can I run trest as a test base for? & I decided to go with alpha 1 for the wet bulk. On cycle plus ai? Wicked PCT + Ostarine + reduce + tudca for post
 
JD70

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I'd be sure to do a good dose of nolva or Clomid with PCT. At least 20/20/10/10 nolva (tamoxifen), Maybe more alpha is not weak.
 

whatsnatty

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How long can I run trest as a base for? And thoughts on ostarine in pct?
 
g0hardorgohom

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How long can I run trest as a base for? And thoughts on ostarine in pct?
Bloodwork is the only way to know for sure. Many guys run it for 8 weeks.

Ostarine in PCT will help to maintain those hard earned gains for sure. It may be slightly suppressive for some people. I think you're good to go if you keep it at 10mg/day.
 

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Should i be using arimidex as an ai or will an otc estrogenblocker/ai like arimistane amd formeron be fine? Inhibit-P for prolactin control?
 

stillchillin

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I would at least keep an ai on hand in case estrogen sides flare up. As to which one to choose, its up to you.
 
Spaniard

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Should i be using arimidex as an ai or will an otc estrogenblocker/ai like arimistane amd formeron be fine? Inhibit-P for prolactin control?
I would recommend a prescription strength AI such as arimidex, which can be obtained via RX
 

whatsnatty

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So with my cycle arimistane and inhibit-p for estrogen and prolactin control wont suffice? Should I get arimidex and nolva? Don't like the fact of free floating estrogen after discontinuing a serm. Any sidesmwoth prescription ai's?
 
g0hardorgohom

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Arimistane won't suffice but TransFORM might - at least it does for me even with 100mg/day of DermaSTRENGTH.
 
Spaniard

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So with my cycle arimistane and inhibit-p for estrogen and prolactin control wont suffice? Should I get arimidex and nolva? Don't like the fact of free floating estrogen after discontinuing a serm. Any sidesmwoth prescription ai's?
In my opinion I would definitely opt for something stronger than arimistane.

Arimidex would be the AI, which yes I recommend. Don't use arimidex and Nolva during the cycle as you'll likely crush your estradiol levels and experience some pretty nasty sides.

Yes, usually with Rx AI's they can be a little more harsh on lipids etc. Just remember though, when it comes to TRT I would venture to say that most clinics are using Arimidex with minimal issues due to its high rate of success of aromatase inhibition and its safety profile
 

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I'm looking into running IM trestolone as base for a 16 week contest prep cycle. What's concerning me is the occasional claims of trestolone causing permanent, irreversible infertility. Wesley Inman claimed this on PHF (though when I asked for proof to back that I got no response) and I've seen one or two other people on various boards claim it as well.

There's a chance of permanent, irreversible infertility with any steroid. And with a million other things in life. Is there anything specific to trestolone that leads us to believe it can cause permanent, irreversible infertility?

I wouldn't think they'd even consider it for male contraception if that were possible. There are no female contraceptives that render a woman permanently sterile.

It seems to me like the 12x more suppression than testosterone is being taken to an extreme by some. When you're shut down, you're shut down. There aren't varying degrees of it. Once your body stops producing testosterone on its own, it stops. It doesn't go negative. It's the same as any other compound, it just happens quicker.
 

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The few things I've read on it suggested it was a viable contraceptive but it only required low doses. Maybe the dose would be the determining factor, I def remember it saying it was reversible simply by stopping use of it.
 

danieltx13

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The few things I've read on it suggested it was a viable contraceptive but it only required low doses. Maybe the dose would be the determining factor, I def remember it saying it was reversible simply by stopping use of it.
Agreed, I've read that as well.

I still don't see how even an extremely high dose for a long period of time could cause it. Testosterone will shut you down, whether it's 150mg for a month or 2g for a year, and the end result is the same. So why would it be different for trestolone?
 

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I dunno but I'm bored and interested in the answer, so I'm gonna see if I can find any case studies or articles lol
 

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DISCUSSION

This study is the first to provide evidence on the capacity of MENT to reverse osteoporosis in a preclinical animal model of male hypogonadism. The effects of MENT were also compared with T replacement, the conventional treatment for male hypogonadism. MENT is approximately 10-fold more potent than testosterone at the androgen receptor [26]. In line with previous studies [14,*17], MENT proved also a more potent androgen than T*in vivo, with the weight of the ventral prostate maintained with a much lower dose of MENT (12 versus 72 µg/day for T) in aged male orchidectomized rats. In contrast with MENT, however, T action is amplified into the more potent androgen DHT by 5?-reductase in the prostate [27]. Nevertheless, the greater potency of MENT is also observed in other androgen-sensitive organs such as the SV and even more in the LA muscle. In this context and in line with previous findings [17], MENT fully restored the integrity of the reproductive organs as well as levator ani in hypogonadal animals without overstimulation of the prostate or amplification by 5?-reductase in the reproductive tract. In accordance with earlier reports [15,28], MENT also suppressed LH more strongly than T. Such strong suppression of LH by MENT may be of clinical interest in its potential use as a male contraceptive. The effect on LH also reflects its greater androgenic potency since androgen action on LH in rats is mainly androgen receptor dependent. In fact, only DHT but not 17?-estradiol has been shown to lower LH levels in this animal model [29].

The most important question addressed in this preclinical study in hypogonadal rats was whether enhanced androgenic potency of MENT - in comparison with T - would be translated into favorable effects on bone and body composition. The aged orchidectomized rat model is a well-characterized preclinical model for overt male hypogonadism as induced by chemical or surgical castration in the elderly [5,*30]. Similar to overt hypogonadism in men, castration in aged male rats results in loss of cortical and trabecular bone mass as well as lean body mass and gain of fat [31]. In addition, androgens - when administered immediately after orchidectomy - prevent these unfavorable changes in this model [17]. However, what is unknown is if, and to what extent, androgens are also able to restore hypogonadal osteoporosis as well as changes in body composition at a later stage of hypogonadism, the focus of the current preclinical study.*

T is testosterone
A comparison of ment and t treatment on rats.


Full article: pretty good read.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204340/
 

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On paper it would appear to be far superior for a base then test, but not everything on paper is how would you say? Proportional to real life results, take msten for example on paper its a beast but its really not that great, good but not great. I'm gonna keep digging for human research if there's any creditable sources that is.
 

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Study on trestolone:

High points first:
  • Testosterone induced azoospermia quicker and in more subjects than ment
  • After 4 weeks, some men on ment had their sperm and FSH levels start to recover - while still taking ment!
  • Testosterone maintains suppression better than ment
  • Guys recovered more quickly from ment than testosterone

Full text of study - http://onlinelibrary.wiley.com/doi/10.2164/jandrol.107.002683/full

Both groups showed profound suppression of spermatogenesis initially (Figure 2). At 12 weeks, 8 of 10 subjects (80%) in the MENT group and 13 of 16 (81%) in the testosterone group demonstrated suppression to less than 1 × 106/mL, with 3 and 11 subjects, respectively, being azoospermic. Thereafter, suppression was inconsistent in the MENT group. Only 4 men maintained less than 1 × 106/mL until 24 weeks, whereas the others showed partial recovery. Overall the mean sperm concentration rose to 11.5 × 106/mL ± 5.2 × 106/mL at that time.
In contrast, the testosterone group showed maintained suppression. At 24 weeks, 14 of 16 subjects (88%) were azoospermic, and by the end of the treatment period all subjects demonstrated azoospermia (n = 14). One of the 2 men not azoospermic at 24 weeks withdrew from the study for personal reasons, and the other became azoospermic at week 44. The range of time to achieve azoospermia was therefore 4–44 weeks (median, 12 weeks). Once azoospermic, sperm were detected only in the centrifuged pellet of the ejaculate in 1 individual on 1 occasion.
Recovery was rapid following implant removal in the MENT group, with 9 of 10 subjects achieving sperm concentration of more than 20 × 106/mL within 16 weeks. Slower recovery was seen in the testosterone group, with a median duration of 28 weeks. One subject continued to show sperm concentrations of 10 × 106/mL–15 × 106/mL after more than 1 year of follow-up, with normal total sperm number, motility and morphology, and gonadotropin concentrations. A second subject underwent vasectomy before his sperm concentration had recovered to more than 20 × 106/mL, 64 weeks after removal of etonogestrel implants.
I've seen multiple people claim trestolone makes you permanently infertile with no chance of reversing it, but each time they haven't given a specific case. So for everyone taking the 12x more suppressive than testosterone and running to wild conclusions with it, educate yourself.
 

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I really don't know how people came to that conclusion I've never even heard of that happening until I came across this thread. The only thing I've read on the matter is that you simple have to stop taking it to reverse the contraceptive effects. I love tr3st, **** keeps me out of trouble with my girl. My first cycle I ran epi solo and couldn't get it up she thought I was cheating on her....
 
Spaniard

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Study on trestolone:

High points first:
  • Testosterone induced azoospermia quicker and in more subjects than ment
  • After 4 weeks, some men on ment had their sperm and FSH levels start to recover - while still taking ment!
  • Testosterone maintains suppression better than ment
  • Guys recovered more quickly from ment than testosterone

Full text of study - http://onlinelibrary.wiley.com/doi/10.2164/jandrol.107.002683/full







I've seen multiple people claim trestolone makes you permanently infertile with no chance of reversing it, but each time they haven't given a specific case. So for everyone taking the 12x more suppressive than testosterone and running to wild conclusions with it, educate yourself.
I'll get you the paper on the 12 x more suppression later but don't come in this thread telling people to educate themselves.

The reality is simple, Trestolone is being looked at for contraception due to its suppression being much higher than testosterone mg for mg. It's MUCH stronger, period, which is why they are also looking at it for HRT. They can use implants at much lower doses with Trestolone vs Testosterone also making it a more viable candidate.

The people saying you will become impotent and infertile permanently is however like you said false. Well, it can happen but the same is true with all hormones and is very unlikely that recovery will not occur.
 

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Not trying to be a smart ass, but I would like read this paper you speak of for informational purposes. I really like learning :D
 
mixedup

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I'm heading into week 7 running 100mg trest td Daily (50mg after my morning shower, 50 mg after my post w/o shower) with 100mg formestane td daily (same schedule as the trest). Stacked with 30 mg of Epi oral and 125mg arimistane daily. Just added the Epi and a-stane a week ago. I've been taking a DHEA sup (Sterone D3- 2 caps AM, 2 caps PM) from jump. My plan is to run the trest for 12 weeks. Does this look like overkill?
If your at week 7 and not having sides I'd go for it unless gains stop. I like trest but need a stronger AI at anything over 50mg
 
Spaniard

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Not trying to be a smart ass, but I would like read this paper you speak of for informational purposes. I really like learning :D
"An androgen implant with potential for contraceptive purposes in men is 7α-methyl-19-nortestosterone (MENT), a synthetic androgen [29] (Figure 2) that inhibits gonadotrophin secretion ∼10 times more than does testosterone [30]. Because MENT cannot be metabolized to 5α-reduced compounds it is hoped that it will be less prostatatogenic than testosterone itself. However, although clinical trials of MENT as a male contraceptive are under way, its efficacy has yet to be demonstrated."
You won't find that in any abstracts it's in the full text
 

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