Trestalone experiences?

[Gonz0]

Using ment ace for the first time, not bulking , going to be eating at maintenance with 1 high day. Just wanted to know if anyone’s used it in a cut/recomp stack and how did they like it ? Currently running 175/280/140/35 test C, primo , mast E , ment ace. May increase the primo and ment once everything saturates, I’m only on day 2 so not really feeling the ment yet.

 

[Gonz0]

With that DHB dose im not sure if he'll need an AI. His e2 might even be crashed..I could be wrong but..

Lol! I need to give DHB another shot. I’ll always get to about 2 weeks and then drop it because of the pip

 

[Gonz0]

I do .5 adex Monday and Thursday. Keeps everything working

I got a couple vials of DHB laying around , you’re making me want to throw some in but every time I try and run DHB I always pussy out from the pip lol

 

[Photon]

Lol! I need to give DHB another shot. I’ll always get to about 2 weeks and then drop it because of the pip

I gave up after the first week..

 

[Sickxlost]

I got a couple vials of DHB laying around , you’re making me want to throw some in but every time I try and run DHB I always pussy out from the pip lol

I gave up after the first week..

Man I’ve heard that for so many years but where I get mine it’s pip free. It has to be the way it’s cooked… I’ve only used from 2 labs (both I’ve been with for years) and it’s gtg

 

[lilchikin]

Im 4 weeks in to mast/ment. Absolutely loving it. This will be my goto cycle from now on. Doing carb cycling with two high days, progressing great so far

 

[Gonz0]

Man I’ve heard that for so many years but where I get mine it’s pip free. It has to be the way it’s cooked… I’ve only used from 2 labs (both I’ve been with for years) and

Im 4 weeks in to mast/ment. Absolutely loving it. This will be my goto cycle from now on. Doing carb cycling with two high days, progressing great so far

Hell yeah bro ! I might increase the mast , it’s my favorite compound but with the shortages I’m trying to use it sparingly lol so only running 140 mg weekly. Carb cycling has been a game changer , I’ve been doing it for almost a year now

 

[Slowww]

i wouldn’t use ment in a cut personally. Too watery. If I’m going to get shredded I want to be as dry as possible by the end, without diuretics, or destroying estrogen. But love ment in off season. Get strength going up like crazy greater to tren probably due to leverages changing, but 0 psychological or sexual side effects.

 

[Gonz0]

i wouldn’t use ment in a cut personally. Too watery. If I’m going to get shredded I want to be as dry as possible by the end, without diuretics, or destroying estrogen. But love ment in off season. Get strength going up like crazy greater to tren probably due to leverages changing, but 0 psychological or sexual side effects.

I would usually run tren with something like this but I really want to experiment with ment lol. Running 175/280/140/52 - test C/primo/mast E/ment A. The thought behind it is to use a lowish dose of ment just to keep e2 in a good spot so I can run my dht’s higher. Very low aromatizer, 1000/300 test/eq crashes my e2. May increase the primo and ment as the cycle progresses , If water begins to be an issue I’ll end up dropping the ment, upping the test and adding in tren.

 

[Slowww]

I would usually run tren with something like this but I really want to experiment with ment lol. Running 175/280/140/52 - test C/primo/mast E/ment A. The thought behind it is to use a lowish dose of ment just to keep e2 in a good spot so I can run my dht’s higher. Very low aromatizer, 1000/300 test/eq crashes my e2. May increase the primo and ment as the cycle progresses , If water begins to be an issue I’ll end up dropping the ment, upping the test and adding in tren.

Yeah that’s fair, up to you man, I’m not criticizing just answering your question haha.

Ment will not increase e2, but will increase methylated estradiol which is much more potent. It will not appear on blood work if you’re doing the basic hormone panel test/e2 etc... Also the dhts— primo & masteron as well as ai will not help you control the type of aromatization that occurs with ment. I ran a decent amount of eq and ai with ment, and it did nothing when it came to side effects regarding methylated estradiol.

 

[Gonz0]

Yeah that’s fair, up to you man, I’m not criticizing just answering your question haha.

Ment will not increase e2, but will increase methylated estradiol which is much more potent. It will not appear on blood work if you’re doing the basic hormone panel test/e2 etc... Also the dhts— primo & masteron as well as ai will not help you control the type of aromatization that occurs with ment. I ran a decent amount of eq and ai with ment, and it did nothing when it came to side effects regarding methylated estradiol.

Damn dude I appreciate the info !! This sounded good on paper but I’m not sure if this will work lol

 

[sliderke]

Ment was good to me. I ran 25mg eod. I ran it in my off-season, I don't see why you would run it in a deficit or maintenance though. Not exactly a compound I would run for the hell of it. Strength seemed never ending with it. Felt like I could lay in bed for 3 months and still come in to hit pr's.

Did you run it with test or something else in conjunction.

 

[accidentaljedi173]

Did you run it with test or something else in conjunction.

I ran it along side test, and eq.

 

[ChemBB]

View attachment 334907
Feel amazing with it right there

Trest won't increase your E2 levels.

It does _not_ aromatize into Estradiol, its aromatase metabolite is 7a-methyl-Estradiol (7a-Me-E2)

For proof: Here is bloodwork 1 month after stopping 350mg Test E
I had been running 200-300mg Trest D (Amino Asylum, I had Jano test it) for months.

You can see my E2 is crushed (13pg/mL) to what you'd expect with ~260ng/dL Test.

It's physically impossible for an E2 LC/MS to detect 7a-Me-E2. The molar mass of the two are different and so are the collision products.

To simplify it: LC/MS looks for very particular "molecular fingerprints" which the machines are calibrated to. Even slight modifications from the target molecule produce significant enough changes that the assay won't detect it.

 

[sliderke]

It doesn’t aromatise to e2. But could give gyno very rapidly if you pair it too high with testosteron.
Maybe your bloods were better because on trest D? Trest D better than ace?

 

[ChemBB]

It doesn’t aromatise to e2. But could give gyno very rapidly if you pair it too high with testosteron.
Maybe your bloods were better because on trest D? Trest D better than ace?

The affinity of 7a-Me-E2 for the Estrogen Receptor is 1% higher than E2.

If you assume a 1-to-1 relative aromatization rate, (e.g. that 100mg of Test and 100mg of Trest produce equivalent amounts of their aromatase metabolite) then the gyno risk is no different than running Testosterone at <whatever Trest dose>.

It doesn’t aromatise to e2. But could give gyno very rapidly if you pair it too high with testosteron.
Maybe your bloods were better because on trest D? Trest D better than ace?

The idea that there is some "synergy" or potency-enhancing of Trest to standard E2 is false.

Because both E2 and 7a-Me-E2 bind to the Estrogen Receptor, they COMPETE for binding at target sites.

This is the same principle behind why you can't squeeze more gains out of taking more gear whose primary target is the AR -- once AR receptor saturation occurs, there literally is nowhere for the steroids to "dock" to exert their effects.

You have to look to compounds whose primary mechanism of action is not via the Androgen Receptor, like Anadrol/Winstrol/Anavar.

----

Honestly, I don't know where people on the internet come up with these absurd broscience ideas, and why others continue to parrot them.

They're so easy to debunk if you do basic bloodwork and scientific research.

 

[ChemBB]

It doesn’t aromatise to e2. But could give gyno very rapidly if you pair it too high with testosteron.
Maybe your bloods were better because on trest D? Trest D better than ace?

The only difference between esters of a compound is the rate at which esterase (Esterase - Wikipedia) is able to cleave the side-chain and yield bio-active free hormone.

Sure, there are differences in potency mg-for-mg due to the molar mass of the ester, but all else equated the only other difference is the Area-under-Curve for serum blood levels.

 

[HKOX]

The affinity of 7a-Me-E2 for the Estrogen Receptor is 1% higher than E2.

If you assume a 1-to-1 relative aromatization rate, (e.g. that 100mg of Test and 100mg of Trest produce equivalent amounts of their aromatase metabolite) then the gyno risk is no different than running Testosterone at <whatever Trest dose>.



The idea that there is some "synergy" or potency-enhancing of Trest to standard E2 is false.

Because both E2 and 7a-Me-E2 bind to the Estrogen Receptor, they COMPETE for binding at target sites.

This is the same principle behind why you can't squeeze more gains out of taking more gear whose primary target is the AR -- once AR receptor saturation occurs, there literally is nowhere for the steroids to "dock" to exert their effects.

You have to look to compounds whose primary mechanism of action is not via the Androgen Receptor, like Anadrol/Winstrol/Anavar.

----

Honestly, I don't know where people on the internet come up with these absurd broscience ideas, and why others continue to parrot them.

They're so easy to debunk if you do basic bloodwork and scientific research.

I believe the issue with trestolone vs. test is in with the former's potency, rather than its affinity to the receptor.

 

[NotHuman]

I used to love as little as 5-10mg MENT daily but it just raises my heart rate too much and now that I’m taking Reta, I’d be worried it would take me into Tachycardia and I’d have to take too much Nebivolol that it would give me way too low blood pressure.

 

[ChemBB]

I believe the issue with trestolone vs. test is in with the former's potency, rather than its affinity to the receptor.

García-Becerra et al. demonstrate "estrogen activity via both ER subtypes with efficiency similar to natural E2":

Comparison of 7α-methyl-19-nortestosterone effectiveness alone or combined with progestins on androgen receptor mediated-transactivation

In the murine uterine, 7a-Me-E2 shows x1.5 the potency of E2: "7 alpha-Methylestradiol-17 beta was 150% as active as estradiol-17 beta as an uterotropic agent."

Structure-activity relationships of estrogens. Effects of 14-dehydrogenation and axial methyl groups at C-7, C-9 and C-11

Casting aside objective literature and diving into anecdata:

I got gyno from 500mg Test E + 50mg Dbol as a teen.

Currently running (w/ no AI) 600mg Test + 150mg Trest D, previously running 200-300mg Trest D solo, and have not so much as a nipple itch.

Like I said, I'm unsure of where this urban legend of "estro monster MENT" originated but it's patently false.

 

[Photon]

The affinity of 7a-Me-E2 for the Estrogen Receptor is 1% higher than E2.

If you assume a 1-to-1 relative aromatization rate, (e.g. that 100mg of Test and 100mg of Trest produce equivalent amounts of their aromatase metabolite) then the gyno risk is no different than running Testosterone at <whatever Trest dose>.

Basically what you're saying is that if one does not aromatise much at all, or if they take an AI like aromasin which inhibits the enzyme, there is little conversion to methyl e2?

And going further..if one takes something like EQ, which increases E1, which prevents conversion of E2, then it will also prevent the conversion to methy e2?