Injectable replacement for tren during a strength cycle
- Thread starter BigNerd
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2kvette
Active member
What are you saying? Trest is an aromatase substrate(the normal pathway), but the normal pathway isnt needed? So AI's which affect the normal pathway in the peripheral tissues shouldn't be useful in dealing with trestolone aromatization.
xR1pp3Rx
Legend
no im saying, from the research ive seen on trest specifically, multiple avenues are available for trest to convert and AIs do have appreciable effects on trests its ability to convert into estrogens.
im not saying everyone can get by with or with out one. everyone reacts differently to trest. I saw some one post they can run it with out any ancillaries, and anecdotally that's not the case for most.
2kvette
Active member
Just two avenues so far are known to be available. One avenue is the aromatase pathway in the periphery, the other is by cyp3A4 mediated dehydrogenation of the A-ring. The A-ring then undergoes keto-enol tautomerization upon its own without interaction with any enzymes at all to 7 methyl estradiol.
The aromatase enzyme pathway is so ineffective at converting trestolone into estrogens that in studies of trestolone on men, they all lost bone density, a common feature of menopausal estrogen decline.
This study: Invalid Link Removed goes in depth at just how much trest can aromatize and how it is slow and inefficient. This is why trestolone was abandoned, it causes an estrogen deficiency that leads to bone loss.
The second pathway is effective, but aromatase inhibitors don't target it.
hairygrandpa
Legend
2kvette , how would you interpret the lab results of T. Huge after 100mg trest ace/d? Supposing they are real and no other aromatizing compound was used.
I'm with you and firmly believe that "trest gyno" is not estrogen related -but by prolactin/progesterone.
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I'm currently using trest-ace without test, next week I'll stop using AI's, when test is out of my system -to prove the point that AI's do not work with trest (or at least , that it doesn't matter whether you take them -or not). I got gyno symptoms twice from trest in the past -but never used caber to curve prolactin, now I do.
I'm with you and firmly believe that "trest gyno" is not estrogen related -but by prolactin/progesterone.
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I'm currently using trest-ace without test, next week I'll stop using AI's, when test is out of my system -to prove the point that AI's do not work with trest (or at least , that it doesn't matter whether you take them -or not). I got gyno symptoms twice from trest in the past -but never used caber to curve prolactin, now I do.
hairygrandpa
Legend
By the way, the link to Tony's lab test is from xR1pp3Rx . It seems to demonstrate that trest heavily converts (aromatizes?) to a lab measurable estrogen (methyl estrogen?). If so -and if AI's do not curve the conversion, how does one control that much estrogen (SERM?).
Edit: 2kvette ,
Tony's lab test is showing ultra high estrogen, that would imply, that somehow methyl estrogen is not beneficial for bone density and is different from regular estrogen. If we assume all that, could we also assume that methyl estrogen may not cause gyno?
Edit: 2kvette ,
Tony's lab test is showing ultra high estrogen, that would imply, that somehow methyl estrogen is not beneficial for bone density and is different from regular estrogen. If we assume all that, could we also assume that methyl estrogen may not cause gyno?
2kvette
Active member
Well, my point was never that it didn't aromatize. Just that it didnt do it through the aromatase enzyme. So AI's are worthless. SERMs are definitely needed. But who knows what that guy was on before then. If you were taking 1g of test a week before that blood work, its gonna take 5 weeks to return that level to normal limits. This and what every else he was doing will be reflected in blood work.
But progesterone and prolactin are big issues as well.
2kvette
Active member
100mg of Ace a day is far beyond what was ever tested clinically. IIRC, the most they used was something like 8mg. Trestolone likely displays what’s called dose dependent pharmacokinetics. In that it displays different metabolic results at different dosages; and not in a linear fashion. This could be one explanation for his wild estrogens.
But also, look at his lab work. Estradiol, the product of aromatase, is low. But total estrogens, the 7 methylestradiol, is high. It didn’t aromatase!
hairygrandpa
Legend
2kvette , what do we know about the so called methyl estrogen (ME)?
-apparently ME is not beneficial to bone density (study), like regular estrogen, or trest dose was to low for study?.
-Does trest convert to it? (apparently so)
-read somewhere that ME does NOT show on regular lab tests, only estrogen does? (maybe false)
-can it be controlled by AI (apparently not if its the product of a different pathway as test-estrogen aromatease)? -solved-
-does ME cause gyno, like estrogen does if high? Studies?
-can it be controlled by a SERM, like estrogen? Studies? Does it need to be controlled (assuming it may not cause gyno)?
-is libido affected by ME? (assuming my ME levels to be high right now -but libido is up, contrary to high estrogen levels)
-apparently ME is not beneficial to bone density (study), like regular estrogen, or trest dose was to low for study?.
-Does trest convert to it? (apparently so)
-read somewhere that ME does NOT show on regular lab tests, only estrogen does? (maybe false)
-can it be controlled by AI (apparently not if its the product of a different pathway as test-estrogen aromatease)? -solved-
-does ME cause gyno, like estrogen does if high? Studies?
-can it be controlled by a SERM, like estrogen? Studies? Does it need to be controlled (assuming it may not cause gyno)?
-is libido affected by ME? (assuming my ME levels to be high right now -but libido is up, contrary to high estrogen levels)
hairygrandpa
Legend
I suspect that:
Estrogen (methyl estrogen) from trest conversion does not cause gyno, as it also does not affect libido -it may be a total different animal.
My believe is, probably ALL gyno from 19-nors is caused by high prolactin. Rendering the use of AI's AND SERMS useless/unnecessary.
Control of prolactin -and in case of trest, progesterone is the key (caber, bromo, prami + winstrol).
I obviously can be dead wrong on this -but all my experiments so far are leading me to believe that.
Estrogen (methyl estrogen) from trest conversion does not cause gyno, as it also does not affect libido -it may be a total different animal.
My believe is, probably ALL gyno from 19-nors is caused by high prolactin. Rendering the use of AI's AND SERMS useless/unnecessary.
Control of prolactin -and in case of trest, progesterone is the key (caber, bromo, prami + winstrol).
I obviously can be dead wrong on this -but all my experiments so far are leading me to believe that.
xR1pp3Rx
Legend
thanks for posting this, its an interesting read.. I did find one thing in the table shown, that the methylestradiol has the slowest rate of clearance across the board, so even though it (trest) has a slow and inefficient conversion via aromatse to m-est, the clearance rates might be whats causing the estro related sides for people.
again excellent find ~
hairygrandpa
Legend
That is the big question! DOES ME indeed cause sides? Which? I assume bloat, is a given (high BP could be assumed as a consequence) -but how comes libido is high with high levels of ME?
I cant find relevant studies comparing estrogen to methyl estrogen, especially when it comes to controlling -or lowering it. Everything we do, like taking AI's and SERM's we do because others do.
2kvette
Active member
And good find for you as well. This 100% explains his sky high E2. If 7methyl-E is cleared slower than normal estradiol, then accumulation occurs. Did you find the half life for 7ME? Because I can tell you just how much is building up by some math.
2kvette
Active member
7-Methyl-Estradiol is 10% more potent than the normal estradiol that test converts to. And, as xR1pp3Rx just pointed out, has a slower clearance half life compared to normal estradiol. So its just a touch stronger than normal estrogen, and lasts longer in the system than normal estrogen. This explains everything reflected in his blood work.
But just a normal SERM will prevent the sides, AI won't prevent anything at all.
xR1pp3Rx
Legend
7a MENT=27.5 min retention time vs 7aMethylEstradiol 33.5 mins respectively.
conversely... testosterone= 34.5 min vs 17b estradiol 31.3 mins <----- notice the lesser time of clearance between these two!!!
hairygrandpa
Legend
That is what all assume.
If its identical to estrogen -and even more potent, why doesn't libido suffer with high ME? But suffer greatly when estrogen is high?
2kvette
Active member
b/c your taking trest with it. Trest has 5x the androgenic (sexual) gene expression effects of testosterone. So its potent at counteracting this. And high estrogen doesnt kill sex drive a lot of times, but low E does. I've been on both sides of this coin and my dick will take high E any day.
hairygrandpa
Legend
Thank you! That makes sense!
I'm about to cruise again. I learned today to be careful coming off of trest, because methyl estrogen will remain high for some time ( thank you xR1pp3Rx ) -and it can not be leveled down by AI. I will lowering the dose of trest slowly, to let m-estro get slowly lower too, while introducing a longer test ester.
Micash3641
New member
I know this is a three year old thread, but had to throw this in here. True progestins can’t aromatize. Nandrolone is both a androgen and progestin. It has minimal if any aromatization. Trestolone though also a 19 NOR aromatizes quite heavily. It aromatizes into the potent methyl estradiol.
Part of the biological effects of testosterone (T) are mediated by its enzymatic reduction to 5 alpha-dihydrotestosterone (DHT) or aromatization to estradiol (E2). 7 alpha-Methyl-19-nortestosterone (MENT) is a synthetic androgen that is considerably more potent than T. Previous studies have shown that MENT is not 5 alpha-reduced. The studies reported here were undertaken to determine whether MENT undergoes enzymatic aromatization in vitro. Human placental microsomes were used as the source of the aromatase. Radioactive or nonradioactive T or MENT was incubated with the microsomes in the presence of NADPH and the metabolites extracted out with ethyl ether. Following evaporation of ether, the residue was dissolved in benzene-petroleum ether and extracted with 0.4 N NaOH which selectively removes phenolic metabolites of the androgens. When either radioactive T or MENT was incubated with the aromatase in the presence of NADPH, there was a 20-fold increase in the amount of radioactivity extracted with NaOH. In contrast, if the incubation was carried out in the absence of NADPH or in the presence of R76713, an aromatase inhibitor, most of the radioactivity remained in the benzene-petroleum ether phase. To further identify the enzymatic reaction products, thin layer chromatography (TLC) was performed. The Rf value for MENT was 0.22 while that of the major reaction product was 0.34, which corresponded with the RF value of the estrogen, 7 alpha-methyl-estradiol (MeE2). This was further verified by using a second solvent system for the chromatographic separation. In an effort to ascertain whether the metabolites bind to estrogen receptors (ER), rat uterine cytosol was used. NaOH extracts of medium following incubation of nonradioactive MENT with microsomes showed competitive inhibition of [3H]E2 binding to rat uterine ER. Furthermore, after [3H]MENT was incubated with microsomes, the radioactive metabolite extracted in NaOH showed specific binding to the ER which could readily be displaced with E2 or MeE2. These results indicate that like T, MENT undergoes enzymatic aromatization.
2kvette
Active member
Correct. They do not aromatize via the aromatase enzyme. They do it via a different enzyme that is specific to the liver.
Joshinator
Active member
Cool info! I never knew that
Matthersby
Well-known member
Ment is so damn amazing. SHBG be damned