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Blast: Trestolone Acetate + Testosterone + Superdrol + LGD / Hairygrandpa blowing up!

Whisky said:
Haha, yeah fair point. Lines have definitely been crossed already......actually decided to invest in 4mg a week cjc dac from next week to see what that dosage does.....

Waiting till september for three reasons (i literally have everything good to go for a test e, tbol, winny 14 weeker)

1) only finished pct from my 10 week trest/epi run 5 weeks back so trying to stick to a sensible time off whilst using the time off to cut (so the cycle can be a lean bulk all the way)

2) i typically travel and work less in the last few months of the year so its easier for me to be consistent with training (i train when i travel with work but lots of hotel gyms don't have a squat rack or enough weight to religiously overload)

3) i have a personal reason to want to look absolutely jacked to fcuk at year end so trying to tie in with that

4) this is probably the real reason - i go on holiday mid august for 2 weeks and have no intention of having a break in my first pin cycle lol
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I actually have thought about this a lot myself - and hairygrandpa asked me a similar question a while back. But in my mind, it's a card that I just don't want to play yet more than anything, but in more detail it's also about legality, the hassle of learning to pin and getting the equipment, etc., money and cost and healthcare (which I don't carry and is a sub category of cost). I've dabbled in things, and moral lines are blurred - but overall I am just not ready to invest and I am still thinking I have a lot of progress to be made on my own. Kind of like - how far can I get before I take that jump?
 
Whisky said:
Haha, yeah fair point. Lines have definitely been crossed already......actually decided to invest in 4mg a week cjc dac from next week to see what that dosage does.....

Waiting till september for three reasons (i literally have everything good to go for a test e, tbol, winny 14 weeker)

1) only finished pct from my 10 week trest/epi run 5 weeks back so trying to stick to a sensible time off whilst using the time off to cut (so the cycle can be a lean bulk all the way)

2) i typically travel and work less in the last few months of the year so its easier for me to be consistent with training (i train when i travel with work but lots of hotel gyms don't have a squat rack or enough weight to religiously overload)

3) i have a personal reason to want to look absolutely jacked to fcuk at year end so trying to tie in with that

4) this is probably the real reason - i go on holiday mid august for 2 weeks and have no intention of having a break in my first pin cycle lol
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All good reasons to wait. I was being a bit philosophical as far as the why wait part. :) Really just meant legally no difference, and you are already pinning so fear of needles shouldn't be a factor. The mental hurdles should pretty much be covered at this point.

I didn't remember or didn't know that you were planning a test cycle later this year. Your post sounded like you were still ambivalent as to if you would go "to the dark side".


HIT4ME said:
I actually have thought about this a lot myself - and hairygrandpa asked me a similar question a while back. But in my mind, it's a card that I just don't want to play yet more than anything, but in more detail it's also about legality, the hassle of learning to pin and getting the equipment, etc., money and cost and healthcare (which I don't carry and is a sub category of cost). I've dabbled in things, and moral lines are blurred - but overall I am just not ready to invest and I am still thinking I have a lot of progress to be made on my own. Kind of like - how far can I get before I take that jump?
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All great reasons as well.
 
xR1pp3Rx said:
idk ... if I drop my ai while on trest the nipps start screaming almost overnight.
likey user dependent.
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IMHO, this happens only when in conjunction with testosterone. To test my hypothesis, I'm going without test now. It was already established that AI's do not affect methyl estro as no aromatease enzyme is involved.
 
The reason I started (too young at my 21st bday) was because of the realization that all the guys whose physiques I admired for one reason or another were using them - and I stand by that decision, as I still believe it to be true. Gear creates a different look and builds you differently. However, I do wish I had spent a few more years learning about proper training first - I feel that I learned it all backwards, with supplements first lol
 
MrKleen73 said:
All good reasons to wait. I was being a bit philosophical as far as the why wait part. :) Really just meant legally no difference, and you are already pinning so fear of needles shouldn't be a factor. The mental hurdles should pretty much be covered at this point.

I didn't remember or didn't know that you were planning a test cycle later this year. Your post sounded like you were still ambivalent as to if you would go "to the dark side".
.
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Haha, hell no, about 4 weeks into my first ph cycle I knew I would be. Based on the fact pinning is significantly better than ph’s and I loved that first cycle I knew I had to get in on the dark side action lol
 
SkRaw85 said:
Agreed. IM trest E has been catching my eye lately....
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Only if you had experience with trest ace. It gave me gyno by week 3 and I was thankful to not have used a long ester.
If I manage to control it I would love to go for a longer ester.

Lets see if my theory is right, it would prove most cycle regimes for trest wrong. Even enhanced athlete (Tony Huge) got off trest, remarking in a video that he could not control gyno, even with ridiculous amounts of letro.... well, if AI's don't work because no aromatization is involved, no letro helps. Also, no SERM will help if the gyno is not estrogen related. That leaves us with prolactin/progesterone as the culprit. Caber is the key -and probably a low dose winstrol for progesterone control. MrKleen73 , mentioned DIM , I don't know anything about that compound -but guess he knows what he is talking about.
 
hairygrandpa said:
IMHO, this happens only when in conjunction with testosterone. To test my hypothesis, I'm going without test now. It was already established that AI's do not affect methyl estro as no aromatease enzyme is involved.
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I'm pretty sure estrogen/prolactin balance is the part of the deca only cycle to lower gyno sides.
 
Newth said:
I'm pretty sure estrogen/prolactin balance is the part of the deca only cycle to lower gyno sides.
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Exactly. By lowering prolactin, because not too much estrogen here, as long as the dosage isn't excessively high.

AND, apparently you CAN'T lower methyl estrogen by AI.
 
Hyde said:
The reason I started (too young at my 21st bday) was because of the realization that all the guys whose physiques I admired for one reason or another were using them - and I stand by that decision, as I still believe it to be true. Gear creates a different look and builds you differently. However, I do wish I had spent a few more years learning about proper training first - I feel that I learned it all backwards, with supplements first lol
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Exactly, I stand by my use as well. I was stuck in the 190's for years and then chose to use it to get to my goals. Now I had trained at least 8 years by the time I did my first cycle though. I was training hard, and eating a lot back then. At the time i wanted to be a bodybuilder and that meant getting on gear. I think I would have done decently well but got in an accident and destroyed my back, dislocated some ribs from my spine, and soft tissue damage out the wazoo. I was 238 at the time wearing 34 inch waist pants and my legs were a ripped 28 inches. Probably could have competed between 195-198 then...

It seems a lot of people are learning things backwards now, but so long as they are getting into it and bettering themselves safely and with awareness then in my opinion it is still better than not getting into the fitness lifestyle at all.


hairygrandpa said:
Only if you had experience with trest ace. It gave me gyno by week 3 and I was thankful to not have used a long ester.
If I manage to control it I would love to go for a longer ester.

Lets see if my theory is right, it would prove most cycle regimes for trest wrong. Even enhanced athlete (Tony Huge) got off trest, remarking in a video that he could not control gyno, even with ridiculous amounts of letro.... well, if AI's don't work because no aromatization is involved, no letro helps. Also, no SERM will help if the gyno is not estrogen related. That leaves us with prolactin/progesterone as the culprit. Caber is the key -and probably a low dose winstrol for progesterone control. MrKleen73 , mentioned DIM , I don't know anything about that compound -but guess he knows what he is talking about.
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Yeah, I am not an expert on this but when estrogen metabolizes it turns into 2 major forms of metabolite, or those 2 are the only ones addressed in what I have read. Either way there are 2 estrogen metabolites, one ends with a 2, and is the healthier version of metabolization, and the other ends with a 7 and is considered the methyl estrogen metabolite. DIM helps to steer the estrogen metabolization toward more of the healthier versions and less of the methyl version or something along those lines. Apparently trest tends to metabolize into methyl estrogen which the DIM should help to mitigate in theory.

Sorry was a while back when I started looking into the two so not 100% on all the details and didn't feel like going back to look.
 
hairygrandpa said:
IMHO, this happens only when in conjunction with testosterone. To test my hypothesis, I'm going without test now. It was already established that AI's do not affect methyl estro as no aromatease enzyme is involved.
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its true this time i am on test.. but the first few times i wasn't. in fact i was using trest as a test base for a few cycles before i felt like i needed to run some test again.

im currently at 300 mgs per week of test. at that dose i typically need to run very little if any AI. yet at 30mgs TD stand alone trest i need and AI
 
xR1pp3Rx said:
its true this time i am on test.. but the first few times i wasn't. in fact i was using trest as a test base for a few cycles before i felt like i needed to run some test again.
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If you can control it that way, than awesome!

You could test it by using caber and lower the AI. It appears that for prolactin gyno symptoms to flare up, it needs a certain amount of estrogen to be present, not too much. You killed that little bit off, while high on prolactin.
Trest affects progesterone -and progesterone has a pathway to convert to estrogen and prolactin (anyone correct me on this, if wrong).
Now, if prolactin is high but you use AI's to control estrogen and e2 gets low enough, gyno from prolactin may not develop. The best approach would be to curb prolactin and let that little e2 and methyl estrogen stay. As we observed, Trests conversion to methyl estro is LOW. Not too much estro here, but too much prolactin, see what I mean?
 
hairygrandpa said:
If you can control it that way, than awesome!

You could test it by using caber and lower the AI. It appears that for prolactin gyno symptoms to flare up, it needs a certain amount of estrogen to be present, not too much. You killed that little bit off, while high on prolactin.
Trest affects progesterone -and progesterone has a pathway to convert to estrogen and prolactin (anyone correct me on this, if wrong).
Now, if prolactin is high but you use AI's to control estrogen and e2 gets low enough, gyno from prolactin may not develop. The best approach would be to curb prolactin and let that little e2 and methyl estrogen stay. As we observed, Trests conversion to methyl estro is LOW. Not too much estro here, but too much prolactin, see what I mean?
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Your lactation when it kicks in is proof of the prolactin theory. Estrogen does not make you lactate.
 
xR1pp3Rx said:
this .. and i have never lactated on trest or tren or dien... ect..
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Lucky fugger... I did not lactate myself but my nipples did feminize a bit. The lumps under them swelled up temporarily, they got a bit puffy too. The little bumps around the nipples got bigger now and never went completely all the way back down. I was running prami @ 1mg a day though too. I think I probably would have lactated without it. I was running TD Trest @90 a day I think or whatever 3 doses was of the OL Dermatr3st.
 
MrKleen73 said:
Lucky fugger... I did not lactate myself but my nipples did feminize a bit. The lumps under them swelled up temporarily, they got a bit puffy too. The little bumps around the nipples got bigger now and never went completely all the way back down. I was running prami @ 1mg a day though too. I think I probably would have lactated without it. I was running TD Trest @90 a day I think or whatever 3 doses was of the OL Dermatr3st.
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1 full pump of ol tr3st was 50......
 
Whisky said:
1 full pump of ol tr3st was 50......
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Okay then it must have been 100 I am sure I didn't go over 100 a day. I would have remembered that for sure! Has been since they first came out with it and I was a rep for them. So I don't remember the particulars.
 
xR1pp3Rx said:
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Well, that would render my assertion: all 19-nors convert less to estrogen as compared to test - void
Sadly, he did not test for prolactin -but progesterone was already high.

xR1pp3Rx said:
BTW who established that ment doesn't aromatise?
is there studys refuting that conversion to estrogen occurs?
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It CONVERTS, but not by aromatazing enzymes. AI's target the enzyme -not estrogen! AI's won't help - this still stands.

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"The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. 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."
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It basically says that no aromatease enzyme is involved ( = AI's do sh1t ) but a process mediated by P450.

Discussed in this thread:

http://anabolicminds.com/forum/steroids/283628-injectable-replacement-tren.html
 
In face of Tony Huge's blood work, I now assume that gyno from Trest can be due to both: prolactin and methyl estrogen.
Since there is no known "killer " for methyl estro, if methyl estro is formed by another path that isn't amromatease, gyno will be an individual response to either estro or prolactin -or both.

Best way to go is:
-a SERM like Ralox at high dose
-cabergoline

AI's may not affect methyl estro.
 
Trestolone is a substrate for aromatase and hence produces the estrogen 7α-methylestradiol as a metabolite. discussed in these somewere:

Jump up ^ Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR (June 2008). "Dimethandrolone (7,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase". The Journal of Steroid Biochemistry and Molecular Biology. 110 (3–5): 214–22. doi:10.1016/j.jsbmb.2007.11.009. PMC 2575079 Freely accessible. PMID 18555683.

and

^ Jump up to: a b c d e f g García-Becerra R, Ordaz-Rosado D, Noé G, Chávez B, Cooney AJ, Larrea F (2012). "Comparison of 7α-methyl-19-nortestosterone effectiveness alone or combined with progestins on androgen receptor mediated-transactivation". Reproduction. 143 (2): 211–9. doi:10.1530/REP-11-0171. PMID 22065861.

basically affirming your claim that it doesn't need aromatase to convert, as it acts like aromatase..

can anyone recover the discussions on the old PHF ??

PA had this all ironed out at one time I think.
 
xR1pp3Rx said:
Trestolone is a substrate for aromatase and hence produces the estrogen 7α-methylestradiol as a metabolite. discussed in these somewere:

Jump up ^ Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR (June 2008). "Dimethandrolone (7,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase". The Journal of Steroid Biochemistry and Molecular Biology. 110 (3–5): 214–22. doi:10.1016/j.jsbmb.2007.11.009. PMC 2575079 Freely accessible. PMID 18555683.

and

^ Jump up to: a b c d e f g García-Becerra R, Ordaz-Rosado D, Noé G, Chávez B, Cooney AJ, Larrea F (2012). "Comparison of 7α-methyl-19-nortestosterone effectiveness alone or combined with progestins on androgen receptor mediated-transactivation". Reproduction. 143 (2): 211–9. doi:10.1530/REP-11-0171. PMID 22065861.
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The highlighted phrase is in contradiction to:

herefore, 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."
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xR1pp3Rx said:
.....basically affirming your claim that it doesn't need aromatase to convert, as it acts like aromatase..
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I understand it as being converted to methyl estro by "other" hepatic enzymes, not via aromatease enzyme.

I repeat, if all that is true:

Best way to go is:
-a SERM like Ralox at high dose
-cabergoline

No AI needed.
 
ralox would block estrogen and thus lessen trests ability to kick ass though... Im down right afraid to come off my AI, but im taking test too so, I wont gamble this time round. maybe next run. im planning to come off everything after this run to clear out my receptors.
 
xR1pp3Rx said:
ralox would block estrogen and thus lessen trests ability to kick ass though... Im down right afraid to come off my AI, but im taking test too so, I wont gamble this time round. maybe next run. im planning to come off everything after this run to clear out my receptors.
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Ralox is selective with preference to breast receptors, not sure that it would affect muscle growth.

I'm not taking a SERM, just caber. Lets see how this goes. I have ralox on hand for getting rid of gyno afterwards, if it happens.
After this run, I'm cruising too, at least for 6 weeks.
 
hairygrandpa said:
Well, that would render my assertion: all 19-nors convert less to estrogen as compared to test - void
Sadly, he did not test for prolactin -but progesterone was already high.



It CONVERTS, but not by aromatazing enzymes. AI's target the enzyme -not estrogen! AI's won't help - this still stands.

Invalid Link Removed



It basically says that no aromatease enzyme is involved ( = AI's do sh1t ) but a process mediated by P450.

Discussed in this thread:

http://anabolicminds.com/forum/steroids/283628-injectable-replacement-tren.html
Click to expand...

I think trest is unlike other 19-nors in many ways. Like I said, I never had estrogen problems on trest and I only used aromatase inhibitors. And I am gyno prone, a little DBOL gives my gyno, as does low dose testosterone. But high dose trest + AI = no gyno. I cant think of any way to explain all of that other than trest works through the aromatase enzyme.Or that I am immune to methyl estrogen, which I doubt seriously.

Again, never used IM. Only oral and TD
 
RickyBlobby said:
I think trest is unlike other 19-nors in many ways. Like I said, I never had estrogen problems on trest and I only used aromatase inhibitors. And I am gyno prone, a little DBOL gives my gyno, as does low dose testosterone. But high dose trest + AI = no gyno. I cant think of any way to explain all of that other than trest works through the aromatase enzyme.Or that I am immune to methyl estrogen, which I doubt seriously.

Again, never used IM. Only oral and TD
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We all can conclude that trest is weird. :)
 
The best
 
One day when i am feeling brave I will try some IM Trest Ace. One of my buddies said it was hands down the best gear he ever used running it at 50mg a day. He blew up and stayed lean on it. It was pretty unreal how fast he made gains!!!
 
Yeah screw testosterone. If I was a single man I would be cruising on TREST year round
 
You guys are talking me into hunting down some IM trest !!
 
Leg and Neck - what the heck

BB squats -smith/slow-mo
135lbs warmup x 20
155lbs 3 sec down/3 sec up x18
200lbs 3 sec down/3 sec up x9/7

linear leg press, 600lbs slow-mo
4 sec lowering
14/14/10

4x Neck exercises with 15kg plate (33lbs)

unilateral leg curls
22.5kg (50lbs) x9/9/8+1

smith reverse shrugs
135lbs quick x 56
240lbs x13/14/11

Leg extensions eccentric, holding 5 sec, lowering 5 sec
155lbs x11/7/9
 
so about that estrogen protocol for trest you plan to use.... I got this today from another member,
"Hey Bro,

Noticing some gyno in trest. I have been taking ralox at 50mg a day and it’s not working very well. I was thinking adding exemestane at 12.5 mg eod. Any recommendations?"

so again, there has to be something aromatizing with trest.
 
xR1pp3Rx said:
so about that estrogen protocol for trest you plan to use.... I got this today from another member,
"Hey Bro,

Noticing some gyno in trest. I have been taking ralox at 50mg a day and it’s not working very well. I was thinking adding exemestane at 12.5 mg eod. Any recommendations?"

so again, there has to be something aromatizing with trest.
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He has gyno from prolactin, damn, that's why ralox, exem, adex and letro does NOT work. Wanna bet?
Caber = mandatory, IMHO.
 
xR1pp3Rx said:
so about that estrogen protocol for trest you plan to use.... I got this today from another member,
"Hey Bro,

Noticing some gyno in trest. I have been taking ralox at 50mg a day and it’s not working very well. I was thinking adding exemestane at 12.5 mg eod. Any recommendations?"

so again, there has to be something aromatizing with trest.
Click to expand...
Oh it aromatizes but not through aromatase. The enzyme has no effect on it, it armoatization is independent of that. Also gyno probably has a lot to do with it's his progesterone activity and prolactin. Winstrol or proviron would help the progesterone activity problem and Caber for prolactin. Ralox is the only option for is estrogen control.

Really should use all 3 with trest.
 
What if we just all get jacked and have wildly overblown D-cup gyno, and it just becomes the new norm?

It’s 2018 people
 
Aromatization of 7 alpha-methyl-19-nortestosterone by human placental microsomes in vitro.

LaMorte A1, Kumar N, Bardin CW, Sundaram K.

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Author information


Abstract

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.










From Wikipedia:

Pharmacodynamics[edit]

As an AAS, trestolone is an agonist of the androgen receptor (AR), similarly to androgens like testosterone and dihydrotestosterone (DHT).[4][3] Trestolone is not a substrate for 5α-reductase and hence is not potentiated or inactivated in so-called "androgenic" tissues like the skin, hair follicles, and prostate gland.[12] As such, it has a high ratio of anabolic to androgenic activity, similarly to other nandrolone derivatives.[4][3] Trestolone is a substrate for aromatase and hence produces the estrogen 7α-methylestradiol as a metabolite.[7][13] However, trestolone has only weak estrogenic activity and an amount that would appear to be insufficient for replacement purposes, as evidenced by decreased bone mineral density in men treated with it for hypogonadism.[5][3] Trestolone also has potent progestogenic activity.[7][3] Both the androgenic and progestogenic activity of trestolone are thought to be involved in its antigonadotropic activity.[









MENT (7alpha-methyl-19-nortestostrone), or trestolone was one of several 19-nortestosterone derivatives to be investigated as a possible male contraceptive therapy due to its unique chemical properties. Initially, drug companies were combining progesterone with testosterone in order to produce a viable male contraceptive option due to progesterone's ability to suppress spermatogenesis. While testosterone can decrease sperm production, the dose for a test-only birth control would be too high to avoid unwanted side effects. Testosterone can also convert to DHT via 5alpha-reductase, it can have deleterious effects on the prostate, as well as increase male pattern balding. [1] Since MENT was incapable of binding to 5alpha-reductase and thus cannot convert to DHT, it made it a perfect candidate for an androgen male contraceptive. The reason for this lies in the unique alpha methyl group on carbon 7 of the molecule. This methyl group sticks out below the steroidal ring structure and sterically inhibits conversion to DHT. However, MENT still can undergo aromatization and undergo other androgen-dependent functions, making it effectively act like testosterone in the body despite being a 19-nortestosterone derivative. [2][3] MENT was also shown to have minimal affinity for the progesterone and mineralocorticoid receptors, despite being a nandrolone derivative.
 
Some have had success using AI's, some have not. I cannot tell you why. However, I am compelled to believe suicidal inhibitors like formestane and exemestane are more effective at deterring the aromatization of trestolone.
 
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