Injectable replacement for tren during a strength cycle

fueledpassion said:
How about Tren? Does this also happen with Tren to some degree? I ask, because I always notice that Tren works much better with much less sides for me when I run low dose of Test. I suppose one reason is because less test = less estrogen in the body, too.

Just trying to find common ground with this information and what I know anecdotally about Tren.
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With tren it's a mixed bag, I've seen so much conflicting information. But off the top of my head I would say it's much much less likely to aromatize due to the tri-ene system possibly balancing the conjugation out of the direction of the A-ring. Some studies have shown it to aromatize a little, others have detected nothing. So I think this one is likely user dependent due to different isozymes of Cyp3A4 in each individual.

What you know anecdotally about tren is absolutely right. Tren is potent at the progesterone receptor, and running it with test is a must. The whole less estrogen = less test is kind of misleading. It's not so much about the amount of estrogen so to speak, but the ratio of T to E. As testosterone levels get lower, estradiol becomes dominate. Estradiol dependent gene transcription begins to out pace androgen dependent gene transcription, leading to increases in estrogenic side effects. Additionally, testosterone acts as an antagonist to estradiol, and balances or neutralizes it's effects. This is why you might get gyno from running test at 300mg/wk, and at 600mg/wk you wil notice a shrinkage of gyno. This is also why testosterone is used as a third tier medication in many breast cancer chemo care plans. Because high enough doses will slow or stop estrogen dependent cell proliferation/differentiation.
 
2kvette said:
With tren it's a mixed bag, I've seen so much conflicting information. But off the top of my head I would say it's much much less likely to aromatize due to the tri-ene system possibly balancing the conjugation out of the direction of the A-ring. Some studies have shown it to aromatize a little, others have detected nothing. So I think this one is likely user dependent due to different isozymes of Cyp3A4 in each individual.

What you know anecdotally about tren is absolutely right. Tren is potent at the progesterone receptor, and running it with test is a must. The whole less estrogen = less test is kind of misleading. It's not so much about the amount of estrogen so to speak, but the ratio of T to E. As testosterone levels get lower, estradiol becomes dominate. Estradiol dependent gene transcription begins to out pace androgen dependent gene transcription, leading to increases in estrogenic side effects. Additionally, testosterone acts as an antagonist to estradiol, and balances or neutralizes it's effects. This is why you might get gyno from running test at 300mg/wk, and at 600mg/wk you wil notice a shrinkage of gyno. This is also why testosterone is used as a third tier medication in many breast cancer chemo care plans. Because high enough doses will slow or stop estrogen dependent cell proliferation/differentiation.
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Interesting. I find the Tren behaves better with a low to moderate dose of Test. My post was meant to distinguish between low Test and high Test with Tren. But I never run Tren without T3 and never without AI's as long as I run T with it.
 
Any consider running tren without test? Like
tren 500mg
Mast 500-700mg
T3(at preferred dose)
In theory(atleast my theory) it would eliminate alot of side because you don't have to worry about estrogen
 
rtmilburn said:
Any consider running tren without test? Like
tren 500mg
Mast 500-700mg
T3(at preferred dose)
In theory(atleast my theory) it would eliminate alot of side because you don't have to worry about estrogen
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If I understand 2k correctly that could possibly make it worse because you could potentially still have estrogen in your body or possibly some sort of aromatization from tren with no testosterone. So then your testosterone to estrogen ratio would be even worse
 
I wanted to say that the no ester TDs are nowhere near as strong as the ace TDs from my experience.. I understand IM this could be a different story.
OLs td had no ester.
POs td had ace ester.
 
CATdiesel76 said:
If I understand 2k correctly that could possibly make it worse because you could potentially still have estrogen in your body or possibly some sort of aromatization from tren with no testosterone. So then your testosterone to estrogen ratio would be even worse
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If I'm not mistaken, 2K stated above that estrogen may not be the biggest problem with nandrolone. It appears 5 AR attacks the nor 19 steroids, and the end result is dihydroandrolone. I believe he also made the point that nandrolone doesn't actually aromatize.
 
CATdiesel76 said:
If I understand 2k correctly that could possibly make it worse because you could potentially still have estrogen in your body or possibly some sort of aromatization from tren with no testosterone. So then your testosterone to estrogen ratio would be even worse
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Nandrolone can amrotize tren cant it also can't be 5a reduce like deca can.
 
rtmilburn said:
Nandrolone can amrotize tren cant it also can't be 5a reduce like deca can.
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You need to read this whole thread.
Nortestosterone can 5 alpha reduce. That was 2K's point earlier in the thread. He explained the entire mechanism.

"Okay takeaways is this. You know the dreaded deca Dick? It's not from estrogen or prolactin(well it does play a big role tbh). What causes this is something called DHN, dihydronandrolone. 19-Nors do get 5a reduced. And and 5a-reduced 19-nors tend to be POTENT anti-androgens. So AI's aren't the biggest concern with 19-nors, it's 5a inhibitors & second prolactin.

So anytime your using deca, go for a 5a-reductive inhibitor and then think about prolactin."

He went into some detail before that, too.
 
BigNerd said:
You need to read this whole thread.
Nortestosterone can 5 alpha reduce. That was 2K's point earlier in the thread. He explained the entire mechanism.

"Okay takeaways is this. You know the dreaded deca Dick? It's not from estrogen or prolactin(well it does play a big role tbh). What causes this is something called DHN, dihydronandrolone. 19-Nors do get 5a reduced. And and 5a-reduced 19-nors tend to be POTENT anti-androgens. So AI's aren't the biggest concern with 19-nors, it's 5a inhibitors & second prolactin.

So anytime your using deca, go for a 5a-reductive inhibitor and then think about prolactin."

He went into some detail before that, too.
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Deca aka nandrolone Can yes. Tren cannot
 
Not trying to sound like a dick either, but 2k is acting like he knows more than he does.

Atleast that my perception. Interpretation on a forum can be a b!tch so he definitely could be a lot smarter than im portraying him.

From all the literature I've read for 19nors to be 5a reduces, it needs to turn in to its ad version(Dione and diol) first. Making it a 2 step for it to convert, which definitely happens. However not in high quantities.

Oh ya conversion definitely happens both ways. So test can turn into androstenedione and androstenediol and even dhea and visa versa. Thats why these dhea prohoromones are so unpredictable

PS I felt like I should add that I admitly acknowledge I not the smartest, and expert, oranything of the sort. I just have a passion for this and use college as an excuse to studies these things more. So I could most definitely be wrong.
 
rtmilburn said:
Not trying to sound like a dick either, but 2k is acting like he knows more than he does.

Atleast that my perception. Interpretation on a forum can be a b!tch so he definitely could be a lot smarter than im portraying him.

From all the literature I've read for 19nors to be 5a reduces, it needs to turn in to its ad version(Dione and diol) first. Making it a 2 step for it to convert, which definitely happens. However not in high quantities.

Oh ya conversion definitely happens both ways. So test can turn into androstenedione and androstenediol and even dhea and visa versa. Thats why these dhea prohoromones are so unpredictable

PS I felt like I should add that I admitly acknowledge I not the smartest, and expert, oranything of the sort. I just have a passion for this and use college as an excuse to studies these things more. So I could most definitely be wrong.
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I am an actual expert, that went to college for 7 years for these things. In two more years, I'll be Dr. 2kvette, I'll post pictures of my state license if people don't believe my credentials.

As for the 5a reduced versions; the ketone or alcohol version isn't going to matter a whole lot. For 19nors to be 5a reduced it depends on whether they are estrene or estrane's. Estranes are already 5a reduced, estrenes are not. Deca is an estrene, there is nothing inhibiting it from being 5a reduced, no steric effects, no stereochemistry, and no function groups that would interfere. Tren is a estrene as well; but it is also a triene. It is unlikely to aromatize due to the triene system, so instead of the electrons being pushed towards c19 and the 19 methyl becoming the leaving group, they'll get pushed towards c18 and the 18 methyl becomes the leaving group.

And yes, alot of these enzymes work both ways, not all though, but many do. This comes down to phase 1 and phase 2 of metabolism, phase one is where a function group handle is added or modified, where a diol or dione will get converted to one or the other. Then, comes phase 2 which is conjugation where it is hooked onto a gluccoronide group. This matters because the reason they get converted to the diol or dione is each time they pass through the liver a portion of the substance undergoes either phase 1 or phase 2. Some will go diol, some will go dione, depending on what specific enzyme it is exposed to.
 
BigNerd said:
Others in this thread are far more knowledgeable than I in this arena. If you look at tren, it is nandrolone-19-nor-δ9,11-testosterone, Δ9,11-nandrolone, or estra-4,9,11-trien-17β-ol-3-one.

I'll await clarification on this, but there was no distinction made in this thread between tren and nandrolone..
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Yep you are correct my friend. tren is nandrolone with two extra double bonds, one at 9 and another at 11
 
Others in this thread are far more knowledgeable than I in this arena. If you look at tren, it is nandrolone-19-nor-δ9,11-testosterone, Δ9,11-nandrolone, or estra-4,9,11-trien-17β-ol-3-one.

I'll await clarification on this, but there was no distinction made in this thread between tren and nandrolone..
 
So, is it safe to say that a very low dose of T3 will be as beneficial with nandrolone and deca as it is on tren?
 
Hyde said:
So, is it safe to say that a very low dose of T3 will be as beneficial with nandrolone and deca as it is on tren?
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I really don't know to be honest with you. Fueled passion says that it helps. But this is something I've never looked into, so maybe. Anecdotal evidence from others as stated above indicates it helps. It wouldn't surprise me if it does help with something; I do remember reading something about certain androgens lowering thyroid activity.

For the naysayers out there who say I'm just some guy rambling on the internet. I just said above I wasn't sure, if there is something I don't know I'll say it honestly. If I'm wrong on something and caught, I'll take my lumps and fess up. Can't be right all the time; and education is overrated. I'm 120k in debt for stuff I could have taught myself with google.
 
rtmilburn said:
Any consider running tren without test? Like
tren 500mg
Mast 500-700mg
T3(at preferred dose)
In theory(atleast my theory) it would eliminate alot of side because you don't have to worry about estrogen
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I just almost guarantee that ED will take place though but maybe not at first. You have to keep excessive estrogen out of the picture and prolactin at bay and maybe Tren is good for keeping normal penile function.
 
2kvette said:
I am an actual expert, that went to college for 7 years for these things. In two more years, I'll be Dr. 2kvette, I'll post pictures of my state license if people don't believe my credentials.

As for the 5a reduced versions; the ketone or alcohol version isn't going to matter a whole lot. For 19nors to be 5a reduced it depends on whether they are estrene or estrane's. Estranes are already 5a reduced, estrenes are not. Deca is an estrene, there is nothing inhibiting it from being 5a reduced, no steric effects, no stereochemistry, and no function groups that would interfere. Tren is a estrene as well; but it is also a triene. It is unlikely to aromatize due to the triene system, so instead of the electrons being pushed towards c19 and the 19 methyl becoming the leaving group, they'll get pushed towards c18 and the 18 methyl becomes the leaving group.

And yes, alot of these enzymes work both ways, not all though, but many do. This comes down to phase 1 and phase 2 of metabolism, phase one is where a function group handle is added or modified, where a diol or dione will get converted to one or the other. Then, comes phase 2 which is conjugation where it is hooked onto a gluccoronide group. This matters because the reason they get converted to the diol or dione is each time they pass through the liver a portion of the substance undergoes either phase 1 or phase 2. Some will go diol, some will go dione, depending on what specific enzyme it is exposed to.
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What about Dienolone? I'm guessing it has a "Dien" system. I'm always told it cannot convert to estrogen - especially by your arch nemesis in this thread, much like you suggest about Nandrolone but a matter of fact is that water weight and estrogen-related, lumpy gyno forms under my nipple not unlike Trestolone only considerably easier to control with mild AI's. I would refer to some random article commentary on the FDA's research with Dienolone, which is here - http://anabolicminds.com/forum/steroids/98883-dienolone-boldione-testing.html for additional thought-provoking data.

This is the compound I really need to understand because this is what I have lying around. Btw, Dienolone is a very anabolic hormone and I've been thinking it would make total sense to replace a more finicky Nandrolone with Dienolone. You get the absurd strength and mass from Dienolone but it works fairly flawlessly with Test - just a little watery. The appetite reduction that the study suggests is probably from estradiol increases.

Anyways, I'm willing to bet Dienolone converts readily to estrogen as much as Test does, if not more. It also interacts with the progesterone receptors, I'm sure. But does it reduce itself like Nandrolone?

also 2kvette, I've quoted you on another forum, Invalid Link Removed, which is the remains of Datbtrue. This is a private forum that is closed atm, but I could pull some strings to have you added over there if needed. The moderators are considerably more intelligent than what we've come to expect on "bodybuilding forums"...
 
fueledpassion said:
What about Dienolone? I'm guessing it has a "Dien" system. I'm always told it cannot convert to estrogen, much like you suggest about Nandrolone but a matter of fact is that water weight and estrogen-related, lumpy gyno forms under my nipple not unlike Trestolone only considerably easier to control with mild AI's.

This is the compound I really need to understand because this is what I have lying around. Btw, Dienolone is a very anabolic hormone and I've been thinking it would make total sense to replace a more finicky Nandrolone with Dienolone. You get the absurd strength and mass from Dienolone but it works fairly flawlessly with Test - just a little watery.
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I'm gonna look at the structure of dienolone, and post up some drawing and diagrams of what I'm talking about. From the structure I can tell a lot of what could potentially happen. You are correct, dienolone is a diene. For what it's worth; another name for trenbolone is trienolone. It's a synonym, it's the same molecule.
 
xR1pp3Rx said:
I wanted to say that the no ester TDs are nowhere near as strong as the ace TDs from my experience.. I understand IM this could be a different story.
OLs td had no ester.
POs td had ace ester.
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Strange. From what the study claimed Id've thought there would be little end-point difference.
 
How, though? Based upon what I've learned before, as well as in this thread, the ED from a nandrolone isn't caused by estrogen, but appears to be a result of the 5 alpha reduction of nandrolone. Again, to cite some things from this thread, dihydronandrolone would be the underlying cause of ED from nandrolone.
Not saying you're wrong. Just looking for a clarification.
 
BigNerd said:
How, though? Based upon what I've learned before, as well as in this thread, the ED from a nandrolone isn't caused by estrogen, but appears to be a result of the 5 alpha reduction of nandrolone. Again, to cite some things from this thread, dihydronandrolone would be the underlying cause of ED from nandrolone.
Not saying you're wrong. Just looking for a clarification.
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Right; if I'm not also mistaken I think it is partially selective for tissues in the prostate as well, which would further explain the ED in deca. But prolactin definately rises with deca from what I hear, and prolactin definately causes ED.
 
fueledpassion said:
What about Dienolone? I'm guessing it has a "Dien" system. I'm always told it cannot convert to estrogen - especially by your arch nemesis in this thread, much like you suggest about Nandrolone but a matter of fact is that water weight and estrogen-related, lumpy gyno forms under my nipple not unlike Trestolone only considerably easier to control with mild AI's. I would refer to some random article commentary on the FDA's research with Dienolone, which is here - http://anabolicminds.com/forum/steroids/98883-dienolone-boldione-testing.html for additional thought-provoking data.

This is the compound I really need to understand because this is what I have lying around. Btw, Dienolone is a very anabolic hormone and I've been thinking it would make total sense to replace a more finicky Nandrolone with Dienolone. You get the absurd strength and mass from Dienolone but it works fairly flawlessly with Test - just a little watery. The appetite reduction that the study suggests is probably from estradiol increases.

Anyways, I'm willing to bet Dienolone converts readily to estrogen as much as Test does, if not more. It also interacts with the progesterone receptors, I'm sure. But does it reduce itself like Nandrolone?

also 2kvette, I've quoted you on another forum, Invalid Link Removed, which is the remains of Datbtrue. This is a private forum that is closed atm, but I could pull some strings to have you added over there if needed. The moderators are considerably more intelligent than what we've come to expect on "bodybuilding forums"...
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yea, pm me. I just really enjoy discussing all the science behind this stuff. It would be lots of fun to discuss this on other boards. It's so fascinating. But from what you just linked up, dienolone definately raises estradiol levels. I've dug around pub med and can't find where anyone has been able to cite a mechanism, I can't even find an ADME study on it, so with out that there is no way to know what metabolites there could be. I can definately say this though, it's not happening through aromatase. The enzyme just won't work without C19.

Here is a thought though, the study you linked also noted a significant increase in testicular size. I propose that dienolone could possibly have some sort of pituitary antagonist activity. Leading to an increase in LH/FSH, which could increase testicular size and activity. Then testicular aromatase could have excess testosterone to convert, leading to estradiol increases. I don't know that this is true, im just trying to think of how it could happen because it definately can't aromatize.
 
Smont said:
2kvette

Can you suggest some good reading material for someone trying to get a better understanding of all this.
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Study up on structure activity relationships, receptor ligand interactions, and metabolism.

A good one that I frequent is the Journal of Steroid Biochemistry and Molecular Biology. All the latest steroid research is there.
 
2kvette said:
Right; if I'm not also mistaken I think it is partially selective for tissues in the prostate as well, which would further explain the ED in deca. But prolactin definately rises with deca from what I hear, and prolactin definately causes ED.
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Well first tren CANT be 5a reduced(2k correct me if I'm wrong there) but even if it does, mast has a very high affinity for the reproductive androgens receptors and should compete(and win for the most part) with dhn. Then without using test estrogen would be low enough that prolactin shouldnt be able to raise. As without enough E prolactin can't raise(again 2k correct me if I'm wrong)
 
rtmilburn said:
Well first tren CANT be 5a reduced(2k correct me if I'm wrong there) but even if it does, mast has a very high affinity for the reproductive androgens receptors and should compete(and win for the most part) with dhn. Then without using test estrogen would be low enough that prolactin shouldnt be able to raise. As without enough E prolactin can't raise(again 2k correct me if I'm wrong)
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Tren can't 5a reduce. Mast has an affinity for the receptor, not other androgens. I don't know what would compete and win, this is a maybe or maybe not type of thing. And you have it backwards, unless you have a prolactinoma, the lower the estrogen the higher prolactin goes. This is why alot of women don't get their periods while breast feeding and has alot to do with the postpartum depression. Because estradiol crashes to bring on the rise in prolactin.
 
2kvette said:
Tren can't 5a reduce. Mast has an affinity for the receptor, not other androgens. I don't know what would compete and win, this is a maybe or maybe not type of thing. And you have it backwards, unless you have a prolactinoma, the lower the estrogen the higher prolactin goes. This is why alot of women don't get their periods while breast feeding and has alot to do with the postpartum depression. Because estradiol crashes to bring on the rise in prolactin.
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Ok so I was mostly right.
 
2kvette said:
yea, pm me. I just really enjoy discussing all the science behind this stuff. It would be lots of fun to discuss this on other boards. It's so fascinating. But from what you just linked up, dienolone definately raises estradiol levels. I've dug around pub med and can't find where anyone has been able to cite a mechanism, I can't even find an ADME study on it, so with out that there is no way to know what metabolites there could be. I can definately say this though, it's not happening through aromatase. The enzyme just won't work without C19.

Here is a thought though, the study you linked also noted a significant increase in testicular size. I propose that dienolone could possibly have some sort of pituitary antagonist activity. Leading to an increase in LH/FSH, which could increase testicular size and activity. Then testicular aromatase could have excess testosterone to convert, leading to estradiol increases. I don't know that this is true, im just trying to think of how it could happen because it definately can't aromatize.
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And I can confirm Testicular size does increase on this stuff.
 
2kvette said:
Tren can't 5a reduce. Mast has an affinity for the receptor, not other androgens. I don't know what would compete and win, this is a maybe or maybe not type of thing. And you have it backwards, unless you have a prolactinoma, the lower the estrogen the higher prolactin goes. This is why alot of women don't get their periods while breast feeding and has alot to do with the postpartum depression. Because estradiol crashes to bring on the rise in prolactin.
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Thanks for the clarification.
So, what is it about tren that makes it impossible to 5 alpha reduce? I'm assuming it must be the order of the molecules? I know dienolone can't aromatize because of the A ring before the ene (I think I know that).
 
rtmilburn said:
Ok so I was mostly right.
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Yes you were. Moreso at least than I. My apologies.
I have an education, but not in any science we would discuss here. Therefore, for future reference, any comment/question that reads like mine above is not intended to be inflammatory. Trust me, there'd be no mistake if that were my intention ;-)
Pretty solid group of guys here. I appreciate everyone's help.
 
NewAgeMayan said:
Strange. From what the study claimed Id've thought there would be little end-point difference.
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for me it made a HUUgE difference. in fact I ran a log here were I introduce the suspension version mid other brand cycle and I sh!T you not, it was like some one threw a switch. and I still have nothing against OL .. it is what it is. we all react differently to these things.
 
xR1pp3Rx said:
for me it made a HUUgE difference. in fact I ran a log here were I introduce the suspension version mid other brand cycle and I sh!T you not, it was like some one threw a switch. and I still have nothing against OL .. it is what it is. we all react differently to these things.
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All good man.

Yeah Im remembering the researchers claiming that ment acetate rapidly hydrolyzed to ment. I took this to imply the acetate would make little difference in terms of gainz.
 
BigNerd said:
Thanks for the clarification.
So, what is it about tren that makes it impossible to 5 alpha reduce? I'm assuming it must be the order of the molecules? I know dienolone can't aromatize because of the A ring before the ene (I think I know that).
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RIght, the bonds are conjugated so they actually exist in an equilibrium between two different states, flopping back and forth between the two.
 
NewAgeMayan said:
All good man.

Yeah Im remembering the researchers claiming that ment acetate rapidly hydrolyzed to ment. I took this to imply the acetate would make little difference in terms of gainz.
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Thats cuz all the estrified stuff are precursors. Test cyp is a prodrug to testosterone. The blood esterases cleave the ester off as the stuff slowly seeps out, this provides a slow sustained blood level and release, allowing more active compound to stay in the system longer.
 
2kvette said:
Thats cuz all the estrified stuff are precursors. Test cyp is a prodrug to testosterone. The blood esterases cleave the ester off as the stuff slowly seeps out, this provides a slow sustained blood level and release, allowing more active compound to stay in the system longer.
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Please humor my layman crudeness...

"Rapidly hydrolyzed to MENT" I take to mean that the ester bonds (to the active compound) are very quickly broken down to leave the non estered compound.

MENT has a halflife of 40mins. If the estered compound is rapidly released from the ester, leaving MENT itself, then this becomes a question of how long is rapid; as this will be the halflife (40mins) PLUS.

So, 40mins + "rapidly". As if 40mins wasnt rapid enough.
 
NewAgeMayan said:
Please humor my layman crudeness...

"Rapidly hydrolyzed to MENT" I take to mean that the ester bonds (to the active compound) are very quickly broken down to leave the non estered compound.

MENT has a halflife of 40mins. If the estered compound is rapidly released from the ester, leaving MENT itself, then this becomes a question of how long is rapid; as this will be the halflife (40mins) PLUS.

So, 40mins + "rapidly".
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yea, however long rapidilly is. who knows. For acetate im gonna guess 1-3 days. And thats a litteral guess based on other acetate stuff ive seen
 
2kvette said:
yea, however long rapidilly is. who knows. For acetate im gonna guess 1-3 days. And thats a litteral guess based on other acetate stuff ive seen
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So here "rapidly" could well just mean "...compared to other esters"

:/

Lol i need to re look at the actual study.
 
Have you tried methyltren? Might be suited with less sides, but I've heard that goes both ways. If it's pure strength you want throw some a bombs in. Or if you really want strength it's halotestin all day sonnnn
 
I appreciate the suggestions, but the only reason I'm looking t'ward something else are the sides, and toxicity. I'd like to do without the methyl group.
I drink...I drink a lot! That's more or less why I'm leaning t'ward an injectable.
I get BW regularly (from a GP, not asteroid doctor), and I've kept my liver enzymes within the normal range through out my last couple of cycles.
Anything methylated probably increases the chance of cholestasis, I'd imagine. I use lecithin regularly.

That, combined with the fact I'm on Lipitor now just seems a bit too hepatotoxic. Thanks, though.
 
Well then your stuck with trest If you can get it or deca. Only thing that fits your criteria that will produce somewhat tren like gains.

Personally, I dislike 19 nors and I think strength gains are largely focused around how you train and what you eat.

My reccomendations: Throw in some EQ at 400-800 a week. Try to run as long as 16-20 weeks, some say you must but 8 weeks is still beneficial. Only other thing I can think of is masteron for the dht agression in the weight room. Good luck man.
 
deeznutsboi said:
Well then your stuck with trest If you can get it or deca. Only thing that fits your criteria that will produce somewhat tren like gains.

Personally, I dislike 19 nors and I think strength gains are largely focused around how you train and what you eat.

My reccomendations: Throw in some EQ at 400-800 a week. Try to run as long as 16-20 weeks, some say you must but 8 weeks is still beneficial. Only other thing I can think of is masteron for the dht agression in the weight room. Good luck man.
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Yeah, you're not the first to recommend EQ, either. Personally, it's never excited me much, but guys are talking about dosages and duration of cycle that I haven't experimented with. That may be a consideration in the future.

I LOVE Masteron, so that's already a done deal.
I agree, the training and diet have to be spot on. I've definitely got that much covered.
Thanks again, dude.
 
BigNerd said:
I appreciate the suggestions, but the only reason I'm looking t'ward something else are the sides, and toxicity. I'd like to do without the methyl group.
I drink...I drink a lot! That's more or less why I'm leaning t'ward an injectable.
I get BW regularly (from a GP, not asteroid doctor), and I've kept my liver enzymes within the normal range through out my last couple of cycles.
Anything methylated probably increases the chance of cholestasis, I'd imagine. I use lecithin regularly.

That, combined with the fact I'm on Lipitor now just seems a bit too hepatotoxic. Thanks, though.
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Assuming we're still talking about replacing Tren, I believe Dienolone is a good substitute and even better would be Desoxy T, if you can find either. Both of those are very effective and can be run at 200-400mg/wk with great results, especially DTA.
 
fueledpassion said:
Assuming we're still talking about replacing Tren, I believe Dienolone is a good substitute and even better would be Desoxy T, if you can find either. Both of those are very effective and can be run at 200-400mg/wk with great results, especially DTA.
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Yeah, you guys have got me sold on dienolone now. I'm just having a bitch of a time finding it.
I used to have a place that had desoxy T. My strength went through the roof on Promagnon 25 (I know, that's forever ago).
I tried the desoxy T oil. I didn't have great luck with it, but I suspect it wasn't legit stuff.

You've already proven to me that you know what you're talking about, so any suggestions within the original parameters are appreciated.
 
Dienolone it is then. It isnt very androgenic and I get no sides from it in that regard. Masteron with it would be perfect. I'd say 75mg EOD.

Other than that, Trestolone is a good alternative to Tren for strength but no better than Dien in this regard. Trest is best at the figure-morphing aspect. It can really melt the fat just as fast as Tren if you can keep the estrogen down.

EQ works but it takes some time to kick in and the strength, while impressive, isnt Tren-like. It offers anaerobic endurance however like no other. Make sure you take plenty of Nattokinase and keep blood pressure low while on. Outside of keeping blood pressure down, there is very little else to concern yourself with while taking EQ. It should be mild mannered in every aspect when it comes to sides, which is why I like it so much.
 
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