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Test enanthate and test propionate

that's not a cycle, those are compounds.

for a cycle, you'd need to list your dosage amount, protocol, PCT, etc.

Also, years training, age, bf, weight, lifts...
 
So u want to run the prop as kick start to the enth I assume?
Bit like dbol preload?
I think it's a good idea, but maybe go 6 weeks?
Or u can run test suspension if u want a straight up kick thats not an oral
 
SFN

there's no need to run 2 different esters...test is test is test....the enanthate ester will take approximately 4 weeks to kick in, so in the meantime you take prop as that's noticeable in just a few days...so take that eod for 4 weeks then drop it and by then you'll be running on the E ester

If you wanna wait a month or so to feel it then no prop...

If you don't mind pinning eod for a few months then no need for the enanthate
 
mav18 said:
This is my cycle give me your opinion on them thank you
Click to expand...

Drop the prop no need if you want a kick start get dbol. Test p is the test of choice when running other short ester injectables like npp, tren ace, mast p. Save it for then. Your just causing your self a headache. If you wanna run 2 injects than go with another long ester then you can mix em and just shoot once or twice a week. Deca or equipoise are good additions. Whats your pct? Do you have on cycle support like an ai, hcg?
 
Nolvidex 40/20/20/20/20 I'm going to look into the options you told me besides deca **** deca Dick. But I will have my final decision of compounds and cycle very soon thanks for the advice man
 
For deca or tren wang ( both are 19-nors) I find cabergoline is the stuff to have to fix those issues...having used both liquid and tab form I def prefer tabs...I read a good bit in liquid suspension caber breaks down and loses effectiveness ...anyway real world for me says use tabs
 
mav18 said:
Nolvidex 40/20/20/20/20 I'm going to look into the options you told me besides deca **** deca Dick. But I will have my final decision of compounds and cycle very soon thanks for the advice man
Click to expand...

Dont run nolva and deca they dont mix well.
 
Any cycle suggestions for test e and equipoise dosages and how long. switching to equipoise need to know how to run cycle
 
mav18 said:
Any cycle suggestions for test e and equipoise dosages and how long. switching to equipoise need to know how to run cycle
Click to expand...

Tell you what.
You've been researching & studying cycles.
You've now chosen Test E & EQ/bold,
Tell us how you would run it!
Tell us how you'd dose it & for how long.
What AI's you would use & how you'd run hcg.
Tell us your pct regime.

Then I'll respond and make suggestions.
Let's see what you have decided first brother
 
Alright get to know me a little better I'm 5 "8" 172 pounds. I've been lifting around 3 years. Ive decided to run equipose and test e everything is ready to go just want my cycle down done some research and this looks like it Will work to me Test 500mg/week 1-15 EQ 400mg/week 1-14. Post cycle Is hcg and clomid. Hope this isnt a stupid question but would estrogenx work for my e blockers or no. Thanks for response ready to get going on my cycle!
 
DetroitHammer said:
Why?
Click to expand...

Because nolva can make receptors more sensitive and deca is a 19 nor which is known to cause prolactin issue. So basically with nolva your making it easier. You should also keep a progesterone antagonist on hand if running a 19 nor like tren or deca. I like dostinex but bromo and prami work.
 
mav18 said:
would estrogenx work for my e blockers or no. Thanks for response ready to get going on my cycle!
Click to expand...

You're not ready to go. EsttrogenX? WTF? is that? from what I've read on amazon, it's a estrogen supplement made from plant estrogen...? WAT?

you need to have an AI on hand, I prefer exemestane from what I've read, but other have used adex and letro. If it's your first cycle, start simple, test-only. But really, it's up to you. Less substances just means less problems/confusion, etc.
 
joeblow1 said:
Because nolva can make receptors more sensitive and deca is a 19 nor which is known to cause prolactin issue. So basically with nolva your making it easier. You should also keep a progesterone antagonist on hand if running a 19 nor like tren or deca. I like dostinex but bromo and prami work.
Click to expand...

Nolva can make what receptors more senstive and how? Prolactin issues are a given, but I'm having a hard time understanding why so many guys say do not use a SERM with deca because it's a 19 nor. Deca does not produce estrogen sides by aromatizing, so any SERM/AI would be worthless anyway, so even "if" a SERM made the AR more sensitive, so what? I mean, it makes no sense at all. I'm just trying to understand the logic to why everyone assumes it's a bad mix and hope someone can give me a little more explaination. And I guess the question is, "Why is a SERM/AI a bad choice if taking a 19 nor?" So if a guy was stacking test, anadrol and deca, a SERM/AI is not recommended?
 
DetroitHammer said:
Nolva can make what receptors more senstive and how? Prolactin issues are a given, but I'm having a hard time understanding why so many guys say do not use a SERM with deca because it's a 19 nor. Deca does not produce estrogen sides by aromatizing, so any SERM/AI would be worthless anyway, so even "if" a SERM made the AR more sensitive, so what? I mean, it makes no sense at all. I'm just trying to understand the logic to why everyone assumes it's a bad mix and hope someone can give me a little more explaination. And I guess the question is, "Why is a SERM/AI a bad choice if taking a 19 nor?" So if a guy was stacking test, anadrol and deca, a SERM/AI is not recommended?
Click to expand...

Nolva can make progesterone receptors more sensitive. Deca can cause prolactin issues. When you combine them your inviting those problems to happen. If you doubt this than give at try. Let me know how it works for you.a
 
joeblow1 said:
Nolva can make progesterone receptors more sensitive. Deca can cause prolactin issues. When you combine them your inviting those problems to happen. If you doubt this than give at try. Let me know how it works for you.a
Click to expand...

The most recent and comprehensive study I've found on deca says the following:

Estrogen-sensitive nandrolone users have always complained about inexplicable estrogen-like symptoms that cannot be treated with conventional anti-estrogen therapies.

One theory blamed a feminizing hormone called prolactin. However that theory never really held up since potent androgens tend to decrease prolactin and prolactin sensitivity whereas estrogens seem to increase its activity. There was also no evidence to assume that prolactin played any significant role in the most common of estrogenic side-effects in the absence of estrogen, which would fail to explain why conventional anti-estrogenic therapy did not work with nandrolone use/abuse, given that nandrolone aromatized considerably less and blood profiles of users generally showed low estradiol and estrone levels in the blood after several weeks of use. Fortunately this theory was only shortlived, and only maintained by a few obscure guru’s eager to draw attention to themselves by claiming to have found a solution, where there wasn’t a problem.

Another theory, that has persisted very long, and remains the most popular belief today was that nandrolone’s progestational activity lay at the base of the perceived estrogenic effects. This theory again held very little ground, but is commonly accepted because it was never thoroughly refuted since the rumour first started circulating. Indeed, nandrolone3 and several of its metabolites4,5 have been identified as being progestins. Meaning they can bind and activate the progesterone receptor. And equally supportive of the theory, studies have demonstrated that progestagenic activity can both stimulate and suppress estrogenic activity6. Whether that holds true for the more common estrogenic side-effects is not really known, but it leant a validity to this theory. However, again, progestins have never been shown to cause estrogenic side-effects in the absence of estrogen. So once again, this did not account for the lack of effect with conventional anti-estrogens.

A third and last theory that has only been circulating of late is that nandrolone was directly estrogenic, binding and activating the estrogen receptor (ER) without metabolizing. Most likely the rumour initiated after the proposed theory that oxymetholone, another non-aromatizing drug, may me directly estrogenic. It was a theory first proferred by Bill Llewellyn7, and found support with people like myself and organic chemist Patrick Arnold. A dutch pseudo-guru even suggested he had found proof in the fact that studies demonstrated that nandrolone bound the estrogenic receptor8. This infamous study however demonstrated that nandrolone had a more estrogenic effect at the ER than testosterone in millimolar doses. However testosterone is not a potent ER activator, nor are millimolar in vitro doses indicative of what a typical steroid user would have in his blood.

All of these theories were shot down by two other studies9,10. The first study is not immediately relevant, but that it contained a table with results from an older study, showing the relative estrogenic properties of several progestins, compared to estradiol.

As you can see from the table above, taken from that study, nandrolone was about 60% as estrogenic in nature as estradiol itself. So far nothing special. All this tells us is that nandrolone has very potent estrogenic action that cannot be explained by aromatization, which is what we already knew. At best this has some shock value by demonstrating just HOW estrogenic it really is. The second study however was undertaken by the same researchers to hopefully shed some light on the situation. It did not. But it disproved all commonly accepted theories supported to date. In the study the researchers administered nandrolone with either an aromatase blocker, a progesterone receptor blocker or an estrogen receptor blocker. As was to be expected the aromatase blocker had no effect whatsoever on the estrogenic activity of nandrolone. More surprisingly, neither did the progesterone receptor blocker. Which also strikes a blow for basically any involvement of progestational activity in the development of common estrogenic side-effects associated with AAS use. And lastly, and even more surprisingly, the estrogen receptor blocker’s effect on the estrogenic activity was just barely significant. This suggests that nandrolone’s direct binding (or that of its metabolites) to the estrogen receptor played a very limited role. At the end of that all we could state was that nandrolone was 60% as estrogenic as estradiol itself, but more than 55% of that could not be explained.

Yours truly dug a little deeper and actually found the answer in a synthetic nandrolone metabolite, named estren (19-Nor-4-androstene-3α,17β-diol)11. Estren was found to only weakly bind the estrogen receptor, showing no real activity at that site and possessing a 300-fold lower binding affinity. Yet it mimicked the actions of estrogens in osteoblasts. Estren was however shown to be as active as DHT at activating certain androgen receptor related transcripts. The same study also demonstrated that estren was capable of activating estrogen specific constructs in the DNA through the androgen receptor. Estren is a metabolite of nandrolone through the 3α-HSD enzyme. So in first instance one might suggest we start looking for something that blocks this enzyme. However I mentioned that this steroid was synthetic. Nandrolone is a natural androgen. So why does estren not appear naturally in the body ? Well mostly because it is a very labile structure, that is quickly converted back to nandrolone. The problem however is that the researchers noted that despite similar activity on several constructs as DHT, it bound with a 200-fold lower activity to the androgen receptor. The researchers found that the high androgenic potency of estren resulted in its conversion to the more stable molecule nandrolone, almost 50% in 4-6 hours, and no less than 95% within 24 hours. From this it can be concluded that the effects of estren via the AR are mediated by its metabolite nandrolone, and it is in fact nandrolone that activates estrogen specific transcripts via binding and activating the androgen receptor. Now the study also noted that binding of DHT activated estrogen-related transcripts, so this is not uncommon, but DHT did so with a 30 to 100-fold lower potency than estren. The authors concluded :

“Finally, the unexpected estren-dependent activation(and by extension nandrolone-dependent activation) of ERE-driven gene expression in cells that express AR, which occurs with far greater potency relative to DHT, predicts the possibility of some troublesome feminizing effects in males, which still await examination."

I have used just about every AAS there is, more than once. I cannot, by way of personal experience, say that Nolva has produced the effects you, and others, say will occur due to a theory based on studies done on women post cancer treatment. So to answer your challenge, I have done just that, and did not see the dire results predicted, and I attribute that to the studies quoted above. I don't think there are enough clinical studies out there to make a sweeping statement like that.



 
DetroitHammer said:
The most recent and comprehensive study I've found on deca says the following:

Estrogen-sensitive nandrolone users have always complained about inexplicable estrogen-like symptoms that cannot be treated with conventional anti-estrogen therapies.

One theory blamed a feminizing hormone called prolactin. However that theory never really held up since potent androgens tend to decrease prolactin and prolactin sensitivity whereas estrogens seem to increase its activity. There was also no evidence to assume that prolactin played any significant role in the most common of estrogenic side-effects in the absence of estrogen, which would fail to explain why conventional anti-estrogenic therapy did not work with nandrolone use/abuse, given that nandrolone aromatized considerably less and blood profiles of users generally showed low estradiol and estrone levels in the blood after several weeks of use. Fortunately this theory was only shortlived, and only maintained by a few obscure guru’s eager to draw attention to themselves by claiming to have found a solution, where there wasn’t a problem.

Another theory, that has persisted very long, and remains the most popular belief today was that nandrolone’s progestational activity lay at the base of the perceived estrogenic effects. This theory again held very little ground, but is commonly accepted because it was never thoroughly refuted since the rumour first started circulating. Indeed, nandrolone3 and several of its metabolites4,5 have been identified as being progestins. Meaning they can bind and activate the progesterone receptor. And equally supportive of the theory, studies have demonstrated that progestagenic activity can both stimulate and suppress estrogenic activity6. Whether that holds true for the more common estrogenic side-effects is not really known, but it leant a validity to this theory. However, again, progestins have never been shown to cause estrogenic side-effects in the absence of estrogen. So once again, this did not account for the lack of effect with conventional anti-estrogens.

A third and last theory that has only been circulating of late is that nandrolone was directly estrogenic, binding and activating the estrogen receptor (ER) without metabolizing. Most likely the rumour initiated after the proposed theory that oxymetholone, another non-aromatizing drug, may me directly estrogenic. It was a theory first proferred by Bill Llewellyn7, and found support with people like myself and organic chemist Patrick Arnold. A dutch pseudo-guru even suggested he had found proof in the fact that studies demonstrated that nandrolone bound the estrogenic receptor8. This infamous study however demonstrated that nandrolone had a more estrogenic effect at the ER than testosterone in millimolar doses. However testosterone is not a potent ER activator, nor are millimolar in vitro doses indicative of what a typical steroid user would have in his blood.

All of these theories were shot down by two other studies9,10. The first study is not immediately relevant, but that it contained a table with results from an older study, showing the relative estrogenic properties of several progestins, compared to estradiol.

As you can see from the table above, taken from that study, nandrolone was about 60% as estrogenic in nature as estradiol itself. So far nothing special. All this tells us is that nandrolone has very potent estrogenic action that cannot be explained by aromatization, which is what we already knew. At best this has some shock value by demonstrating just HOW estrogenic it really is. The second study however was undertaken by the same researchers to hopefully shed some light on the situation. It did not. But it disproved all commonly accepted theories supported to date. In the study the researchers administered nandrolone with either an aromatase blocker, a progesterone receptor blocker or an estrogen receptor blocker. As was to be expected the aromatase blocker had no effect whatsoever on the estrogenic activity of nandrolone. More surprisingly, neither did the progesterone receptor blocker. Which also strikes a blow for basically any involvement of progestational activity in the development of common estrogenic side-effects associated with AAS use. And lastly, and even more surprisingly, the estrogen receptor blocker’s effect on the estrogenic activity was just barely significant. This suggests that nandrolone’s direct binding (or that of its metabolites) to the estrogen receptor played a very limited role. At the end of that all we could state was that nandrolone was 60% as estrogenic as estradiol itself, but more than 55% of that could not be explained.

Yours truly dug a little deeper and actually found the answer in a synthetic nandrolone metabolite, named estren (19-Nor-4-androstene-3?,17?-diol)11. Estren was found to only weakly bind the estrogen receptor, showing no real activity at that site and possessing a 300-fold lower binding affinity. Yet it mimicked the actions of estrogens in osteoblasts. Estren was however shown to be as active as DHT at activating certain androgen receptor related transcripts. The same study also demonstrated that estren was capable of activating estrogen specific constructs in the DNA through the androgen receptor. Estren is a metabolite of nandrolone through the 3?-HSD enzyme. So in first instance one might suggest we start looking for something that blocks this enzyme. However I mentioned that this steroid was synthetic. Nandrolone is a natural androgen. So why does estren not appear naturally in the body ? Well mostly because it is a very labile structure, that is quickly converted back to nandrolone. The problem however is that the researchers noted that despite similar activity on several constructs as DHT, it bound with a 200-fold lower activity to the androgen receptor. The researchers found that the high androgenic potency of estren resulted in its conversion to the more stable molecule nandrolone, almost 50% in 4-6 hours, and no less than 95% within 24 hours. From this it can be concluded that the effects of estren via the AR are mediated by its metabolite nandrolone, and it is in fact nandrolone that activates estrogen specific transcripts via binding and activating the androgen receptor. Now the study also noted that binding of DHT activated estrogen-related transcripts, so this is not uncommon, but DHT did so with a 30 to 100-fold lower potency than estren. The authors concluded :

“Finally, the unexpected estren-dependent activation(and by extension nandrolone-dependent activation) of ERE-driven gene expression in cells that express AR, which occurs with far greater potency relative to DHT, predicts the possibility of some troublesome feminizing effects in males, which still await examination."

I have used just about every AAS there is, more than once. I cannot, by way of personal experience, say that Nolva has produced the effects you, and others, say will occur due to a theory based on studies done on women post cancer treatment. So to answer your challenge, I have done just that, and did not see the dire results predicted, and I attribute that to the studies quoted above. I don't think there are enough clinical studies out there to make a sweeping statement like that.
Click to expand...

So are you willing to be the guinea pig. You personally run deca and nolva and keep a log on it. Are you willing to put your research to the test?
 
joeblow1 said:
So are you willing to be the guinea pig. You personally run deca and nolva and keep a log on it. Are you willing to put your research to the test?
Click to expand...

If you read my post, you'll see I answered that already. The results were predictable; no problems. However, I do not run deca now because it's one of the worst compounds you can put in your body. I'd ask you to actually read my post in its entirety.
 
yea i was just looking at he structure of test, nandrolone, estrogen, and estrone... nandrolone could easily go to estrone

and i've read literature stating significant increases in both estrone AND estradiol from nandrolone

what's funny is no AI will help you with nandrolone going to estrone, and then estrone goes to estradiol through 17a-hsd (not aromatase) so no aromatase inhibitor will stop any of the estrogen production from nandrolone

so besides all the nolva-deca no no stuff... f*ck nandrolone all together
 
joeblow1 said:
So are you willing to be the guinea pig. You personally run deca and nolva and keep a log on it. Are you willing to put your research to the test?
Click to expand...
The whole "no nolva on a progestin" thing is bro-lore at its finest.

I have run 10mg nolva on tren on more then one occasion. ;)
 
DetroitHammer said:
If you read my post, you'll see I answered that already. The results were predictable; no problems. However, I do not run deca now because it's one of the worst compounds you can put in your body. I'd ask you to actually read my post in its entirety.
Click to expand...

Not everyone will respond the same to drugs or anything for that matter. My self personally, I use deca and I do not use nolva. I wont use nolva on any cycle, its a personal choice. I use what works for me clomid, arimadex, dostinex. I stay free of prolactin issues on deca. There is no reason for me to run nolva. If you can get away with it then go for it. So if you ran nolva and deca with out any negative effects why do you consider it to be one of the worst compounds? Like I said I run it and get good results, and I recover fine. I do however discontinue deca a few weeks before test because it takes a little longer to clear your system.
 
joeblow1 said:
Not everyone will respond the same to drugs or anything for that matter. My self personally, I use deca and I do not use nolva. I wont use nolva on any cycle, its a personal choice. I use what works for me clomid, arimadex, dostinex. I stay free of prolactin issues on deca. There is no reason for me to run nolva. If you can get away with it then go for it. So if you ran nolva and deca with out any negative effects why do you consider it to be one of the worst compounds? Like I said I run it and get good results, and I recover fine. I do however discontinue deca a few weeks before test because it takes a little longer to clear your system.
Click to expand...

Man, I wish you would actually read my post so I don't have to repeat myself. I don't use deca for the very reasons stated in my post above. I can't make it any clearer than that. I used deca long ago and used tamoxifen without gyno problems, but did have libido issues. As clearly stated above, none, not a one, nada, no SERM or AI will protect you against deca sides, none, not a one, zero. So I am not advocating using nolva/tamoxifen because it would be contrary to what I just posted. I wanted to know what proof you have other than bro sci that demonstrates that using nolva/tam will increase progesterone receptors and effectively increase progesterone. Besides a study where post cancer women...agh, I'm not going to repeat that again... Point is proliferation of bad info doesn't make it true; it just makes it a popular misconception. I've used deca with and without a SERM with no difference at all. Why? The answer is painfully obvious.
 
DetroitHammer said:
Man, I wish you would actually read my post so I don't have to repeat myself. I don't use deca for the very reasons stated in my post above. I can't make it any clearer than that. I used deca long ago and used tamoxifen without gyno problems, but did have libido issues. As clearly stated above, none, not a one, nada, no SERM or AI will protect you against deca sides, none, not a one, zero. So I am not advocating using nolva/tamoxifen because it would be contrary to what I just posted. I wanted to know what proof you have other than bro sci that demonstrates that using nolva/tam will increase progesterone receptors and effectively increase progesterone. Besides a study where post cancer women...agh, I'm not going to repeat that again... Point is proliferation of bad info doesn't make it true; it just makes it a popular misconception. I've used deca with and without a SERM with no difference at all. Why? The answer is painfully obvious.
Click to expand...

I have read it. Despite the theories and studies you have noted
 
DetroitHammer said:
Man, I wish you would actually read my post so I don't have to repeat myself. I don't use deca for the very reasons stated in my post above. I can't make it any clearer than that. I used deca long ago and used tamoxifen without gyno problems, but did have libido issues. As clearly stated above, none, not a one, nada, no SERM or AI will protect you against deca sides, none, not a one, zero. So I am not advocating using nolva/tamoxifen because it would be contrary to what I just posted. I wanted to know what proof you have other than bro sci that demonstrates that using nolva/tam will increase progesterone receptors and effectively increase progesterone. Besides a study where post cancer women...agh, I'm not going to repeat that again... Point is proliferation of bad info doesn't make it true; it just makes it a popular misconception. I've used deca with and without a SERM with no difference at all. Why? The answer is painfully obvious.
Click to expand...

I have read it. Despite the theories and studies you have noted, I know from personal experience that when I have used deca without nolva I did not have any issues. I know of people that have used nolva with it and had issues. That does not mean everyone is the same. How many people were these studies done on? You say that you used serms and ai's on deca what about a progesterone antagonist like caber or bromo? How high was your test dosage? These will affect your libido on deca. If your test dose is too low than the deca sides can become more prominent. This is why I use test as a base line for cycles. It tends to keep everything else in check. This is based on my own experimentation and may not hold true for anyone else. I also do make use of aromotase inhibitors, serms, hcg, and progesterone antagonists. I base my choices on what works best for me.
 
joeblow1 said:
I have read it. Despite the theories and studies you have noted, I know from personal experience that when I have used deca without nolva I did not have any issues. I know of people that have used nolva with it and had issues. That does not mean everyone is the same. How many people were these studies done on? You say that you used serms and ai's on deca what about a progesterone antagonist like caber or bromo? How high was your test dosage? These will affect your libido on deca. If your test dose is too low than the deca sides can become more prominent. This is why I use test as a base line for cycles. It tends to keep everything else in check. This is based on my own experimentation and may not hold true for anyone else. I also do make use of aromotase inhibitors, serms, hcg, and progesterone antagonists. I base my choices on what works best for me.
Click to expand...

Was the Nolva the "people you know" pharmacy grade, or "research"? If the latter it has no validity.

Secondly I think you need to read this thread. ;) I think your understanding of caber, bromo, and "progesterone antagonists" is flawed.
http://anabolicminds.com/forum/steroids/123701-progesterone-prolactin.html
 
Frank Reynolds said:
Was the Nolva the "people you know" pharmacy grade, or "research"? If the latter it has no validity.

Secondly I think you need to read this thread. ;) I think your understanding of caber, bromo, and "progesterone antagonists" is flawed.
http://anabolicminds.com/forum/steroids/123701-progesterone-prolactin.html
Click to expand...
Everyone is entitled to their own opinion. I have mine and everyone has theirs. Yes I familiar with both pharmacy grade and research chems. And I know what a progesterone antagonist is. I will continue to avoid nolvadex,because I choose not to use it. If anyone else wants to use it than do as you please. I am done beating a dead horse.
 
joeblow1 said:
Everyone is entitled to their own opinion. I have mine and everyone has theirs. Yes I familiar with both pharmacy grade and research chems. And I know what a progesterone antagonist is. I will continue to avoid nolvadex,because I choose not to use it. If anyone else wants to use it than do as you please. I am done beating a dead horse.
Click to expand...
Obviously you don't..lmao
 
I use caber on deca/tren cycles and both nolva and clomid for pct and never had issues
 
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