Clomid is usually stacked withh Nolvadex for the first few weeks. The idea being to kickstart HPTA recovery without the 'weird' clomid side effects. Clomid is actually a special estrogen, and when you're on it, you definitely act like a little b*tch.

Underrated? A little bit. Some people (like Chad) are oldschool and run clomid-only PCT's.

Sinner,

I want to know if I should build up and taper off (pyramid) cycle my anti-estrogen/natural test boooster after my main cycle to restore my hormonal levels and prevent estrogen excess and gyno.

or should i just take it like it says, two/three caps a day for four weeks?

thanks

I guess it really depends on what you're talking about.

Check out this thread. It's a good'n :
Running Serm inverse to ADT??

Will Anabolics xtreme advanced PCT give me regular hormonal levels, lower estrogen/ increase natural test production enough to use as a stand alone coming off of a Halodrol/Maxodrol/Hemadrol cycle?

or is it a no good product and a ripoff?

tried doing research on it, and really couldnt find conclusive evidence as whether or not it would be smart to use that alone to come off a cycle. It would suck ass to try it, and then have gyno problems. i would be pissed

APCT looks like it would be a decent test booster, but a SERM it is not. A common approach used with such products is to use in conjunction with the SERM. As you lower your SERM dosages, increase your APCT dosages (start with zero your first week, one cap your second week, and build up to a full dose).

right, i understand that. but since i am currently in iraq, it is quite hard for me to find a SERM. unless there is some good BUDDIES on here that would be kind to hook me up

EDIT: This edit is to exhaust the emphasis on how fuking hard it is to acquire in Iraq

This thread should be a STICKY!

Reps to The Sinner.

I agree with what some say, that ON cycle hormone balancing would be the best way to lessen the permanent risk associated with shutdown, as well as the side effects and health risks associated with post-cycle hormone levels. going back to thesinners original quotes,

if testosterone is synthetically raised to very high on cycle levels, then compensation will occur and estrogen will raise, and probably cortisol as well.

So after a cycle when the synthetic testosterone element is removed, we are left with very low levels of test, and yet high levels of estrogen and cortisol, whiich not only make our gains dissapear, but make us feel like crap, and can lead to various health problems in the long run if left untreated.

so instead of bombarding the system with a sort of Shock treatment to aid in the restoration of our once treasured equilibrium, wouldnt it seem like a better idea to prevent as much shutdown as possible while ON?

I havent really heard alot of talk about this besides HCG use, but all that does is keep Testicular atrophy at a minimum and can even worsen the fact that LH production is low since it takes the place of it.

Although i agree with HCG use to minimize atrophy and help keep natural test levels sort of going, i think its only a part of the puzzle. there are arguments for the use of opiod modulators but i dont think the emotional and psychological effects of these drugs would benefit the bodybuilder and the risk\benefit ratio isnt favorable.

i do think that careful monitoring of estrogen and cortisol while on cycle is important to make recovery a breeze.

such a protocol would involve using a SERM at a small dose while ON like ralox or tamox ( i would use ralox) to protect against to the negative side effects of high estrogen, aid in the axis balance required to keep natural test pumping.

Of course putting a special synthetic estrogen into ones system would add to the high serum estrogen levels, so an AI like aromasin or adex at a small dose to control and curb estrogen all together would keep the equilibrium balanced as well.

The other issue is cortisol, now it depends on the steroid compound being used, but for an easy reference if one is using Test which is of course going to suppress ones system without taking any care, cortisol will probably shift in either a favorable or unfavorable way while ON. now being that cortisol is sometimes an overlooked part of HPTA homeostasis, it should also be monitored and controlled while ON cycle. THis can be done with the various compounds listed earlier in this thread.

I would also suggest the use of HCG on long cycles like 10+ weeks along with all of these other steps to ensure a quick and easy (hopefully) recovery..

IGF-1 is a great add on to any PCT

** this is not to say that a SERM taper after cycle should be ignored. I think it would only further restore ones system and add to naturally high test levels post cycle. I am a fan of the SERM being tapered inversely to an AI like hyperdrol X2 and continuing a cortisol blocker like retain 2 throughout post cycle.

after this a natural LH stimulator and test booster like Massfx etc would help transition into being completely natural once again.

Althogh it wasnt mentioned above, to stimulate LH while on cycle, does anyone have any input as to whether herbs like trib or fen or longjack would be beneficial while ON for this purpose and this purpose only?

Originally Posted by pudzian2

IAlthogh it wasnt mentioned above, to stimulate LH while on cycle, does anyone have any input as to whether herbs like trib or fen or longjack would be beneficial while ON for this purpose and this purpose only?

There's not enough data out there to be able to make a 'for sure' suggestion as to the effectiveness of these.


In my opinion, proactive on-cycle test stimulation is not going to be of much effect because the amount of exogeneous test/steroids will far too greatly outnumber whatever you are taking to combat against downregulation. Also note that a lot of these steroids have a higher anabolic ratio that testosterone. So what would be the benefit of increasing endogeneous testosterone if it is only going to be competing with the the steroids you are using for androgenic receptors?

Some people like the idea. Then again, some people like Muscletech Products. I can't tell you which path to take, but I can at least show you the one I walk, and why I walk it.

Originally Posted by thesinner

There's not enough data out there to be able to make a 'for sure' suggestion as to the effectiveness of these.


In my opinion, proactive on-cycle test stimulation is not going to be of much effect because the amount of exogeneous test/steroids will far too greatly outnumber whatever you are taking to combat against downregulation. Also note that a lot of these steroids have a higher anabolic ratio that testosterone. So what would be the benefit of increasing endogeneous testosterone if it is only going to be competing with the the steroids you are using for androgenic receptors?

Some people like the idea. Then again, some people like Muscletech Products. I can't tell you which path to take, but I can at least show you the one I walk, and why I walk it.

I agree with you in part, but I like to compare both sides. As for the on cycle test stimulation that was only part of my point. I think that indirectly the test stimulation and at least "control" would need to come from balancing the body's response with respect to the other two hormones: cortisol and estrogen. IF PCT uses compounds that regulate these hormone levels in hopes of restoring the missing link-testosterone, then why wouldnt the opposite apply; regulating these hormone levels on cycle to lessen the severity of the shutdown, while continuing to make good ganes, and furthering the likelihood of a smooth and quick rebound while at the same time minimizing the negative side effects related to hormone levels being thrown out of whack. whether or not the natural test is competing with the exogenous test, you will make gains either way and there probably wouldnt be much of a difference if one were to compare.

It always scares me to hear stories of young men needing to go on HRT becuase of using steroids, but then they usually dont do a proper PCT and have little knowledge of whats actually going on in their body..but when considering all of the information that many of AM's board members know with respect to, well basically, Endocrinology, there seems to be no way that ones body would not eventually recover, especially when using some of the methods described above this thread and given the appropriate amount of time.

Pudzian, I think this article is somewhat relevant to what your saying. It really is more of a matter of control of these hormones than anything and finding the right balance to maximize gains/minimize sides.....the problem is figuring out where that balance is of course. Anyway....

______________________________ ______________________

The Role of Estrogen in Muscle Growth
William Llewellyn
Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced[i]. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

What does this all mean?
It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.

Originally Posted by Travis

Pudzian, I think this article is somewhat relevant to what your saying. It really is more of a matter of control of these hormones than anything and finding the right balance to maximize gains/minimize sides.....the problem is figuring out where that balance is of course. Anyway....

______________________________ ______________________

The Role of Estrogen in Muscle Growth
William Llewellyn
Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced[i]. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

What does this all mean?
It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.

Hey, agreed and nice article. I hope people start to look into this some more. I would like to see more emphasis on ON cycle hormone control or at least equal emphasis between ON cycle control and PCT

bump

Originally Posted by p5sky

bump

GREAT idea

Sinner,

Someone who is willing to field newbie questions....bless you!

I have more people telling me so many differing opinions I am completly lost.

I am not planning on doing a roid cycle for two reasons. One I am a diabetic and take insulin and to be honest, don't want to mess with it yet and two I do not think I am far enough along in my training that I would derive the full benefits of it. Sort of that I still need to put in my dues as I have only been working at this seriously for about a year.

With that said, feeling like I am standing at the bar with my sippy cup filled with cola....

I have been directed to take some OTC items for a boost. I have been told that I would need to do a post cycle and that I don't need a post cycle. The number of opinions on how to cycle the following is so vast there is not enough webspace to contain them all.

I have the following and think I need to cycle them for a 4 week period.

17-HD- take 30 minutes before workout
T-Bomb II- take twice daily
Viraloid- take twice daily
6-OXO- take twice daily

Do I need to take a post cycle with the mild test boosters? If so, would it have to be as serious as a post cycle from a real cycle ? Heck, is my baby cycle even the right way to take these items?

Sorry for the newb questions but I would rather admit I don't know, be beaten about the head and neck with a large trout for being a newb, and get some decent information.

Thanks for everyones input.

Originally Posted by ticktwo

Sinner,

Someone who is willing to field newbie questions....bless you!

I have more people telling me so many differing opinions I am completly lost.

I am not planning on doing a roid cycle for two reasons. One I am a diabetic and take insulin and to be honest, don't want to mess with it yet and two I do not think I am far enough along in my training that I would derive the full benefits of it. Sort of that I still need to put in my dues as I have only been working at this seriously for about a year.

With that said, feeling like I am standing at the bar with my sippy cup filled with cola....

I have been directed to take some OTC items for a boost. I have been told that I would need to do a post cycle and that I don't need a post cycle. The number of opinions on how to cycle the following is so vast there is not enough webspace to contain them all.

I have the following and think I need to cycle them for a 4 week period.

17-HD- take 30 minutes before workout
T-Bomb II- take twice daily
Viraloid- take twice daily
6-OXO- take twice daily

Do I need to take a post cycle with the mild test boosters? If so, would it have to be as serious as a post cycle from a real cycle ? Heck, is my baby cycle even the right way to take these items?

Sorry for the newb questions but I would rather admit I don't know, be beaten about the head and neck with a large trout for being a newb, and get some decent information.

Thanks for everyones input.

From the reviews I've seen on the products you plan to be using, 6-oxo is the only one that's been positive. The others are herbal testosterone boosters, and here's my issue with them:

1) There is little (if any) data that would suggest that they work.
2) There is little (if any) data that would suggest their safety. Some of them are downright dangerous.

If you were to ask about running these in the supplements forum, you'd get about 9 other people telling you to drop 17-HD: more dangerous than it is effective.

T-Bomb has a lot of stuff in it. In fact, some of the components in T-Bomb have been proven to actually LOWER your testosterone. It also contains Long Jack, which can be toxic if taken in high enough dosages, and here's the kicker: there isn't enough data to say what a toxic dose of Long Jack is.

Viraloid, I've gotta be honest, I don't have any clue what the heck this stuff is.

Lastly, no you would not need a Post Cycle therapy regime for such a 'stack'. In fact, many of these "test boosters" are often implemented during post cycle therapy to optimize endogeneous testosterone.

Sinner,

I appreciate the help.

It seems to me that if I truly want some sort of medicinal/herbal assistance I need to put my sippy cup away and belly up to the bar. It sounds as if no non-steroid options exist.

Originally Posted by ticktwo

Sinner,

I appreciate the help.

It seems to me that if I truly want some sort of medicinal/herbal assistance I need to put my sippy cup away and belly up to the bar. It sounds as if no non-steroid options exist.

Oh, they are out there. Check out the Supplements forums, and try reading some supplement logs. There's some products out there that are very effective. Are the as powerful as steroids? No, but they can sure get the job done my friend.

Best of luck to you,

thesinner

Sinner, good stuff man!

I really like the idea of running a SERM inversly with ATD. But what about using something like HDx2? Would it matter if I just ran it at 4 pills a day while tapering the SERM or would I need to start off with 0 and work my way up like I would with an ATD?

Reps!

Originally Posted by UNCfan1

Sinner, good stuff man!

I really like the idea of running a SERM inversly with ATD. But what about using something like HDx2? Would it matter if I just ran it at 4 pills a day while tapering the SERM or would I need to start off with 0 and work my way up like I would with an ATD?

Reps!

I ran cissusdrol (GL's version of AX's hyperdrol) during my last PCT. I just ran it straight at the recommended dosage. After I was done doing the SERM thing, I knocked it up a little higher to get more of an effect.

Originally Posted by thesinner

I ran cissusdrol (GL's version of AX's hyperdrol) during my last post cycle therapy. I just ran it straight at the recommended dosage. After I was done doing the SERM thing, I knocked it up a little higher to get more of an effect.

Thanks, reps when I can, it will not let me now.

Don't worry 'bout it. It's the thought that counts.

Originally Posted by thesinner

Don't worry 'bout it. It's the thought that counts.

Ok guys after alot of reading and reading post here about SERM's I can now understand the importance of them.

Jomi maybe u can help out a bro.

Torem mainly, After my Epi cycle I will be running some PP and superdrol bridge. Not right after lol. Hopefully my cholestrol will be back up to par. Have u came over any studies on how much of a positive effect it has on HDL cholestrol?

No one answered that for me. Stupid question maybe. Can u help a brother out?

Originally Posted by UNCFan1

Ok guys after alot of reading and reading post here about SERM's I can now understand the importance of them.

Jomi maybe u can help out a bro.

Torem mainly, After my Epi cycle I will be running some PP and superdrol bridge. Not right after lol. Hopefully my cholestrol will be back up to par. Have u came over any studies on how much of a positive effect it has on HDL cholestrol?

No one answered that for me. Stupid question maybe. Can u help a brother out?

I just ran a quick search on Pubmed and found this little fella (see below). It would appear Torem is about 3x more effective at raising HDL than Nolvadex, if that can put things into perspective for ya.

Antiatherogenic effects of adjuvant antiestrogens: a randomized trial comparing the effects of tamoxifen and toremifene on plasma lipid levels in postmenopausal women with node-positive breast cancer.Saarto T, Blomqvist C, Ehnholm C, Taskinen MR, Elomaa I.
Department of Oncology, Helsinki University Central Hospital, Finland.

PURPOSE: To evaluate whether a novel antiestrogen, toremifene, has similar antiatherogenic effects as tamoxifen. PATIENTS AND METHODS: Forty-nine postmenopausal patients with node-positive breast cancer were randomized in a trial that compared the effects of tamoxifen and toremifene on serum lipoproteins. Tamoxifen was given at 20 mg and toremifene at 60 mg orally per day for 3 years. Serum concentrations of apolipoprotein (apo) A-I, A-II, and B, and lipoprotein(a) [Lp(a)], cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol were measured before and after 12 months of antiestrogen therapy. RESULTS: Both antiestrogens significantly reduced serum total and LDL cholesterol and apo B levels. However, the response of HDL cholesterol to treatments was clearly different between the groups. Toremifene increased the HDL level by 14%, whereas tamoxifen decreased it by 5% (P = .001). As a consequence, both cholesterol-to-HDL and LDL-to-HDL ratios decreased more in the toremifene than tamoxifen group (P = .008 and P = .03, respectively). Toremifene also increased the apo A-I level (P = .00007) and apo A-I-to-A-II ratio (P = .018). Both tamoxifen and toremifene decreased the Lp(a) concentration significantly (change, 34% v 41%). CONCLUSION: These results provide positive evidence that toremifene has antiatherogenic properties with potency to improve all lipoproteins that are associated with increased coronary heart disease (CHD) risk.

PMID: 8636753 [PubMed - indexed for MEDLINE]

Originally Posted by thesinner

I just ran a quick search on Pubmed and found this little fella (see below). It would appear Torem is about 3x more effective at raising HDL than Nolvadex, if that can put things into perspective for ya.

Very nice, many thanks!!!

Originally Posted by UNCfan1

Very nice, many thanks!!!

Keep in mind that this study was done using people who's cholesterol values are not f*cked up worse than Britney Spears. After you're done with a SD cycle, your Cholesterol levels will want to go back to the way they were before the cycle about as much I want to bone Jolene Blalock. With that being said, the HDL raising capabilities of Toremifene will be much more pronounced than 14%.

Props thesinner. Mad props yo.

Oh... eccck... and that hairdolls out of taint hairs thing is the grossest thing I've heard in a long time.

Originally Posted by Force of Green

Oh... eccck... and that hairdolls out of taint hairs thing is the grossest thing I've heard in a long time.

what's really funny is that I had to explain to Trip what a taint was.