Zero sex drive post sustanon cycle:<

[Conciliator]

Wouldn't low estrogen levels influence the body to cause aromatistion as soon as testosterone is available,thus making and A1 worth including to elevate test levels higher before aromatisation?

I don't think research has really demonstrated how estrogen regulates aromatase. I've seen conflicting results (i.e. upregulation of aromatase both with increasing and decreasing estrogen levels). It's not clear that with lower estrogen levels, aromatase will be upregulated.

 

[BBC3]

Also, nolva doesn't stimulate LH, it blocks estrogen at the pituitary, reducing negative feedback, so that GnRH can better stimulate LH.

Also, I think the aromasin is unnecessary. Most experts on PCT (e.g. Llewellyn, Brink, Swale, Scally) recommend that you take only SERMs during PCT, and not an AI. Why don't they recommend an AI? Because 1) estrogen levels are already very low, since there is little testosterone to aromatize, and 2) so you can still get the positive effects of estrgeon on blood lipds, bone, etc. It's not worth his time or money tracking down some aromasin. The major impediment to his recovery is not going to be restoration of LH levels (which can happen pretty quaickly even without anti-estrogens), but restoration of testicular response to LH.

STOP IT STOP IT STOP IT STOP IT STOP IT STOP IT STOP IT........ Conciliator, I demand you get a new avatar...........................

This drug is used as a first line defense against breast cancer. In the late 80s, Dan Duchaine speculated that it could also be used by bodybuilders to halt the development of another type of tumor in the mammary glandGynocomastia. He introduced this find to the Steroid-using-community in his Contest Prep issue of the UnderGround Steroid Handbook Update Newsletters (the contest prep-issue was actually 3 issues in one, for those who had a subscription to the newsletter). Nolvadex is commonly referred to in quite a few ways: as a SERM (Selective Estrogen Receptor Modulator), as an anti-estrogen (that is actually incorrect, as we will later see), and finally as a triphenylethylene. I happen to stick with calling Nolvadex a SERM, because out of my three options, it happens to be correct (as we know that calling it an anti-estrogen is incorrect), and pronouncable (as we know that I have no idea how to say "triphenylethylene")... ...Selective estrogen receptor modulators (SERMs) act as either estrogen receptor agonists or antagonists in a tissue-selective mannerlets see what that means to us Nolvadex actually has quite a few applications for the steroid using athlete. First and foremost, its most common use is for the prevention of gynocomastia. Nolvadex does this by actually competing for the receptor site in breast tissue, and binding to it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor blockade of breast tissue (1)especially since total body estradiol increases with use of tamoxifen. Clearly, if you are on a cycle which includes steroids which convert to estrogen, you may want to consider nolvadex as a good choice to run along side them. Nolvadex, however, is not the most potent ancillary compound we can use on a cycle, but it is probably the safest considering it doesnt actually reduce estrogen in your body Keeping some estrogen floating around could have many benefits on muscle growth, as well. Estrogen is also important for a properly functioning immune system, and not only that, but your lipid profile (both HDL and LDL) should also show marked improvement with administration of tamoxifen (4). Many bodybuilders actually use this stuff during their cycle for the health benefits provided by it. If, however, you are preparing for a bodybuilding contest, you need to use something which will suck most (if not all) of the estrogen out of your body. I am speculating that you may be able to use Nolvadex for the majority of a contest prep cycle, to keep yourself relatively healthy, and then switch over to Letrozole for the last 8 weeks. Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (2)(3). The best (rough) estimate I can give you from my research is that 20mgs of Nolvadex will raise your testosterone levels about 150% (5)...and this would of course greatly aid post-cycle-recovery. What this means to us is that if you take Nolvadex after a cycle, when you are trying to raise your levels of testosterone, LH, and FSH back to normal, it will greatly aid recovery. In fact, if I were limited to just one compound to aid me in post-cycle-recovery, Nolvadex would be my choice. If you want a comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but nolvadex also significantly increased the LH (Leutenizing Hormone) response to LHRL (5), after 6 weeks. Some of the more harsh ancillary compounds available today will give you a more dry look that nolvadex cant, but nolvadex is simply safer to use in long (over 16 week) cycles. Unfortunately, Nolvadex isnt perfect. Anecdotally, it has been linked to reduced gains in some bodybuilders. This isnt due, as previously thought, to its reducing estrogen levels (which it doesnt), but rather to its ability to possibly reduce IGF (Insulin-like-Growth-Factor) levels, which are important for muscle growth.

Anonymous.......

People, A GRAIN OF SALT PLEASE........................... iT IS A BLOCKER, A FUCKING RECEPTOR HOG bLOCKER AAUUGGHHHHHH !!!!!!! PITUITARY MY ASS...... STOP!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

 

[Conciliator]

STOP IT STOP IT STOP IT STOP IT STOP IT STOP IT STOP IT........ Conciliator, I demand you get a new avatar...........................

People, A GRAIN OF SALT PLEASE........................... iT IS A BLOCKER, A FUCKING RECEPTOR HOG bLOCKER AAUUGGHHHHHH !!!!!!! PITUITARY MY ASS...... STOP!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

What the hell are you going on about? From what I can gather, you're trying to stress that nolva is a "blocker" while at the same time saying it has nothing to do with the pituitary. Do you even know what the pituitary is? It's a tiny gland at the base of the brain that produces, among other things, LH and FSH.

I don't know what point you think you're making by posting that article. You'll see that it says "In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (2)(3)." Do you know why there was an increase in LH and subsequent to that, testosterone? Because the pituitary contains estrogen receptors. Nolvadex is an estrogen receptor antagonist. It binds to the estrogen receptor in the pituitary and, as an antagonist, it blocks estrogen at the pituitary.

Settle the fuck down, especially when you have no idea what you're talking about.

 

[Conciliator]

I just realized that it was BBC3 who played the fool in this thread as well. Looks like he has a track record of idiocy.

I'd nominate you as one of the most confused and misinformed people on this forum, BBC3. Seriously.

 

[Conciliator]

Nolvadex is an estrogen receptor antagonist.

Just to be clear, novladex is taken for it's effect as an estrogen receptor antagonist (i.e. the anti-estrogenic effect). However, it can also be an agonist, depending on the tissue, which is why they call it a selective modulator.

 

[brang]

Just to be clear, novladex is taken for it's effect as an estrogen receptor antagonist (i.e. the anti-estrogenic effect). However, it can also be an agonist, depending on the tissue, which is why they call it a selective modulator.

Wooo! this is one of my favorite subjects!

So, just to rephrase this:
Nolva does NOT stimulate the HPTA directly (it can't right?). It simply blocks the receptor at the pituitary and the breast tissue receptors (amoung others possibly).
The LH and FSH production is due to the secondary effect of Pitutary not detecting the estrogen as it slowly builds up because the receptors are blocked.

Is that correct?
That has been my understanding of Nolva's action, which conflicts with many expert opinions.

If the above is correct, then i don't understand why PCT cannot be done well with an AI like Arimidex to prevent estrogen from building up (as natural Test comes back online) rather than binding to the Pitutary receptors.
Seems like just another way to skin a cat to me. Both prevent the detection of Estrogen, one by preventing Estrogen being created(Arimidex) and the other by hiding the estrogen that is there from the Pituitary..

Perhaps the use of Nolva is some of the reason that some people say they get depressed during PCT - its not that they have no Test, its that they have TOO much Estrogen!
I'm a beliver in prevention is better than cure. Therefore and AI should be better than a SERM for some respects of PCT.

A common argument against Arimidex for PCT is that Estrogen will be low due low Testosterone at the end of cycle so an AI will be ineffective (as there is nothing to arimatize).
But this is the same even if your using Nolva, it can't block what is not there, right?!

As natural Test comes back online the AI will be there to prevent aromatization just as Nolva would be there to block the receptor.
And, if Nolva is NOT stimulating the HPTA directly (it cannot, that's not how SERM or a negative feedback loop works - my understanding) then what's it doing when there is no Test to aromatize? Sweet-fuck-all i imagine..

It seems to me that an AI would work equally well as Nolva, as both achieve the same end result but via different mechanisms.
I concede that AI has less than positive effects on lipid profile(I have read this but haven't looked into it at any length) and from what i have read Nolva has positive effects? Or is this just more internet dogma?

Thoughts? Comments? Abuse?

I just want to learn!

regards,
- b

 

[dennis]

Bro, you screwed your PCT up to hell. THATS why you are like that. You NEVER run that much HCG and NEVER run it DURING your PCT. You use a small amount BEFORE PCT or your just wasting your time. All the Nolva did during those three weeks was prevent any gyno. Your estrogen levels are prob high as HCG at high doses cause an estrogen rebound from hell. Not to mention you only did 3 real weeks of Nolva. I would run another couple of weeks of Nolva and Aromisan and you should be back to normal in no time. The Aromisan will regulate your estrogen levels and the nolva will properly stimulate the LH and FSH

I could not agree more bench.he was not very clear on how much hcg he used..i hope it ws not 5000 ius daily for 3 weeks.restart pct with just nolva,take natural supps too like zma,hmb,tribulus,force yourself to workout and eat.Dont worry about the sex drive..it all hopefully will come back on line..how old are you ???

 

[Oxygen]

Friends, your argument is only helping me get further confusion I don't know what to use or not use anymore !!! one thing I know though, that right now I feel like crap.

Please, what I need from you is wisdom, that insane pct protocol was from some respectable body building forum & it turned out to be the stupidest thing I could ever do, why do body building experts swear by things when they are really not sure

dennis;

I took 5000 iu hcg once every week for 2 weeks & 2500 iu for the 3rd week. during the 3 weeks period I was feeling good & my sex drive was fine, but things went down gradually the following weeks, which gave me an indication that hcg is only helpful temporarily !! maybe it has delayed my recovery and/or increased my estrogen levels drastically, because I felt so depressed & emotional afterwards, I suspect that stress is also a big player in my problem, I am really forcing myself to hit the gym even though I feel that I don't want to....

to rule out any other causes for lack of libido, I made further testing for my cholestrol, blood pressure, liver, cbc test, LDL, HDL, diabetes, creatinine......all were fine.

now I conclude that I should go on 20 mg nolvadex for say 3-4 weeks & then take a week off then re-test my hormons including total test, free test, LH, estradiol, TSH, prolactin, cortisol,,,,did I miss anything? suppose (I hope) that results were fine then, would that mean my leydig cells are functioning & responding to LH,, any thoughts ?

also, do I need aromasin ? please confirm

 

[bigbench]

How were estro levels? Were they above normal? If not, then the aromisan may not be needed. Yes, another course of Nolva will help out as you were keeping yourself shutdown while on the HCG.

 

[Conciliator]

So, just to rephrase this:
Nolva does NOT stimulate the HPTA directly (it can't right?). It simply blocks the receptor at the pituitary and the breast tissue receptors (amoung others possibly).
The LH and FSH production is due to the secondary effect of Pitutary not detecting the estrogen as it slowly builds up because the receptors are blocked.

Is that correct?
That has been my understanding of Nolva's action, which conflicts with many expert opinions.

Yes, that's correct. What "expert opinions" conflict with that?

If the above is correct, then i don't understand why PCT cannot be done well with an AI like Arimidex to prevent estrogen from building up (as natural Test comes back online) rather than binding to the Pitutary receptors.

Seems like just another way to skin a cat to me. Both prevent the detection of Estrogen, one by preventing Estrogen being created(Arimidex) and the other by hiding the estrogen that is there from the Pituitary.

PCT can be done with an AI. The problem is that AIs kill estrogen completely, including the positive effects that estrogen has on blood lipids, bone, energy levels, etc.

On the other hand, nolva is selective. While it blocks estrogen at the HPTA (which includes the pituitary), it acts like estrogen where you WANT estrogen, like in the liver (where it affects lipds) and bone.

Perhaps the use of Nolva is some of the reason that some people say they get depressed during PCT - its not that they have no Test, its that they have TOO much Estrogen!
I'm a beliver in prevention is better than cure. Therefore and AI should be better than a SERM for some respects of PCT.

I don't think depression during PCT is from too much endogenous estrogen, which will be low. Much more likely, it's due to low androgen levels. SERMS can also cause changes in mood in some people.

A common argument against Arimidex for PCT is that Estrogen will be low due low Testosterone at the end of cycle so an AI will be ineffective (as there is nothing to arimatize).
But this is the same even if your using Nolva, it can't block what is not there, right?!

Well estrogen is there, levels are just low. My opinion is that SERMS do a better job at blocking a small amount of estrogen than AIs do at reducing an already small amount of estrogen. And as I've mentioned, having little to no estrogen is not optimal.

As natural Test comes back online the AI will be there to prevent aromatization just as Nolva would be there to block the receptor.
And, if Nolva is NOT stimulating the HPTA directly (it cannot, that's not how SERM or a negative feedback loop works - my understanding) then what's it doing when there is no Test to aromatize? Sweet-fuck-all i imagine..

In tissues where Nolva blocks estrogen, yes, it's going to be doing "sweet-fuck-all" when there's no estrogen around to block. However, nolva is selective. In tissues where it acts like an estrogen (an agonist of the estrogen receptor) it will produce estrogenic effects, which is beneficial.

Hope that helps,
Conciliator

 

[Oxygen]

__________________________________________________________________________
QUANTIFICATION OF LEYDIG CELLS AND MEASUREMENT OF LEYDIG-CELL SIZE FOLLOWING ADMINISTRATION OF HUMAN CHORIONIC GONADOTROPHIN TO NORMAL MEN
C. G. HELLER and D. R. LEACH
Summary.: Six normal men were injected with 4000 i.u. of HCG intramuscularly three times a week for 6 weeks or every 2nd day for 16 weeks. Levels of urinary testosterone and oestrogens were measured. Leydig cells were quantified on the basis of the Leydig cell/Sertoli cell ratio, and Leydig-cell size was measured.

Following both 6 and 16 weeks HCG administration, four subjects showed no change in Leydig-cell numbers. The remaining subjects showed slight increases or decreases. Levels of urinary testosterone and oestrogen increased. It is concluded that there is no consistent increase in Leydig-cell numbers following HCG administration. Measurements of Leydig-cell nucleus and cytoplasm revealed a significant increase in the size of both at 6 and 16 weeks in all but one subject. It is concluded that the increased activity of the Leydig cells is related to their increase in size and not to an increase in number as had been reported.
__________________________________________________________________________


I came across this study, its not about the HCG-induced-desensitization, but you can see that those NORMAL men were injected with 4000 iu hcg 3 times a week for 6 weeks,,,, shouldn't that cause them desensitization ?

 

[brang]

Firstly, I apologize to the original poster for hijacking this thread.
I'm just going to reply quickly here and then i'll shut right up.

Yes, that's correct. What "expert opinions" conflict with that?

I've read posts by some people who attempt to come across as experts; that have said things along the lines of: "Nolva stimulates the HPTA".

When in fact it doesn't stimulate anything. It merely blocks receptors and the natural feedback loop does the rest. Using that logic, i could claim that Arimidex "stimulates" the HPTA - which it does not. Just semantics? - i think not. There is clearly (to me anyway) a logical difference.

Hope that helps,
Conciliator

Absolutely it does. Thanks for the detailed response. it's much appreciated.

Sincerely, i am not trying to give anyone shit or point the finger here.. just wanting to understand the actual mechanism of these drugs, before i use them.

peace.
- b

 

[jasthace]

I've read posts by some people who attempt to come across as experts; that have said things along the lines of: "Nolva stimulates the HPTA".

When in fact it doesn't stimulate anything. It merely blocks receptors and the natural feedback loop does the rest. Using that logic, i could claim that Arimidex "stimulates" the HPTA - which it does not. Just semantics? - i think not. There is clearly (to me anyway) a logical difference.

I don't know who claimed nolvadex stimulates the HPTA,but they are correct.
It does so by blocking the estrogen receptors {that is the initial mechanism} as would arimidex would by inhibiting aromatisation.
It is the final result that they were referring to.
Its like saying you don't put your hand brake on with the level inside he car, it is actually the cable that pulls the brake pads on,unnecessary and slighty pedantic

 

[jasthace]

__________________________________________________________________________
QUANTIFICATION OF LEYDIG CELLS AND MEASUREMENT OF LEYDIG-CELL SIZE FOLLOWING ADMINISTRATION OF HUMAN CHORIONIC GONADOTROPHIN TO NORMAL MEN
C. G. HELLER and D. R. LEACH
Summary.: Six normal men were injected with 4000 i.u. of HCG intramuscularly three times a week for 6 weeks or every 2nd day for 16 weeks. Levels of urinary testosterone and oestrogens were measured. Leydig cells were quantified on the basis of the Leydig cell/Sertoli cell ratio, and Leydig-cell size was measured.

Following both 6 and 16 weeks HCG administration, four subjects showed no change in Leydig-cell numbers. The remaining subjects showed slight increases or decreases. Levels of urinary testosterone and oestrogen increased. It is concluded that there is no consistent increase in Leydig-cell numbers following HCG administration. Measurements of Leydig-cell nucleus and cytoplasm revealed a significant increase in the size of both at 6 and 16 weeks in all but one subject. It is concluded that the increased activity of the Leydig cells is related to their increase in size and not to an increase in number as had been reported.
__________________________________________________________________________


I came across this study, its not about the HCG-induced-desensitization, but you can see that those NORMAL men were injected with 4000 iu hcg 3 times a week for 6 weeks,,,, shouldn't that cause them desensitization ?

Estrogen can have a negative effect on the leydigs,this is why tamoxifen is a must have with pct and especially with and after the use of hcg which can have a negative impact on the leydig via it's estrogen properties.


It is generally agreed that estrogens, principally estradiol-17?, are synthesized by and act in the testis of mammals, including humans. The site of estradiol synthesis in the testis is generally believed to begin in the Sertoli cell and switch to the Leydig cell during neonatal development where a gonadotropin-regulated aromatase is present. Numerous studies suggest that the primary target cell of estradiol in the testis at all ages is the Leydig cell. In fact, the Leydig cell is known to possess an estrogen receptor that binds estradiol in the classic manner. The mechanism of estradiol action and the role of its receptor in the testis, however, remain unresolved. In Leydig cells, estradiol appears to induce several alterations that are dependent in large part on the developmental stage of the Leydig cell. In the fetal and neonatal testes, estradiol appears to block the ontogenic development of Leydig cells from precursor cells. There is also evidence that estradiol similarly blocks the regeneration of Leydig cells in the testis of mature, ethane dimethylsulfonate-treated animals. Evidence indicates that the precursor cell possesses high levels of estrogen receptors relative to that of the Leydig cell. It is postulated that estradiol is a paracrine factor involved in regulating the interstitial population of Leydig cells. Evidence also indicates that estradiol acts directly in the mature testis to block androgen production. It appears to do so by inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis. Although the more conventional receptor-mediated mode of action is feasible, several studies have suggested that this action might entail direct competitive inhibition of key steroidogenic enzymes by estradiol. In summary, the net biologic effect of estradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell.

ScienceDirect - Steroids : The potential roles of estrogens in regulating Leydig cell development and function: A review

 

[brang]

I don't know who claimed nolvadex stimulates the HPTA,but they are correct.

I'd say they are being vague and inaccurate.
---------
stimulate |?stimy??l?t|
verb [ trans. ]
raise levels of physiological or nervous activity in (the body or any biological system)
---------
Nolva does not raise levels, it binds to receptors, blocking messages - that's it. Nothing more. There is a clear difference; yes it ends up causing a comparable outcome but that's not the point.

It does so by blocking the estrogen receptors {that is the initial mechanism} as would arimidex would by inhibiting aromatisation.
It is the final result that they were referring to.
Its like saying you don't put your hand brake on with the level inside he car, it is actually the cable that pulls the brake pads on,unnecessary and slighty pedantic

Heh, cute analogy Ok, so let me put that to you in another light:
If i'm a apprentice mechanic(there are lots of us here on meso , it IS important that i know that it's cable that exerts pressure on the brake pads, not the lever in the car!
Understanding the mechanism is absolutely necessary to make an informed choice.

The usual comments go something like this:
Nolva stimulates the HPTA so it should be used in PCT. (Inferring that it has some magical power that an AI does not . Now, it might just be me, but that is a misleading and uninformed statement. It makes it seem as thought the HPTA is actually being directly acted upon by Nolva - which it is not.

To me it's important to be as accurate as possible when it comes to giving advice regarding drugs for very important things such as PCT.

Research is not really worth much if it's inaccurate information being used, is it?

Anyway, lets agree to disagree; you say it stimulates the HPTA, i say it doesn't.
peace.
- b

 

[Conciliator]

I agree with brang. When you say that something "stimulates" something else, it gives the impression of a direct, positive action. But here, we have a negative action on an inhibitor (removing the brakes, so to say).

In your car, you can think of pressing the gas as "stimulating" speed. You can think of pressing the brake as "inhibiting" speed. Now what about easing off the brake, so you're not pushing on it so hard? Does that "stimulate" speed? I think not. You're just reducing the inhibition of speed. And so it is with SERMS and LH/Testosterone production.

Along the same lines, I wouldn't call easing off the gas as "inhibiting" speed. You're not really inhibiting anything, you're just reducing the stimulus.

 

[Oxygen]

Good news is: I had a morning wood today ! first in several weeks!!! also my mood is more stable & feeling better in general, interesting that these positive effects coincided the usage of the following:

0.5mg arimidex ED
25mg DHEA ED
Activate Xtreme ED

I wanted to use nolvadex instead of arimidex, but I just ran out & based on your cold war I was convinced somehow that inhibiting % estrogen is the way to go.

I hope that things will even get better in the upcoming days/weeks,,, any comments ? btw, "agree to disagree" doesn't seem bad at all

 

[jasthace]

Ok
But then if we were to state in the same specific terms the effect of AAS,we would not be able to say that anabolic/androgenic steroids stimulate protein synthesis and glycogen retention.
We'd have to say the they stimulate gene regulation which in turn stimulates cell up regulation,
More specifically the steroid receptor complex activates transcription of transcriptional factors and aporepressors that then function in the transcription of active transport proteins specific to amino acids and glucose.

 

[jasthace]

Good news is: I had a morning wood today ! first in several weeks!!! also my mood is more stable & feeling better in general, interesting that these positive effects coincided the usage of the following:

0.5mg arimidex ED
25mg DHEA ED
Activate Xtreme ED

I wanted to use nolvadex instead of arimidex, but I just ran out & based on your cold war I was convinced somehow that inhibiting % estrogen is the way to go.

I hope that things will even get better in the upcoming days/weeks,,, any comments ? btw, "agree to disagree" doesn't seem bad at all

I was wondering if DHEA might be your answer
Thats good news bro.

 

[brang]

Ok
But then if we were to state in the same specific terms the effect of AAS,we would not be able to say that anabolic/androgenic steroids stimulate protein synthesis and glycogen retention.
We'd have to say the they stimulate gene regulation which in turn stimulates cell up regulation,
More specifically the steroid receptor complex activates transcription of transcriptional factors and aporepressors that then function in the transcription of active transport proteins specific to amino acids and glucose.

LOL. I don't think so.
Claiming stimulation where there is none is the issue here, not using the exact scientific terminology and defining the biological process in as much detail as possible.
Surely you can see a difference? TBH i think you're just being argumentative for the sake of it.

FWIW, there IS a transitive stimulation affect in both of the above statements describing the actual biological process; one process stimulates another which stimulates another.
So saying AAS stimulates protein synthesis and glycogen retention is reasonable IMO.
However, it it not reasonable to claim that a SERM like Nolva stimulates the HPTA when it provides no stimulus at all.

Is it really too much to ask to describe the real mechanism of a SERM or an AI?
They can be easily described accurately and require nothing like the long-winded description of the affects of AAS you have provided above. But you already know that.

If you want to describe the process that way for brevity sake then by all means go right ahead, its no skin off my nose. I believe i do understand the actual mechanism sufficiently now, so i'm happy either way.

I wont post on this subject anymore as i don't want to piss people off anymore than i probably already have.

And again, sorry to Oxygen for hijacking.

peace.
- b

[edited as some of what i wrote came out wrong.]