1-Test - Anabolic/Androgenic?

[pa1ad]

I never said increasing gonadotropins was irrelevant. What I said was that gonadotropins return quickly on their own, and with estrogenic and androgenic inhibition both reduced post-cycle there seems no notable mechanism for AE's to help. The testes are screwing everything up post cycle, not LH levels. You are trying to fix something with AE's that isn't really broke.

I am not trying to knock your aromatase inhibitor. I just strongly feel that bodybuilders are missing the issue when relying on anti-estrogens, and are forgetting the truly important post-cycle drug: HCG.

So what you are trying to say is that you have to increase gonadotropins to supraphysiological levels to get the testes to jump back into play. I can buy that.

Now, I think where we disagree here is whether or not anti-estrogens can increase gonadotropins in someone with low androgen and estrogen levels. The literature that I have read on the subject seems to indicate that they can. You seem to think that they cannot.

 

[Bill Llewellyn]

So what you are trying to say is that you have to increase gonadotropins to supraphysiological levels to get the testes to jump back into play. I can buy that.

Now, I think where we disagree here is whether or not anti-estrogens can increase gonadotropins in someone with low androgen and estrogen levels. The literature that I have read on the subject seems to indicate that they can. You seem to think that they cannot.

What I am saying is that if anti-estrogens could somehow have a slight effect on LH, in spite of the fact that estrogen is low already and LH often rises to supraphysiological levels on its own in this window anyway, I don't think it would significantly alter post-cycle recovery.

I think AE's are very useful for fighting gyno here, but not for kicking testosterone back up. If you want to keep muscle size you'd be better off spending the money on another cycle.

 

[rush]

Is it possible from a 10 day 1 test cycle 6 months ago
that I would be experiencing estrogen problems even
now, as I have mentioned on this board before I have
been getting very paranoid regarding the hair on my
head and body which has become very fine, and easy
to remove, shouldnt my body have rightened itself by
now in terms of hormonal function

 

[pa1ad]

What I am saying is that if anti-estrogens could somehow have a slight effect on LH, in spite of the fact that estrogen is low already and LH often rises to supraphysiological levels on its own in this window anyway, I don't think it would significantly alter post-cycle recovery.

I think AE's are very useful for fighting gyno here, but not for kicking testosterone back up. If you want to keep muscle size you'd be better off spending the money on another cycle.

Well Bill, I adamantly feel that you are wrong. Here is one case study that supports my contention (WJM, Vol 162,#2, 1995):

29 year old bodybuilder, chronic steroid user, off the drugs for a year.

FSH - 0.6 (normal 1.6 - 17.8)
LH - 1.9 (normal 1.4 - 11.1)
free testosterone - 7.1 (normal 19.0 - 41.0)

After a month on clomiphene 50mg a day, FSH, LH and free test showed mild improvements.

The dose was then increased to 100 mg and after a month at this dose serum FSH, LH, and free testosterone levels had reached normal for his age.

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Typical case of post cycle hypogonadotropic hypogonadism successfully treated with an anti-estrogen.

I do admit however that not all bodybuilders respond to anti-estrogens alone, and sometimes HCG is needed either alone or in combination with the anti-estrogens.

But to say that anti-estrogens are not of any use in treating post cycle testosterone suppression is really wrong.

 

[pa1ad]

What I am saying is that if anti-estrogens could somehow have a slight effect on LH, in spite of the fact that estrogen is low already and LH often rises to supraphysiological levels on its own in this window anyway, I don't think it would significantly alter post-cycle recovery.

I think AE's are very useful for fighting gyno here, but not for kicking testosterone back up. If you want to keep muscle size you'd be better off spending the money on another cycle.

I think that instead of us just butting heads on this and getting nowhere, we should consult someone who has the practical real world hands on experience in treating anabolic steroid induced hypogonadism. I am gonna email Dr. Mauro DiPasquale and ask him what his experience has taught him about this.

The two issues that we differ on here are

1) Whether post cycle suppression is typically characterized by low gonadotropins and low testosterone (as I contend) or by normal or high gonadotropins with low testosterone (as Bill contends)

2) Whether anti-estrogens can successfully be used to restore testosterone production after anabolic steroid cycles.

Now, if Dr. DiPasquale sides with Bill I am going to have to swallow my pride and accept it. And vice versa. I am going to report here what he tells me, if he responds to my email

 

[Bill Llewellyn]

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Typical case of post cycle hypogonadotropic hypogonadism successfully treated with an anti-estrogen.

The reference you cite is not really relevant. I agree that he has suffered exactly what is stated. But someone who has suppressed gonadotropins 1 year after steroid discontinuance is not a good example of the typical post-cycle rebound window.

My article should be out on Par's site very soon. I would like you to reference it before passing judgement. It does show clearly a long post cycle window characterized by normal LH and low T. I don't have the key reference to my article here, but I did post it on Elite once before if you want to search.


- Bill

 

[pa1ad]

The reference you cite is not really relevant. I agree that he has suffered exactly what is stated. But someone who has suppressed gonadotropins 1 year after steroid discontinuance is not a good example of the typical post-cycle rebound window.

My article should be out on Par's site very soon. I would like you to reference it before passing judgement. It does show clearly a long post cycle window characterized by normal LH and low T. I don't have the key reference to my article here, but I did post it on Elite once before if you want to search.


- Bill

I will say this much. I have seen blood tests of people after they came off of 1-AD and after they have come off of other prohormones as well as steroid cycles. What I saw was suppressed gonadotropins as well as suppressed testosterone. The time frame of these was anywhere from a week to 2 months. Were all these anomalies?

 

[Bill Llewellyn]

I will say this much. I have seen blood tests of people after they came off of 1-AD and after they have come off of other prohormones as well as steroid cycles. What I saw was suppressed gonadotropins as well as suppressed testosterone. The time frame of these was anywhere from a week to 2 months. Were all these anomalies?

I didn't say your bodybuilder was an anomalie, just that his condition does not represent the healthy bodybuilder. As for your 1-AD users, I couldn't comment without seeing the bloodwork, but could guess recovery of T took a hell of a lot longer than LH.

I am not saying gonadotropins pop up within an afternoon, but that the post-cycle window is drawn out because of testicular insensitivity to gonadotropins, not low levels of gonadotropins. I am sure you have heard of the concept of testosterone rebound therapy as a means of increasing male fertility. This takes advantage of the high levels of gonadotropins that result in the post-cycle window after T has been suppressed for a long time, and the testes atrophied, from testosterone administration.

Plus, estrogn is not the cause when gonadotropins are low, because estrogen too is low.

 

[pa1ad]

I didn't say your bodybuilder was an anomalie, just that his condition does not represent the healthy bodybuilder. As for your 1-AD users, I couldn't comment without seeing the bloodwork, but could guess recovery of T took a hell of a lot longer than LH.

I am not saying gonadotropins pop up within an afternoon, but that the post-cycle window is drawn out because of testicular insensitivity to gonadotropins, not low levels of gonadotropins. I am sure you have heard of the concept of testosterone rebound therapy as a means of increasing male fertility. This takes advantage of the high levels of gonadotropins that result in the post-cycle window after T has been suppressed for a long time, and the testes atrophied, from testosterone administration.

Plus, estrogn is not the cause when gonadotropins are low, because estrogen too is low.

Are you trying to tell me that atrophying the testicles is a treatment for male infertility? So you want to lower the sperm count, and shut down the sertoli cells? Please tell me more about this. On the surface it makes as much sense as putting the country into a deep depression as a means to stimulate the economy

Yes, T takes longer to recover than gonadotropins. But T won't recover at all unless we raise gonadotropins high. That is why we use anti-estrogens

The problem is that you seem to think that you need high or normal estrogen levels for anti-estrogens to raise gonadotropins. I am pretty sure you are wrong about this. Have you checked into this to make sure this is the case?

 

[Bill Llewellyn]

Are you trying to tell me that atrophying the testicles is a treatment for male infertility? So you want to lower the sperm count, and shut down the sertoli cells? Please tell me more about this. On the surface it makes as much sense as putting the country into a deep depression as a means to stimulate the economy

You should have at least bothered to look up the term Pat. Here is a quote re:TRT.

"Other androgens have been used to produce a rebound effect. These androgens are administered to suppress gonadotrophin secretion and spermatogenesis. After androgen therapy is discontinued there is a surge of FSH and LH and spermatogenesis is recommenced."

Cochrane Database Syst Rev 2000;(2):CD000150 Androgens versus placebo or no treatment for idiopathic oligo/asthenospermia.

I didn't say this therapy was a great, effective idea. But the discussed effect does a good job of illustrating my point.

Yes, T takes longer to recover than gonadotropins. But T won't recover at all unless we raise gonadotropins high. That is why we use anti-estrogens

The problem is that you seem to think that you need high or normal estrogen levels for anti-estrogens to raise gonadotropins. I am pretty sure you are wrong about this. Have you checked into this to make sure this is the case?

If estrogen and androgen levels are low enough to produce a surge in LH and FSH, where do the anti-estrogen comes in? We have already done a great job of lowering estrogen and androgen inhibition. If it takes a little time for LH to get back up, it is obviously not due to sex steroids, nor does it make sense that blocking estrogen will do anything significant.