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1-Test - Anabolic/Androgenic?

3000GT

New member
I'd like to know everyone's thoughts on the androgenic activity of 1-test. There's been a lot of posts saying that it is very androgenic (more than test), but then why the decreased sex drive that users report? Is this because it's a DHT derivative, and there isn't actually any DHT, once your own test is suppressed? Typically people complain about a loss of sex drive, when a cycle doesn't have enough androgens (i.e. deca dick). I know people complain about hair loss, but winny and primo have very low androgenic activity and can still cause hair loss. Also, it sounded like Bill thought that 1-test may not be a very strong androgen (at least not compared to test). Has anyone noticed strong androgenic side effects (acne, hair growth) when using 1-AD, 1-test products? It just seems like all of the signs point to 1-test being a strong anabolic, weak androgen. :confused:
 
According to the assays, 1-Test is both more androgenic and anabolic than testosterone mg for mg. It is overall more anabolic than androgenic in nature though (it has a favorable ratio), which means that for a given level of activity in the muscle tissue you have comparably less activity in androgenic target tissues. The reverse is true with testosterone.

In my experience, even at 400mg daily (Ethergels), 1-test could not replace the full androgenic action of testosterone in regards to libido.
 
doffmaster said:
Since 1-Test is supposedly so potent, should regular post-cycle precautions be followed (i.e. clomid, nolvadex)?

:confused:

The standard precaution of using an anti-estrogen only works with Gyno. It doesn't effect testosterone levels really, as estrogen levels are actually lower post-cycle, not higher.

If you are not using HCG there is probably not much need for the AE alone, unless of course you are sensitive to gyno (estrogen isn't high post cycle, but is at a greater imbalance than normal with androgens, which can cause gyno).

Look for my article on this in the next Mind And Muscle (Formerly BMFR). www.avantlabs.com
 
w_llewellyn said:


The standard precaution of using an anti-estrogen only works with Gyno. It doesn't effect testosterone levels really, as estrogen levels are actually lower post-cycle, not higher.

If you are not using HCG there is probably not much need for the AE alone, unless of course you are sensitive to gyno (estrogen isn't high post cycle, but is at a greater imbalance than normal with androgens, which can cause gyno).

Look for my article on this in the next Mind And Muscle (Formerly BMFR). www.avantlabs.com



YOu do not need high estrogen levels to experience an increase in gonadotropins from an anti-estrogen. Also, as Bill said, you may experience an androgen / estrogen imbalance post-cycle. Therefore, it is my opinion that it is prudent decision to take an anti-estrogen post cycle
 
3000GT said:
I'd like to know everyone's thoughts on the androgenic activity of 1-test. There's been a lot of posts saying that it is very androgenic (more than test), but then why the decreased sex drive that users report? Is this because it's a DHT derivative, and there isn't actually any DHT, once your own test is suppressed? Typically people complain about a loss of sex drive, when a cycle doesn't have enough androgens (i.e. deca dick). I know people complain about hair loss, but winny and primo have very low androgenic activity and can still cause hair loss. Also, it sounded like Bill thought that 1-test may not be a very strong androgen (at least not compared to test). Has anyone noticed strong androgenic side effects (acne, hair growth) when using 1-AD, 1-test products? It just seems like all of the signs point to 1-test being a strong anabolic, weak androgen. :confused:


The piece of the puzzle you are missing is the fact that estrogen is necessary for the libido sustaining effects of androgens. That is probably why strong androgens that do not aromatize sometimes lower libido. Case in point: trenbolone acetate
 
pa1ad said:
YOu do not need high estrogen levels to experience an increase in gonadotropins from an anti-estrogen.

I agree you do not need high estrogen levels for anti-estrogens to have an effect, but have seen nothing to suggest that offer a benefit when gonadotropins are already elevated due to subnormal estrogen and androgen levels.
 
w_llewellyn said:
According to the assays, 1-Test is both more androgenic and anabolic than testosterone mg for mg. It is overall more anabolic than androgenic in nature though (it has a favorable ratio), which means that for a given level of activity in the muscle tissue you have comparably less activity in androgenic target tissues. The reverse is true with testosterone.

In my experience, even at 400mg daily (Ethergels), 1-test could not replace the full androgenic action of testosterone in regards to libido.


cant say that i agree. im on hrt but find that 1-test spikes my libido to a much greater extent .
 
stoomp said:
cant say that i agree. im on hrt but find that 1-test spikes my libido to a much greater extent .

We are speaking about when taken with no other androgens.

Libido is a funny thing anyway. You will never get a consistent opinion on how a particular steroid effects this. Some people are totally unaffected by Deca, while others are ready to jump off a roof within a couple of weeks.
 
w_llewellyn said:


We are speaking about when taken with no other androgens.

Libido is a funny thing anyway. You will never get a consistent opinion on how a particular steroid effects this. Some people are totally unaffected by Deca, while others are ready to jump off a roof within a couple of weeks.


true, maybe 1-test and test have a sinergistic affect with regard to libido. wonder whether par's libido is increased when using one+
 
w_llewellyn said:


I agree you do not need high estrogen levels for anti-estrogens to have an effect, but have seen nothing to suggest that offer a benefit when gonadotropins are already elevated due to subnormal estrogen and androgen levels.


MOst people suffering from post cycle hypoandrogenism have low LH/FSH levels. I have never seen a case of high LH/FSH and low testosterone from someone suffering from simple post cycle suppression
 
pa1ad said:
MOst people suffering from post cycle hypoandrogenism have low LH/FSH levels. I have never seen a case of high LH/FSH and low testosterone from someone suffering from simple post cycle suppression

Please post a reference to this, as the only thing I see is a rapid LH/FSH return post cycle, and this is after long-term use.

I can't see logically how LH would be more slow to return on small cycles, yet rapid after more suppressive cycles.
 
w_llewellyn said:


Please post a reference to this, as the only thing I see is a rapid LH/FSH return post cycle, and this is after long-term use.

I can't see logically how LH would be more slow to return on small cycles, yet rapid after more suppressive cycles.



I don't get it. I have seen many blood tests of people post cycle and there is always an LH/FSH deficit along with the testosterone suppression. I know what I have seen firsthand, but if you want references this is what i find on medline:

Pol Merkuriusz Lek 2001 Dec;11(66):535-8 Related Articles, Books, LinkOut


[Treatment strategies of withdrawal from long-term use of anabolic-androgenic steroids]

[Article in Polish]

Medras M, Tworowska U.

Anabolic-androgenic steroid (AAS) withdrawal is established to be an important, though poorly known medical problem, because of AAS potency to cause physical and psychological dependence. Thus discontinuation of high-dose, long-term anabolic steroid use, apart from endocrine dysfunction (hypogonadotropic hypogonadism),

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Notice the term HYPOgonadotropic

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Postgrad Med J 1998 Jan;74(867):45-6 Related Articles, Books, LinkOut


Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin.

Gill GV.

Endocrine Unit, Walton Hospital, Liverpool, UK.

A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months. Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse.
----------

ONce again HYPOgonadotropic (meaning due to lack of LH/FSH) hypogonadism

-----------------


Hum Reprod 1997 Aug;12(8):1706-8 Related Articles, Books, LinkOut


Conservative management of azoospermia following steroid abuse.

Gazvani MR, Buckett W, Luckas MJ, Aird IA, Hipkin LJ, Lewis-Jones DI.

Reproductive Medicine Unit, Liverpool Women's Hospital, UK.

As well as athletes and competitive body builders, recreational body builders attending gymnasia are known to abuse anabolic steroids, using doses from 10- to 40-fold above physiological levels. Androgenic steroids induce hypogonadotrophic hypogonadism with associated azoospermia, leading to infertility. Little literature exists on the treatment of steroid-induced azoospermia following the cessation of abuse. We present four cases of steroid-induced azoospermia, its conservative management and eventual return of normal semen density.

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hypogonadotropic again Bill

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Am J Sports Med 1990 Jul-Aug;18(4):429-31 Related Articles, Books, LinkOut


Anabolic steroid-induced hypogonadotropic hypogonadism.

Jarow JP, Lipshultz LI.

Department of Surgery (Urology), Bowman Gray School of Medicine, Winston-Salem, North Carolina 27103.

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No abstract but the title says it all

--------

My search revealed nothing to support your view on the subject so i am interested in what you have to support your view
 
Pat, you are not looking at the whole picture. Of course gonadotropins become suppressed with steroids. Nobody is arguing against hypogonadotropic hypogonadism, this occurance is common sense. You references do not detail LH and T levels for the weeks and months post cycle however, and therefore explain only the cause of suppression, not the process in which T is restored naturally by the body.

I wrote an referenced article for the next Mind and Muscle, with graphs of LH, T, and everything. It will be easy for you to follow, and shows clearly that LH comes back quickly, while T is delayed for weeks/months. Gonadotropins are not the weak link in the post-cycle window, the testes are.

- Bill
 
w_llewellyn said:
Pat, you are not looking at the whole picture. Of course gonadotropins become suppressed with steroids. Nobody is arguing against hypogonadotropic hypogonadism, this occurance is common sense. You references do not detail LH and T levels for the weeks and months post cycle however, and therefore explain only the cause of suppression, not the process in which T is restored naturally by the body.

I wrote an referenced article for the next Mind and Muscle, with graphs of LH, T, and everything. It will be easy for you to follow, and shows clearly that LH comes back quickly, while T is delayed for weeks/months. Gonadotropins are not the weak link in the post-cycle window, the testes are.

- Bill


So what you are saying is that there is a delay between LH/FSH restoration and testicular response. I don't doubt that. The testes probably take some time to prime after a period of atrophy.

However, none of this changes anything. You still need to restore gonadotropins to get the testes working again. And that can be done using HCG, menotropins, anti-estrogens, or a combination of all of these.

I do not understand your logic in regards to determining that this testicular response lapse indicates that increasing gonadotropins is irrelevant. Unless you know of some other way to stimulate the testes - perhaps dipping them in hot or cold water? I dunno
 
pa1ad said:
I do not understand your logic in regards to determining that this testicular response lapse indicates that increasing gonadotropins is irrelevant. Unless you know of some other way to stimulate the testes - perhaps dipping them in hot or cold water? I dunno

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.
 
w_llewellyn said:


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.
 
pa1ad said:
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.
 
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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
 
w_llewellyn said:


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.

-----------

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.
 
w_llewellyn said:


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
 
pa1ad said:
-----------

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
 
w_llewellyn said:


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?
 
pa1ad said:
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.
 
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w_llewellyn said:


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?
 
pa1ad said:
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.
 
w_llewellyn said:


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.



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. [/B]


Why don't you end the mystery and tell me what the references are for everything you are talking about.
 
pa1ad said:
Why don't you end the mystery and tell me what the references are for everything you are talking about.

Here is the one that I reference regarding the post-cycle recovery of gonadotropins and T. I know I posted this before.

Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84

Here, blood hormone levels were monitored before, during, and after a long cycle of test enanthate (250mg weekly). LH levels started to rise withing a few weeks after the last shot, while T was still declining, but there was no significant movement in endogenous testosterone production for about 10 weeks.
 
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w_llewellyn said:


Here is the one that I reference regarding the post-cycle recovery of gonadotropins and T. I know I posted this before.

Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84

Here, blood hormone levels were monitored before, during, and after a long cycle of test enanthate (250mg weekly). LH levels started to rise withing a few weeks after the last shot, while T was still declining, but there was no significant movement in endogenous testosterone production for about 10 weeks.


Thanks Bill, but I got an answer from Mauro. It seems that your contention on LH is right - in about 20% of cases. Other than that, its hypogonadotropic hypogonadism. I think you will find what Mauro has to say very interesting, as well as pretty indisputable given his vast experience over the years with treating HPTA dysfunction secondary to AAS abuse. I am glad I got this answer before you printed your article on the subject. Take care.

----------

Hi Patrick,

It's good to hear from you. I hope everything is going well.

I'll briefly tell you what I know on the two issues off the top of my head.
If needed I can enlarge on anything I say below.

Of the several hundred cases I've seen and treated over the past three
decades over 80% have shown a low LH and a low testosterone, secondary to a
refractory HTPA (an acquired hypogonadotropic hypogonadism). About 10% have
shown a normal LH and low testosterone and the rest, less than 10%, have
shown an elevated LH and a low testosterone. One thing you have to keep in
mind is that in many of these cases the lab work was not done immediately
after the cessation of anabolic steroids, but usually a few months and often
time more, after. As such, what the results may or may not be relevant to
the average person within a few weeks after they've discontinued the use of
anabolic steroids. In the few dozen times that I have done serum LH and
testosterone levels within less than a week of going off steroids the almost
universal finding was a low LH and low testosterone (and BTW a low
epitestosterone - another BTW, the FSH responds differently, depending on
what the person was on). It's true however, that the Hypothalamic/pituitary
axis usually recovers first, leading to increases in LH and subsequent
increases in testicular steroidogenesis.

There are several factors involved in the way all of these people have
presented after using AS. The most important, in my view, are the type,
amount and time the AS are used, interindividual variability, which of
course includes the presteroid makeup of the individual, and the response to
AS, and the age of the individual. I suspect that much of the
interindividual variability or phenotypic differences in the HPTA response
to AS, in cases where the use of AS is similar, is due to single-nucleotide
polymorphism within the various relevant human gene coding sequences
(including the various receptors [GnRH, LH, androgen, etc.], hormone levels
and other factors [such as SHBG levels, in which deficiencies and excess of
may be inherited]).

Treatment will also vary according to the individual response to the use of
AS and the person's genetic makeup, including the many polymorphisms that
are invariably present in our population that may have an effect on one or
more factors that make up the overall phenotypic presentation.

In general, I've found anti-estrogens very effective when both of the
following conditions were present, along with a low serum testosterone. A
low testosterone/estrogen ratio, and a low to normal LH. The low LH usually
results from a refractory hypothalamic/pituitary axis while a normal LH
(with a low testosterone) is indicative of dysfunction along the whole HPTA
when essentially what has happened is that the body has reset it's
testosterone thermostat, so to speak, so that a low level is now considered
normal.

Anti-estrogens have been less effective when the testosterone/estrogen ratio
was high, even when serum testosterone levels were low. Anti-estrogens were
not effective in cases where the LH levels were high. In these cases the
problem was not in the HP axis but was mainly one of low testicular
steroidogenesis due to primary testicular (Leydig cell) refractory state
(hypergonadotropic hypogonadism - something I see in every age group but
more commonly in older men and in those who are compromised in some way, as
in HIV infected men. In these cases HCG injections can be effective while
anti-estrogens are not.

In general the refractory HPTA that is present after the discontinuation of
anabolic steroids will respond to either the anti-estrogens or HCG, mainly
because there are no real defects present in the hypothalamic, pituitary,
testicular tissues, and they recover once the physiological damper, the
exogenous anabolic steroids, are removed. The use of HCG is a potent
stimulus for increasing testicular steroidogenesis, although it likely
extends the refractory state as far as the HP axis. On the other hand, as
noted above, in most cases the HP axis recovers first and then the increased
LH leads to increased testicular steroidogenesis, but it may take a while.
As such, stimulating the testicular machinery and getting it up to par may
make the whole process as efficient, and perhaps in some cases more
efficient (if the HP axis recovers quickly) as using anti-estrogens. In
cases where the HPTA axis suppression is prolonged, the usual result is a
low LH and testosterone and in these cases I've found that HCG is not as
effective in kick-starting the HPTA as the anti-estrogens. In some cases you
can increase testosterone levels by the use of a variety of compounds,
including GnRH, LH, HCG, and the anti-estrogens but it just doesn't stick.
In these cases some suprahypothalamic regulatory pathways have been
disrupted and the only treatment is replacement therapy.

I apologize for the rambling but I hope that this information helps,
although I may have muddled the issues. If things weren't so hectic I would
have spent more time on giving you a more complete answer. On the other
hand, if you have any questions or concerns with any of the above don't
hesitate to write.

All the best,

Mauro
 
pa1ad said:
Thanks Bill, but I got an answer from Mauro. It seems that your contention on LH is right - in about 20% of cases. Other than that, its hypogonadotropic hypogonadism. I think you will find what Mauro has to say very interesting, as well as pretty indisputable given his vast experience over the years with treating HPTA dysfunction secondary to AAS abuse. I am glad I got this answer before you printed your article on the subject. Take care.


Thanks for the post, and thank Mauro for his time. It is certainly an informative letter, and it was nice of him to rattle it off so fast.

In regards to our argument, I still disagree with you. Mauro is talking about treating patients with dysfunction long after steroids are withdrawn. I do not believe this represents the healthy bodybuilder that we are talking about, who just needs to hasten a window that will normally close for him without help. Cartainly many people screw themselves up with long-term steroid use, and require a much different approach.

Mauro did support my point when he said ,"It's true however, that the Hypothalamic/pituitary axis usually recovers first, leading to increases in LH and subsequent increases in testicular steroidogenesis." This is the basis of my argument. The weak link is the testes, not LH. You will see in the reference that I gave you that LH was rebounding rapidly for the subjects (as T was still declining), while T was deadpan for months. It was very characteristic of the hypergonadotropic hypogonadal condition Mauro was referring to as being poolry responsive to AE's. This is closest to the model we are arguing about I think, not the hypo.

I'll give you that it is not such a black and white thing, with HCG being the golden drug and AE's totally worthless. I'm sure if the subjects of my study took tamoxifen in the post-cycle window we might have seen a higher peak LH, and perhaps even a slightly quicker onset. But I strongly feel that with the way the healthy body restores LH, focusing on anti-estrogens alone is a waste of money. For the minimal, probably unnoticable, difference they make they aren't worth the money. I myself take HCG + anti-estrogen, or nothing at all.

I'll end by pointing you to Mauro's letter again, when he says ,"On the other hand, as noted above, in most cases the HP axis recovers first and then the increased LH leads to increased testicular steroidogenesis, but it may take a while. As such, stimulating the testicular machinery and getting it up to par may make the whole process as efficient, and perhaps in some cases more efficient (if the HP axis recovers quickly) as using anti-estrogens. "

Isn't that pretty close to what I am saying Pat?
 
w_llewellyn said:


Thanks for the post, and thank Mauro for his time. It is certainly an informative letter, and it was nice of him to rattle it off so fast.

In regards to our argument, I still disagree with you. Mauro is talking about treating patients with dysfunction long after steroids are withdrawn. I do not believe this represents the healthy bodybuilder that we are talking about, who just needs to hasten a window that will normally close for him without help. Cartainly many people screw themselves up with long-term steroid use, and require a much different approach.

Mauro did support my point when he said ,"It's true however, that the Hypothalamic/pituitary axis usually recovers first, leading to increases in LH and subsequent increases in testicular steroidogenesis." This is the basis of my argument. The weak link is the testes, not LH. You will see in the reference that I gave you that LH was rebounding rapidly for the subjects (as T was still declining), while T was deadpan for months. It was very characteristic of the hypergonadotropic hypogonadal condition Mauro was referring to as being poolry responsive to AE's. This is closest to the model we are arguing about I think, not the hypo.

I'll give you that it is not such a black and white thing, with HCG being the golden drug and AE's totally worthless. I'm sure if the subjects of my study took tamoxifen in the post-cycle window we might have seen a higher peak LH, and perhaps even a slightly quicker onset. But I strongly feel that with the way the healthy body restores LH, focusing on anti-estrogens alone is a waste of money. For the minimal, probably unnoticable, difference they make they aren't worth the money. I myself take HCG + anti-estrogen, or nothing at all.

I'll end by pointing you to Mauro's letter again, when he says ,"On the other hand, as noted above, in most cases the HP axis recovers first and then the increased LH leads to increased testicular steroidogenesis, but it may take a while. As such, stimulating the testicular machinery and getting it up to par may make the whole process as efficient, and perhaps in some cases more efficient (if the HP axis recovers quickly) as using anti-estrogens. "

Isn't that pretty close to what I am saying Pat? [/B]


Well you are admitting now that anti-estrogens are not a total waste of time so it least thats a start.

I think Mauro's letter pretty much speaks for itself, so I won't comment any more on this
 
w_llewellyn said:



In regards to our argument, I still disagree with you. Mauro is talking about treating patients with dysfunction long after steroids are withdrawn. I do not believe this represents the healthy bodybuilder that we are talking about, who just needs to hasten a window that will normally close for him without help. Cartainly many people screw themselves up with long-term steroid use, and require a much different approach.
[/B]


But earlier in this thread you said:

"Please post a reference to this, as the only thing I see is a rapid LH/FSH return post cycle, and this is after long-term use."

So which is it Bill?
 
w_llewellyn said:



In regards to our argument, I still disagree with you. Mauro is talking about treating patients with dysfunction long after steroids are withdrawn. I do not believe this represents the healthy bodybuilder that we are talking about, [/B]



So you think a 1975 study on what happens after a cycle of 250mg of testosterone a week to be more typical of modern day post cycle suppression?

How many bodybuilders do you know that do cycles of just 250mg of test a week?

I am guessing that the people that Mauro treats represent more typical steroid users of today
 
pa1ad said:
I am guessing that the people that Mauro treats represent more typical steroid users of today

Pat, are we reading the same letter here?

Mauro is basically saying: I have these patients, who months after steroids are withdrawn suffer this type of dysfunction, and I need to treat them in this manner. But in most normal cases the HP (hypothalamic-pituitary) axis recovers first, with the testes more slowly responding to LH, which makes priming them with HCG more effective than Anti-estrogens. Please read his email more slowly.
 
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pa1ad said:

So which is it Bill?

What is with the semantics? I use long-term to describe 4-5 months use where the HPTA was maredly suppressed. Not long-term where a pathological condition developed preventing a normal rebound.
 
pa1ad said:
I am guessing that the people that Mauro treats represent more typical steroid users of today

My cited study represents what happens to healthy men who take steroids for several months, then get their test levels back naturally. This is representitive of our target audience. We are not talking about people who need medical treatment. This group should not be taking advice from us.
 
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w_llewellyn said:


Pat, are we reading the same letter here?

Mauro is basically saying: I have these patients, who months after steroids are withdrawn suffer this type of dysfunction, and I need to treat them in this manner. But in most normal cases the HP (hypothalamic-pituitary) axis recovers first, with the testes more slowly responding to LH, which makes priming them with HCG more effective than Anti-estrogens. Please read his email more slowly.


Once again, his letter stands on its own merits. People here can read it and see what it says. All I know is that it confirms everything that i have held to be true about this subject. Whether or not it confirms or denies what you believe to be true is your business. I really don't have much more to say
 
pa1ad said:
Once again, his letter stands on its own merits. People here can read it and see what it says. All I know is that it confirms everything that i have held to be true about this subject. Whether or not it confirms or denies what you believe to be true is your business. I really don't have much more to say

If that is how you want to read it, all the power to you Pat.
 
People here can read it and see what it says



This is where the problem is. You have to have a general understanding/knowledge base to follow this conversation. I think many people (regardless of which board this was posted on) will be able to decipher the text and draw a conclusion. The general public (at least from what I experience in this store) just want to know the answer without doing the work behind it. If people come in and ask about which protein is the best, they don't care why, they just want to know which one. Some people don't comprehend the fact that science isn't always clear cut. There isn't always a yes or no answer. When reading this topic (which I've printed out and let some customers read) they just look at me and say, so what does this mean? It would be interesting to have another reputable mind debate this topic with you two. I've really enjoyed it and enjoy any topic you two engage in.
 
1fast400 said:




This is where the problem is. You have to have a general understanding/knowledge base to follow this conversation. I think many people (regardless of which board this was posted on) will be able to decipher the text and draw a conclusion. The general public (at least from what I experience in this store) just want to know the answer without doing the work behind it. If people come in and ask about which protein is the best, they don't care why, they just want to know which one. Some people don't comprehend the fact that science isn't always clear cut. There isn't always a yes or no answer. When reading this topic (which I've printed out and let some customers read) they just look at me and say, so what does this mean? It would be interesting to have another reputable mind debate this topic with you two. I've really enjoyed it and enjoy any topic you two engage in.



the bottom line that i hope people can conclude from Mauro's letter is that anti-estrogens can often be quite effective in restoring testosterone production after steroid cycles. that is all I want people to get from this
 
pa1ad said:
the bottom line that i hope people can conclude from Mauro's letter is that anti-estrogens can often be quite effective in restoring testosterone production after steroid cycles. that is all I want people to get from this

What I have been saying from the beginning is that in normal situations (not those who suffer a long-term hypogonadotropic dysfunction and are seeking medical treatment) LH returns much more rapidly than the testes do in their ability to respond to it. The testes are the weak link that drags out recovery, not LH, which you seemed to be stuck focusing on.

Did he Mauro not state almost exactly what I did? He said generally the HP axis (LH) recovers first, and it may take some time for the testes to be able to respond. With LH recovering quickly HCG is preferred over AE's for its ability to stimulate the "testicular machinery".

Pat, I think you are confusing his earlier comments about how he treats patients with long-term conditions with his later comments on how normally the whole HPTA rebounds in exactly the order I stated. Yes, there are numerous disorders characterized by low androgen levels, and some may respond to anti-estrogens while other may benefit mostly from HCG. But people with such conditions do not represent the average healthy bodybuilder, nor are they the subject of our discussion. These people should not be treating themselves with OTC products.

My bottom line is that bodybuilders need to stop relying solely on AE's, and start remembering HCG if they want to make any real progress here at all.
 
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w_llewellyn said:


What I have been saying from the beginning is that in normal situations (not those who suffer a long-term hypogonadotropic dysfunction and are seeking medical treatment) LH returns much more rapidly than the testes do in their ability to respond to it. The testes are the weak link that drags out recovery, not LH, which you seemed to be stuck focusing on.

Did he Mauro not state almost exactly what I did? He said generally the HP axis (LH) recovers first, and it may take some time for the testes to be able to respond. With LH recovering quickly HCG is preferred over AE's for its ability to stimulate the "testicular machinery".

Pat, I think you are confusing his earlier comments about how he treats patients with long-term conditions with his later comments on how normally the whole HPTA rebounds in exactly the order I stated. Yes, there are numerous disorders characterized by low androgen levels, and some may respond to anti-estrogens while other may benefit mostly from HCG. But people with such conditions do not represent the average healthy bodybuilder, nor are they the subject of our discussion. These people should not be treating themselves with OTC products.

My bottom line is that bodybuilders need to stop relying solely on AE's, and start remembering HCG if they want to make any real progress here at all.


You seem fixated on thinking that LH returns quickly to normal in the "average" steroid user. And you base this on what, a study using 250mg of testosterone a week?

Bill, as I have stated before and will continue to state, i have always seen low LH and low testosterone in people coming off of prohormones and coming off of steorids. Additionally, these cases more often than not have high estrogen relative to their testosterone. This, Bill, is the typical bodybuilder coming off of steroids/prohormones as i know it and they respond quite well to anti-estrogens.

Now, some people that have been suppressed for longer periods have some pretty marked testicular atrophy and these people probably need HCG to get the testes back to size before the whole HPTA kicks in.

I took issue to your blanket statement that anti-estrogens are useless in restoring testosterone in people coming off of steroids. I think Mauro made it quite clear that this is untrue. Furthermore, I have seen blood results of typical users get their testosterone levels back to high normal very quickly using anti-estrogens. All your theorizing based on one study using 250mg of test won't change the facts
 
w_llewellyn said:


What I have been saying from the beginning is that in normal situations (not those who suffer a long-term hypogonadotropic dysfunction and are seeking medical treatment) LH returns much more rapidly than the testes do in their ability to respond to it. The testes are the weak link that drags out recovery, not LH, which you seemed to be stuck focusing on.

Did he Mauro not state almost exactly what I did? He said generally the HP axis (LH) recovers first, and it may take some time for the testes to be able to respond. With LH recovering quickly HCG is preferred over AE's for its ability to stimulate the "testicular machinery".

Pat, I think you are confusing his earlier comments about how he treats patients with long-term conditions with his later comments on how normally the whole HPTA rebounds in exactly the order I stated. Yes, there are numerous disorders characterized by low androgen levels, and some may respond to anti-estrogens while other may benefit mostly from HCG. But people with such conditions do not represent the average healthy bodybuilder, nor are they the subject of our discussion. These people should not be treating themselves with OTC products.

My bottom line is that bodybuilders need to stop relying solely on AE's, and start remembering HCG if they want to make any real progress here at all.


OK, I want to see if we can reach some common ground here. Mauro stated that anti-estrogens alone do work on some of these long term users - users who undoubtedly have suffered some testicular atrophy. So, obviously LH does matter, in sofar as it is possible to increase LH using AE's and this increased LH is sufficient to stimulate the testes, even though they are in the atrophied state.

The way to look at this is that getting atrophied testicles back working you must "prime the pump". That is, you must increase gonadotropins in the body to high (hopefully supraphysiological levels) in order to wake up the sleepy gonads. This can be done using HCG, or in many circumstances it can be done using anti-estrogens.

I think you are too quick to recommend HCG to users. HCG can cause problems in and of itself (high estrogen levels and testicular insensitivity) and does not address the full axis. Yes, in many cases HCG is needed, but in the cases that it is not you are much better off stimulating the entire axis using anti-estrogens.
 
pa1ad said:
OK, I want to see if we can reach some common ground here. Mauro stated that anti-estrogens alone do work on some of these long term users - users who undoubtedly have suffered some testicular atrophy. So, obviously LH does matter, in sofar as it is possible to increase LH using AE's and this increased LH is sufficient to stimulate the testes, even though they are in the atrophied state.


Yes of course, but you have to remember he is dealing with people who have long-term hypogonadotropic hypogonadism. They need to get LH levels up, as this is at the root of their problem. The people we are speaking about here do not have the same problem, and do restore LH levels quickly (well before testosterone) on their own. They need to get the testes up to speed more quickly than waiting for LH to do the job on its own.

The way to look at this is that getting atrophied testicles back working you must "prime the pump". That is, you must increase gonadotropins in the body to high (hopefully supraphysiological levels) in order to wake up the sleepy gonads. This can be done using HCG, or in many circumstances it can be done using anti-estrogens.


This we can agree on, but I will also remind you that the dragging issue post cycle is not LH. LH will reach normal or supraphysiological levels rather quickly without the use of an anti-estrogen, and even with, will not reach a point where it is rapidly affecting testicular mass without the concurrent use of HCG. I feel that in many regards by lowering androgen and estrogen inhibition (removing exogenous steroid) we have done much of the job of the AE already. Levels are low enough to produce a surge in gonadotropins after all, that says a lot.

I think you are too quick to recommend HCG to users. HCG can cause problems in and of itself (high estrogen levels and testicular insensitivity) and does not address the full axis. Yes, in many cases HCG is needed, but in the cases that it is not you are much better off stimulating the entire axis using anti-estrogens.

I recommend HCG because for the normal steroid user who has LH levels return within a couple of weeks, it more directly addresses the core issue of testicular atrophy. This is the group that I am speaking to, and I'm sure the same group Mauro is suggesting gets better benifit from HCG as well. This drug does have issues, which is why I recommend short-term use instead of regular on-cycle use like BR.

I do not disagree that Mauro in on the mark with his patients. Clearly there is a group, those with perisitently low LH levels, that are much better served better by anti-estrogens.


What I hope we can agree on are:

1) The healthy bodybuilder, not suffering a prolonged condition, should restore gonadotropins first, and T much later due to atrophy of the testes.

2) In this group HCG is more effective at shortening the post-cycle window, as it directly "stimulates the machinery" so to speak.

3) anti-estrogens are most effective at stimulating testosterone when LH is low, and estrogen levels normal to high.

4) There are issues with HCG, and as such it should be used cautiously and probably always with an anti-estrogen.

5) Hypoandrogenism is quite encompassing, and includes a number of different medical conditions. There are validy some where anti-estrogens are the preferred method of treatment, probably moreso than HCG. But the healthy group most relevant to us should consider HCG the more effective post-cycle drug than AE's.
 
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pa1ad said:
You seem fixated on thinking that LH returns quickly to normal in the "average" steroid user. And you base this on what, a study using 250mg of testosterone a week?


Yes, it caused suppression that lasted for a few months, and returned to normal without medical treatment. Typical, no?

Bill, as I have stated before and will continue to state, i have always seen low LH and low testosterone in people coming off of prohormones and coming off of steorids.


Immediately post cycle that is what you will see of course. I didn't say LH rebounds on day one. But if you follow the whole window, most will be spent with normal or high LH and low T because the testes do not read it.

Additionally, these cases more often than not have high estrogen relative to their testosterone. This, Bill, is the typical bodybuilder coming off of steroids/prohormones as i know it and they respond quite well to anti-estrogens.


They could not have high estrogen levels unless testosterone was still high from steroids. They are lower than pre-cycle no doubt, just imbalanced with T. This is not realy relevant because androgens and estrogens do not play opposing roles here like they do with gyno.

I took issue to your blanket statement that anti-estrogens are useless in restoring testosterone in people coming off of steroids. I think Mauro made it quite clear that this is untrue. Furthermore, I have seen blood results of typical users get their testosterone levels back to high normal very quickly using anti-estrogens. All your theorizing based on one study using 250mg of test won't change the facts

I tend to be overly dramatic. I suspect AE's would increase LH a little bit over and above what the post-cycle gonadotropin surge would do on its own. But I think without addressing the core issue with HCG, it won't make much of a difference overall. I think your anti-estrogen group would have been much better served in the long run by purchasing more 1-AD (sorry 1-T Ethergels) :)
 
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I thought that estrogen came from aromatization AND some other sources(I have no idea where), thats why you need nolva, not just anastrozle when using HCG. Its also the consensus of most steroid users I know of that HCG prolongs recovery, because the HPTA recognizes the elevation in LH and ceases production of LH.

For all of you coming off extended pro-hormone cycles:

Do a search on the anabolic forums for proper post cycle recovery. Dont be fooled by thinking that because PH's arent as strong as steroids that they dont cause inhibition. You will recover naturally, but studies show that naturally typically means 8 weeks.
 
Flash_75 said:
I thought that estrogen came from aromatization AND some other sources(I have no idea where)


Estrogen comes from androgens aromatized in the testes, as well as other tissues. There is an imbalance post cycle, because although you diminish gonadal source of estrogen, you still have it from androstenedione aromatization in other tissues.

thats why you need nolva, not just anastrozle when using HCG. Its also the consensus of most steroid users I know of that HCG prolongs recovery, because the HPTA recognizes the elevation in LH and ceases production of LH.

The hypothalamus reads the elevated estrogen, not LH. HCG is therefore not inhibitive here until it starts working and T/E levels come back up. But overused it most certainly can prolong recovery.

Most steroid users sorely misunderstand what is going on unfortunately. I think we have been debating the technical specifics of this issue pretty well here though, and I thought my case was well stated. But it seems you have missed it.

I guess the best point made in the whole thread was 1fast400's after all.

Maybe Pat and I should just arm wrestle next time.


- Bill
 
Thanks bill :)


P.S. I sell the sh*t out of your book here, yet still get questions that are easily answered by pulling the same book I sold them and pointing to the page.
 
1fast400 said:
P.S. I sell the sh*t out of your book here, yet still get questions that are easily answered by pulling the same book I sold them and pointing to the page.

Thanks for the support 1F4. I appreciate it. As for the humerous questions, we should chat sometime. I've got a long list of them :)
 
If HCG increases testicular mass independent of LH and FSH levels would it be more useful to use HCG during the cycle to prevent testicular atrophy in the first place?
 
Jacob Creutzfeldt said:
If HCG increases testicular mass independent of LH and FSH levels would it be more useful to use HCG during the cycle to prevent testicular atrophy in the first place?

In theory this is just as good or better than trying to fix testicular atrophy at the end of the cycle. But the potential issues such as LH desensitization and increased estrogen with HCG, IMO, make it safer to use for a short period at the end of the cycle.
 
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w_llewellyn said:


Yes of course, but you have to remember he is dealing with people who have long-term hypogonadotropic hypogonadism. They need to get LH levels up, as this is at the root of their problem. The people we are speaking about here do not have the same problem, and do restore LH levels quickly (well before testosterone) on their own. They need to get the testes up to speed more quickly than waiting for LH to do the job on its own.

[/B]

This we can agree on, but I will also remind you that the dragging issue post cycle is not LH. LH will reach normal or supraphysiological levels rather quickly without the use of an anti-estrogen, and even with, will not reach a point where it is rapidly affecting testicular mass without the concurrent use of HCG. I feel that in many regards by lowering androgen and estrogen inhibition (removing exogenous steroid) we have done much of the job of the AE already. Levels are low enough to produce a surge in gonadotropins after all, that says a lot.



I recommend HCG because for the normal steroid user who has LH levels return within a couple of weeks, it more directly addresses the core issue of testicular atrophy. This is the group that I am speaking to, and I'm sure the same group Mauro is suggesting gets better benifit from HCG as well. This drug does have issues, which is why I recommend short-term use instead of regular on-cycle use like BR.

I do not disagree that Mauro in on the mark with his patients. Clearly there is a group, those with perisitently low LH levels, that are much better served better by anti-estrogens.


What I hope we can agree on are:

1) The healthy bodybuilder, not suffering a prolonged condition, should restore gonadotropins first, and T much later due to atrophy of the testes.

2) In this group HCG is more effective at shortening the post-cycle window, as it directly "stimulates the machinery" so to speak.

3) anti-estrogens are most effective at stimulating testosterone when LH is low, and estrogen levels normal to high.

4) There are issues with HCG, and as such it should be used cautiously and probably always with an anti-estrogen.

5) Hypoandrogenism is quite encompassing, and includes a number of different medical conditions. There are validy some where anti-estrogens are the preferred method of treatment, probably moreso than HCG. But the healthy group most relevant to us should consider HCG the more effective post-cycle drug than AE's.
[/B]



The healthy group can get testosterone production back in a timely fashion using anti-estrogens alone. Or maybe all those blood tests I have seen over the years were filled with typos?
 
Jacob Creutzfeldt said:
If HCG increases testicular mass independent of LH and FSH levels would it be more useful to use HCG during the cycle to prevent testicular atrophy in the first place?



Yes, this is how I have always thought it should be used. And anti-estrogens post cycle
 
w_llewellyn said:


In theory this is just as good or better than trying to fix testicular atrophy at the end of the cycle. But the potential issues such as LH desensitization and increased estrogen with HCG, IMO, make it safer to use for a short period at the end of the cycle.


Why would LH desensitization be less likely to happen when you use it post cycle as opposed to using it intermittently during the cycle? Why is estrogen elevation ok for the short period after the cycle and not during the cycle?

Also, why is increased estrogen such a problem during the cycle if you are already taking androgens that aromatize as part of your cycle? And if you are afraid of the estrogen from the HCG during the cycle, why not just take anti-estrogens?

Take HCG during the cycle, and anti-estrogens after is good idea
 
w_llewellyn said:


3) anti-estrogens are most effective at stimulating testosterone when LH is low, and estrogen levels normal to high.
[/B] [/B]


Mauro made it quite clear that it is low testosterone/estrogen ratio that is the factor here and not high absolute estrogen levels.

I have seen many a bodybuilder post cycle with a low test/estrogen ratio. These bodybuilders should be able to stimulate their gonadotropins effectively with anti-estrogens and therefore shorten the time that their testes come back to order. They can use HCG perhaps and get their testes back quicker, however there may be a temporary secondary suppression after HCG is ceased.
 
pa1ad said:
Mauro made it quite clear that it is low testosterone/estrogen ratio that is the factor here and not high absolute estrogen levels.

You are starting to babble Pat. That makes absolutely no sense at all. Androgens are inhibitive. It is not like gyno, where the two play opposing roles and the ratio is most important. The lower androgen and estrogen levels post cycle, even if differently balanced, serve only to increase LH. With your logic non-aromatizable androgens would stimulate the HPTA.

I am quite certain you are misunderstanding Mauro's explaination of how hypogonadrotropic hypogonadism is characterized.
 
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pa1ad said:
Why would LH desensitization be less likely to happen when you use it post cycle as opposed to using it intermittently during the cycle?

Because you are using it for a very short period of time post-cycle. It is difficult to guess exactly how much to use so that testicular mass is maintained, yet the testes are not overstimulated, if you are taking it throughout the course of the cycle. If you have the perfect dosing routine for this I am all ears.
 
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Bill if LH levels elevate post cycle and you compound that elevated LH with a synthetic LH like HCG aren't you more apt to cause LH resistance using HCG post cycle? If LH levels fall by say the 2nd week of a cycle and you administer HCG following the LH decrease I would think LH resistance is less likely. Also does HCG tend to increase aromatization? If so then could you be more apt to end up increasing estrogen levels thus inhibiting natural LH production?
 
Jacob Creutzfeldt said:
Bill if LH levels elevate post cycle and you compound that elevated LH with a synthetic LH like HCG aren't you more apt to cause LH resistance using HCG post cycle?


I think if done correctly you should shorten the recovery window rather than extend it. The whole problem is that it takes too long to wait for physiological, or slightly above physiological, levels to do the job. We need to kick start them, otherwise why bother with a T recovery program.

If LH levels fall by say the 2nd week of a cycle and you administer HCG following the LH decrease I would think LH resistance is less likely.


I understand your point, but repeat my above. This works well in theory, but I think you run the risk of not really having a clue what is going on down there and desensitizing the LH receptor inadvertently in practice. We don't know enough about this type of use to say it is recommended. But if that is what you find works, by all means, do it.

Also does HCG tend to increase aromatization? If so then could you be more apt to end up increasing estrogen levels thus inhibiting natural LH production?

It increases testicular aromatase specifically, and therefore should not really increase estrogen levels until it is already working to increase testosterone. If used past this point it will suppress the HP axis.

If it works for you either way it is great. The big point I am trying to make here is that HCG is the most important recovery drug because testicular atrophy is the biggest roadblock to recovery, not LH.
 
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Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.
 
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Jacob Creutzfeldt said:
Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.

You are absolutely right JC. What the hell was I thinking.

We certainly wouldn't want our testosterone levels to return to normal or anything, now would we? :rolleyes:

- Bill
 
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Re: Re: 1-Test - Anabolic/Androgenic?

pa1ad said:
The piece of the puzzle you are missing is the fact that estrogen is necessary for the libido sustaining effects of androgens. That is probably why strong androgens that do not aromatize sometimes lower libido. Case in point: trenbolone acetate

Sorry to be the asshole once again Pat, but where does Mesterolone fit in ? Its probably the best libido booster in the world, yet it does not aromatize. Its an anti-aromatase.
 
Jacob Creutzfeldt said:
Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.

The whole point of HCG is to increase testicle size once again so that larger amounts of natural testosterone can be produced once LH production resumes, after treatment with HCG AND either clomid or Nolvadex.
 
QUESTION for PA and BILL

First of all great thread.

I'm still puzzled by one thing though. If long term androgen use causes a depression of gonadotrophins, starting at the base with GnRH, and the androgen used does not form estrogen, so there is no circulating estrogen in the system at the time the androgen use is discontinued, then how on earth is it possible to have rebound estrogen without increasing GnRH and subsequently LH/FSH first ?
 
Re: QUESTION for PA and BILL

Big Cat HH said:
I'm still puzzled by one thing though. If long term androgen use causes a depression of gonadotrophins, starting at the base with GnRH, and the androgen used does not form estrogen, so there is no circulating estrogen in the system at the time the androgen use is discontinued, then how on earth is it possible to have rebound estrogen without increasing GnRH and subsequently LH/FSH first ?

There is no rebound. Estrogen is actually lower post-cycle than pre. Since you get a good amount of estrogen from extragonadal sources however, you do get an imbalance (androgens get suppressed more extensively).

- Bill
 
w_llewellyn said:


You are starting to babble Pat. That makes absolutely no sense at all. Androgens are inhibitive. It is not like gyno, where the two play opposing roles and the ratio is most important. The lower androgen and estrogen levels post cycle, even if differently balanced, serve only to increase LH. With your logic non-aromatizable androgens would stimulate the HPTA.

I am quite certain you are misunderstanding Mauro's explaination of how hypogonadrotropic hypogonadism is characterized.



It is what Mauro said Bill. anti-estrogens tend to work well on those with a low testosterone to estrogen ratio and low LH

Yes, the absolute levels of the androgens and estrogens are below normal but that does not mean that anti-estrogens cannot still increase LH output in this state.

Unless you have some evidence that they cannot? I provided evidence in that case study with the clomid guy that they can, and Mauro pretty clearly is saying that they can
 
w_llewellyn said:


Because you are using it for a very short period of time post-cycle. It is difficult to guess exactly how much to use so that testicular mass is maintained, yet the testes are not overstimulated, if you are taking it throughout the course of the cycle. If you have the perfect dosing routine for this I am all ears.


Bill, HCG is not traditionally used continuously throughout the cycle. It is used for short periods intermittently throughout the cycle.

No one knows the perfect dosing regimen for either during or post cycle use.
 
Jacob Creutzfeldt said:
Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.



then why would one use HCG? After all you are basically increasing LH levels for all intents and purposes.

ONe can increase LH high enough to kick start the testes without using HCG by using anti-estrogens.

The key here is to raise gonadotropin levels high enough to prime the testes. In some cases this requires HCG but in many cases anti-estrogens are good enough.

Mauro made this quite clear in his letter
 
Re: Re: Re: 1-Test - Anabolic/Androgenic?

Big Cat HH said:


Sorry to be the asshole once again Pat, but where does Mesterolone fit in ? Its probably the best libido booster in the world, yet it does not aromatize. Its an anti-aromatase.


You have no idea what you are talking about big cat
 
Re: Re: QUESTION for PA and BILL

w_llewellyn said:


There is no rebound. Estrogen is actually lower post-cycle than pre. Since you get a good amount of estrogen from extragonadal sources however, you do get an imbalance (androgens get suppressed more extensively).

- Bill


It is quite possible that estrogen depletion, whether through the use of non-aromatizing androges or through the use of anti-estrogens, can cause an up-regulation of aromatase. Hence an imbalance of estrogen to testosterone in the post-cycle period
 
Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

w_llewellyn said:


For some reason without an in-vivo Human study you will never convince Pat of this.


There is not even in-vitro evidence that it is an anti-aromatase. It may very well be but I certainly am not going to say its for certain without evidence
 
Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

w_llewellyn said:



Hey Bill,

Can you just answer the following for me?

You must agree that these long term suppressed subjects of Mauros with the low LH and low test/estrogen ratio are undoubtedly suffering from testicular atrophy, correct?

And you noticed that Mauro said that anti-estrogens often are sufficient to restore testosteorne production in these subjects. Correct?

Does this not completely contradict your theory that anti-estrogens are useless for those with testicular atrophy?

Furthermore, these subjects are hypogonadotropic and so must therefore have lower than normal estrogen levels, correct? Why then are anti-estrogens still working in these people? That too seems to contradict what you have been saying?


????????????????????
 
w_llewellyn said:


Here is the one that I reference regarding the post-cycle recovery of gonadotropins and T. I know I posted this before.

Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84

Here, blood hormone levels were monitored before, during, and after a long cycle of test enanthate (250mg weekly). LH levels started to rise withing a few weeks after the last shot, while T was still declining, but there was no significant movement in endogenous testosterone production for about 10 weeks.



So Bill, are you assuming that the effect (qualitatively speaking) of ALL steroids (or combinations thereof) on the HPTA are just like testosterone at 250mg a week? You think that you can make a blanket statement (that post cycle recovery is typically characterized by a hypergonadotropic hypogonadal state) based on ONE study using a low dose of testosterone?

Also, where in this study do they demonstrate that anti-estrogen treatment is ineffective in accelerating the testicular recovery?
 
pa1ad said:
It is what Mauro said Bill. anti-estrogens tend to work well on those with a low testosterone to estrogen ratio and low LH

Yes, the absolute levels of the androgens and estrogens are below normal but that does not mean that anti-estrogens cannot still increase LH output in this state.


I never said anti-estrogens didn't work on these people. I just said that your claim that the ratio was important was way, way incorrect.
 
Re: Re: Re: QUESTION for PA and BILL

pa1ad said:
It is quite possible that estrogen depletion, whether through the use of non-aromatizing androges or through the use of anti-estrogens, can cause an up-regulation of aromatase. Hence an imbalance of estrogen to testosterone in the post-cycle period

That is an interesting idea actually Pat. I can't imagine that with the loss of gonadal estrogens levels could really be elevated post-cycle though. Right now IMO there is no evidence to support a true estrogen rebound, but certainly there is to support a rebound imbalanced T/E ratio.
 
Re: Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

pa1ad said:
w_llewellyn said:
Can you just answer the following for me?

You must agree that these long term suppressed subjects of Mauros with the low LH and low test/estrogen ratio are undoubtedly suffering from testicular atrophy, correct?

of course.

And you noticed that Mauro said that anti-estrogens often are sufficient to restore testosteorne production in these subjects. Correct?

I never said they wouldn't be sufficient. I'm sure they work well, especially since HCG doesn't seem to address the issue for these people at all. They have atrophy, yes, but the lazy LH is the big problem.

Does this not completely contradict your theory that anti-estrogens are useless for those with testicular atrophy?

No. They are useless in a sense that practically I expect they will work little better than waiting for your body to do the job on its own. Certainly not worth the hard-earned $$ for third generation aromatase inhibitors. For the healthy person, the removal of external steroid and suppression of natural test/estrogen will already have created favorable conditions for heightened LH levels.

Furthermore, these subjects are hypogonadotropic and so must therefore have lower than normal estrogen levels, correct? Why then are anti-estrogens still working in these people? That too seems to contradict what you have been saying?

No actually, it doesn't. The bodybuilder can certainly take AE's as well, and wait for the testes to have enough time under normal or slightly above normal LH stimulation to get the testes and T back. Maybe the anti-estrogen would even help a tiny bit in spite of low estrogen and androgen levels. But it will be far less effective than hitting the testes with bolus LH right off the bat in terms of atrophy, no?
 
pa1ad said:
So Bill, are you assuming that the effect (qualitatively speaking) of ALL steroids (or combinations thereof) on the HPTA are just like testosterone at 250mg a week? You think that you can make a blanket statement (that post cycle recovery is typically characterized by a hypergonadotropic hypogonadal state) based on ONE study using a low dose of testosterone?


I think it is a good example of typical suppression. Normal men took steroids, which suppressed natural T, for about 20 weeks. They then stopped, and had testosterone rebound without any lagging dysfunction in the HPTA. The HP axis came back first, with the testes much slower to respond due to the atrophied state. Yes, in my mind it is very representitive of the average healthy male looking to shorten the post-cycle window.

That given, I'm sure some heavy steroid users will have unknowingly aquired hypo-hypo states. For them likely the HCG would be wholy ineffective. That I do not disagree with, but this is not the person I am addressing.

I am talking to the healthy male that would have his T levels rebound normally without drugs, and would not be in the doctors office 3 or 4 months after his cycle still bitching about a poor libido.
 
w_llewellyn said:


I never said anti-estrogens didn't work on these people. I just said that your claim that the ratio was important was way, way incorrect. [/B]



Its not my claim bill, its Mauro's claim.

"I've found anti-estrogens very effective when both of the
following conditions were present, along with a low serum testosterone. A
low testosterone/estrogen ratio, and a low to normal LH."

And he bases it on hundreds of case studies. And you base your assertion to the contrary on what?

????????????
 
Re: Re: Re: Re: QUESTION for PA and BILL

w_llewellyn said:


That is an interesting idea actually Pat. I can't imagine that with the loss of gonadal estrogens levels could really be elevated post-cycle though. Right now IMO there is no evidence to support a true estrogen rebound, but certainly there is to support a rebound imbalanced T/E ratio.


Yeah, I agree with that
 
Re: Re: Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

w_llewellyn said:


of course.



I never said they wouldn't be sufficient. I'm sure they work well, especially since HCG doesn't seem to address the issue for these people at all. They have atrophy, yes, but the lazy LH is the big problem.



No. They are useless in a sense that practically I expect they will work little better than waiting for your body to do the job on its own. Certainly not worth the hard-earned $$ for third generation aromatase inhibitors. For the healthy person, the removal of external steroid and suppression of natural test/estrogen will already have created favorable conditions for heightened LH levels.



No actually, it doesn't. The bodybuilder can certainly take AE's as well, and wait for the testes to have enough time under normal or slightly above normal LH stimulation to get the testes and T back. Maybe the anti-estrogen would even help a tiny bit in spite of low estrogen and androgen levels. But it will be far less effective than hitting the testes with bolus LH right off the bat in terms of atrophy, no?




I think often anti-estrogens work more than just "a tiny bit" Bill. I know I have seen levels bounce back quickly and strongly after the use of clomid. And sure, HCG will get the testosterone back quicker but then what happens when you stop the HCG? YOu once more have depressed LH and you have to wait for that to kick back in again.

LOts of people would be better off getting their WHOLE axis back in line using the anti-estrogens, however for those cases where anti-estrogens don't work (due to more serious testicular atrophy) HCG might do the job.


Why do you hate anti-estrogens so much?
 
pa1ad said:




Its not my claim bill, its Mauro's claim.

"I've found anti-estrogens very effective when both of the
following conditions were present, along with a low serum testosterone. A
low testosterone/estrogen ratio, and a low to normal LH."

And he bases it on hundreds of case studies. And you base your assertion to the contrary on what?

????????????

You are misreading him Pat. Anti-estrogens are effective in these people BECAUSE they need to restore LH. What does HCG do for LH? Nothing. Anti-estrogen are therefore the preferred treatment here, that's all.
 
w_llewellyn said:


I think it is a good example of typical suppression. Normal men took steroids, which suppressed natural T, for about 20 weeks. They then stopped, and had testosterone rebound without any lagging dysfunction in the HPTA. The HP axis came back first, with the testes much slower to respond due to the atrophied state. Yes, in my mind it is very representitive of the average healthy male looking to shorten the post-cycle window.

That given, I'm sure some heavy steroid users will have unknowingly aquired hypo-hypo states. For them likely the HCG would be wholy ineffective. That I do not disagree with, but this is not the person I am addressing.

I am talking to the healthy male that would have his T levels rebound normally without drugs, and would not be in the doctors office 3 or 4 months after his cycle still bitching about a poor libido. [/B]



I don't think what you are getting my point Bill. Different steroids have different effects on the HPTA. Anabolic steroids have different activities that can potentially efffect the HPTA - these including estrogenic, androgenic, and progestational properties. Furthermore, effects on the HPTA at high dosages may be markedly different than those at low dosages - qualitatively different and not just quantitiatively. Your hypergonadotropic hypogonadism hypothesis may be valid in reference to a low dose testosterone cycle, but may completely off base in regards to a trenbolone / halotestin cycle (which may be associated with a severe HYPOgonadotropic hypogonadal post cycle state)

I think you did a poor job in forming your widely encompassing theory (that covers all steroids and types of cycles) based on extrapolation of a study using one steroid at one low dosage
 
w_llewellyn said:


I think it is a good example of typical suppression. Normal men took steroids, which suppressed natural T, for about 20 weeks. They then stopped, and had testosterone rebound without any lagging dysfunction in the HPTA. The HP axis came back first, with the testes much slower to respond due to the atrophied state. Yes, in my mind it is very representitive of the average healthy male looking to shorten the post-cycle window.

That given, I'm sure some heavy steroid users will have unknowingly aquired hypo-hypo states. For them likely the HCG would be wholy ineffective. That I do not disagree with, but this is not the person I am addressing.

I am talking to the healthy male that would have his T levels rebound normally without drugs, and would not be in the doctors office 3 or 4 months after his cycle still bitching about a poor libido. [/B]


How do you know that testosterone at 750mg a week might not be sufficient to induce a post cycle hypo hypo state? Or deca at 600mg a week?

IMO, the only sound scientific conclusion one could gather from that study is that 250mg a week of test for extended cycle may result in a post cycle hyper hypo state that resolves itself over a few months.

I think you were too eager to come up with a revolutionary theory on post cycle suppression
 
w_llewellyn said:


You are misreading him Pat. Anti-estrogens are effective in these people BECAUSE they need to restore LH. What does HCG do for LH? Nothing. Anti-estrogen are therefore the preferred treatment here, that's all.


Thats the answer that i thought you were going to give, but you miss my point.

If they had testicular atrophy (which you agreed that they must have had) then according to you simply raising LH would not be sufficient to restore testosterone production. Yet anti-estrogens enough were sufficient, Mauro made that quite clear. This is where your theory completely breaks down.
 
Re: Re: Re: Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

pa1ad said:
I think often anti-estrogens work more than just "a tiny bit" Bill. I know I have seen levels bounce back quickly and strongly after the use of clomid. And sure, HCG will get the testosterone back quicker but then what happens when you stop the HCG? YOu once more have depressed LH and you have to wait for that to kick back in again.


I think we are finally making some progress here. You are correct, which is why I never suggest taking HCG alone. It is a bad idea. You need anti-estrogens during and for at least a few weeks after the HCG has been cut for this very reason. You also need to be careful not to overuse the drug as well. But we are finally hitting on the point that this is the quickest way to get T levels back up.

Why do you hate anti-estrogens so much?

Actually I don't hate ant-estrogens at all Pat. I happen to think Nolvadex was one of the best drugs ever made in fact.

I am just faced with what is logical, and has worked, for me. By removing steroids post-cycle we have already created favorable conditions for heightened LH release. We see a pretty rapid recovey of the HP, and the couple of weeks it does take to get back seem hard to attribute to estrogenic or androgenic inhibition with the lower levels we know to be present. It takes far longer for T levels to come back up, due to testicular atrophy. I don't see anyway to justify the current "forget HCG and stick with Clomid" sentiment. It doesn't make sense given the parameters of a normal post-cycle window. Atrophy is by far the bigger issue, and HCG is no doubt the quickest way to address it.

It is really nothing personal here Pat, with you or the Anti-estrogens.
 
Last edited:
My comment about the dual quads on the three cylinder engine is taken out of the context of my previous statements. I assert that it makes sense to keep the testes at full functioning capacity during the cycle to reduce natural testosterone recovery time as it must take time for the atrophied testes to reach full functional size, hence a longer recovery period. If you only have x number of leydig cells that produce a maximum of y units of testosterone each you can only produce a maximum of xy units of testosterone. If you start recovery with 2x number of leydig cells which produce a maximum of y units of testosterone each then you can produce a maximum of 2xy units of testosterone. Why drown them in synthetic LH and wait for the testes to hypertrophy in response to the increased demand when you can start recovering post cycle at full working potential?
 
pa1ad said:
Thats the answer that i thought you were going to give, but you miss my point.

If they had testicular atrophy (which you agreed that they must have had) then according to you simply raising LH would not be sufficient to restore testosterone production. Yet anti-estrogens enough were sufficient, Mauro made that quite clear. This is where your theory completely breaks down.

Even just restoring LH to physiological levels would accomplish this. Of course it will counter atrophy, just as waiting without anything but your own LH will. It doesn't "kick the babies back in gear" though, which is what we want to happen when spending $$ on post-cycle drugs.
 
Jacob Creutzfeldt said:
My comment about the dual quads on the three cylinder engine is taken out of the context of my previous statements. I assert that it makes sense to keep the testes at full functioning capacity during the cycle to reduce natural testosterone recovery time as it must take time for the atrophied testes to reach full functional size, hence a longer recovery period. If you only have x number of leydig cells that produce a maximum of y units of testosterone each you can only produce a maximum of xy units of testosterone. If you start recovery with 2x number of leydig cells which produce a maximum of y units of testosterone each then you can produce a maximum of 2xy units of testosterone. Why drown them in synthetic LH and wait for the testes to hypertrophy in response to the increased demand when you can start recovering post cycle at full working potential?

You don't actually grow new cells. Your present ones just increase or decrease in mass.

Your theory makes sense, but I reiterate that it is a guessing game with unwelcome consequences if you are wrong.
 
w_llewellyn said:


Even just restoring LH to physiological levels would accomplish this. Of course it will counter atrophy, just as waiting without anything but your own LH will. It doesn't "kick the babies back in gear" though, which is what we want to happen when spending $$ on post-cycle drugs.


So why didn't Mauro use HCG on these subjects also? I think I know the answer but I would like to hear yours
 
pa1ad said:
So why didn't Mauro use HCG on these subjects also? I think I know the answer but I would like to hear yours

It does not address the issue at hand I think, and I'll admit possibly could even interfere with HP recovery. If you focus on the HP with an anti-estrogen, the testes should come up to speed slowly without issue. This I am not debating at all.

If you read his letter again though, you will see that there are situations (those which relate most to the healthy BB mind you) where he states that HCG is more effective than AE. It is a few pages back, but remember when Mauro stated, "As such, stimulating the testicular machinery and getting it up to par may make the whole process as efficient, and perhaps in some cases more efficient (if the HP axis recovers quickly) as using anti-estrogens.".

Read: If the HP axis recoverys quickly (i.e. is healthy), HCG can make the recovery process more efficient than AE's.
 
Last edited:
Re: Re: Re: Re: 1-Test - Anabolic/Androgenic?

pa1ad said:
You have no idea what you are talking about big cat

Do I not ? Ok, then, I'll prove it :

Arch Sex Behav 1985 Dec;14(6):539-48 Related Articles, Books, LinkOut


Human male sexual functions do not require aromatization of testosterone: a study using tamoxifen, testolactone, and dihydrotestosterone.

Gooren LJ.

This study was designed to examine whether testosterone needs to be converted to estradiol in order to exert fully its effects on sexuality in the human male. Administration of the estrogen receptor antagonist tamoxifen and the aromatase inhibitor testolactone were without effect on parameters of sexual functions. Replacement of testosterone substitution therapy of agonadal men by dihydrotestosterone was likewise not associated with any change of sexual functioning. Administration of dihydrotestosterone to eugonadal men led to a transient increase of nocturnal sexual dreams and erections and irritability, waning after 3-4 weeks of dihydrotestosterone administration. It is concluded that aromatization of testosterone is not required and that dihydrotestosterone maintains sexual functions in the adult male with an established sex life.

There you have it, estrogen does not effect libido. Period.so now will you stop talking to me like a little child and tell me where mesterolone fits in ? I mean if estrogen is needed for libido, kindly explain the above study. Thank you.
 
Well gentlemen, I find this debate VERY educational, especially since I have recently argued that you should use post-cycle therapy with 1-test and I was slammed pretty hard, being told it wasnt needed.

Anyway, looking at this from a totally different angle, Bill is stating that testicle size must return ASAP to bring levels of nat test back online (from my interpretation) Now as a fina user, I saw that testicle shrinkage occours slowly..it isnt like they go to rasins overnight. THEREFORE, if testicle size is imperative, wouldnt this mean it is better to do shorter cycles, (i.e. 4 weeks, as opposed to 8 or 12) when using a hard shutdown combo like fina and test, and just go with higher dosages of the androgens? From what I read, your body begins shutting down as soon as ANY outside androgen is introduced, no matter the dosage level. In other words, the gradual decline will go at the same rate if I am using 250mg/week or 1 gram a week of test. I know it is diminishing returns as I raise my androgen levels, but it seems from your debate here, that it would be wiser to do say

weeks 1-4 100/mg test prop/day
75/mg TA/day

versus

weeks 1-8 50/mg test prop/day
37/mg TA/day

I am not saying I will get as great of gains off the 4 week cycle, yet it should be within perhaps 75% of the gains off the 8 week cycle, and I should be able to keep a higher percentage of those gains due to faster testicular recovery time, because they shrank less, therefore it takes less time for them to recover.

Am I completely off base here? If so, Pat and Bill please tell me, I am just trying to learn here and it is not too often I get to hear the opinions of two experts.

Thanks!
 
wardog said:
I am not saying I will get as great of gains off the 4 week cycle, yet it should be within perhaps 75% of the gains off the 8 week cycle, and I should be able to keep a higher percentage of those gains due to faster testicular recovery time, because they shrank less, therefore it takes less time for them to recover.

Am I completely off base here? If so, Pat and Bill please tell me, I am just trying to learn here and it is not too often I get to hear the opinions of two experts.

This type of schedule does make some sense actually. In theory it would avoid pronounced atrophy, and might even eliminate the need for recovery drugs altogether. I tend to think a month would be pushing it though, and might opt for 3 weeks on, 2 off or something myself. Maybe even the BT 2 on 2 off (did I just say that).

I would find it hard to start and stop like that myself though, and am more likey just to run the cycle and deal with atrophy later. But you certainly raise a good point.

- Bill
 
Let me ask the gurus here a question. I'm doing a mild test cycle right now, was thinking of using 1AD or 1Test in the beginning for the 1st 2 weeks followed by a break then start up again when my test finishes.
What would be better, the 1st way or running it throughout?
 
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