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1-Test - Anabolic/Androgenic?
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pa1ad 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.
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w_llewellyn 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.
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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 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:
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:
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:
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:
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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