Inhibitioan and Recovery of Natural Testosterone Production
One of the most significant side effects of anabolic/androgenic steroid (AAS)
use is inhibition of natural testosterone production. There is no way to entirely
avoid the problem, but there are ways to minimize the problem and recover natural
testosterone levels reasonably quickly after a cycle. In this article, we will
look at the problem of inhibition, its causes, and the best solutions currently
known.
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The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone
production. Many bodybuilders have come to believe that elevated estrogen levels
alone are the sole cause of inhibition, and believe that by blocking estrogen,
they can block inhibition.
This is not true. For example, consider the results seen in the second 2-on
/ 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone
acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize,
with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as
an estrogen receptor blocker. His estrogen levels remained in the normal range,
though elevated from baseline, since apparently the Cytadren was not sufficient
to block aromatization completely. The Clomid should easily have been able to
overcome normal estrogen levels, and so if the estrogen-only theory of inhibition
were correct, Jim should have been suffering no inhibition. But the fact is,
his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone
was not the cause of his inhibition. It could not have been the cause of any
of it, given the normal levels and the Clomid use.
So much for the estrogen-only theory of inhibition that has been claimed by
other writers. That isn’t to say, though, that estrogen is not also inhibitory:
it is.
What then besides estrogen can cause inhibition? DHT, which does not aromatize,
has been extensively shown to cause inhibition of testosterone production. Androgen
alone, then, is sufficient to cause inhibition. In Jim’s case, androgen
use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term.
Paradoxically, in the short term it can be stimulatory. Other relevant factors
include beta agonists, opiates, melatonin, prolactin, and probably other compounds.
With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates
(natural endorphins on the one hand being inhibitory, and Nubain blocking such
inhibition) manipulation of these would not seem useful in bodybuilding.
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The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first
how it is produced and how production is controlled. The broad general picture
is that the hypothalamus receives a variety of inputs, for example, levels of
various hormones, and decides whether or not more sex hormones should be produced.
If the inputs are high, for example, high estrogen or high androgen or both,
then it decides that little or no sex hormones should now be produced, but if
all inputs are low, then it may decide that more sex hormones should be produced.
It seems that the hypothalamus doesn’t respond only to current hormone
levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones – instead it produces
LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin
releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how
much LH it should produce. Proper response depends on having sufficient receptors
for LHRH. These receptors must be activated for LH to be produced. The pituitary
also uses sex hormone levels, both current and the past history, in deciding
how much LH to produce. Some aspects of the pituitary’s behavior are peculiar.
For example, too much LHRH results in the pituitary downregulating LHRH receptors,
with the result that very high LHRH production, which one would think should
result in high testosterone production, actually lowers testosterone production.
Another oddity is that while high estrogen levels inhibit the pituitary, still
some estrogen is required to maintain a high number of LHRH receptors. So both
very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone.
Here, the amount of LH is the main factor, and high levels of sex hormones do
not seem to cause inhibition at this level.
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Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition,
traditional cycles simply cannot avoid inhibition of LH production while on
cycle. There are three ways to avoid it:
Avoid having high androgen levels around the clock. This can be done, for example,
by using oral AAS only in the morning, with the last dose being approximately
at noontime. Even 100 mg/day Dianabol can be used in this fashion with little
inhibition. The problem with this approach is that gains are not very good compared
to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan
at 200-400 mg/week may achieve this effect. Again, gains will be compromised
compared to a more substantial cycle. Testosterone esters and Deca are substantially
inhibitory even at 100 mg/week so using a low dose of these drugs will simply
result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the
purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen.
For the first two weeks of the cycle, only the hypothalamus is inhibited, and
it produces much less LHRH as a result of the high levels of sex hormones it
senses. The pituitary is not inhibited at all: in fact, it is actually sensitized,
and will respond to LHRH (if any is provided) even moreso than normally. After
two weeks however, the pituitary also becomes inhibited, and even if LHRH is
provided, the pituitary will produce little or no LH. This then is a deeper
type of inhibition. After this point, there seems to be no definite further
"switching point" where inhibition again becomes deeper and harder
to reverse. As a general rule, I would say that there seems to be little difference
between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either
way. Between 8 and 12 weeks, it becomes more and more likely that recovery will
be difficult and slow, though even at 12 weeks it is common for recovery to
not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much
more likely to cause substantial problems with recovery. In the hundreds of
consultations I have done for people with recovery problems, very few (I can
recall two) were for very short cycles such as 6 weeks, while most were for
usages of 12 weeks straight or more.
I do not know what changes take place in the hypothalamus and pituitary over
a long period of time that result in this problem, but it certainly is true
that long-term inhibition makes recovery more difficult on average. I suspect
the problem may have to do with change in the "clock" that regulates
the pulse rate of LHRH secretion, but I am not sure that that is so.
Drugs of Use With Regard to Inhibition
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol,
and Equipoise (not an exclusive list of aromatizable AAS, but the main ones)
to estrogen. Some feel that when estrogen levels are kept under control during
the cycle, recovery is faster after the cycle is over, though that is not proven.
It is a good idea though. And if testosterone esters were used prior to ending
the cycle, some levels of these will remain for weeks, and continued use of
Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition.
The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on
arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren
than this, or a different pattern, may lead to an adverse effect on cortisol
production, with subsequent cortisol rebound after discontinuing the drug. Some
individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness)
from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible
side effects mentioned above. It is however far more expensive. A typical dose
is 1 mg./day. The timing of the dosage does not matter, since the drug has a
long half-life.
Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective
in restoring natural testosterone production. It acts by blocking estrogen receptors
at the hypothalamus and pituitary. If androgen levels are not elevated, this
is enough to cause production of at least normal amounts of LH, or often more
LH than normal. During the cycle Clomid cannot prevent inhibition, though some
think using it during the cycle will allow a faster recovery afterwards. That
is not proven though. If nothing else, though, it is useful as an antigyno/antibloating
agent during the cycle.
Nolvadex: This works in the same manner as Clomid, but not nearly so well with
regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating
agent, if at all. If Clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary.
Rather it acts like LH, and causes the testicles to produce testosterone just
as if LH were present. It is useful then for avoiding testicular atrophy during
the cycle. The best dosing method is to use small amounts frequently: 500 IU
per day is sufficient, and 1000 IU may optionally be used. The amount may be
given as a single daily dose or divided into two doses. Administration may be
intramuscular or subcutaneous. More is not better: too much HCG can result in
downregulation of the LH receptors in the testes, and is therefore counterproductive.
Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these
drugs may assist in recovery. Personally, I do recommend the use of ephedrine
post-cycle to those who can use it. Clenbuterol has the same effect but acts
around the clock, having a longer half life, and allowing a higher effective
dose (amount times potency) due to having less relative effect on beta receptors
in the heart. I am not sure that Clenbuterol has any better effect with regard
to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production,
but if used only in the morning, can help sustain muscle mass while in the recovery
phase, with little or no adverse effect on recovery.
Tribulus: If this is of benefit, I have not been able to observe it myself.
I have only tried the Tribestan brand, but this is the brand that earned tribulus
its reputation.
Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have
seen no evidence that taking melatonin at night speeds recovery. It is useful
though for those who have allowed their sleep patterns to be disrupted and who
wish to reset their natural clocks.
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General Recommendations
Pharmaceutical drugs should of course not be self-prescribed: the following
are simply recommendations of what works well, not of what to do without physician’s
advice. Enough said.
The best cycle plans are either brief two week cycles with short acting drugs,
which allow a very fast recovery (less than one week) or cycle of approximately
6-10 weeks, which usually allow reasonable recovery and allow quite a bit of
time to make gains. Cycles in the 3-5 week range are less efficient because
they combine the disadvantage of relatively little time gaining with the disadvantage
of slower recovery.
If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the
cycle if possible, as described above. HCG should not be used during the recovery
itself since it will increase androgen and estrogen levels, which will be inhibitory
to the hypothalamus and pituitary. Clomid use should begin, if it was not used
during the cycle, as soon as androgen levels drop enough that recovery becomes
possible. This would be about two weeks after the last injection of long acting
steroid esters, assuming reasonable doses such as 500 mg/week. Clomid use should
start with 300 mg on the first day (50 mg six times) to quickly get blood levels
as high as needed, and then maintained with 50 mg/day. This is needed because
of the half-life of the drug. It should be continued until one is sure that
natural testosterone production is back and testicle size is returned to normal,
with the exception that if use has been more than about 6 weeks, one might try
dropping it for a few weeks to see what happens. If no further improvement occurs,
then Clomid would be resumed. It has been studied medically for long-term use
and found safe for periods of at least a year. However, a small percentage of
users develop vision problems from Clomid, which are generally reversible upon
discontinuing the drug. So if you have this problem, certainly the drug should
be discontinued.
If aromatizable injectables were used, an antiaromatase would be useful for
3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram
per week or more.)
Lastly, ephedrine seems to be of some help. The same dose as used for dieting
(e.g. 25 mg three times per day) seems quite sufficient.
Long term inhibition can potentially be a serious side-effect of AAS use, and
this risk should be minimized by avoiding excessively long cycles. This really
does not compromise gains greatly, since the body cannot grow rapidly week in,
week out, 52 weeks per year anyway. And even moderate post-cycle inhibition
is something we wish to minimize, since it is frustrating to lose much of one’s
gains in the first few weeks after a cycle as a result of low natural testosterone
and no AAS being used. The advice given above is generally successful in minimizing
such losses, and I hope you will find it useful
- Inhibitioan And Recovery Of Natural Testosterone Production - Steroidology.com