posted July 07, 2000 11:47 PM
here it is, very informative, I dug this up, thought it would be helpful to all of u bros...LP
May 96
I need to clear up a few things and instead of answering posts, I have
redone it so it is more comprehensive and understandable.
(Some of the stuff in the first one was slightly off in terms, but that
is not my fault. The research and articles are at times interchanging
DHT and estrogen.)
Aromatizing means that test converts to estrogen (in most literature).
5-alpha reductase (5-ar) converts testosterone to DHT in the liver
prostate and skin. I also think this enzyme converts test to estrogen.
Arimidex is an anti-aromatase with of half life of 30-60 hrs and will
totally eliminate estrogen in a few days at 1mg a day. Does not affect
thyroid levels.
Chrysin is also an anti-estrogen and some say that it may be more so
than Cytadren, however, Chrysin also messes with thyroid.
Citrimax otherwise known as hydroxycitric acid because it inhibits NaDPH
which is needed for 5-alpha reductase enzyme activation. It may be mild,
but it is better than nothing. This may work on DHT and as an
anti-estrogen.
Cytadren is an inhibitor of adrenocortical steroid synthesis which leads
to a reduction in production of estrogens and androgens via stopping
conversion of cholesterol to pregnenolone. This is very interesting here
because while it is definately an anti-estrogen by stopping production
of the 5-ar enzyme working through hydroxylations, but it may also
inhibit production of normal testosterone! It may be at a higher dose
than the 250mg a day that we use to stop aromatization, but if it is, as
I suspect, working to some degree to eliminate natural test production
then this makes the Gufus (pronounced �goof-oos') look really dumb! They
are stating that you can keep testicular function going with the use of
a drug that stops dead the precursor to testosterone production! Can you
say, �TOTALLY INEPT! This does not even address the information to come
on hypothalamus suppression via high doses and alternate mechanisms.
Permixon or saw palmetto extract inhibits the 5-alpha reductase at the
type-1 receptors which are what makes you go bald, while Proscar hits
the Type-II. Saw palmetto is also anti-estrogenic! 320 mg a day or more
of standardized saw palmetto extract would likely be more effective, as
saw palmetto inhibits the binding of DHT to the receptors. So, it should
work for DHT based exogenous steroids, too!
Proscar is a specific 5-ar inhibitor at the site and can reduce serum
DHT by 70% at 5mg a day. Suppression of 5-ar by finasteride does not
have an effect on serum estradiol, cortisol, TSH or thyroxine. It is
suspected that Teslac also works by inhibition of 5-ar. This is where I
may have goofed in the last post. If Teslac lowers serum estradiol by
5-ar mechanism and Proscar works at the 5-ar as well, I deducted that
Proscar could lower estrogen levels as well. My further research to this
point showed that Proscar did not lower serum estrogen and therefore it
is NOT the same as Teslac. I have to research this more and it is not
going to matter as you will see below. Finasteride (Proscar) is
available as Propecia and you may be able to wiggle a �script away from
your liberal docs.
Halotestin and Anadrol are both notorious causers of hair loss which
means that they are being converted to DHT. Methyltestosterone causes
significant hair loss in low dosages as does methandrostenolone (D-bol).
Winstrol converts to DHT, and dosages over 100 mg/week can cause hair
loss, although usually not as dramatic as testosterone hair loss. The
same is true of Primobolan and Masterone (Permastril), but you really
have to take a lot of it (over 300 mg/week) to lose hair.
These are the steroids you would want to take the Proscar or Teslac
with, to stop the conversion to DHT.
Proviron and Teslac are steroidal anti-aromatases. (Teslac is really an
antineoplastic agent) Proviron competes for the site receptors which is
not the best.
Teslac stops conversion at the 5-ar enzyme (suspected) and keeps any
estrogen from even being produced. Teslac may also have IRREVERSIBLE
benefits in this area as its benefits continue even AFTER dosage has
stopped. Teslac is an AS and is C-III and is expensive. Teslac, however,
does not have any blocking capabilies for progesterone conversion which
means it won't stop the hypo from shutting down from Deca use or
blocking progesterone side effects like gyno which our friend Franz
found out!
Ru486 is a progesterone blocker! This is what you would want to use if
you are on Deca or trenbolone! I have to look up the mechanism for this,
but I expect it will work because some were trying it as an
anti-cortisol when it first became available. And the misinformation
morons said there was no use for this drug! (I haven't researched
dosage, yet.)
Nolvadex and Clomid are estrogen antagonists which mean they sit in the
receptor site and block the estrogen from getting in.
Clomid interacts with the hypothalamus as well at least for a short
time. The literature is not totally clear on mechanism, but that may
just indicate that Clomid can mimic LH which keeps your testicles
producing testosterone no matter what you take! The first response to
taking Clomid is release of pituitary gonadotropins. This is why you
don't need to take HCG, ever! This leads me to believe, and although I
could be wrong, that Clomid has the capability of keeping the
hypothalamus functioning through any cycle! Not just keeping the
testicles functioning through mimic of LH.
HCG mimics the actions of LH and FSH and can be used to jump start the
gonads' Leydig cells. This is only a short-term solution as HCG does
nothing to increase secretion of LH and FSH and GnRH AND because the
bigger response you get from the Leydig cells the more the hypothalamus
will down regulate GnRH, LH, and FSH because of increased estrogen which
is why you have to take an anti-estrogen with HCG. Estrogen is one of
the controlling factors in the secretion of GnRH, LH, FSH and
testosterone when you are using HCG.
This is only part of the story as I also found evidence that my other
theory was true about large amounts of ANY AS shutting down the
hypothalamus.
The following is a quote from one of the many misinformation articles by
a certain
group of �Gufus'( pronounced �goo-foo' ). I will show again, as I have
many times before, that their misinformation is wrong.
This is what was said, �If you use an anti-aromatase Like Cytadren or
Teslac while on a heavy cycle, you won't experience much, if any, nut
shrinkage. Right. I agree. Blocking the aromatization won't affect
natural testosterone production. Despite cramming in like 1,000 mg of
testosterone cypionate a week, you'll still produce the same amount of
testosterone as you were before you went on the juice.'
Absolutely wrong! Not only because of the mechanism through which
Cytadren works, but because with those AS doses the hypothalamus can
still be shut down!
Oxandrin, Primobolan, trenbolone, Halotestin, and Deca don't convert to
estrogen and shouldn't cause decreased testosterone production.
Studies show the presence of estrogen is not required to reduce
testosterone production! This is what makes the quote by the �Gufus'(
pronounced �goof-foo') totally inaccurate. Many on the board have seen
and/or experienced this anecdotally (sp?) as many of us have experienced
reduced sex drive or no sex drive on cycles of Deca and/or trenbolone!
(Deca and trenbolone do not aromatize to estrogen)
It is a fact that two other hormones in the body, testosterone and
progesterone, also cause the down-regulation of testosterone production.
Desaulles, et al., have demonstrated that none of the presently used
anabolic steroids are free of the capacity to inhibit gonadotropin
secretion." This study was done in the 60's which makes the quoted
statements above look very foolish.
If estrogen were the only thing shutting down natural testosterone
production, why does one recent study show that Oxandrin, which doesn't
convert to estrogen at all, reduces testosterone production by about
600ng/dl at dosages of only 10mg a day?
Other studies have shown Parabolan, Halotestin, and even
dihydrotestosterone (DHT) all substantially decrease testosterone
production even though they don't convert to estrogen.
Deca Durabolin converts to estrogen at only about 200% the rate of
testosterone, (the Gufus said it does not convert at all!) but still
appears to down-regulate this natural mechanism more than testosterone.
Trenbolone, which produces no estrogen at all, causes about three times
as much down regulation as testosterone and like Deca, Trenbolone has a
progesterone-like effect. Trenbolone causes about three times as much
inhibition of GnRH as testosterone and researchers also found that
trenbolone is approximately three times more androgenic than
testosterone. It appears that it's the androgenic potential which
reduces natural testosterone.
If a steroid works at all it will affect the hypothalamic sensing
mechanisms and down regulate testosterone production!!!!!!!!!
There are androgen receptors in the hypothalamus. And if androgens like
testosterone or dihydrotestosterone bind to the hypothalamic androgen
receptors, they'll cause the hypothalarnus to react and decrease natural
testosterone production.
The hypothalamus also has receptors for the female hormone progesterone
which will also stop the body's production of testosterone. This
progesterone mechanism is one reason that Deca, which produces less
estrogen than testesterone but has a stronger progesterone-like effect,
elicits more testosterone inhibition. Testesterone regulation is
definitely more complex than estrogen alone knocking your testosterone
production down.
Estrogen can attenuate testosterone production and the aromatase
inhibitors (Arimidex, Cytadren , Teslac, and maybe even Proscar (mech?))
can reduce estrogen. However, steroids that don't produce estrogen can
still diminish your body's production of testosterone because of their
androgenic or progesterone-like properties. Also, if the dosage is high
enough these steroids WILL challenge or negate the benefit that
aromatase inhibitors exert by raising testosterone production via
estrogen suppression. People on 1g of Arimidex a day which TOTALLY
eliminates estrogen, will STILL SHOW NO SERUM TESTOSTERONE if the are
using large doses of non-aromatizing AS.
Nevertheless, using aromatase inhibitors will probably result in some
improvement in serum levels and increased effectiveness of a steroid
that does aromatize, like Deca, Anadrol, D-bol and the testosterones if
conversion to estrogen/progesterone is blocked with an aromatase
inhibitor. If the steroid doses you're using aren't high, you might get
very good results using an aromatase inhibitor like Teslac, Arimidex, or
Cytadren(?) during the cycle to kick the testosterone factory into gear,
so you can prevent the testicles from shrinking.
More evidence that AS suppresses everything within 4 weeks!.
Testosterone suppression of the HPT axis.
MacIndoe JH, Perry PJ, Yates WR, Holman TL, Ellingrod VL, Scott SD
BACKGROUND: Although studies have demonstrated the suppression of normal
gonadal function in the experimental setting, the specific mechanisms by
which androgenic-anabolic steroids impact male gonadal function remain
ill defined.
Following 2 consecutive weekly injections of an identically appearing
testosterone cypionate (TC) placebo, subjects were randomized to a TC
dose of 100 mg/wk, 250 mg/wk, or 500 mg/wk. Following the last weekly
injection of active agent the subjects received 12 consecutive weeks of
TC placebo injections.
RESULTS: Spermatogenesis was impaired by each of the doses of TC
employed in this study, but the observed decreases in, sperm count were
neither strictly dose dependent nor consistent between individuals
treated with the same dose.
Basal leuteinizing hormone (LH) and follicle stimulating hormone (FSH)
became undetectable 2 weeks after the start of 250 and 500 mg/wk TC
injections and were lost within 5 to 6 weeks of starting 100 mg doses.
Pituitary gonadotropin responses to leutinizing hormone releasing
hormone (LHRH) disappeared more slowly with FSH responses being lost 1
to 3 weeks after the loss of basal FSH activity. Leuteinizing hormone
responses to LHRH appeared to be suppressed last, disappearing 4 to 6
weeks after FSH responses to LHRH.
CONCLUSIONS: Exogenous testosterone-mediated inhibitory influences on
the hypothalamic-pituitary-testicular axis were reversed following the
cessation of drug treatment.
Publication Types:
�Clinical trial �Randomized controlled trial
PMID: 9394096, UI: 98055891
Then there is this info: Over the last year or so, we've seen research
which shows that the higher aromatizing steroids (ones that more easily
convert into estrogen) cause more IGF-I production in the body. We also
know that as men get older, there's more aromatase in the body, and
testosterone will more readily convert to estrogen.
So what do we do now to keep your testicles online or hypothalamus
working?
Don't listen to the so called, published Gufus!
High doses of AS WILL shut you down no matter what anti-estrogens you
take.
If just keeping your nuts from shrinking is the goal, then I recommend
taking Clomid AFTER week 3 or 4 when everything has been suppressed.
Clomid is also an anti-estrogen and will block aromatization at the site
like Nolvadex does.
Clomid is the only thing I can see that would be efficacious because if
you are trying to use Arimidex, Cytadren, or Teslac to suppress estrogen
to fool the hypothalamus it won't work because the high volumes of AS
are still detected by the hypo.
Clomid was shown to restore test secretion because it is an
anti-estrogen and mimics LH. Therefore, the hypothalamus �sees' less
estrogen and starts test production if you are not on high doses which
most of us are.. You could take Clomid during the entire cycle and it
will not hurt anything but will be a good anti-estrogen via site
mechanism. Clomid does is ACT LIKE LH and therefore there is no
drop-off. However, Clomid may also have a short-term effect on the hypo
as I stated above.
If you are on an aromatizing AS like test and you don't care about
shrinkage, and you have the money you could take Cytadren. If you want
to keep things functioning then you could stack Clomid in here as well.
I see no need for Proviron at ALL! It competes for the receptor site and
is an AS. Take Nolvadex or Clomid if you are worried about gyno!
Nolvadex competes, too but is breast tissue specific.
Teslac is a very good anti-estrogen although expensive and will do
nothing to keep your nuts online with high AS doses.
Cytadren does the same thing as Teslac through a different mechanism and
will probably stop balding, too because it stops production of the 5-ar
enzyme! (I don't know if it stops it in the Type-1 cell and that is why
I said � probably.')
Permixon (saw palmetto extract) may be the cheapest of all and has the
dual function of blocking DHT and being an anti-estrogen. If you want to
stop balding and Proscar is not available then you may want to look into
this. I may try this just to see if it inhibits hair growth.
Hydroxycitric acid (Citrimax) may be used as a last resort.
If you are cycling only with or stacking with Deca or trenbolone then
you need to try and get Ru486 as an anti-progesterone.
How and what to taper?
First, no matter what you do your strength will drop because as the East
Germans discovered, the very androgenic steroids, with virtually no
anabolic effect, cause a significant boost in central nervous system CNS
neuron firing. This is the nerve recovery that I have talked about
before. You lose this excitation AND you automatically lose the
concomittant ability to recover when your cycle ends. You have to
increase the intervals between training days.
STOP the androgenic AS DEAD (do not taper at all these AS) Taper your
cycle with non-androgenics like deca or primo or trenbolone.
A good non-aromatizing steroid to taper with would be trenbolone
(Finaplix, Parabolan) An anabolic steroid that can actually down
regulate the whole cortisol receptor, which means that there are less
receptors avail able to cortisol (trenbolone does this). This would be
the best drug to taper with! Does not convert to estrogen AND it
destroys cortisol receptors, therefore when you go off you don't have
the receptors to take in the cortisol flood and you don't loose your
gains!
If you are tapering with trenbolone or Deca you may want to try and get
some Ru486 to stop the progesterone effect from fooling your
hypothalamus into staying shut down even though you are not on
androgenic steroids.
Start taking PS or upping your dose of Cytadren to the cortisol blocking
dose.
Start taking Creatine to keep your cells full and protein synthesis up.
After all AS are stopped.
DO NOT take HCG!
That will just cause a blast of estrogen and wreck everything you worked
for and does not help your hypothalamus at all! .
------------------
"This is George the owner, and Tony the Guru... Tony knows everything." -Lee Priest
[This message has been edited by The_Blond_Myth (edited July 08, 2000).]
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George Spellwin's ELITE FITNESS Discussion Boards
posted July 07, 2000 11:47 PM
