posted June 25, 2000 11:25 PM            

get big or get out

posted June 26, 2000 05:13 AM            

Dexter

Redo on: NO HCG, anti-estrogens post. (more comprehensive and cleared up)

Posted by Animal on Friday, 6 February 1998, at 1:49 p.m.

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! .
Keep taking your anti-estrogens!

Bump your Cytadren up to 1000mg a day to suppress the gains killing cortisol. If it was me I would take the Clomid all the way through and then save my money for the Cytadren for the 2 weeks post cycle.This is just a suggestion and the dosage may be lower as I don't know how much joint pain people will be able to handle.

If you can't get Cytadren then you may want to try Phosphatidylserine.
Take the PS the 2 weeks of Cytadren and if it doesn't work as good you will know real fast! I am getting some and will let you know if it works at all.

Keep taking the creatine.

Add in your clen or DNP or Mazindol or e/c/a stack.

Feel free to abuse!
It is futile and you will be assimilated into Animals Anarchy System!
(Damn that Borg on ST Voyager is hot! Assimilate me!)
Anarchy in the USA!

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Strength and Honor.

posted June 26, 2000 01:12 PM            

good post BUT your post states that,

"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."

i disagree with this bc ONLY TEST CAN CONVERT TO DHT. the reason winny and primo can cause hairloss is because they themselves are agonists in the scalp. finasterdide will not help with winny and primo bro.

posted June 26, 2000 04:28 PM         

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legend

posted June 26, 2000 06:30 PM            

"This hormone is not a male hormone but mimics the natural hormone LH (Luteinizing Hormone) almost identically. LH stimulates the production of testosterone by the testis in males. HCG sends the same message and results in increased testosterone production by stimulating the leydig cells of the testis."

CLOMID:

"In men, the application of Clomid causes an elevation of follicle stimulating hormone and luteinizing hormone. As a result, natural testosterone production is also increased."

The key word here is mimics LH. Clomid will make your body produce it's own LH. Once you stop HCG your body asn't normalized yet cause your natural LH is still suppressed.

If using HCG and for test atrophy great. It's also good post cycle if you don't mind the increased estrogen (read gyno, wr) but you must follow up with clomid the normalise the LH production.

CLOMID and HCG:

"Since an immediate boost in testosterone is often desirable, athletes will commonly use HCG (human chronic gonadotropin) for a couple of weeks, and the continue treatment with Clomid. Clomid is also effective as an anti-estrogen. Most athletes will suffer from an elevated estrogen level at the conclusion of a cycle. A high estrogen level combined with a low testosterone level puts an athlete in serious risk of developing gynocomastia. With the intake of Clomid, the athlete gets the dual effect of blocking out some of the effects of estrogen, while also increasing endogenous testosterone production.

Later,