"Estrogen Control, Treatment, and PCT by WARMachine"

**WARMachine** · 03-22-2009, 09:25 PM

Ok now guys, i wrote this thread because i see a million posts every week about the subject. So I thought to myself why not make a thread about gyno and ways to prevent it, because i felt its one of a few subjects that is touched on, but not fully explained for most out there. As well as inform these new guys about prevention opposed to waiting till there is a problem.

I'm posting this in Q&A because no one goes into the PCT section, especially new guys. So i thought it'd be best seen here.

Now it seems to me, most newbies do little to no research before coming in here, asking dumb questions that can easily be found with limited effort. Granted, i was once one of those newbies, and i even admit, i have changed my opinion on certain topics more than once. But its because of listening and learning from more experienced guys than myself, finding new medical articles on said topics, and the good ol' trial and error system. So don't post here saying 'Oh yeah! This isn't what you said on x/x/08! Or you said something different on time.' This is why i will periodically be updating this thread with new info.

Now here we go!

So i put this together to include my opinions on how to avoid estrogen related side effects (namely gyno for this particular thread) among other things, namely how Tamox does in fact cure gyno, but well get to that later.

Now there are a few schools of thought on this subject;

The first one being that once you get gyno, begin the reversal ASAP. I feel the issues with doing so on cycle are as follows.

Letro is the most powerful AI you can use, it will inhibit as much as 98+% of estrogen using a dose as low as .25mg. Running a gyno reversal during the cycle will cause a few problems because of this. Now as i'm sure you know, estrogen is needed as much as testosterone is when it comes to muscle building. Running the reversal during the cycle will cause you to maintain a low level of estrogen throughout the cycle (This causes serious gain losses IMO).

The reason for this is because of the estrogen rebound effect that comes with taking Letro. The body will try to re-stabilize the testosterone:estrogen balance, and the issue is your estrogen has been completely inhibited(due to the letro) and thus causing a rebound, sending your estrogen levels to go though the roof. Now because this happens, you will need to prevent this by supplementing further with another AI or SERM.

This means that you need to begin taking Nolva throughout the rest of your cycle until PCT, and with the help of the other PCT drugs(Aromasin , Clomid etc..), it should handle the estrogen rebound effect. (Using Nolva on the last day of your letro will eliminate estrogen's ability to bind to the receptors in the breast thus preventing the onset of estrogen related side effects, or in this particular case, cause the levels to stay lowered.)

Now Mammon put it this way, and it makes perfect sense in what I'm saying.

With starting letro during cycle when symptoms start, i don't know.. sure it will eliminate 98% of estrogen.. stopping the conversion of test to estrogen.. but what about the circulating estrogen that is already present and causing the problem.. does letro have the ability to eliminate already present estrogen.. I'm not sure..

Now the another school of thought;

Waiting till the cycle is over.

Now the only real issues Ive found with waiting to begin a Gyno Reversal is that Letro kills your sex drive, and when used on cycle, since we are using high levels of Testosterone , it should cancel it out. Well i don't know if i really agree, but Ive found nothing in terms of medical articles that either support, or oppose that idea. (Would love to read if you have found some!)

The other problem people seem to have is that if you are running a Gyno Reversal while not on cycle, you have to taper with Nolva for two weeks. Again, not an issue in my opinion considering if you get gyno say week 5 on a 12 week cycle, you'd be using Nolva for another 6 weeks, PLUS PCT. (Just an example)

So, now onto my way! It is as follows.

Prevent gyno before it happens!

Prevention is always best guys! Not preventing these problems would be like not wearing a condom, and then getting AIDS, and treating it! Its always best to prevent problems before they occur!

1) The most obvious way is to control your BF% before and during your cycle. Let me try to make this as clear as possible. The higher your BF% is, the higher risk of developing ERSEs are. The lower the BF%, the lower the risk. Keep in mind these are NOT the only factors, but they are some of the biggest. This of course doesn't mean that you wont get estrogen or progesterone (topic for another day) related side effects, but it does in fact reduce the likelihood. It should also be taken up under advisement to watch your diet and water retention. That bloat and poor diet only adds to problems.

2) Use an AI if you know you're gyno prone. Now Adex on cycle is the same basic concept as using Letro, the difference being that it doesn't inhibit as much estrogen as Letro. The problem here is finding out the hard way if you're Estrogen Related Side Effect Prone (i say estrogen related side effect, because there are more side effects than just gyno such as, lethargy, suppressed gains, suppressed sex drive, acne, bloating etc..). The only way i know how to see if youre ERSEP is the old fashioned way, run a cycle. No sides, no worries! Obviously if you don't follow the first set of rules (above) you'd be best advised to use an AI just in case.

3) If you do get ERSE's, then begin administering Nolvadex immediately! Nolvadex is a SERM. It selectively will block the estrogen from binding to the receptors in the breast, now the circulating estrogen can still be elevated, it just wont have the ability to bind to the receptors in the breast and cause breast growth, i.e. gyno! This making Nolvadex effective in blocking the estrogen and stopping unwanted sides such as gyno. Or in the case of gyno beginning or already occurring, it will stop the symptoms from worsening.

And now onto the big part. Tamox does in fact cure gyno. Yes, shocking to some, to others, not so much. I have long suspected (thanks to the guide from Mammon) that it was possible. Originally i didn't include this in the thread because to be honest i rushed this out. But now time for the big reveal.

Taken from C Bino's thread "All you need to know about gyno"

This brings me to my next point. Do not listen to anyone who tells you to bump up your nolvadex to 60+mg ED if you get gyno. I have no idea where this idea started but I have seen it suggest far too many times recently. Nolvadex will do nothing to reverse your gyno…let me make that clear IT WILL DO NOTHING FOR GYNO. If you are running nolva as your anti-e and start to develop gyno than sure you can bump the dosage a small amount to try to prevent it from progressing further, but letrozole must begin ASAP.

I strongly disagree in the red highlighted areas. He is just plain wrong to put it frankly. Not to mention the terms of stopping symptoms from progressing! Now nothing against C Bino, cause i know people who have used his Gyno Reversal method, and they have said it does work. That being said, i have also heard of its many failures from firsthand users.

I have been waiting for more than just first hand experience to present this case, because lets face it, C Bino and his method are well respected. So now due to discussions with Mammon and Medical articles from my boy Peachfuzz, were ready to present the cases.

Here are five different case studies that provide us with the info that Tamox does, and more importantly CAN cure gyno.

Ill post up the first one for everyone to see.

"Management of physiological gynecomastia with tamoxifen

References and further reading may be available for this article. To view references and further reading you must purchase this article.

H. N. Khan, , R. Rampaul and R. W. Blamey

Professorial Unit of Surgery, Department of Surgery, Nottingham City Hospital, Nottingham NG5 1PB, UK

Abstract
Aims: We aimed to confirm suggestions that tamoxifen therapy alone may resolve physiological gynaecomastia.

Methods: A prospective audit of the outcome of tamoxifen routinely given to men with physiological gynaecomastia was carried out at Nottingham. Men referred with gynaecomastia had clinical signs recorded, e.g., type (diffuse ‘fatty’ or retro-areolar ‘lump’), size and possible aetiology. They were offered oral tamoxifen 20 mg once daily for 6–12 weeks. On follow-up patients were assessed for complete resolution (CR), partial resolution where patient is satisfied with outcome (PR) or no resolution (NR). Success was either CR or PR.

Results: Thirty-six men accepted tamoxifen for physiological gynaecomastia. Median age was 31 (range 18–64). Tenderness was present in 25 (71%) cases. Sixteen men (45%) had ‘fatty’ gynaecomastia and 20 had ‘lump’ gynaecomastia. Tamoxifen resolved the mass in 30 patients (83.3%; CR=22, PR=8) and tenderness in 21 cases (84%; CR=21, PR=0). Lump gynaecomastia was more responsive to tamoxifen than the fatty type (100% vs. 62.5%; P=0.0041).

Conclusions: Oral tamoxifen is an effective treatment for physiological gynaecomastia, especially for the lump type"

*This is just the abstract, for the full article click on the link.

http://www.sciencedirect.com/science...67cb56f35979ec

http://www.ncbi.nlm.nih.gov/pubmed/3664552

http://www.ncbi.nlm.nih.gov/pubmed/3123765

http://www.cababstractsplus.org/abst...No=20043004430

http://www.sciencedirect.com/science...7bea0fc991c05b

Now to make it clear. Can Tamox cure gyno? It seems it can. Does that mean its a fool proof method that will work for anyone? No of course not. To put it frankly, im very skeptical about the Gyno Reversal method as a whole. Weather it be with Tamox or Letro. The point is, its not a proven method. In reference to the Letro Reversal, it was put together by someone who had first hand experience, and until some medical researchers put it to the test, we cannot definitively say it does or does not work.

As for the Tamox reversal, ive found countless articles stating its success. It should be noted however that it doesnt mean that the gyno cannot reoccur. As a matter of fact ive found that it likely will return if the proper precautions of prevention arent taken before you cycle again. And even if you dont cycle, it still can return. Here is a source for this below.

"Am Surg 2000 Jan;66(1):38-40
Comparison of Tamoxifen with danazol in the management of idiopathic gynecomastia.

Ting AC, Chow LW, Leung YF.

Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Pokfulam.

Idiopathic gynecomastia, unilateral or bilateral, is a common physical finding in normal men. Successful treatment using Tamoxifen (antiestrogen) and danazol (antiandrogen) has recently been reported. We compared the efficacy of Tamoxifen and danazol in the treatment of idiopathic gynecomastia. We reviewed the clinical records of patients with idiopathic gynecomastia presenting to the Department of Surgery, University of Hong Kong, between August 1990 and September 1995. Medical treatment with either Tamoxifen (20 mg/d) or danazol (400 mg/d) was offered and continued until a static response was achieved. The treatment response was compared. Sixty-eight patients with idiopathic gynecomastia were seen in the Breast Clinic. The median age was 39.5 years (range, 13-82), with a median duration of symptoms of 3 months (range, 1-90). The median size was 3 cm (range, 1-7). Twenty-three patients were treated with Tamoxifen and 20 with danazol.Complete resolution of the gynecomastia was recorded in 18 patients (78.2%) treated with Tamoxifen, whereas only 8 patients (40%) in the danazol group had complete resolution. Five patients, all from the Tamoxifen group, developed recurrence of breast mass. In conclusion, hormonal manition is effective in the treatment of patients with idiopathic gynecomastia. Although the effect is more marked for Tamoxifen compared with danazol, the relapse rate is higher for Tamoxifen. Further prospective randomized studies would be useful in defining the role of these drugs in the management of patients with idiopathic gynecomastia."

Basically what it says is that i can be reversed with Tamoxifen. But it does have a high % chance to reoccur. Supporting my claim that it will certainly shrink and possibly remove gyno, but its not 100% accurate method. The only way to have that is surgery. But thats not to say if you catch it while its forming you have a chance at reversing, once its formed the best you can hope for is some shrinkage, you aren't going to make it disappear. It will always be there even if you cant feel it, it will come back on your next cycles if you don't take proper precautions. Which is my main point in writing this thread.

All that put aside for a moment, i included the different schools of thought in a way that would help those who would like to attempt the method. I see no problem with trying it, as it seems it has worked for some in the past. I just wanted to make the point of taking preventitive measures before the problems occur. As well as other things such as Tamox indeed being somewhat effective when it comes to treating gyno. More so than the Letro method in my opinion. As far as who's way of doing things is better, thats up to everyones personal opinions. I just happen to think that my way is the best way. It works for me, and the people who follow it. Im sure some will disagree with my way of thinking, but for the most part, ive found people to be open and have positive things to say about my advice.

Now heres my recomendations for doses.

"FOR ON CYCLE ESTROGEN CONTROL"

Adex - .5mgs EOD (For first time users.)

If sides do not decrease much, you may increase the dose to .25mgs ED, or as high as .5mgs ED. I would not exceed 1mgs ED use under any circumstances, at that point, the use of Letro should be looked at.

"FOR GYNO REDUCTION"

Tamox - 40mgs ED (for the first 5 days.)

From there you can drop the dose to 20mgs ED, and if symptoms subside, continue use of 10mgs throughout the remainder of your cycle and into PCT.

This concludes the section for GYNO and Estrogen Control.

__________________________________________________ _____________________________________________

Now im gonna touch on an issue that is commonly asked.

The use of Proviron as an AI.

Ive heard this being used as an AI for quite some time now. This is perhaps the most persistent myth in AAS user circles. There are all kinds of stories with this drug. One of them being that it is supressive to the HPTA (hypothalamic-pituitary-testicular-axis for you new guys.). Well actually ive found studies that show Proviron to not be highly suppressive. Our own profile here on Steroid .com quotes part of the study im referring to.

Big Cats profile on Proviron, Amended by Lawnsaver.

" Mesterolone is an orally active, 1-methylated DHT. Like Masteron , but then actually delivered in an oral fashion. DHT is the conversion product of testosterone at the 5-alpha-reductase enzyme, the result being a hormone that is 3 to 4 times as androgenic and is structurally incapable of forming estrogen. One would imagine then that mesterolone would be a perfect drug to enhance strength and add small but completely lean gains to the frame. Unfortunately there is a control mechanism for DHT in the human body. When levels get too high, the 3alpha hydroxysteroid dehydrogenase enzyme converts it to a mostly inactive compound known as 3-alpha (5-alpha-androstan-3alpha,17beta-diol), a prohormone if you will. It can equally convert back to DHT by way of the same enzyme when low levels of DHT are detected. But it means that unless one uses ridiculously high amounts, most of what is administered is quite useless at the height of the androgen receptor in muscle tissue and thus mesterolone is not particularly suited, if at all, to promote muscle hypertrophy. Proviron has four distinct uses in the world of bodybuilding. The first being the result of its structure. It is 5-alpha reduced and not capable of forming estrogen, yet it nonetheless has a much higher affinity for the aromatase enzyme (which converts testosterone to estrogen) than testosterone does. That means in administering it with testosterone or another aromatizable compound, it prevents estrogen build-up because it binds to the aromatase enzyme very strongly, thereby preventing these steroids from interacting with it and forming estrogen. So Mesterolone use has the extreme benefit of reducing estrogenic side-effects and water retention noted with other steroids, and as such still help to provide mostly lean gains. Its also been suggested that it may actually downgrade the actual estrogen receptor making it doubly effective at reducing circulating estrogen levels. The second use is in enhancing the potency of testosterone. Testosterone in the body at normal physiological levels is mostly inactive. As much as 97 or 98 percent of testosterone in that amount is bound to sex hormone binding globulin (SHBG) and albumin, two proteins. In such a form testosterone is mostly inactive. But as with the aromatase enzyme, DHT has a higher affinity for these proteins than testosterone does, so when administered simultaneously the mesterolone will attach to the SHBG and albumin, leaving larger amounts of free testosterone to mediate anabolic activities such as protein synthesis. Another way in which it helps to increase gains. Its also another part of the equation that makes it ineffective on its own, as binding to these proteins too, would render it a non-issue at the androgen receptor. Thirdly, mesterolone is added in pre-contest phases to increase a distinct hardness and muscle density. Probably due to its reduction in circulating estrogen, perhaps due to the downregulating of the estrogen receptor in muscle tissue, it decreases the total water build-up of the body giving its user a much leaner look, and a visual effect of possessing "harder" muscles with more cuts and striations. Proviron is often used as a last-minute secret by a lot of bodybuilders and both actors and models have used it time and again to deliver top shape day in day out, when needed. Like the other methylated DHT compound, drostanolone, mesterolone is particularly potent in achieving this feat.

Lastly Proviron is used during a cycle of certain hormones such as nandrolone , with a distinct lack of androgenic nature, or perhaps 5-alpha reduced hormones that don't have the same affinities as DHT does. Such compounds, thinking of trenbolone , nandrolone and such in particular, have been known to decrease libido. Limiting the athlete to perform sexually being the logical result. DHT plays a key role in this process and is therefore administered in conjunction with such steroids to ease or relieve this annoying side-effect. Proviron is also commonly prescribed by doctors to people with low levels of testosterone, or patients with chronic impotence. Its not perceived as a powerful anabolic, but it gets the job done equally well if not better than other anabolic steroids making it a favorite in medical practices due to its lower chance of abuse. Mesterolone is generally well liked nonetheless as it delivers very few side-effects in men. In high doses it can cause some virilization symptoms in women. But because of the high level of deactivation and pre-destination in the system (albumin, SHBG, 3bHSD, aromatase) quite a lot of it, if not all simply never reaches the androgen receptor where it would cause anabolic effects, but also side-effects. So its relatively safe. Doses between 25 and 250 mg per day are used with no adverse effects. 50 mg per day is usually sufficient to be effective in each of the four cases we mentioned up above, so going higher really isn't necessary. Unlike what some suggest or believe, I will post an abstract to refute these next statements at the bottom of the page. Its not advised that Proviron be used when not used in conjunction with another steroid, as it too is quite suppressive of natural testosterone, leading to all sorts of future complications upon discontinuation. Ranging from loss of libido or erectile dysfunction all the way up to infertility. One would not be aware of such dangers because Proviron fulfills most of the functions of normal levels of testosterone.

Stacking and Use:

Mesterolone is an oral alkylated steroid. If used primarily as an anti-aromatase drug, using it throughout a longer cycle (10-12 weeks) of injectables may elevate liver values a little bit, though much, much less than one would expect with a 17-alpha-alkylated steroid. Eventhough
instead of inhibiting gains, mesterolone may actually contribute to gains. So that's a bit of a shame. Its not quite as toxic since its not alkylated in the same fashion, but at the 1 position, which reduces hepatic breakdown, but not like 17-alpha alkylation. The reason for the change of position I assume, is because alkylating at the 17-alpha position has been shown to reduce affinity for sex hormone binding proteins. This would in turn decrease its ability to free testosterone. Nonetheless the delivery rate is quite good. Its taken daily in 50-100 mg doses.

The best thing to stack it with is testosterone of course. Its most easily bound to SHBG and albumin, and deactivated for up to 98%. Since the DHT can compete for these structures with higher affinity it would naturally lead to a higher yield of whatever testosterone product you
stacked it with. Since DHT levels are notably higher now there is also more stimulation of the androgen receptor causing more strength gains, and because of its affinity for aromatase the overall estrogen level decreases as well. This has as a result that gains are leaner, and once
again the overall testosterone yield is increased as less I converted at the aromatase enzyme. It's of course used in other stacks with products such as methandrostenolone , boldenone and nandrolone to reduce estrogenic activity and increase muscle hardness. The addition of
proviron makes boldenone a dead lock for a cutting stack and for some may even make it possible to use nandrolone while cutting, although the use of Winstrol or a receptor antagonist in conjunction is wishful as well. The benefit of adding it to a nandrolone stack is that it may
also help you reduce the decrease in libido suffered from nandrolone, since the latter is mostly deactivated by 5-alpha reductase, an enzyme that makes other hormones more androgenic. Proviron is an anti-aromatase, so obviously anti-estrogens would be futile and redundant.
Blood pressure medication for those prone to hypertension may be wise, as this DHT can increase the blood pressure.

Abstract refuting that Proviron is not highly suppressive

Here is the study I was referring to. Only 85 men out of 250 showed any suppression. Proviron did not shut down the HPTA in any of the subjects and that was at 150mg for 1 year. I would say its pretty safe and has very little effect on one's HPTA.

This study shows no effect on normal LH and FSH with 100-150mg/ d mesterolone, and decrease of FSH/LH that were elevated. Proviron doesn't substitute Clomid as hpta therapy, but doesn't get in the way, either. The effect of mesterolone on sperm count, on serum follicle stimulating hormone, luteinizing hormone, plasma testosterone and outcome in idiopathic oligospermic men.

Varma TR, Patel RH. Department of Obstetrics & Gynaecology, St. George's Hospital Medical School London, U.K.

Two hundred fifty subfertile men with idiopathic oligospermia (count less than 20 million/ml) were treated with mesterolone (100-150 mg/day) for 12 months. Seminal analysis were assayed 3 times and serum follicle stimulating hormone (FSH) luteinizing hormone (LH) and plasma
testosterone were assayed once before treatment and repeated at 3, 6, 9 and 12 months after the initiation of treatment. One hundred ten patients (44%) had normal serum FSH, LH and plasma testosterone, 85 patients (34%) had low serum FSH, LH and low plasma testosterone.
One hundred seventy-five patients (70%) had moderate oligospermia (count 5 to less than 20 million/ml) and 75 patients (30%) had severe oligospermia (count less than 5 million/ml). Seventy-five moderately oligospermic patients showed significant improvement in the sperm
density, total sperm count and motility following mesterolone therapy whereas only 12% showed improvement in the severe oligospermic group. Mesterolone had no depressing effect on low or normal serum FSH and LH levels but had depressing effect on 25% if the levels were elevated. There was no significant adverse effect on testosterone levels or on liver function. One hundred fifteen (46%) pregnancies resulted following the treatment, 9 of 115 (7.8%) aborted and 2 (1.7%) had ectopic pregnancy. Mesterolone was found to be more useful in patients with a sperm count ranging between 5 and 20 million/ml. Those with severe oligospermia (count less than 5 million) do not seem to benefit from this therapy.

PMID: 2892728 [PubMed - indexed for MEDLINE]

One more...

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. "

Proviron is basically a mild DHT derived androgen, it's so mild that it's often ran in PCT to help with libido issues as it will not cause suppresion of the HPTA, it also has some mild anti e properties. Proviron is not gonna make a difference in restoring the HPTA in the way SERMs do. I personally dont use it as an addition to PCT, despite the medical article from Abstract. Its advisable to keep in mind that though this article states that roughly 66% of men in this study didnt show any suppression, 33% did. In my opinion that more than constitutes enough reason to be cautious in using Proviron in PCT. Personally i wouldnt run it at a dose above 50mgs in PCT. Somewhere in the range of 25-50mgs ED is appropriate.

The simple facts amongst all this contradicting information is that Proviron, though not highly suppressive, is indeed somewhat suppressive. At least in a large percentage of cases. This coming from both personal and other peoples experiences. Nonetheless it is still debatable. So im presenting you with this information to make your own decision. IMO, Proviron is a drug that when used for the RIGHT reasons, can be a great addition.

Now heres my recomendations for doses.

"FOR ON CYCLE USE"

Proviron - 50-100mgs ED (I hear people use up to 150mgs ED with no issues, but id error on the side of caution until you are familar with the compound.)

"FOR PCT USE"

Proviron - 25-50mgs ED (Personally wouldnt exceed 50mgs ED in PCT for the reason i discussed in the article.)

Hopfully this will clear a few things up for some people.

Now again, this is just my opinions and my research. I have factual research and tests thanks to those wonderful medical researchers. I have a selective list of works compiled to show where part of my opinions are based, but im lazy and this has taken long enough. But here are some other opinions on PCT, gyno, and other things where you can formulate and compare ideas and opinions.

This is where research begins, and never ends!)
Steroid Profiles
http://www.steroid.com/drugprof.php

C Bino's Gyno Reversal
All you need to know about GYNO.

Swifto's hCG and PCT Advice
http://forums.steroid.com/showthread.php?t=349581

**Phate** · 03-22-2009, 09:28 PM

let's keep this bumped guys, it's a great read

***RAGE*** · 03-22-2009, 09:44 PM

God, I love these threads.....

WarMachine you did an outstanding job!!!!!!!!!!!!!!!!!!!!!!!!!

**WARMachine** · 03-22-2009, 09:47 PM

PCT by WARMachine

Now like promised guys, im (finally) adding to the thread.

Now the following is a list of definitions of Estrogen, Progesterone and Cortisol, as well as the drugs that control them.

SERM's (Selective Estrogen Receptor Modulator) : These block certain estrogen receptors, ***ending on the drug, and dont actually lower estrogen in the blood. Estrogen is left to circulate with nowhere to go. Because of this, SERMS have a positive effect on cholesterol levels. They have a negative effect on IGF-1, so if bulking, only take them if totally necessary. They are good at blocking gyno. Commonly used during PCT, and less often used while cycling. A SERM like nolvadex is widely used in PCT to help kickstart the HPTA back to normal function, in conjunction with other beneficial drugs.

AI's (Aromatase Inhibitors) : There are 2 types of AI's. Type I (suicide inhibitor) attaches to the aromatase enzyme and permanently disables it. Type II compete for the enzyme, but dont destroy it. Both are effective at lowering estrogen substantially. Both are commonly used during both cycling and PCT. Used mainly when low estrogen levels are desired, like contest preparation/cutting. Beware that lowering estrogen with strong AI's can have a negative effect on cholesterol levels and low estrogen levels can lead to sore joints, cause your losing estrogens anti-inflammitory effect. Can also have a negative impact on your libido. Estrogen has an important role in mass building and joint health, as noted below where "estrogen" is explained.

RI's (Reductase Inhibitors) : These drugs stop the conversion of testosterone into DHT wherever 5-alpha reductase enzymes are present. RI's work by blocking the action of the 5-alpha. There are 2 5a's. Type I 5a and Type II 5a. Different RI's block one or both of these 5a's. The main reason someone uses RI's is to stop hairloss. They are common anti hairloss drugs. The problem is, when you block the dht conversion, there are less androgens available and may reduce your gains. Sometimes people report less strength, aggression and drive to train.

Estrogen : The first hormone we need to keep an eye on. Many AAS convert to estrogen via the aromatization process. Some AAS are worse than others. Also, estrogen spikes after a cycle. High levels of estrogen leads to gyno, water retention, fat storage etc. Estrogen plays a key role in progesterone related gyno. We either block its receptors with SERMS or reduce its production with AIs. We watch estrogen levels during a cycle and in PCT. Lowering estrogen too much will mess up your blood lipids. Letting it get out of control will cause sides like gyno, water retention etc. Estrogen plays a role in IGF-1 levels, may lower IGF-1 when blocked with a SERM. Estrogen is also beneficial hormone when bulking, promoting higher androgen receptor concentrations (!). It also is beneficial in another way - its supposed to act as an anti-inflammatory - this means blocking or reducing it too much during a heavy bulking cycle can result in injury to joints. Obviously different estrogen levels are desired for different goals, and it is not always good to block its action or its production. Usually, while bulking, estrogen is allowed to rise unless gyno or water retention (leading to high blood pressure) becomes a problem. When cutting and shedding water and lifting a little lighter (contest prep for example) estrogen is usually dropped with an AI. Proper diet and training can help the bad side effects high estrogen can have.

Progesterone : Its not so much progesterone that we watch, which is actually a healthy hormone, but progestins which may act upon its receptors. Progestins, like Tren or Deca (nor-9's), may act on its receptor or lower progesterone in the blood. Gyno and lactating are more common side effects. Some people use progesterone receptor blockers to combat this, or a prolactin production inhibitor.

Cortisol : The third hormone, the stress hormone. When elevated to long, it will store fat. Eat muscle. Cause lethargy. Moodiness. You may crave carbs by the boat load. Cortisol spikes after a cycle because AAS blocks it while on cycle, upping cortisol production and receptor sites. IMO not enough attention is payed to this. It has special functions in the body that are absolutely necessary, like its anti-inflamitory ability. However, when elevated for long periods, it turns into a muscle eating beast. The most important time to watch cortisol is after a cycle, when it spikes. There are a couple ways to help control this, explained below.

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

Now that you brushed up on some defentions, here are some useful compounds :

SERMS (Selective Estrogen Receptor Modulation)

Nolvadex (Tamoxifen Citrate) : Nolvadex is a SERM. It selectively binds to certain estrogen receptors, effectively blocking the estrogen and stopping unwanted sides such as gyno. It DOES NOT lower estro levels in the blood, it only blocks it from binding to certain receptors. It also helps your blood fat levels. It does not suppress LH, blocks desired estro receptors and helps stop HCG from desensitizing your testicles to natural LH. Nolva should be used during HCG therapy, at 20 mg a day, for the reason i just mentioned. Can be used during cycle if you see signs of gyno. Its mainly used to block the estrogen spike when you come off cycle, and should be used right through to the end until natural test levels are back. One drawback to consider about Nolva is that it may cause progesterone receptors to become more sensitive. This means that while using progestins such as Deca or Tren, you may become more sensetive to progestin related gyno.

Faslodex (Fulvestrant) : Approved for use in 2002 for breast cancer research, this drug is unlike most we have seen. It is classified as an estrogen receptor downregulator. It prevents estrogen from exerting its influence on the estrogen receptor. Similar to Nolvadex, but is not selective. It hits all estrogen receptors. It also does this to progesterone receptors to a lesser degree. It is injectable, at 250mg a month. No information on how it affects blood lipids. It is also very expensive.

Clomid (Clomiphene Citrate) : This drug is also a SERM, almost identicle to Nolva. It is said to be a weaker blocker mg for mg than Nolva. Its common use is in PCT, usually for about a month, used after HCG and all AAS esters have run out of your body. Even though it is weaker than Nolva at blocking, it is believed to be quicker at bringing HPTA back to balance. Both are commonly used during PCT. It binds to different receptors than Nolva. There is a lot of debate on this, but until there is solid proof, it may be prudent to include this in your PCT. Commonly taken at about 100mg a day.

Fareston (Toremifene Citrate) : This is a second generation SERM. Approved for use in 1997. Chemically very similar to Nolva and Clomid, it is less powerful mg for mg. Fareston may have a stronger posotive effect on your cholesterol levels. For those who find this an important issue, this is a drug of choice. Used every day at around 60mg.

Evista (raloxifene) : A newer SERM, Evista is shown to be a blocker in breast tissue, but acts as a receptor agonist in bone tissue (unlike Nolvadex). This action promotes bone density. Taken at about 60mg a day. Evista may prove to be very beneficial, as it also helps cholesterol levels (like Nolvadex). Evista is supposed to have a more powerful gyno blocking effect than Nolvadex.

Cyclofenil : Much like Nolvadex, this is also a SERM. Used at about 600mg a day, it is weaker mg for mg. A good alternative if Nolva is not available, which is usually not the case.

AI (Aromatase Inhibitors)

Teslac (Testolactone) : This is a first generation steroidal aromatase inhibitor. Like a suicide, it permanently attaches to the aromatase enzyme. Taked at a maximum of 250mg a day. It is not as strong as the newer AI's, but some people still like to use it. It can lower estrogen about 50%. Streroidal in structure, it has no anabolic effect.

Aromasin (Exemestane) : This drug is classified as a Type I Suicide AI. It binds to the aromatase enzyme and kills it. It is effective at lowering estrogen up to 85%. Once again, you have to watch out for your cholesterol levels. Used mainly for cutting when low estrogen levels are desired. Aromasin is shown to help bone density. Clinical doses are about 25mg a day, but it has been shown that as little as 2.5mg a day can be as effective.

Lentaron (Formestane) : A Type I Suicide AI. Lentaron is not classified as a drug, and can be sold over the counter as a suppliment. Not as strong as the third generation AIs (arimidex , femera). Can lower estrogen by about 60%. Used as an injectable, it is dosed at about 250mg every 2 weeks. Due to poor bioavailability, daily doses of oral Lentaron are about 250mg.

Arimidex (Anastrozole) : This is a widely used type II AI. It competes with estrogen for the aromatase enzyme. This effectively lowers estrogen up to 80% in the blood. Approved for use in 1995 to fight breast cancer. At doses up to 1mg a day, it has been shown to be very effective at controlling estrogen while on cycle or in PCT. It is usefull for curbing the effects that come with aromatizing AAS's while in cycle, and can be used in PCT. Nolvadex is shown to decrease the effectiveness of Arimidex when used together. In this case a suicide inhibitor may be more well suited, like in PCT. It is also called L-dex, in its liquid form.

Femera (Letrozole ) : Letro is a competative Type II AI also. Also farely new compared to other compounds, it is shown to be effective at lowering estrogen by blocking the aromatase enzyme. Doses up to 2.5mg a day are used, but usually as low as .5mg a day can be just as effective. Clinical studies show Femera to lower estrogen by 75-78%, sometimes up to 95%. Once again, watch out for your blood lipids (cholesterol) to get out of whack. There may a noted rebound effect of estrogen levels that goes along with Letro use.

Cortisol Control

Cytadren (aminoglutethimide) : This drug has the ability to reduce cortisol at higher doses (1000mg a day), and act as an AI at lower doses (250mg a day). The cortisol effect is shortlived if taken for a number of consecutive days. Can lower estrogen a lot, anbout 90%. The higher dose has a long list of sides. More effective as an AI.

Mirtazapine :This is used to lower cortisol. Even though it may be effective in cortisol control, Johan has pointed out that it may cause some phycological side effects, like making you feel like a zombie. Here is a pubmed abstract for is effects on cortisol levels, among other things.http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract

Cytodyne (Phosphatidylserine) : This is also used to lower cortisol, but is only effective in lowering about 30%. There are other ingredients in Cytodyne than Phosphatidylserine. Phosphatidylserine is the only real proven ingredient to lower cortisol, or so ive gathered so far. Effective at 800mg a day of PS as an ingredient.

Relacore : This over the counter cocktail of herbs and vitamins and minerals is supposed to reduce the amount of cortisol in your blood. I find it chills me out a little, however i read some places that it may raise estrogen. I used it for a bit, however I dont bother any more.

Vitamin C: At doses of about 1.5 grams a day, can have a lowering effect on elevated cortisol, not to mention its other healthy effects.

LH Repalacement Therapy - Testosterone Stimulating Drugs

HCG (Human Chorionic Gonadotropin ) : HCG is a replacement for your natural LH (luteinizing hormone). LH is what your body produces to tell your testicles to produce natural testosterone. LH levels drop when using AAS (HPTA suppression). Using HCG while on cycle prevents testicular shrinkage, speeding PCT when the time comes. Using Nolva while using HCG helps stop HCG from de-sensitizing your testicles to natural LH. In my opinion, any decent cycle/PCT should include HCG. It has been suggested to me that HCG can be used throughout a cycle at 500iu E4D, but im unsure of this from practical experience. The most favorable way is to use it in the last couple weeks of your cycle at a higher dose, like 500iu ED. The trick is to end the use of HCG just as the last AAS is running out of your system. So, 3 weeks before the the last ester leaves your blood, you would start the HCG/nolva combo. HCG at about 500iu ED and Nolva 20mg ED. This is done before Nolva/aromasin (for example) PCT starts, and runs about a few weeks longer than the end of the HCG. Always include Nolva with your HCG, they work together well. Be careful not to overdose on HCG and permanently desenstize your testicles to LH. HCG has an active life of about 3 days. Vitamin E is a booster, read the next one :

Vitamin E : As Anthony Roberts pointed out to me, vitamin E increases the response to HCG. This may be useful in making the low doses of HCG we use more effective at growing back shrunken testicles. Doses can be generally 1000iu a day while using HCG.

Progesterone Control

Lilopristone, Onapristone: These are progesterone blockers also, said to be safer and possibly more effective than RU-486 when it comes to progesterone blocking. They were developed after RU-486 in an attempt to make more effective, less harsh drugs to block progesterone.

Dostinex (Cabergoline), Bromo (Bromocriptine), B-6 : These are used for Deca/Tren gyno sides. This type of gyno is related to progesterone and its receptors. Tren/Deca may act on the progesterone receptor, as they are progestins, and may increase prolactin in the blood (causing lactating). These drugs stop production of prolactin at the pituitary gland. Controlling estrogen levels with an AI also helps here, as progestins themsleves haven't been proven to cause gyno.

RU-486 (Mifepristone - abortion pill) : This drug has the ability to block estrogen, progesterone AND cortisol. It may or may not be very well tolerated, but I would like to find out more about it, as it is used in the bodybuilding world. In PCT it is used to block cortisol and progesterone. A powerful drug that may turn out to be a good choice, but i need more evidence and feedback from experience useing RU-486. Check out this thread i have going if you would like to learn more about it :
RU-486 - Mifepristone (abortion pill)

RI's (5a Reductase Inhibitors)

Proscar (Finasteride) : This is primarily a Type II 5-alpha blocker. This means that when you are taking a high dose of testosterone, the resulting conversion of test to DHT in certain parts of the body become to high for ones own comfort, mainly hairloss and prostate enlargement. This is where the type II 5a enzymes are mainly found. This will not work against AAS that are already highly androgenic by design, without conversion. AAS like Tren will still exhibit high androgenic properties. Used at doses up to 5mg a day.

Avodart (Dutasteride) : Like Proscar but newer and more effective at blocking the effects of DHT in not only the scalp and prostate (which are Proscar's main strengths) but also in the skin, effectively reducing acne. This is because Avodart will block both Type I and Type II 5-alpha enzymes, covering more of the problem areas due to DHT. Available in .5mg softgels, this is an effective dose. Approved for use in 2002.

Fat Burning, Anti-Catabolic

Clen (Clenbuterol ) : Clenbuterol is a bronchodilator. Everyone knows clen is used to burn fat. Why am I listing it here in a PCT thread? Well, for its anti-catabolic properties. Clen may lower the effect of AAS while on cycle, so I personally dont use it while cycling. It does, however, have an effect on cortisol levels. While on cycle, cortisol is not to much of a problem if you eat right. AAS use increases cortisol production, and increases receptor sites. This means that when you finish a cycle, cortisol spikes along with estrogen. This is a part of the "crash" that is often overlooked. People have reported that blocking cortisol in PCT speeds along fat loss. Clen is supposed to have a blocking effect on cortisol. So, along side of its ability to burn fat, it is anti catabolic in it ability to block cortisol until desired hormone levels are achieved in PCT. For me, it makes sense to use clen in PCT until desired hormone levels are achieved, as it also burns away fat in the process.

SUMMARY and RECOMMENDATIONS

All AAS can supress the HPTA, even in small doses, thus lowering natural LH. Factors that affect ones ability to recover quickly are genetics, cycle length or steroid type. Some AAS will shut you down hard and fast, some not so bad. Some lucky people can rebound quickly without medications, but many need it to avoid a crash and losing muscle/gaining fat. It is in our best interest to use the appropriate medications in the CORRECT doses to keep sides down (like bloat), grow quickly and keep quality mass when we are done our cycles. Most of us can get away with using 2 or 3 compounds to keep sides to a minimum, rebound quickly, and keep gains we worked hard for. Higher levels of AAS (and therefore higher estrogen/progestins) may require more intense hormone control and heavier PCT. Remember, we are aiming to level out estrogen, progesterone, cortisol and testosterone. In PCT, we are trying to achieve equilibrium of the HPTA, getting FSH (follicle stimulating hormone) and LH (luteinizing hormone) back to normal. Keeping our hard earned gains is obviously our first priority.

In short, we generally use :

AI's - While on cycle to "dry up" or lower estrogen because of a persons sensetivity to it (if needed). Used in PCT for the same reason and to help get back to homeostasis. Usually used with a SERM in PCT.

SERM's - to block estrogen while on cycle (if needed) or to help kickstart the HPTA during PCT (most common use). Usually used with an AI in PCT.

HCG - To prevent testicular shrinkage during a cycle, or to encourage them to grow back more quickly. Usually used with an AI and SERM in PCT as the last AAS run out of your body, and stopped a few weeks before your SERM and AI.

As im sure some of you have realized, this is Drummerboys thread. The reason i added this is because it does get the information across to the newbies.

Now after reading this, youre probably thinking, "What does the best PCT consist of?". Well that is matter if opinion. For the most part, the census is the following.

Tamoxifen
Clomid
Tormifene

Now newbies are starting to ask, "Arent Nolva and Clomid both SERMS? Why do i need both?". Well im glad you guys asked that.

There has been far more research on Clomid for male hypogonadism and infertility, than Tamoxifen.

Now Tamoxifen increases the Leutenizing Hormone, but I prefer Clomid at a low dose, than Tamoxifen. I blame Anthony Roberts for this preference of Tamox over Clomid. He (supposedly) got horrible sides from Clomid, hence is biased view towards Tamox over Clomid in PCT. Clomid doesnt exert the majority of its emotional, vision and skin issues on doses of 50-100mg/ED. Problems seem to be encountered when users exceed 150mg/ED. (I know Swifto is bound to get on me here, but nonetheless i refute the agurement that Tamox doesnt increase the LH. Im not sold on this theory, and until i see several supporting articles, im inclined to believe what ive been reading for years. Not saying it isnt true, just saying im yet to be convinced. )

Despite the ''PCT by Steroid.com" A.K.A Pinnacle's PCT, where he states the following.

Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (35)It can also block a bit of estrogen in the pituitary, which is a great benefit when used with HCG (more on that later) (36)(37). The increase in testosterone Nolvadex can give someone with a dysfunctional is basically that 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Why don’t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH
(Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I’m suggesting…and in fact, avoided in general…it’s simply not as good as Nolvadex.

Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid…and no, using it along with Nolvadex will provide no “synergy” that I’ve ever seen in any relevant study."

Addvocating not using Clomid at all is just plain wrong IMO. can do things that Nolvadex cannot.

Case in point is the following. Taken from Pheeno's PCT Sticky.

[I]"Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur. With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary...

Follow thus far?

Here is yet another case and point.

In just 7 days of Clomid use at 100mgs ED is enough to raise LH and FSH by as much as 50%. You will need nolva also, as the point of these serms is to block estrogen receptors in the HPTA to fool it, and to tell the pituitary to start producing it's own LH and FSH. (Will find the supporting study asap.)

Now real quickly onto AI's in PCT.(NOTE: We already covered Proviron.)

Now ive also been from the school of thought that suggests the use of an AI during PCT for some time now. Like many reading this, i was unsure as to why, but just did as i was told. Well after researching the use of AI's a little, ive uncovered the following. I now see that the point in using AI's during PCT is skewed. It is not worth it because youre lowering estrogen levels to subphysiological levels (unhealthy levels too) which in turn can cause a nasty rebound when all Anti-E's are stopped. SWALE advocates NEVER to use them post cycle for a host of reasons.

(Here is the exception. Its advisable to use an AI if you did not use one while on cycle to control estrogen. From Swifto- *AI's are not always needed, especially if one has been used to control estrogen (aromatse activity) during the cycle. There is a high risk of lowering estrogen too low and that can bring its own side effects; Lowered labido, aching joints, poor cholesterol and can negatively effect the immune system. We need some estrogen, not alot, not zero, but one cannot afford a too low an estrogen level at this time of PCT.* I will go into AI's and why not to use them below. In short, Femara is too strong & Adex will likely lead to strong rebound effect when it is stopped. So that leads me to believe suggestion of using Aromasin (25 mgs ED) during PCT is a good one in particular cases, since it does not block all estrogen (a bad thing) nor does it cause a rebound effect. But i will go into detail below.)

First off, Anastrozole (L-dex, A-dex) doesn't stimulate the HPTA. Thats enough reason right there to void its use in PCT. Now the other main point, is that Tamoxifien reducess the effectiveness of Adex. Clinical endo studies generally show a 28-30% reduction in the efficancy when using both.
(Feel free to do some research and not take my word for it.)
http://content.nejm.org/
http://www.bmj.com/

Now onto Femera (Letrozole). If you read my first section, youll know my distaste for Letro already. First off. Letro and your sex drive; Letrozole can and likely will suppress your sex drive. Making it not such a great drug when on PCT for Mr. Happy reasons. The Estrogen Rebound Effect will be the biggest reason why you shouldnt use it in PCT. We've all heard of it. Its quite severe when coming off a dose of Letro. When using Letro, youre lowering estrogen to a point that is below normal. Recovery from a suppressed state can take much longer and Test levels can drop drastically when use is discontinued. The inverse is true also. Estrogen levels will go above normal then slowly fall back to normal after discontinued use.

Here's one helpful thing from C Bino's gyno thread.

With your estrogen being completely inhibited there is a definite estrogen rebound as your body tries to re-stabilize the testosterone:estrogen balance. We can prevent this rebound effect by supplementing further with another AI or SERM. So, I suggest that when you are coming to the end of your cycle you will more than likely be using Nolva in your PCT so just make sure that you begin taking nolva the last day you are going to take your letro and then continue on as you would with regular PCT.

Now, about Letro stimulating the HPTA. Heres a post i found on a board months back that'll save me some time in writing.

The IGF-1 levels that are raised with Letro are really of no signifigance because they don't seem to have an effect on localized IGF-1 (most important for growth). So to me, its a waste and won't help in raising testosterone any faster. Its the response of the testes to LH pulses which will signal natural production to occur, and Letro will not have an positrive effect on this. In this area more is not better as the body will only repsond so fast. Stacking Anti-e's won't have much of an effect. I thought it would a year ago until I tried it, then read SWALES recommendations. TO me, recovery wasn't any faster. I have better recovery with blunting cortisol with the addition of Nolva than anything out there (didn't need HCG though).

Now with AI's in PCT covered, lets move onto the topic of a "Standard PCT". Personally think that the whole 'standard' 4 week PCT needs to be trashed. The idea that 3-4 weeks is the standard of PCT retarts your natural test production, as many people who get bloodwork done on a regular basis can attest to, is not accurate. It can take months after PCT (or even years before full HPTA function is restored) and only in part in some cases. The idea of time on + PCT = time off is a sound one, but in truth, even that amount of time off is insufficient in many cases to restore full HPTA function. With that said, its important to remember to get blood tests done before you begin the cycle, during the cycle, and after PCT.

That being said, im here to deliever.

(These are all, mgs, per day, per week.)

PCT

*Tamox - 40/40/20/20 --(Until Blood Results have confirmed the HPTA has indeed began to recover.)
*Clomid - 100/100/50/50 --(Above)
*Tormifene - 60/40/40/40 -- (Above)
**Aromasin - 20/20/20/20 --(Above)

*Use 2 SERMs, not all 3. I prefer Tamox and Clomid, but only because im yet to use Tormifene. From what i hear, Tormifene has recently been reported to be the best SERM at restarting an inhibited HPTA.(I will talk more about it later, just waiting on some info from Swifto.)

**See Italics above

Hopefully this helps Newbies and Vets alike with question they may have.

Special thanks to Swifto, Mammon, LATS60,Peachfuzz, SWALE, Phate, Pinnicle, Drummerboy, and C Bino. Thanks fellas!

Basically what it comes down to is, do your own research, think for yourself, ask questions, and most importantly,

DO WHAT WORKS BEST FOR YOU!