# STEROIDS FORUM > SARMs (Selective Androgen Receptor Modulators) Information Forum >  Letro while on cycle? HELP PLEASE

## growthgift

Im currently using Test Prop and Masteron , im not gyno prone but recently felt a small lump behind my left nipple after using tren acetate, i used nolvadex and arimadex it made the lump smaller but its still there and my nipples are still puffy a little. I have letrozole i wana use it while im on my cycle of

Test Prop 100 mg EOD
Masteron 100 mg EOD 

and when i get my hands on winny il introduce it 50mg ED

My main question is will letrozole make me loose muscle i do want the puffy tender nips to go away but at the same time i dont wana loose muscle and gains it would just be a waste of the cycle.

Can anyone help me with this asap THANKS  :Smilie: .

----------


## RowRow

why on earth did you use nolva with a 19-nor? nolva uprgulates the prolactin site and can increase the risk of gyno when using tren or deca !!!!
don't see the need for winny with mast but thats me, they are both dht derivatives nast does as good a job and unless yout stepping on stage soon no need for that additional dryness :/ 
you won't lose muscle due to letro you may however lose strength, have achey joints and libido issues due to letros strength, it will destroy your estrogen. 
But to resolve your issue;
start letro at .25mg then the day after increase to;
.5mg follow the outlined pattern
1.0mg
1.5mg
2.0mg
2.5mg
At this point maintain 2.5mg of letro to reduce the size and symptoms of this gyno and eventually ramp back down in the same manner. Additionally take 25mg aromasin every 12 hours until you have completely stopped letro usage then gadually reduce aromasin down to usually 12.5mg ed.

just trust me on the two compounds, you want to stop estrogen gyno thats your best bet, unless its progestrone but thats another kettle of fish

----------


## Sgt. Hartman

That's terrible advise. Tamox works wonders for gyno whether using a 19-nor or not. Where exactly is the "prolactin site"?

There is no point in tapering up the letro dosage unless you're just testing your bodies' tolerance to it. 

Progesterone gyno? Care to explain how a male can grow new breast tissue without an excess of estrogen? The answer is it can't.

----------


## RowRow

Are you for real? Nolva Does work well for estro gyno but not prolactin gyno. Nolva and a 19 nor can increase prolactin issues. And site was just a throw away term.

The point of the taper at the end is to prevent estro rebound. which is also why the aromasin is extended beyond the letro. So its not pointless at all really is it?

And in a situation where we have gyno I'm going to hazard a guess there may be excessive estrogen around. Hence why estorgen blockers and aromatase inhibitors are you used gee whizz who'd have thunk it!?

----------


## Sgt. Hartman

I said there's no point in tapering* UP* the letro, not down. Obviously there will be an estro rebound that will need to be addressed with another AI or tamox.

Read please:


More from Nandi....

PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA 


Before delving into this subject, I’d like to say first and foremost, that in users of anabolic /androgenic steroids (AAS) the first step in combating the development of gynecomastia , or male breast enlargement, is to eliminate the causative agent: the anabolic steroid . Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use . 

In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia , in lieu of more traditional drugs like tamoxifen .

In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF -1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno , and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno . But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:


The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

GH and IGF -1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:




Since elevated GH and IGF -1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF .

Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF -1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia . So perhaps a viable strategy would be to combine DHT gel with tamoxifen . I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.




Summary:

Estrogen regulates prolactin. 

AI's will regulate prolactin by controlling estrogen. Please show me 1 study of healthy males (not females with breast cancer) that shows that tamox has a negative correlation on PrL or PrG. You can't.

Edit: credit to D7M for originally posting this article.

----------


## RowRow

Okay I taper as that's how I was taught. 

I'm sorry for sounding like a douche, on the prolactin side it's from what i've learnt first time seeing that article. 

Can I just clarify though (being genuine here) nolva reduces igf-1 and blocks the estrogen receptors correct? So using nolva would not only prevent estrogen binding and so prevent issues with Prl and Prg, but also reduce IGF-1 and so prevent gyno from that standpoint too? 

But then according to that article as tren does not aromatise and is a strong androgen, that means that prolactin issues cannot arise from the tren itself but rather it is the presence of test that causes them and that the fact tren is present is irrelevant on the interactions between gyno and Nolva? 

I apologise again if I came across like a twat, just repeating what I have learnt elsewhere.

----------


## RowRow

Sorry I can't edit as I'm on my phone. But does that then also imply that usage of a DHT compound may make the need for an AI obsolete?

----------


## Sgt. Hartman

....

----------


## Sgt. Hartman

No, DHT doesn't make an AI obsolete as they are not nearly as effective as an AI. 

I thought/believed the same thing as you until I read articles on this site and did my own research, which confirms what i posted above. 

The whole point of the article is that estrogen regulates PgR and PrL and that controlling E is the primary mechanism of controlling prolactin related sides. 

There are studies that show that tamox does upregulate PrL but they are ALL regarding female breast cancer patients. That is where the no tamox with 19-nor myth comes from. 

When gyno occurs with a 19-nor it is either because not enough test is being run with it so E is high, thereby increasing PrL, or test is being run with it and aromatizing so it elevates E, allowing excess E to upregulate PrL. Either way, I'm not advocating running a 19-nor without a dopamine agonist on hand.

Just saying that the primary way to control PrL and PgR is by controlling estrogen, which is different for all of us.

----------


## Sgt. Hartman

....

----------


## RowRow

Okie dokie I'm with you now. Thanks Sgt!

----------


## D123

> Okie dokie I'm with you now. Thanks Sgt!


Thank you both, I have been historically a Test Prop guy, just branching out a bit and I do plan on running the 19-nor's with Test of course in the near future, just researching. Very educational.

Cheers

----------


## Donjuice

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
http://forums.steroid.com/showthread.php?t=236880

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

----------


## Blergs

> Im currently using Test Prop and Masteron , im not gyno prone but recently felt a small lump behind my left nipple after using tren acetate, i used nolvadex and arimadex it made the lump smaller but its still there and my nipples are still puffy a little. I have letrozole i wana use it while im on my cycle of
> 
> Test Prop 100 mg EOD
> Masteron 100 mg EOD 
> 
> and when i get my hands on winny il introduce it 50mg ED
> 
> My main question is will letrozole make me loose muscle i do want the puffy tender nips to go away but at the same time i dont wana loose muscle and gains it would just be a waste of the cycle.
> 
> Can anyone help me with this asap THANKS .


only thing your gonna lose is water lbs, so dont worry, 
i rec letro at 0.6-1.2mg e3d

----------


## Blergs

> Im currently using Test Prop and Masteron , im not gyno prone but recently felt a small lump behind my left nipple after using tren acetate, i used nolvadex and arimadex it made the lump smaller but its still there and my nipples are still puffy a little. I have letrozole i wana use it while im on my cycle of
> 
> Test Prop 100 mg EOD
> Masteron 100 mg EOD 
> 
> and when i get my hands on winny il introduce it 50mg ED
> 
> My main question is will letrozole make me loose muscle i do want the puffy tender nips to go away but at the same time i dont wana loose muscle and gains it would just be a waste of the cycle.
> 
> Can anyone help me with this asap THANKS .


only thing your gonna lose is water lbs, so dont worry, (unless abusing an AI)
i rec letro at 0.6-1.2mg e3d

----------

