Using Drugs to treat Gyno

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  1. Quote Originally Posted by jbryand101b View Post
    that's pretty bad ass. I want to see chuck Norris do that.
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  2. How to turn a beer can into a camping stove;

  3. motivational music


    And some more motivation to fire this bitch up full blast

  4. Full-Service PCT

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    Quote Originally Posted by Austinite
    There are 2 major components involved in recovery. Testosterone production and Spermatogenesis.

    LH and FSH are both required for the equation. LH is produced by the pituitary and stimulates the Leydig cells to produce testosterone. Once testosterone is in production it works alongside FSH and stimulates sertoli cells to produce sperm. Sperm production is hindered if either of these are unhealthy. They both work in synergy. You need BOTH to be at healthy levels.

    clomid has multiple effects. It's an anti-estrogen, so it obviously decreases the estrogenic effects in your body by stimulating the Hypothalamus back to life and sending gonadotropin releasing hormone (GnRH) to your pituitary, so that LH/FSH can be secreted.

    Nolva boosts the effects of clomid because it put clomid into "competition" mode where they both fight for a receptors to bind to. This competitiveness will only occur with the presence of BOTH nolva/clomid, and will inevitably resolve the issue of excess estrogen in the Hypothalamus. This will trigger both LH and FSH to crank UP, as the high estrogen in this cluster is suppressive. This entire scenario is not as effective with only one drug.

    Furthermore varying the compounds; Since we know both stimulate LH, what most don't know is that the act is different. clomid boosts the amplitude of LH serum, but has no effect on the frequency. Nolvadex is the complete opposite in that area, where it boosts the actual frequency of LH and has no effect on its amplitude.

    You're probably assuming they're identical and overpowering... clomid is a mixed agonist/antagonist for the estradiol receptor. Nolva is also mixed, however.... it is a pure antagonist in the E receptor in breast tissue. There is a reason that clomid is not recommended for gynecomastia reversal, but Nolva is.

    Can you recover with just Nolvadex, or just clomid? Well, anything is possible. But why would you take that risk if the combination gives you a much better chance? To save a few bucks and risk your health? clomid when coupled with Nolvadex is clearly the safer choice over using either compound individually.
    HCG Myth Debunked

    Quote Originally Posted by Austinite
    There are 2 ways that could potentially desensitize Leydig Cells:

    1. Prolonged LH deprivation: When you inject steroids, your LH production is halted at the pituitary, remember? So if you continue in a suppressed state for weeks upon weeks, your Leydig Cells could potentially become unresponsive, or desensitized. It is possible to reverse desensitization of the cells, but that has been proven to be quite a difficult task. So when you use hCG on cycle, the mimicked LH analog will maintain stimulation of Leydig cells so that you don't run the risk of rendering them useless. This level of maintenance will ensure a much healthier and speedy recovery and one of the most important reasons to use hCG on cycle.

    2. Over stimulation/supplying of Leydig cells: There is no reason to use more than 500 IU of hCG at one time. And certainly not a good idea to run even that dose on a daily basis. You do not have an unlimited-ever-flowing-supply of Leydig cells. There is only so much stimulation hCG can do. What happens when you dose hCG really high, is that you're increasing intra-testicular estrogen. So you're thinking that you could use an aromatase inhibitor in that case, right? Nope. AI's are not effective treatment for intra-testicular e2. Furthermore; high doses is a surefire way to desensitize Leydig Cells. So we have a double whammy here. And this is just another reason to use hCG on cycle, and not "blast" hCG post cycle leading up to and/or during PCT.

    For the sake of preventing another debate, Rich Piana is clueless.
    Quote Originally Posted by biggiesmallz
    Now, I understand the proper usage of HCG on-cycle... generally advised at 250iu bi-weekly, sometimes at 500iu bi-weekly, but from the source I came across they referenced a study that basically said there's marginal benefit from HCG when pinning 250 vs 500 bi-weekly, so with that understanding I don't see the need to pin more than 250. That said, is there some limited duration to which HCG should be used on-cycle?

    I also heard conflicting information on long-term HCG use can possibly desensitize lydig cells to natural LH response. Any truth to that?
    There's only so many cells to stimulate, and the doses of 1500 weekly max, spread over 3 or more doses is sufficient enough. If long term therapy was dangerous at those doses, it would mean that our very own production would desensitize cells, doesnt make sense, does it? 250 IU is not necessarily the magic number. Your goal should be to use the least amount of hCG that works for you. Recently, discussing my concerns with the lead urologist in (some magical place out there somewhere), we came to conclude that for me, as a TRT patient, my usual dose of 250 twice weekly is excessive. So we are planning on reducing the dose to 100 IU, 3 times weekly. Note that this urologist is not my doctor, but a friend and partner in a clinical trial.

    Blasting hCG is unhealthy, and the increase in intratesticular E2, which cannot be managed with the commonly readily available aromatase inhibitors, is damaging.
    Also, HCG is generally started 4th week into a cycle, and ran till about 3 days prior to PCT. HCG is suppressive to natural LH production, since it mimics LH, so PCT and natural recovery doesn't start untill you're off HCG.



    Also useful tid-bit of info regarding sexual fluids;
    in reference to male/female sexuality, look into this:

    OM-CHI Herbs - EPISANDRA Enhanced Stamina and Sexual Drive
    Episandra compound is a proprietary blend of Chinese herbal extracts shown to have strong aphrodisiac properties and to improve general health. The herbs in this compound have all been used for centuries for these purposes in China, with excellent results.

    This product can be used by both men and women with no undesirable side effects and is safe for all people.

    Active Ingredients:
    Epimedium sagittatum: "Epimedii is a very powerful yang (male) tonic herb. It’s power ranks almost with the animal yang tonics…It’s name can be translated as "the herb for the man who likes sex too much, like a goat" or "passionate goat weed"…This is what Epimedii is famous for. Women, too, take this herb to increase their sexual drive…

    Schisandra is said to increase circulation in and sensitivity of the female genitals. Many women claim increased genital warmth and sensation after using Schisandra for a period of time "…for both men and women, Schisandra is considered to have aphrodisiac qualtities…it tends to contain sexual fluids until the appropriate time for their release. Thus, consuming Schisandra for a period of time, one tends to build up sexual fluids."
    Attached Images Attached Images  

  5. Careful biggiesmalls. No sourcing.

  6. I am careful brother, I'm so full of care that I wanted to share quality products from a very respectable company to add to the list, variety is the spice of life... meant no harm, just spreading resources; happy cycling for everyone

    They're also not a stranger to this board, and I see plenty of ads for all kinds of RCs

  7. Quote Originally Posted by biggiesmallz View Post
    I am careful brother, I'm so full of care that I wanted to share quality products from a very respectable company to add to the list, variety is the spice of life... meant no harm, just spreading resources; happy cycling for everyone

    They're also not a stranger to this board, and I see plenty of ads for all kinds of RCs
    Sponsored rc companies=okay. Non sponsored = nokay
    Representative of Chaos and Pain, LLC Like us on facebook!

  8. Quote Originally Posted by pyrobatt View Post
    Sponsored rc companies=okay. Non sponsored = nokay
    gotcha, thanks for the heads up

  9. Don't believe that nonsense

  10. Quote Originally Posted by pyrobatt View Post

    Sponsored rc companies=okay. Non sponsored = nokay
    They aren't technically sponsors. And that's not actually true.
    Serious Nutrition Solutions Representative

  11. Quote Originally Posted by biggiesmallz View Post
    I'm still running the same cycle I was running that caused the lump, and since I treated it a month ago, I haven't had the need to use an AI, nor had I had to buy more letro, nor had any more lumps grown from it. Truth be told tho I did lower the dosage (test/EQ) a little for the treatment, and haven't picked it back up since then.

    Soo make of that what you will, but I'm having no issues whatsoever
    still no lump by the way

  12. wut we waitin 4, guize? Name:  isee.png
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  13. ralox I would rec for the gyno IMO
    LG Sciences Board Rep
    These statements have not been evaluated by the FDA, do not constitute medical advice, and are not official or authorized comments by LG Sciences, LLC.

  14. good info as far as legal angle is concerned

  15. Steroid Control Ban has officially been overturned in hear;

  16. Quote Originally Posted by biggiesmallz View Post

    Attachment 91755
    by Mike Arnold
    Out of all the side effects a steroid user could potentially experience, gynecomastia (aka bitch tits) is one of the worst…and it certainly tops the list when it comes to cosmetic side effects. Being heavily associated with womanhood, the very nature of this side effect is an affront to our masculinity. Not only is it embarrassing, but in some cases it can destroy the entire appearance of one’s physique. We have all seen pictures of the more extreme cases, where the BB’r literally looks like he has grown a small pair of tits on an otherwise normal body. The severity of this condition can range from only slight swelling, which is often imperceptible from a visual standpoint, to the more extreme cases, as mentioned above Fortunately, gynecomastia does not develop over night and its progression is easily halted and reversed if the proper steps are taken in a timely fashion. There really isn’t any good excuse for a steroid user to experience permanent, visible breast tissue growth. Those that do either don’t care or rather (and much more likely), they weren’t prepared and/or educated to deal with this side effect ahead of time. While there are numerous potential causes of this condition, the BB’r generally only has to worry about a few of them and the available treatment options are simple in their application. Through minimal self-education and a small financial investment we have all the tools we need to keep this side effect at bay.

    Why are my nipples sore?
    The most important factor in the prevention of gyno is knowing how it occurs in the first place. Since this article is targeted mainly towards the steroid-using BB’r, we will only address the causes which are directly attributable to PED usage. There are 4 types of steroids which can cause gynecomastia, the most prominent of which are the aromatizable steroids. Aromatizable steroids are those AAS which are capable of converting to estrogen. This includes many steroids, such as testosterone, methyltestosterone, methandrostanolone (Dianabol), and to a lesser degree, nandrolone (Deca/NPP), and boldenone (EQ). This conversion process is initiated when aromatizable AAS interact with aromatase, which is an enzyme necessary for the biosynthesis of estrogen. See below for a depiction of this interaction:
    Attachment 91756
    When low dosages of these steroids are administered, the degree of conversion is not sufficient to cause this side effect. However, this threshold is regularly crossed by BB’rs who utilize dosages well in excess of those required to avoid estrogenic side effects. The problem with being able to pin-point the dose at which this side effect occurs is that not all individuals are affected equally by the same dose. Some can get away with using fairly large dosages of highly aromatizing drugs, such as testosterone, while others seem to develop problems even with minimal use. I know a powerlifter who was able to use a full gram of pharmaceutical-grade testosterone per week without experiencing any gyno symptoms, while other people have encountered early signs of gynecomastia at only 250 mg weekly. For this reason, assumptions should not be made beforehand regarding personal tolerance. When it comes to learning your limit, real-world experience must be your teacher. However, if I had to guess, I would say that most individuals will begin to experience the early stages of gyno by the time they reach 400-500 mg per week when using testosterone, assuming preventative action is not taken.
    The 2nd type of steroid which can potentially cause gyno are those which appear to exhibit inherent estrogenic activity, despite lacking the ability to aromatize. One example would be oxymetholone (Anadrol). This steroid is not capable of converting to estrogen to any degree, yet it causes gyno in a moderate percentage of users. The most plausible explanation for this side effect is that the Anadrol molecule itself demonstrates estrogenic activity, likely by attaching directly to the estrogen receptor. While we cannot yet conclusively state this to be fact, it seems more probable than the other theories which have been put forward over the years.
    The 3rd type of AAS associated with the development of gynecomastia are the progestin-based steroids, which promote their effects through direct stimulation of the progesterone receptor. Two examples which fit this description would be trenbolone and nandrolone. However, these drugs differ from the previously mentioned AAS in that they rarely cause gyno on their own. Typically, they require the presence of estrogen (usually at above normal levels) in order to have an impact on the growth of breast tissue. In essence, their progestagenic effects tend to exacerbate the effect of estrogen, thereby acting more as a contributor rather than the primary offender.
    The last category of AAS with a history of exhibiting this side effect are those which result in estrogen-rebound. Anticipating the effects of these drugs can be difficult, as they are much less predictable in their behavior. Not only does personal response vary tremendously between individuals, but there is often a lack of consistency even among the same individual. For example, a particular steroid may be employed multiple times without incident, only to cause troubling gyno symptoms under nearly identical circumstances at a later date.
    We’ve looked at particular types of AAS and how they work to cause gyno, but there are other causes which should not be overlooked, one of which is an out of balance androgen to estrogen ratio. DHT itself, as well as many DHT derivatives, possess natural anti-estrogenic activity. Therefore, even in the face of stable estrogen levels, a reduction in these hormones may lead to the appearance of estrogenic side effects. In turn, an increase in DHT or its related metabolites will enable an individual to more effectively deal with increased levels of estrogen. This is why a steroid user is much more likely to encounter estrogenic side effects using testosterone alone, compared to a combination of testosterone and drostanolone (Masteron), which was developed specifically for the management of female breast cancer (i.e. Advancement of breast cancer is heavily dependent on the availability of estrogen).
    The last cause of gyno in the steroid user is prolactinemia, which is an elevation of prolactin levels outside of the normally recognized limits. The most common cause of prolactinemia in the general population is prolactinoma (tumor of the pituitary gland), although this condition can be caused by administering prolactin elevating steroids, such as trenbolone and nandrolone. However, just like progesterone, prolactin rarely causes gyno by itself. This is not because prolactin is not able to accomplish this. Rather, AAS generally aren’t able to elicit elevations in prolactin adequate for causation. Most of the time, prolactin acts to exacerbate the effects of estrogen (similar to progesterone), making it a contributing factor and not the primary cause in the large majority of cases. Still, there have been instances in which these steroids were able to cause gyno and/or lactation independent of aromatizable AAS. I want to emphasize the fact that lactation rarely occurs in steroid users, but when it does, it is almost always attributable to excessive dosing with the offending steroids, in combination with poor personal response.

    The Cure
    Once you’ve indentified the root of the problem, deciding on the best course of action is relatively simple. With that said, let’s get right to the nuts-n-bolts of how to get rid of gyno. When excess estrogen levels are the culprit (aromatizable AAS), there are multiple treatment methods available to us. Ideally, you want to stop the problem before it even begins. Therefore, when planning your cycle, if you know you will be using a dose of aromatizable drugs likely to raise estrogen into a problematic range, the concomitant administration of an A.I. (anti-aromatase) from the outset of your cycle is the best bet. By making an A.I. an integral component of your program right from the start, you will never find yourself in an emergency situation.
    While A.I’s can be used in either the prevention or reversal of gyno symptoms, they are best employed as a preventative measure…and with good reason. You see, the job of an A.I. is to prevent testosterone from aromatizing into estrogen, which it does very well, but the problem is that it does absolutely nothing to prevent currently circulating estrogen from continuing to cause problems. As long as A.I’s are utilized as a preventative measure and not for the treatment of an emergency situation, they are preferable to other gyno remedies, but that is not all. The primary mechanism by which A.I’s inhibit gyno formation (management of systematic estrogen) also provides numerous other benefits not found elsewhere, such as: reduced water retention, lowered blood pressure, decreased fat storage, and others. Lastly, A.I.’ do not reduce IGF-1 levels, as will tamoxifen (Nolvadex).
    Should you find yourself in a situation where gyno symptoms manifest unexpectedly, you should turn to tamoxifen (Nolvadex) for assistance. Why? The body is programmed to convert a percentage of our naturally produced testosterone into estrogen. This is a necessary and healthy process, as estrogen is required for a variety of male physiological functions. However, as the dose of androgens continues to rise, the body continues to convert roughly the same amount of androgens into estrogen. This becomes a problem once we begin administering supraphysiological quantities of these drugs. The much greater amounts of estrogen now floating through the bloodstream are free to attach to any estrogen receptor sites they come in contact with, including those in breast tissue. The end result is gyno formation…also known as “growing boobs”. This is great in teenage girls, but not in grown men.
    The only way to put an immediate stop to this is by deactivating estrogen in breast tissue. Tamoxifen does just that. Due to its greater binding affinity, Tamoxifen is able to dislocate estrogen from the receptor site and take its place, leaving the estrogen with nowhere to attach. The main downside of Tamoxifen relative to the A.I.’s, aside from its IGF-1 lowering effect, is that it is powerless to reduce systematic estrogen levels. Because whole-body estrogen levels remain elevated, the user is subject to side effects such as water retention, increased fat storage, increased blood pressure, etc.
    The 3rd way to treat estrogen-induced gyno is through the use of anti-estrogenic steroids, such as Masteron or Proviron. Of this we can be certain, as Masteron has been proven effective, in a clinical setting, at modulating estrogen levels in breast tissue. In fact, Masteron was originally designed for use in women afflicted with breast cancer. Like A.I.’s, Masteron and gang work to keep estrogen levels low by preventing aromatization. As mentioned above, this is a decisive advantage compared to a drug like Tamoxifen, which is completely ineffective at managing whole-body estrogen. This also means it is best used as a preventative measure and not in emergency situations. As a whole, anti-estrogenic steroids are not as potent as the A.I’s. Therefore, these steroids should be utilized right from the start of a cycle, at a dosage commensurate to the amount of aromatizable drugs being used. In my opinion, Masteron is usually the best steroid for this purpose, as it not only provides an anti-estrogenic punch similar to Proviron, but it also increase the muscle-building value of a cycle, unlike Proviron, which has virtually no muscle building effect. Lastly, Masteron provides the additional benefit of enhanced sex drive.
    We’ve spoken a lot on estrogen-induced gyno, but not all gyno is estrogen dependent. Prolactin has the ability to cause gyno if levels get high enough, as does progesterone. While AAS do not directly increase progesterone levels, some steroids themselves are progestins (ex. trenbolone & nandrolone), exhibiting progestagenic effects on the body. Generally, this progestagenic effect is not strong enough to cause gyno by itself, but it can certainly exacerbate the effects of estrogen, making the problem worse. In the same way, AAS are generally not able to increase prolactin high enough in order to cause gyno by itself, yet it can certainly contribute to the problem. In extreme cases, individuals using large doses of Trenbolone have been known to lactate. Although this is rare and typically only occurs in heavy users with an unfavorable response, it does occasionally happen.
    The most effective treatment for normalizing prolactin levels are the anti-prolactin drugs, such as cabergoline, pramipexole, or bromocriptine. Bromocriptine is a 1st generation anti-prolactin drug. It is not as potent as the other two and since it is less specific in its actions, it comes with an increased risk of side effects. There is no longer any good reason to choose bromocriptine when seeking relief from elevated prolactin. While cabergoline and pramipexole will both get the job done, in terms of compatibility and ease of use, caber is usually preferred due to its reduced side effect profile and longer active life. If there is one downside, it would be its greater cost. Pramipexole must be dosed daily, while cabergoline is usually only administered once every 2-3 days, depending on need. As for the progestagenic effects of AAS, a stated above, gyno is rarely ever a concern as long as estrogen levels are properly managed. Therefore, no specific treatment is indicated. Rather, you indirectly treat the problem by maintaining a normal estrogen level.
    That about sums it up, guys. If there is one take home message here, it is that prevention is preferable to correction. Stop gyno before it starts by keeping your estrogen level stable and it is very unlikely that you will ever have gyno issues. For those who are very sensitive to the effects of prolactin, yet like to use high doses of trenbolone or nandrolone, you may require the additional use of an anti-prolactin drug. However, most of us will not need these in order to avoid gyno.
    Obviously, personal experience will play a key role in showing us what we can and cannot do as we attempt to stay gyno-free, so as you go about experimenting with different steroids & dosages, make sure you have the appropriate ancillaries on hand just in case they are needed. It is always wise to have a back-up supply of Tamoxifen lying around, simply because it’s almost universally effective for stopping gyno, regardless of the cause.

    If you have observed some erect nipples, and a small 'lump' underneath the nipple; will Tamoxifen & an Ai (formeron) reverse these symptoms?


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