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  1. #1
    Mike Guest

    Lightbulb A MUST READ!! Progesterone unveiled...the hidden benefits and common myths...

    Ok guys - I have been researching the misconceptions of progesterone lately and it came up in a thread with some other people. Since I spent the time writing it there I have just decided to cut and copy my response on that thread to this one for you guys to read.

    ------ This was the response ------


    I am glad you asked - I have been researching this a bit actually and have come up with some interesting things about progesterone, it's effects on the body, and how to deal with it appropriately.

    Progesterone is found in men and is actually beneficial in a lot of ways contrary to popular belief. It is the primary precursor of adrenal cortical hormones and testosterone . Males synthesize progesterone in amounts less than women (in fact men have about half what women do) but it is still vital. It also can be very useful for steroid users in preventing prostate cancer due to large amounts of testosterone. Progesterone regulates testosterone levels in males just as it does estrogen levels in females. It does this by preventing the body from converting testosterone to di-hydro testosterone. It does this by inhibiting the enzyme 5-alpha reductase.

    As for gyno, progesterone alone does not cause gyno. But at any rate - gyno, in the literal sense of the word is not a feminizing characteristic. It's a fatty build up in the breast.

    BUT....if you ask me I don't think that progesterone alone causes gynecomastia . Everyone thinks that there is such thing as progesterone induced gyno....I tend to disagree. I have been studying this a bit and have found that it seems that progesterone is only a risk for gynecomastia when in combination with C-17 components or others that cause activity at the progesterone receptor.

    There have been studies done regarding the interaction with spironolactone. Spironolactone, trade name - Aldactone, was originally developed in the early 1970's as a competitive antagonist of aldosterone for the treatment of hyperaldosteronism, edematous states, and hypokalemia. In studies where Spiro was being test to combat heart failure it was noticed that the drug had interactions with the testosterone and progesterone receptors, thus causing gynecomastia. There were noticeable differeces in the levels of pre-existing progesterone in the trial patients. The difference correlated with those who did, and those who did not run into problems with gynecomastia.

    So to make a long story short - it's my theory that nobody gets gyno from deca cycles alone converting to progesterone. I dont think gyno can be derived from progesterone levels alone. I think this excess progesterone is a vital part of the process BUT I would argue that it is the 17aa components that activate the progesterone receptors and let the excess amounts of progesterone start to create gynecomastia. I cannot possibly say what other elements would activate the receptors that would lead to increased risk of gynecomastia. I am sure that 17aa'a are not the only ones though. So how would you combat that risk?

    RU-486. I know you didn't ask HOW RU-486 works but I figure if I explain how it is that RU-486 helps prevent and eradicate gyno, you would understand that RU-486 is most likely NOT the only compound to have this capability. RU486 (mifepristone) is a synthetic steroid related to progesterone. Unlike most progestins that mimic the action of progesterone, RU-486 blocks the action of progesterone. In other words, RU-486 renders progesterone biologically inactive.

    RU-486 is a progesterone antagonist. It binds to the progesterone receptor, and in so doing prevents progesterone itself from occupying its receptor. Thus the gene transcription normally turned on by progesterone is blocked, and the proteins necessary to begin the process of gynecomastia are not synthesized.

    So, that being why RU-486 actually helps progesterone RELATED gyno, it is also true that other progesterone antagonists will help in the same way. The only other commercially available progesterone antagonists that I know of is Onapristone (ZK 89.299). The only difference between these two progestrogen antagonists, is the difference in antiglucocorticoid activities for the glucocorticoid receptor (GR). RU-486 provokes this action while Onapristone does not. So, my point being that RU-486 actually blocks corticoid action, thus - the healthiest choice of progesterone related gyno combat tools, would actually be Onapristone. For which I am trying to research what the effective dose would be.

    So my conclusion is that RU-486 is, contrary to popular believe, NOT the only way to combat this gyno and in fact - probably not even the healthiest way.

    whew...sorry I know you didn't ask for all that but i's something I have been stewing on for a bit and I think what I am finding is very interesting.

    Mike


    **Note - another important fact about progesterone.

    Progesterone is a natural and powerful inhibitor of the 5-alpha reductase enzyme. This means - that when on a testosterone/deca cycle and worried about DHT....proscar may not be the answer....

    You don't need to take saw palmetto or proscar with a Test/Deca cycle to prevent testosterone from converting to DHT. Deca acts as progesterone which actually inhibits 5 alpha reductase far more effectively than Proscar and Saw Palmetto which are the more standard agents employed in traditonal and natural medicine.

    Just a thought......

  2. #2
    Triple Plates's Avatar
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    intresting stuff... good post bro

  3. #3
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    Damn, why do they call you God again???? One thing I got from this and correct me if I misunderstood, is that you're saying taking winny with deca , contrary to popular belief, can actually cause prog gyno? That's kinda scary. Thanks for all the info bro.

  4. #4
    Mike Guest
    First off I am surprised even 3 people read that whole thing! lol

    JP - you bring up a VERY good point. Thank you - first off I have stated my stance on winny combatting deca 's 'gyno' properties in another post in 'educational threads'. Personally I never thought it was effective in doing so in the first place. Now this kind of explains to me why it wouldn't be preventative.

    I don't think that deca will cause gyno in the first place. I think when you over activate the receptors with pre-existing excess of progesterone - you will increase your susceptibility to it, but nothing more. But in theory at least - yes I think winstrol in conjunction with deca would actually do more harm than it would good. Though I don't feel it a particularly dangerous combination either. I think that 'deca gyno' as it's commonly referred to, is overstated if it actually exists at all.

    And yes I know I am spitting in the face of popular belief on this one and I fully expect to get flamed LOL

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    Re: A MUST READ!! Progesterone unveiled...the hidden benefits and common myths...

    Originally posted by Mike
    Ok guys - I have been researching the misconceptions of progesterone lately and it came up in a thread with some other people. Since I spent the time writing it there I have just decided to cut and copy my response on that thread to this one for you guys to read.

    ------ This was the response ------


    I am glad you asked - I have been researching this a bit actually and have come up with some interesting things about progesterone, it's effects on the body, and how to deal with it appropriately.

    Progesterone is found in men and is actually beneficial in a lot of ways contrary to popular belief. progesterone is beneficial.. absolutely It is the primary precursor of adrenal cortical hormones and testosterone . Males synthesize progesterone in amounts less than women (in fact men have about half what women do) but it is still vital. It also can be very useful for steroid users in preventing prostate cancer due to large amounts of testosterone. Progesterone regulates testosterone levels in males just as it does estrogen levels in females. It does this by preventing the body from converting testosterone to di-hydro testosterone. It does this by inhibiting the enzyme 5-alpha reductase. the inhibition of 5a is limited.....actually its most important benefit is the role that it plays in male sexual arousal.. at least from all the cries about deca and fina "dick"

    As for gyno, progesterone alone does not cause gyno.true, there are many things that cause "gyno" and some of them are completely unrelated to the sex hormones.. growth factors have a stronger causal link, though usually in the presence of elevated hormones But at any rate - gyno, in the literal sense of the word is not a feminizing characteristic. It's a fatty build up in the breast. true gyno is the growth of the milk gland, fatty tissue gyno(which is actually called pectoral feminization) is caused by estrogen alone.. the puffyness of nipples is caused by estrogen, progesterone and prolactin to varying degrees (this is one of the least understood elements)

    BUT....if you ask me I don't think that progesterone alone causes gynecomastia . Everyone thinks that there is such thing as progesterone induced gyno....I tend to disagree. I have been studying this a bit and have found that it seems that progesterone is only a risk for gynecomastia when in combination with C-17 components or others that cause activity at the progesterone receptor. there is no such thing as progesterone induced gyno, PROGESTIN induced gyno on the other hand is very real.. but you are right on target with the importance of 17aa.. its increase of growth factors and effects on the liver are HIGHLY implicated in development of gyno

    There have been studies done regarding the interaction with spironolactone. Spironolactone, trade name - Aldactone, was originally developed in the early 1970's as a competitive antagonist of aldosterone for the treatment of hyperaldosteronism, edematous states, and hypokalemia. In studies where Spiro was being test to combat heart failure it was noticed that the drug had interactions with the testosterone and progesterone receptors, thus causing gynecomastia. There were noticeable differeces in the levels of pre-existing progesterone in the trial patients. The difference correlated with those who did, and those who did not run into problems with gynecomastia.

    So to make a long story short - it's my theory that nobody gets gyno from deca cycles alone converting to progesterone. I dont think gyno can be derived from progesterone levels alone. I think this excess progesterone is a vital part of the process BUT I would argue that it is the 17aa components that activate the progesterone receptors and let the excess amounts of progesterone start to create gynecomastia. I cannot possibly say what other elements would activate the receptors that would lead to increased risk of gynecomastia. I am sure that 17aa'a are not the only ones though. So how would you combat that risk?

    RU-486. I know you didn't ask HOW RU-486 works but I figure if I explain how it is that RU-486 helps prevent and eradicate gyno, you would understand that RU-486 is most likely NOT the only compound to have this capability. RU486 (mifepristone) is a synthetic steroid related to progesterone. Unlike most progestins that mimic the action of progesterone, RU-486 blocks the action of progesterone. In other words, RU-486 renders progesterone biologically inactive.

    RU-486 is a progesterone antagonist. It binds to the progesterone receptor, and in so doing prevents progesterone itself from occupying its receptor. Thus the gene transcription normally turned on by progesterone is blocked, and the proteins necessary to begin the process of gynecomastia are not synthesized.

    So, that being why RU-486 actually helps progesterone RELATED gyno, it is also true that other progesterone antagonists will help in the same way. The only other commercially available progesterone antagonists that I know of is Onapristone (ZK 89.299). The only difference between these two progestrogen antagonists, is the difference in antiglucocorticoid activities for the glucocorticoid receptor (GR). RU-486 provokes this action while Onapristone does not. So, my point being that RU-486 actually blocks corticoid action, thus - the healthiest choice of progesterone related gyno combat tools, would actually be Onapristone. For which I am trying to research what the effective dose would be.

    So my conclusion is that RU-486 is, contrary to popular believe, NOT the only way to combat this gyno and in fact - probably not even the healthiest way.

    whew...sorry I know you didn't ask for all that but i's something I have been stewing on for a bit and I think what I am finding is very interesting.

    Mike


    **Note - another important fact about progesterone.

    Progesterone is a natural and powerful inhibitor of the 5-alpha reductase enzyme. This means - that when on a testosterone/deca cycle and worried about DHT....proscar may not be the answer....

    You don't need to take saw palmetto or proscar with a Test/Deca cycle to prevent testosterone from converting to DHT. Deca acts as progesterone which actually inhibits 5 alpha reductase far more effectively than Proscar and Saw Palmetto which are the more standard agents employed in traditonal and natural medicine.

    Just a thought......

    you make some good points.. progesterone is not the enemy it is actually a friend (at reasonable levels) HOWEVER PROGESTINS ARE "the ENEMY" AND THEY ARE STRONGLY IMPLICATED IN THE DEVELOPMENT OF GYNO... EVEN IN THE ABSENCE OF C-17 ALKYLATION-- THOUGH THIS DOES INCREASE RISK..thus the use of an oral with deca (even winstrol ) will increase risk of gyno.. one of the reasons that fina and deca are highly implicated, is the fact that they both SUPRESS NATURAL PROGESTERONE.. thus you have high levels of progestins in the absence of progesterone.. a bad combination

    btw- agree about ru- 486.. anti progestins are bad news.. part of the reason that many have sexual problems on winstrol (though its not a strong.. so less problems.. and across less of the population.)

  6. #6
    Mike Guest
    SK -

    Yeah see that was my thinking too! I mean I dont know of ONE real case of someone who did JUST deca and got gyno. It's always a friend of someone's cousin or whatever ya know? So I can't subscribe to that.

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    Originally posted by Mike
    SK -

    Yeah see that was my thinking too! I mean I dont know of ONE real case of someone who did JUST deca and got gyno. It's always a friend of someone's cousin or whatever ya know? So I can't subscribe to that.
    just a little side note-

    know(personally, not on the net) 2 people that have gotten gyno from a nandrolone only cycle.. one from ttokyo deca (last year) and one from laurobolin(about 3 years ago).

  8. #8
    Mike Guest
    do you know of any other medications they were possibly on at the time? Specifically ACE Inhibitors, beta blockers, calcium channel blockers, anti-hypertensives and other heart meds? I think there are compounds that have interactions with the testosterone and progesterone receptors that need to activate these receptors per se in order for progesterone to create gyno.

    just my thoughts.....

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    99% sure none of the above

  10. #10
    Billy Boy's Avatar
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    Are you saying that using 17aa like Winny may not prevent progesterone it may actually be opening the receptors for gyno?As no clinical studies have ever shown Winny to prohibit progesterone could we all be wrong in assuming that it does?

    RU-486 is the Abortion pill right? If this stops the progesterone from binding to the receptors which it does obviously there are still high levels of progesterone in the body-what happens to that and what effects does that have?
    Last edited by Billy Boy; 02-14-2002 at 03:54 AM.

  11. #11
    Billy Boy's Avatar
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    Just thought I would add this here as there maybe people who don,t know what the RU-486 is this refers to the female side but is worth a quick read over.DOES CONTAIN FACTS ABOUT ABORTIONS SO IF EASILY OFFENDED DON,T READ.

    . INTRODUCTION

    RU486 (also known as Mifepristone) has been a drug with a great deal on controversy surrounding it. Early research was directed as a glucocorticoid receptor blocker for possible anti-cancer applications, (1). But the drug’s most promising application was as an abortifacient. There in lies the true controversy.


    2. MECHANISM

    RU486 acts as an abortifacient. The drug’s actions are effective for the first 49 days after conception. The mechanism of action is as follows.

    RU486 blocks progesterone receptors in the uterine lining. Progesterone is necessary in the woman to maintain the lining of the uterus, which, during pregnancy is loaded with blood vessels, acts as a life support system for the developing embyro (life). (NOTE: the developing life for the first 60 days post conception is medically referred to as an embryo, whereas after 2 months it is referred to as a fetus.) As the embryo implants into the uterine lining, the embryo grows dependent upon the mother’s uterine blood supply for nutrients, oxygen, and waste removal. Thus, any cut off of the blood supply would lead to the rapid death of the developing life.

    RU486 acts to block the effects of progesterone to maintain the uterine lining. As the progesterone signal is cut off in the uterus, the uterine blood vessel lining begins to breakdown and subsequently the embryo dies (1).

    Now as the embryo is dead, the uterus may try to expel the embryo and its surrounding tissues. But, using RU486 alone results in only about a 60-65% (3,4) success rate. Therefore many doctors give a second very powerful drug-prostaglandins (the best known is Misoprostol-also known as Cytotec TM ), which causes very strong (and sometimes very painful) uterine contractions to expel the dead embryo. Using the dual drug system, RU486 and Cytotec TM, the success rate rises to 84 to 95% (5). In small cases, 5 to 15% of patients, the patient is required to undergo a surgical procedure called a dilation and curettage (D&C) to remove any remaining embryonic tissue (6). In some reports (7), the women report discharging the embryo into the toilet under great pain due in part to the powerful uterine contractions.

    3. RU486 PHARMACOLOGY BASICS

    Several important points must be observed at this point. Use of RU486 to induce an abortion is not like a surgical abortion. The most widely used technique for surgical abortion (8) is a D&C, whereby the embryo is scraped off the uterine wall. A surgical abortion occurs at a certain moment of time and the patient then returns home. The process using RU486 requires that the woman be given the drug at the clinic and then return back to the clinic within 24 to 48 hours for the second drug (the prostaglandin-usually Cytotec TM ), where upon within 12 to 24 hours the woman will via strong uterine contractions expel the embryo.

    What this means is that the process requires more time for the action to occur (the abortion) as well as less monitoring by medical authorities for any complications. The patient must decide on her own IF complications warrant a return visit to the clinic or to the emergency room. This decision making could be hampered by guilt, desire to maintain the abortion as a secret, or problems of obtaining transportation to the clinic or hospital. Each delay factor increases the risk of death or further trauma. We will discuss this shortly.

    Also the drug process (RU486) is different as the drug remains in the woman for a prolonged period of time. A drug "half life" is a pharmaceutical term to describe the time period by which ½ (one half) of the active drug is broken down by the body and/or removed from the body. Also, a drug "metabolite" is the drug by-product, produced by the body’s metabolic enzymes (usually from the liver) acting to breakdown or chemically alters the active drug. It must be noted that drug metabolites can still retain some of the original drug’s properties!

    With regard to RU486, the half-life is 25.5 to 47.8 (9) hours, depending if the drug is given in a single or multiple does. Also, one study has shown that the active drug may linger in the woman’s blood stream up to 10 days AFTER taking the drug (10). Finally, the RU486 metabolites are partly active (they also will bind to progesterone and glucocorticoid receptors) and the metabolites can linger up to 5 days after administration (11, 12). This is important to remember as some effects of the drug RU486 may last well past (10 to 15 days) after administration and the time of the actual abortion. This writer questions whether women are properly informed of these aspects of the drug. The actions of having the drug last so long in the body may play a role in the following complications.

    4. ADVERSE EFFECTS

    A. IMMUNOSUPPRESSION

    In many of the studies with RU486, a common side effect is infections, usually in the pelvic or genital tract (13,14). One medical study stated that patients required a 6-week follow up treatment of antibiotics (15). Whenever the RU486 treatment led to an incomplete abortion (thus, requiring a D&C for a follow-up), up to 29.4% of the women reported an infection requiring antibiotic treatment (15).

    WHY?

    Several factors are now understood. RU486 will itself suppress the immune system by causing the patient’s cortisol to rise (16). Cortisol, a glucocorticoid hormone, acts to suppress the immune system by diminishing the ability of certain white blood cells (leukocytes) to migrate to sites of tissue infection; acts to suppress lymphocyte (another type of white blood cell) gene expression; and acts on neutrophils (another type of white blood cell) capacity to kill ingested bacteria cells (thus blocking this white blood cells’ capacity to stop infection). All of these effects hinder the immune systems capacity to fight off bacterial infection (17).

    Also, a study by Van Voorhis et al (18) demonstrated that RU486 alone acted to hinder white cell activity, but, the effect of suppressing white cells is MAGNIFIED greatly by the combined presence of cortisol and RU486!

    Finally, one study by Moran et al (19) mentioned unpublished data that Cytotec TM (the prostaglandin given to enhance the uterine expulsion of the embryonic remains) can work in a synergistic manner with steroids (like cortisol) to suppress immune function.

    This may explain the persistence of infections in RU486 patients. The scenario is that first RU486 acts to damp down immune function, while cortisol levels rise, then cortisol and RU486 act together and further magnify immune system suppression, and finally, as Cytotec TM is given to the patient, the presence of Cytotec TM and high cortisol levels render the immune system incapable of defending against infection, especially an infection brought on by the ensuing abortion and subsequent uterine bleeding. This allows bacterial infections to gain a significant foothold in the pelvic or genital region and would require strong antibiotics to fight off and finally defeat the infection.

    Since the risk of infection is so prevalent, ALL users of RU486 need to be warned of the infection hazard. The problem is further complicated if the woman using RU486 has AIDS/HIV or other immunosuppressive diseases, since any infection would almost certainly run rampant in the patient and become a cause for a possible patient death.

    One final note on this topic. Margie Profet produced a study examining (20) menstruation as a defense factor against the development of female reproductive infection. In her work, she notes the dynamic microbiological activity within the female reproductive tract and lists various methods that infection can be introduced. Should the immune system weaken (as via RU486) any infection from a hostile microorganism could cultivate in the female reproductive tract. Also, beyond the natural microbiological activity within the female reproductive tract, microorganisms can be transported into the tract by either seminal fluid or via attachment to sperm. These various pathogens that "hitch a ride" in seminal fluid or on sperm, include E. Coli, Chlamydia, N. Gonorrhea (pathogen that causes Gonorrhea), Trichomonad (which causes Vaginitis), or even Cytomegalovirus (21, 22, 23, 24, 25,26, 27). With the immune system suppressed via RU486 (as well as elevated cortisol levels and Cytotec TM) and with the half life of the active drug and its partly active metabolites lasting as a long as 10 to 15 days after administration, ANY RU486 patient may have to refrain from active sexual relations for a significant period after receiving the drug to avoid a serious infection. Again, this writer wonders how many doctors will inform their patients of this point!

    B. PAIN

    During use of RU486 and Cytotec TM, medical studies cited patients reporting pain (79.1%, SEE 28) or severe uterine cramps (80.5%, SEE 7) to such a degree that many required opiate based painkillers. The percentage of patients in the studies reporting pain ranged from 57.1% to as high as 79.1%. Many patients required and were treated with injections of VERY strong analgesics (13).

    The problem with this issue is that many patients go home after receiving RU486 and may not have easy access to powerful narcotic painkillers (which require a doctor’s prescription). Furthermore, in this pill popping, "self medicating", instant pain relief nation; use of over the counter medications would be dangerous, if not fatal. HOW?

    Use of nonsteroid anti-inflammatory drugs (NSAIDs) will not relieve pain, BUT due to the NSAIDs capacity to block blood clotting, these drugs could enhance bleeding (SEE CHART 1). One case was reported in January 1996 (29) of a near death due to massive hemorrhaging (bleeding) by a patient using RU486. It must be noted that by the very nature of the RU486 abortion, the woman will bleed significantly during the process of expelling the embryo and associated tissues.

    NSAIDs will only enhance the blood loss incited by a RU486 abortion and will only increase the risk of death to the woman!

    One other curious research paper reported in 1990 (30) that women who use RU486 to abort their first pregnancy and then used the pain reliever acetaminophen (commonly know by its trade name TYLENOL TM) has an INCREASE in reported pain. Scientists do not know why, but acetaminophen increased painful suffering in the presence of RU486.

    C. BLEEDING

    As previously mentioned, bleeding is a serious issue when dealing with RU486 abortions. A series of studies (13, 15, 31, 32) demonstrates that 1 to 11% of the women using RU486 suffered profuse bleeding. Some cases even required blood transfusions! (15, 29, 31, 32)

    If a woman is not told to avoid over the counter pain medications, like NSAIDs, this could clearly INCREASE the incidence of severe bleeding and possible death.

    D. SLEEP

    Sleep is a necessary component for the maintenance of health of any individual. BUT more so, it is the various components of sleep that are important to both physical and mental well being of a person.

    With that much in mind, one study (33) by Wiedemann et al demonstrated how RU486 disrupts sleep: including total sleep time, slow wave sleep, and REM (Rapid Eye Movement) sleep. RU486 diminished total sleep time, reduced both slow wave and REM sleep, and caused increased sleep time re-awakenings (i.e. "kept waking up in the middle of the night").

    REM sleep is referred to as Dream sleep. This is the stage of sleep when most dreaming occurs. There are various theories as to why we sleep, but many psychologists believe dream sleep is useful in helping the individual cope with stress and stressful events of life (34).

    As with undergoing an abortion will put the woman under psychological stress and tension; it is sad to note that the very same drug used to induce the abortion, will also suppress the woman’s dream mechanisms (in the brain) which are needed to help the individual cope with the psychological stresses (e.g. guilt, shame, remorse, grief, etc.) of the event. It maybe interesting to note that after several days of REM sleep suppression (which could occur since RU486 may linger up to 10 days in the woman’s blood stream), the brain then increases the amount of REM sleep each night. This is referred to as REM REBOUND (35). This may help to explain (in part) any incidents where RU486 patients have extended periods of dreams or nightmares.

    One must wonder that since RU486 induced the abortion, and its subsequent physical and psychological stress; how many women suffered further physical or psychological harm due to sleep reduction, REM sleep (dream) deprivation, and the subsequent REM rebound (as the RU486 drug blood levels have dissipated)?

    5. THE FUTURE PATHWAY

    One other important point must be noted regarding RU 486 and its marketing. It will become much more freely available in the not so distant future. HOW?

    Note that many pharmaceutical manufacturers convert over their products from prescription only (RX) to over the counter (OTC) products after a decade or so. This is called RX to OTC conversion. These conversions have been demonstrated by the successful marketing of such products as Aleve TM (sodium naproxen), Rogaine TM , Motrin TM (ibuprofen), and Tagamet TM. This process occurs when the pharmaceutical manufacturer’s patent is about to expire. With the RX to OTC conversion, the pharmaceutical manufacturer gets a new lease on the life of the drug product. The FDA has banned RX to OTC conversions on only narcotic drugs. Therefore, when the RU486 patient approaches expiration (in 2002, SEE 36), it is conceivable that somewhere in the near future, RU486 will be as easy to buy at the discount drug store as aspirin, condoms, and mouthwash. At that time, how many abortions will occur to women and female minors (under age 17)? Only God may know.

    Rather than surgical abortion, RU486 has been a herald towards a new method of abortions-pharmaceuticals. This method can reduce the need for clinics, allowing doctors to shield patients from surgical procedures, and yet allow women the expulsion of pregnancies in the privacy of their home bathrooms. Although this may appear efficient, the murder of the unborn life and the physical and psychological harm to the mothers are certainly unconscionable.

    But, this technology has its risks. Patients must know ALL and ANY warning signs of complications to allow time for the woman to take the necessary steps (e.g. emergency room treatment, blood transfusion, antibiotics, etc.); steps necessary to prevent injury or death. In light of the paucity of information regarding complications, both physical and psychological, prolife forces at present have a strategic advantage avenue to warn women from not just the point of saving the unborn life (some unfortunately will not listen to this avenue), but provide information to warn women about the complications of almost certain hemorrhaging, infection, intense pain, sleep disruption, and psychological trauma.

    The challenge to prolife is clear. It is necessary to become quite familiar with this technology and its complications as the drug RU86 enters U.S. and foreign markets. Prolife forces with the necessary technical, medical and psychological knowledge could save unborn children from death and save their mothers from tremendous agony (both physical and mental) or even death.

  12. #12
    Iron horse's Avatar
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    I got a question. So what your saying is that deca with test help stop conversion to DHT right?

    lets say this is an average cycle

    500mgs/test -week
    400mgs/deca- week

    10 weeks


    would the cycle down below prevent DHT even more?

    500mgs/test - week
    600mgs/deca - week

    10 weeks

  13. #13
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    Great thread guys...learning more every day... this is the reason why I'm on this god**** site all the time!

    Sorry Mike, no blasphemy intended,lol...

  14. #14
    RUSSIANBEAR is offline Member
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    I got gyno from a Deca only cycle at 450mg/week. Can you explain why???

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    Billy Boy's Avatar
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    Just curious why 450mg a week?

  16. #16
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    1 1/2cc of deca 300 by Ttokkyo a week whats wrong with that. 400-500mg is about what deca dosage should be around.

  17. #17
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    Wow cool it bro!!

    I was just curious thats all I never said for a moment there was anything wrong with it

  18. #18
    RUSSIANBEAR is offline Member
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    Bro i am as cool as they come,I did not mean to come at you in any wrong way.

  19. #19
    RUSSIANBEAR is offline Member
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    I just want to make it clear that it was not full blown gyno. I had a lump under my left nipple. I took some EAS protein and ZMA so i dont think it was any of those that could have caused it.

  20. #20
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    You mess with your own hormones(or lack there of) and shit happens. Comes with the territory. Maybe nandrolone decanoate is not the only chemical in ttokkyo brand 300. Maybe after you used it the progesterone became progestin. Maybe it happened before it.

    From this I would say that RU-486 is to progesterone receptor sites as nolvaldex is to estrogen receptor sites. After the use of the drug, all the progestin "floating" around your body hits the sites just like the estrogen. Is that correct?

    From this it seems that 17aa tabs would hinder progestin build up even more than without the use of 17aa tabs. (I never believed the winny vs. progesterone debate)

    This leads me to ask "What else dont we know about AS?" Obviously a lot. Anyone wanna be lab rats in a National experiment?? Sign me up!

  21. #21
    NightOp is offline Member
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    my main question from all of this is> does this mean that winny and other 17aa drugs can possibly cause gyno? sorry if this is a dumb question, but i just want to know the bottom line.

  22. #22
    Mike Guest
    Well I have to remind you guys that what I found the most interesting in all of this is that there is a drug out there that would appear to be more effective for fighting progesterone gyno than RU-486, when initially it was thought that this would be the only drug out there for this use.

    Billy - free floating progesterone in the body has a life of about 5 minutes I believe. So it wouldn't be a problem.

    Iron Horse - yes, I am saying precisely that.

    Macro -

    I am surprised that you are "99%" sure of the meds that your friends were taken. For two reasons, first being that we live in an age where over prescription is habbit and second being that one of your friends got this THREE years ago. That's quite the memory.

    So for you and for Russian -

    I am not invalidating anything that you are saying. I think that is MOST cases atleast, progesterone cannot act alone without another agent "clearing the path" so to speak, by activating progesterone receptors in order to start creating gynecomastia . While it is also true that it may be that some people may have over active receptors and perhaps the conversion of deca or laurabolin etc may just be enough to induce gyno, I would just be very curious to see what other agents those people have been on in the six months prior to that cycle. Including any other meds (prescription or not) and especially including other steroids like test or C17s.

    Also - for those who say they have gotten gyno from a deca ONLY cycle, I would be very interested to see what other agents you were taking at the time.

  23. #23
    Mike Guest
    Nightop -

    No winny is not CAUSING gyno. I think that by this theory it may be a catalyst for turning free floating progesterone into early stages of gyno. It reacts at the receptor sites to aid in the process of creating gyno. I think winny and other drugs may make it easier for gyno to be created. But they wont do this alone.

    And it is very possible that those agents are NOT needed to induce gyno, but my curiousity lies in the incidence rate. Of all the people who really thought they had deca gyno, I would like to know how many of those people were on any other forms of medication or hormones etc.

    I don't have that data - so I am not really in a place to be completely and totally conclusive about this. It's just a theory....

    HOWEVER...how we fight prgesterone is not just a theory. I have found that RU-486 is not the only antagonist NOR the best.

  24. #24
    Mike Guest
    Here's the thing. Winny alone will NOT cause gyno. Won't happen.

    Progesterone CAN cause gyno but I think it's ability to cause gyno without having some sort of help at the progesterone receptor (hence C-17's etc) is grossly overstated. I do believe it possible but to those who have gotten gyno from deca only cycles - I think that they carried a pre-existing natural disposition. I think it is very rare that deca alone will cause gyno but in some cases where the user may be prone, it is possible.

    No I do not think that winstrol will aid in the inhibition of progesterone build up when taking deca. In fact I think that the opposite is true. I think that using winstrol (or dbol etc for that matter) will actually have the reverse effect and cause a bigger incidence rate for progestin induced gynecomastia .

    Once someone already has gynecomastia from a build up of progestins, it appears that two options are available. One being that you take RU-486 and the other being that you take ZK 89.299. The latter of the two being the one that will NOT stop corticoid action by causing antiglucocorticoid activity at the G receptor.

    Please people - I know that some of this is contrary to the current stance on some things but dont let THAT be your main argument. I think some of you will disagree just because "the masses" do. I have presented real clinical data. If you want to object or disprove anything - it'd be wise that you do the same.

  25. #25
    Mike Guest
    Sk* (or god if it pleases you LOL)

    No not the vet version. ZK 89.299 (Onapristone) I explained in the above response.

  26. #26
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    Originally posted by Mike


    Macro -

    I am surprised that you are "99%" sure of the meds that your friends were taken. For two reasons, first being that we live in an age where over prescription is habbit and second being that one of your friends got this THREE years ago. That's quite the memory.
    1. for some odd reason the people i know consult with me regarding the medications that they take- cant figue out why

    2. yes.. it is quite a memory

  27. #27
    GenuinePL's Avatar
    GenuinePL is offline Senior Member
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    Great posts Mike and Billy. Great stuff, it makes you think and has very usefull info in it. Great Job guys

  28. #28
    RUSSIANBEAR is offline Member
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    "Mike" it was Deca 300 by ttokkyo labs. I ran a 7 week cycle over the summer just deca nothing else bro. By week 5 or 6 my nips got sore as hell and by the end of my cycle i noticed a lump under my left niple. Why just Deca??? I was not a memeber of this board so i did not know much about AS thats the only reason i did not stack.

  29. #29
    Mike Guest
    Macro - read my above post. I am not disputing that it happened. I believe it IS possible to acheive gyno from deca alone and other related compounds. I just think that the incidence rate of that actually happening is FAR lesser than most will believe. I think it is grossly overstated and that in most cases where people think that it was simply the deca, the deca had "help" so to speak.

    By the way - my friends do the same thing to me! lol

  30. #30
    big_guy is offline Associate Member
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    ok.. im puttin in my vote to put this in the Educational threads.. so everyone in the future can see it!!... GREAT STUFF

  31. #31
    Mike Guest
    SK -

    I NEVER once said that 17aa's are the only things to trigger it. I stated pretty clearly above that 17aa's will probably raise risk factor of getting gyno because of it's interaction with the receptors.

    BUT I do believe that people can have predispositions that raise that risk factor W/OUT 17aa's or other compounds. Hence - Macro's friends and RussianBear. I just believe that without those additional agents or predispositions - it would take extreme amounts of progesterone from the deca - more than most people currently think.

  32. #32
    JP1570's Avatar
    JP1570 is offline Senior Member
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    This is some great stuff. I'm voting for educational threads too.

  33. #33
    Mike Guest
    bump

  34. #34
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    This needs to be clarified.

    progesterone has many benefits. progesterone itself is VERY unlikely to cause gyno though it may aggravate it a higher doses.

    deca and tren do not increase progesterone.

    deca and tren are progestins.. they bind to the PR and activate it. Thus any benefits that accrue from progesterone CANNOT be attributed to them.. in fact quite the opposite.

  35. #35
    Billy Boy's Avatar
    Billy Boy is offline Retired Moderator
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    Ok thanks for answering my question Mike

    Just to summarize everything up in one post and for myself what you are saying is

    1 The chances of getting gyno from a deca only cycle is very rare but those that do get it may have an existing natural diposition for gyno

    2 Adding 17aa may increase the chance of gyno related incidents due to the fact that these may trigger an action within the receptors

    3 Other forms of medication may increase the chances of getting Progestrone related gyno.

    4 It is unlikely that Progestrone gyno is caused just by progestrone and that it may need some sort of help at the receptor

    5 Progesterone is only a risk for gynecomastia when in combination with C-17 components

  36. #36
    Mike Guest
    Macro -

    No, deca and tren do not convert to progesterone. They don't need to. They act as progesterone would at the receptor. This is what ultimately leads to gyno (and to be redundant, I repeat that I don't believe that incidence level is high without other compounds such as but ot limited to certain C-17 agents.)

    Also - I set out to dispel common myths about Progesterone and why it wasn't "so bad for us". I never said that Deca and tren actually create progesterone and thus it's benefits. Though for some reason, I have noticed a correlation between using deca and decreasing DHT levels in a testosterone cycle.


    By the way...here's somethig else you can disagree with
    Deca will aromatize in small amounts to estrogen.

  37. #37
    Mike Guest
    Points 4 and 5 Billy....

    4. It is unlikely that Progestrone gyno is caused just by progestrone and that it may need some sort of help at the receptor

    "Progesterone Gyno" is not caused by progesterone but by progestins, for example - deca is a progestin, it 'ACTS AS' progesterone at the progetserone receptor. These levels are increased with other agents at the receptor (so yes you are very close)

    5 Progesterone is only a risk for gynecomastia when in combination with C-17 components

    No. Refer to the above answer as to why it is not progesterone itself that is the risk. It is the progestins that create activity at the progesterone receptor. Also, look at your own point on #3. C-17 components are most likely not the only ones to enhance this process at the PR.

  38. #38
    Mike Guest
    Oral anabolic steroids that are modified by the addition of a side chain or group of molecules at the alpha position of the number 17 carbon atom through alkylation. These are C-17, 17aa steroids.

    Orals like winstrol , dianabol , anavar , anadrol etc.

  39. #39
    Mike Guest
    LOL

  40. #40
    Mike Guest
    I've thought about that - it's hard to say really. I have my suspicions though, it is a small amoutn of estrogen but an amount that cannot easily be prevented by normal anti-aromatize like with testosterones

    I have a feeling that it is very possible that everyone who thinks they have gotten gyno from "deca converting into progesterone" (which doesnt even happen) really may have just gotten it from estrogen, but in all honesty there is no way to tell. Nobody is going to come on here with PROOF that themselves or their friend got it from progestins rather than estrogen, it's all just heresay. So until i find a guinea pig it's really inconclusive as to how much progestins actually lead to gyno in these cases and how much does estrogen

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