Question For All The Experts

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    Question Question For All The Experts


    We know Superdrol is not an aromatizable androgen.
    We know its structure does not even remotely resamble a progestin.
    We know(at least who has actually used it)it has a pretty weak androgenic activity(my skin,prone to acne,gets even better on it and I've never lost one hair).
    There are 3 known pathways for negative feedback in the brain,none of theese seems apparently affected to a great degree by SD on paper.

    So the question is: why that little bastard causes that commonly reported very hard shutdown of the HPTA?

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    I dont understand? You think only androgens cause suppression and not anabolics?

    holy
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    Obviously NOT.
    But I'm wondering why SD is so hard on HPTA since it is not a strong androgen(YES,a potent anabolic)not a progestin and doesn't convert to estradiol at any degree.
    On paper,but not in real life,shold be pretty mild on HPTA like oxandrolone.
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    Questions, Questions


    Jay Edit: Please read all of the Rules and the FAQ's on anabolics especially. Do not try to find sources here.
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    Excuse me sir,have you read this thread's title?
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    Quote Originally Posted by xtyler View Post
    Excuse me sir,have you read this thread's title?

    I couldn't figure out how to start a new thread...sorry.
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    when you click on the "STEROIDS" forum there's a botton on the upper left part of the page, "NEW THREAD".
    If you make a quick search here you'll probably not need to start a new thread at all.
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    Quote Originally Posted by xtyler View Post
    when you click on the "STEROIDS" forum there's a botton on the upper left part of the page, "NEW THREAD".
    If you make a quick search here you'll probably not need to start a new thread at all.

    Thanks
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    ...and before you post a new thread you make want to take a glance at the board rules regarding source posting
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    someone answer this mans question. Has anyone actualy used SD and DID lose hair on it? .. Im contemplating this or turinabol for my next cycles jump start.
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    also, i think masteron was origanly used to treat breast cancer or gyno like epi. So why is it so well known for causing gyno, delayed gyno?
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    I think all that the experts are on an extended Labor Day weekend holiday vacation. I'll have all the experts check in as soon as they return to grace us with their presence

    Superdrol does possess androgenic characteristics in real world application and yes there is some scalp itchiness and mild shedding reported by some.
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    Quote Originally Posted by citystreets View Post
    also, i think masteron was origanly used to treat breast cancer or gyno like epi. So why is it so well known for causing gyno, delayed gyno?
    estrogen rebound
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    Any steroid, whether its an androgen or not can cause gyno AFTER the cycle due to either an estrogen rebound (if you used an AI during cycle), or simply by your test levels being suppressed for a long time post cycle.

    I think you'll find that masteron exhibits more androgenic activity than its given credit for.

    holy
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    Quote Originally Posted by citystreets View Post
    someone answer this mans question. Has anyone actualy used SD and DID lose hair on it? .. Im contemplating this or turinabol for my next cycles jump start.
    Yea, i've used SD and some clones (mdrol,methyldx3) and have never lost one hair...........
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    Quote Originally Posted by lennoxchi View Post
    Yea, i've used SD and some clones (mdrol,methyldx3) and have never lost one hair...........

    glad to hear it, are you prone to balding though?
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    Quote Originally Posted by citystreets View Post
    glad to hear it, are you prone to balding though?
    not that i know of.
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    i think that it shuts you down hard because it activates the estrogen receptor, not necessarily aromatizeing.

    and estrogen (too much and little test) will shut down the hypothalmus.
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    direct interaction with ERs? What on heart lets you think so???
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    Quote Originally Posted by xtyler View Post
    direct interaction with ERs? What on heart lets you think so???
    well lets see, direct ? no, but DHT dervitives

    i think of it this way
    5a reduced steroids dont aromatize at all, yet phera, epi, and SD, tren (that just being a progestin itself) also. all gave prolactin sides. and when used with NOLVA it only enhanced the effect.

    DHT derivites or interacts with the 5a enzyme causeing a possible interaction with the estrogen receptor.


    as well as that theory i think people dose the nolva too high causing a flux of hormone which signals the adrenal glands to make DHEA and a lot of it and that aromatizes (converts to andro then it converts to test/estrogen) and being that nolva doesnt reduce estrogen, you have your problem
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    I wasn't talking about nolva!
    The question is still here: why SD lead to a so deep suppression if its profile is close to something like anavar or winstrol(no aromatization,no progestational activity and low androgenic potential).
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    I believe this is due to superdrol's similarities to anadrol. The only differance between SD and anadrol is that anadrol has an OH group bonded to a carbon and hydrogen, which is then double bonded to carbon 2. Superdrol has a methyl group (CH3) at carbon 2. If you look at the structure of anadrol on paper, it doesn't look like it would aromatise because it lacks a double bond between carbons 4 and 5. However, we all know that anadrol induces heavy bloating and estrogen related sides. It is believed that this is due to direct stimlulation of the receptor.

    I think this may hold true for SD to a certain extent as far as prolactin goes. I think that SD may directly stimulate receptors to cause prolactin induced sides.

    My other thought refers to SD's similarities to masteron. Masteron is extremely dry and has been shown to reduce estrogen. Now too much E2 supression can lead to a rise in prolactin, which I think may also be a problem here.

    Through personal experience, I have found that while on superdrol, I dry out a lot. When I had gyno(had it removed), I found that while on SD, my gyno actually shrunk somewhat significantly. (I am talkting about original SD from AX, there has been talk of SD being tainted with anadrol in some clones so users of clones may not have experienced this effect). Although the actual lump may have gotten smaller, I often has problems with prolactin (minor lactation) towards the end of my cycle.

    What do you guys think?

    ps. I still have some more chemistry to learn so if i made any mistakes please point them out.
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    Quote Originally Posted by xtyler View Post
    I wasn't talking about nolva!
    The question is still here: why SD lead to a so deep suppression if its profile is close to something like anavar or winstrol(no aromatization,no progestational activity and low androgenic potential).

    i think of it this way
    5a reduced steroids dont aromatize at all, yet phera, epi, and SD, tren (that just being a progestin itself) also. all gave prolactin sides. and when used with NOLVA it only enhanced the effect.

    DHT derivites or interacts with the 5a enzyme causeing a possible interaction with the estrogen receptor.


    as well as that theory i think people dose the nolva too high causing a flux of hormone which signals the adrenal glands to make DHEA and a lot of it and that aromatizes (converts to andro then it converts to test/estrogen) and being that nolva doesnt reduce estrogen, you have your problem

    the reson is in there, ESTROGEN will shut down the hypothalmus, and by having an effect on it you get a highly anabolic subbstance with no chance to aromatize with severe shut down.

    i forgot to add that in im sorry.
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    Quote Originally Posted by xtyler View Post
    I wasn't talking about nolva!
    The question is still here: why SD lead to a so deep suppression if its profile is close to something like anavar or winstrol(no aromatization,no progestational activity and low androgenic potential).
    winstrol will shut you down....

    ALTERATION OF HORMONE LEVELS IN NORMAL MALES GIVEN THE ANABOLIC STEROID STANOZOLOL
    M. SMALL 1 G. H. BEASTALL 1 C. G. SEMPLE 1 R. A. COWAN 1 C. D. FORBES 1
    1 University Department of Medicine and Pathological Biochemistry, Royal Infirmary, Glasgow
    Correspondence: Dr M. Small, University Department of Medicine, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK.
    Copyright 1984 Blackwell Publishing Ltd
    ABSTRACT
    Abstract REFERENCES

    Anabolic steroids have widespread metabolic effects but, to date, their proven clinical indications have been limited. Recently the 17 α-alkylated steroid, stanozolol, has been shown to be of value in a variety of commonly occurring vascular diseases. Its endocrine effects have received little attention and we have investigated the effect of administering a 14 d course of stanozolol (10 mg orally per day) on a variety of important hormonal pathways in nine healthy male subjects. Significant changes occurred as follows: a 55% reduction in serum testosterone levels was noted and was accompanied by reductions in 'derived' free testosterone, sex hormone binding globulin and LH levels; total T4 and T3 levels fell in association with a decrease in thyroxine binding globulin, but no alteration was detected in TSH or free T4 levels. Changes in vitamin D status, with falls in 25-hydroxycholecalciferol and vitamin D binding globulin were also observed. These effects were reversible on stopping treatment. Stanozolol therapy therefore leads to a number of hormonal changes, probably by an action at both pituitary and hepatic levels.

    and again these cause shut down at higher levels,... minimally with anavar at 10mg per day but ....... still the interaction with the 5a reductase enzyme i believe has a lot to do with it,.
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    Quote Originally Posted by dice404 View Post
    I believe this is due to superdrol's similarities to anadrol. The only differance between SD and anadrol is that anadrol has an OH group bonded to a carbon and hydrogen, which is then double bonded to carbon 2. Superdrol has a methyl group (CH3) at carbon 2. If you look at the structure of anadrol on paper, it doesn't look like it would aromatise because it lacks a double bond between carbons 4 and 5. However, we all know that anadrol induces heavy bloating and estrogen related sides. It is believed that this is due to direct stimlulation of the receptor.

    I think this may hold true for SD to a certain extent as far as prolactin goes. I think that SD may directly stimulate receptors to cause prolactin induced sides.

    My other thought refers to SD's similarities to masteron. Masteron is extremely dry and has been shown to reduce estrogen. Now too much E2 supression can lead to a rise in prolactin, which I think may also be a problem here.

    Through personal experience, I have found that while on superdrol, I dry out a lot. When I had gyno(had it removed), I found that while on SD, my gyno actually shrunk somewhat significantly. (I am talkting about original SD from AX, there has been talk of SD being tainted with anadrol in some clones so users of clones may not have experienced this effect). Although the actual lump may have gotten smaller, I often has problems with prolactin (minor lactation) towards the end of my cycle.

    What do you guys think?

    ps. I still have some more chemistry to learn so if i made any mistakes please point them out.
    i believe it makes it a supersaturated form or anadrol, but Ziquor knows this better then me.

    but from all the research ive done. phera some people had prolactin sides with, epi, Super, i think it INDIRECTLY involves the estrogen receptor, because if it was a direct effect i believe there would be much more bloat.
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    Quote Originally Posted by crazyfool405 View Post
    winstrol will shut you down....
    Of course it does....and so does anavar....and every other anabolic or androgen out there. I tried to point that out in the first post, but apparantly there is a magical explanation out there as to why a steroid would shut you down that hes looking for...

    holy
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    Quote Originally Posted by holyintellect View Post
    Of course it does....and so does anavar....and every other anabolic or androgen out there. I tried to point that out in the first post, but apparantly there is a magical explanation out there as to why a steroid would shut you down that hes looking for...

    holy
    AHAH. Poor sarcasm.
    Even my cat knows that dear captain obvious.
    I hope you can understand the difference between suppression and shutdown and different levels of suppression.
    I try to be kind,but useless posts like this one make me crazy.
    No e-**** sizing match please,I posted an answer in a pretty easyly understandable fashion and I'm looking for some expert's only opinion.
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    Quote Originally Posted by xtyler View Post
    AHAH. Poor sarcasm.
    Even my cat knows that dear captain obvious.
    I hope you can understand the difference between suppression and shutdown and different levels of suppression.
    I try to be kind,but useless posts like this one make me crazy.
    No e-**** sizing match please,I posted an answer in a pretty easyly understandable fashion and I'm looking for some expert's only opinion.
    Ok. I'm going to try to make this thread a little less hostile.

    For anyone who isn't clear on this, I think he knows that superdrol, like any other AAS will cause supression of the HPTA, but comparativly speaking, superdrol causes faster supression of the HPTA than it seems like it would on paper. Other steroids, like trenbolone and nandrolone cause shutdown very quickly (exactly how quickly depends on many factors like the individual, dose, etc.) and there are known reasons for this. Anavar has a mild androgenic profile and therefore it takes longer for complete HPTA supression to take place (also keep in mind the factors above). each of these compounds when looked at on paper show reasons why the concurent effects on the speed of HPTA supression occur, but the speed of SD's action on the HPTA is somewhat mysterious.

    hopefullly I clarified what the OP was trying to get across.

    Holy, you seem very knowledgable and I would appreciate it if you gave this another look. If the OP or I are wrong on any accounts please point them out. We are all here to learn and I value your opinion greatly.
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    i'm no expert but i think you'll find that the tighter an androgen binds to the receptor the more supression will occur... superdrol compared to phera plex or even epistane actually has a lower anabolic/androgenic rating on paper. In reality though superdrol binds a lot tighter to the receptor which causes harder shutdown, more sides and generally more gains hope this helps and it was a perfectly legitimate question too...
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    i can't see how this wasn't a perfectly legitimate question...
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    Quote Originally Posted by ezza View Post
    i can't see how this wasn't a perfectly legitimate question...

    I agree....I dont think its a stupid question or a question without merit. I do think however, that sometimes things that involve chemicals (and I make a living in the chemical field) arent black and white, but grey. We all know that anabolics and androgens cause suppression/shutdown. We also know that certain chemicals sometimes look fantastic on paper yet exhibit a different activity in the real world than we would have anticipated based on their structure/Q factor/ etc...Then you get into a situation where chemicals affect everyone differently. I take it and have no hair loss/ you take it and lose handfuls....There are just lots of variables to factor in when talking about why something suppressed you. I just didnt see the big mystery with this compound as it relates to the original question, and I actually thought there were three decent responses (not mine) that gave theories.

    I didnt mean to belittle the question, just the fact that there is no real answer to be gotten. Instead of throwing something sarcastic out there, I should have just made this point and left it alone. Im not fond of people trolling in my posts either....

    holy
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    Quote Originally Posted by dice404 View Post
    Ok. I'm going to try to make this thread a little less hostile.

    For anyone who isn't clear on this, I think he knows that superdrol, like any other AAS will cause supression of the HPTA, but comparativly speaking, superdrol causes faster supression of the HPTA than it seems like it would on paper. Other steroids, like trenbolone and nandrolone cause shutdown very quickly (exactly how quickly depends on many factors like the individual, dose, etc.) and there are known reasons for this. Anavar has a mild androgenic profile and therefore it takes longer for complete HPTA supression to take place (also keep in mind the factors above). each of these compounds when looked at on paper show reasons why the concurent effects on the speed of HPTA supression occur, but the speed of SD's action on the HPTA is somewhat mysterious.

    hopefullly I clarified what the OP was trying to get across.

    Holy, you seem very knowledgable and I would appreciate it if you gave this another look. If the OP or I are wrong on any accounts please point them out. We are all here to learn and I value your opinion greatly.
    Apparently someone's able to read.
  

  
 

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