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  1. #1
    Big M's Avatar
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    Stupid question, I know.....

    Just wondering If I took Armidex only.. that would stop my natural testosterone from becoming estrogen right, And since estrogen is just as suppresive on your HPTA as testosterone? would´nt the result be that I could raise my natural testosterone levels without increasing the total androgen amount in my body and therefor not get a negative feedback loop that would decrease my testosterone production again???

  2. #2
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    IMO... That's a very good question...

    Q: In your question,,,define your use of "total androgen amount"...please...

  3. #3
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    Quote Originally Posted by Big M
    Just wondering If I took Armidex only.. that would stop my natural testosterone from becoming estrogen right, And since estrogen is just as suppresive on your HPTA as testosterone? would´nt the result be that I could raise my natural testosterone levels without increasing the total androgen amount in my body and therefor not get a negative feedback loop that would decrease my testosterone production again???
    This might be a good read for ya bro.


    The Causes of Inhibition

    copied @ anabolic -paradise.com


    Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.

    This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol , which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the Clomid use.

    So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.

    What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.

    Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol ) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.


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    The Hypothalamic/Pituitary/Testicular Axis (HPTA)

    To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.

    The hypothalamus itself cannot produce any sex hormones - instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.

    The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.

    LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.


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    Inhibition From AAS Cycles

    Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:

    Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
    Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
    In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
    Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.

    I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.


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    Drugs of Use With Regard to Inhibition

    Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.

    Arimidex : This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.

    Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.



    Nolvadex : This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.

    HCG : This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia .

    Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.

    Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.

    Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.

    Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.

  4. #4
    Big M's Avatar
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    VERY VERY INTERESTING!!! Primopup But i mean, if you´ve never taken AAS and by taking Cytadren /armidex would prevent your naturaly produced testosterone from becoming estrogen... Then since (this is what i mean Froggy) the total amount of Testosterone AND estrogen would remain the same Just shifting into favour of testosterone (more testosterone to expence of the estrogen) should´nt that mean that your testosterone production will remain the same?

  5. #5
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    Quote Originally Posted by Big M
    Just wondering If I took Armidex only.. that would stop my natural testosterone from becoming estrogen right, And since estrogen is just as suppresive on your HPTA as testosterone? would´nt the result be that I could raise my natural testosterone levels without increasing the total androgen amount in my body
    Testosterone is an androgen...how can you raise test levels without raising androgen levels? Thats like me saying I'm going to drink a glass of water without raising the amount of water in my body....

  6. #6
    Nicky B's Avatar
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    Taking something strong like armidex without a real need for it good be bad. Because yes estrogen is somewhat bad but it essential to daily life for man and woman. And armidex can raise test levels by over 50%.

  7. #7
    stupidhippo is offline Anabolic Member
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    i agree but beyond the wordplay does he have a point there?

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    I don't know...if the point is that you can raise testosterone without taking steroids , by simply taking arimidex ...yeah...he has a point. It's about a decade late, but ya, he has a point.

  9. #9
    Big M's Avatar
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    Aight... You see, I know that Armidex raises your testosterone levels . But I was thinking that since estrogen levels are simultaniusly lowerd, Baybe the testes dont give a damn (about the rise in testosteron that would normaly leed to a decrease in testosterone production) and just keep pruducing normaly.

  10. #10
    Nicky B's Avatar
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    What I want to know is there a reason for this question.

  11. #11
    Big M's Avatar
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    Hi Nicky B Not really (as in i´m not planning on doing it) just a Q that popped up in my head Maybe I can refraise my question to... (how does long time use of armidex effect testosterone levels ??)

  12. #12
    stupidhippo is offline Anabolic Member
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    I am also interested in the question, not that I wanna do it but just to know....to me the question is about the feedback to hypothalamus. If the total amount of estrogen + testosterone is the same (with increased test to estro ratio) will this cause some shutting down or not. Basically my question is what causes the feedback. If it was only estrogen (which I think really that it is not) the non-aromatizing steroids wouldnt do anything to the HPTA axis.

  13. #13
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    Quote Originally Posted by PrimoPup
    This might be a good read for ya bro.


    The Causes of Inhibition

    copied @ anabolic -paradise.com



    This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, .
    Since Trenbolone is progesitin you have to use RU486. I use RU486 with Femara and Nolvadex together with 1500mg test/week 450mg trenbolone/week and after a 12 week cycle I made a blood check 5 weeks later without any PCT my test level increases %14 and LH increases %32 compared to beginning of cycle. With Deca , tren nolvadex and femara, arimidex ..etc are totally useless. You need progestin antogonist and cortisol blocker. There are many options however because of toxicity best is RU486.

  14. #14
    Big M's Avatar
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    of course it´s not only the estrogen that effects HPTA. But maybe if the total amount Test+est is unalterd (just tipping over in favour of testosterone ) the HPTA will not care... or are there different receptors maybe And the 2 hormones will effect the HPTA independently

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