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  1. #1
    TheMindOfRoss is offline Banned
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    Did You Know? Proof!

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    Inhibition/HPTA

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    The Causes of Inhibition

    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.


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    General Recommendations

    Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.

    The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.

    If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary.

    Clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. Clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then Clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from Clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.

    If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)

    Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.

    Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful.



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  2. #2
    TheMindOfRoss is offline Banned
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    ..

    http://jcem.endojournals.org/cgi/content/full/84/8/2705

    FROM ABOVE STUDY:

    "Although natural androgens such as T clearly stimulate muscle protein synthesis, they also possess androgenic or virilizing effects. Often this limits the clinician’s use of these androgens to specific patient populations such as hypogonadal men. However, efforts have been made to find alternative anabolic agents that can be used in women and children suffering from muscle-wasting diseases or trauma. Oxandrolone [Oxandrin (OX) Bio-Technology General, Iselin, NJ], a synthetic analog of T, is an oral anabolic steroid currently used as an adjunctive therapy to promote weight gain in patients after surgery, chronic infections, and severe trauma. OX improved weight gain in patients experiencing AIDS-wasting myopathy (10) as well as in convalescing burn patients (30–50% total body surface area burns) (11). In addition, OX is used by clinicians to treat children with growth disorders such as Turner’s syndrome and constitutional delay of growth and puberty (12, 13). A recent pilot study in boys with Duchenne muscular dystrophy found that OX, given at a dose of 0.1 mg/kg·day, improved muscle strength over a 3-month period (14). Given that OX is administered orally, as opposed to im as with TE, its ease of administration makes it attractive to clinicians and patients alike. Further, OX is purported to have a much greater anabolic potential than T, with fewer of the androgenic effects.

  3. #3
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    Which of your arguments does this provide proof for? Here you have "Jim" using Tren and Dbol , along with two drugs which stimulate testosterone production, and his natural testosterone levels dropped to 1/10th of their baseline! And you think those gains are more keepable than gains from test?

    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.
    Once again, the author of this article doesn't have any medical studies backing him up...he has one "case study" done without a control group....what does this article proove? If anything...?

  4. #4
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    Quote Originally Posted by TheMindOfRoss
    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.
    While some research has shown that 100mgs of Dbol (the study is cited in my dbol profile) leaves you with some of your natural hormones circulating...some other research has shown that a mere 5 and 10 mg of dbol administered daily can reduce endogenous testosterone by 66 and 73% respectively*. And this is noteworthy because it didn't depres LH, meaning it is strongly possible that dbol is having a direct effect on testicular testosterone production without any hypothalamic or pituitary action.

    So...I'd say 66-73% inhibition of testosterone is pretty hefty...and that's 1/10th of the dose the author of that article claims is "little inhibition"! Little inhibition my ass....73% is alot of inhibition!

    Also...how can taking it in the morning be said to lessen the effect? Because your body has a spike of LH, FSH, and testosterone in the morning, you can take methandrostenolone and your body won't notice? Because it's hiding? There is 0 evidence that the human body functions in the manner of being able to hide a totally foriegn compound among a spike in natural hormones.


    Reference:

    *Scand J Clin Lab Invest. 1977 Nov;37(7):577-86.
    Effect of short-term treatment with an anabolic steroid (methandienone) and dehydroepiandrosterone sulphate on plasma hormones, red cell volume and 2,3-diphosphoglycerate in athletes.
    Remes K, Vuopio P, Jarvinen M, Harkonen M, Adlercreutz H.

  5. #5
    TheMindOfRoss is offline Banned
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    Quote Originally Posted by hooker
    While some research has shown that 100mgs of Dbol (the study is cited in my dbol profile) leaves you with some of your natural hormones circulating...some other research has shown that a mere 5 and 10 mg of dbol administered daily can reduce endogenous testosterone by 66 and 73% respectively*. And this is noteworthy because it didn't depres LH, meaning it is strongly possible that dbol is having a direct effect on testicular testosterone production without any hypothalamic or pituitary action.

    So...I'd say 66-73% inhibition of testosterone is pretty hefty...and that's 1/10th of the dose the author of that article claims is "little inhibition"! Little inhibition my ass....73% is alot of inhibition!

    Also...how can taking it in the morning be said to lessen the effect? Because your body has a spike of LH, FSH, and testosterone in the morning, you can take methandrostenolone and your body won't notice? Because it's hiding? There is 0 evidence that the human body functions in the manner of being able to hide a totally foriegn compound among a spike in natural hormones.


    Reference:

    *Scand J Clin Lab Invest. 1977 Nov;37(7):577-86.
    Effect of short-term treatment with an anabolic steroid (methandienone) and dehydroepiandrosterone sulphate on plasma hormones, red cell volume and 2,3-diphosphoglycerate in athletes.
    Remes K, Vuopio P, Jarvinen M, Harkonen M, Adlercreutz H.

    The study referenced at the bottom mentions NOTHING of LH/FSH levels, or total effect on plasma T levels in the blood.

    63% Inhibition--IN PROPORTION TO THE ANABOLIC EFFECT--is nothing. I gain lbs a week off of 15mg dbol.

  6. #6
    TheMindOfRoss is offline Banned
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    Have you

    Have you, or do you KNOW anyone that has used LOW DOSES of dbol ? 10, 15 mgs ED? Or even dosing schemes of 5 ON 2 OFF?

    Everyone with dbol experience knows that its MISUSE is what gives it a bad name.

  7. #7
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    Quote Originally Posted by TheMindOfRoss
    http://jcem.endojournals.org/cgi/content/full/84/8/2705

    FROM ABOVE STUDY:

    "Although natural androgens such as T clearly stimulate muscle protein synthesis, they also possess androgenic or virilizing effects. Often this limits the clinician’s use of these androgens to specific patient populations such as hypogonadal men. However, efforts have been made to find alternative anabolic agents that can be used in women and children suffering from muscle-wasting diseases or trauma. Oxandrolone [Oxandrin (OX) Bio-Technology General, Iselin, NJ], a synthetic analog of T, is an oral anabolic steroid currently used as an adjunctive therapy to promote weight gain in patients after surgery, chronic infections, and severe trauma. OX improved weight gain in patients experiencing AIDS-wasting myopathy (10) as well as in convalescing burn patients (30–50% total body surface area burns) (11). In addition, OX is used by clinicians to treat children with growth disorders such as Turner’s syndrome and constitutional delay of growth and puberty (12, 13). A recent pilot study in boys with Duchenne muscular dystrophy found that OX, given at a dose of 0.1 mg/kg·day, improved muscle strength over a 3-month period (14). Given that OX is administered orally, as opposed to im as with TE, its ease of administration makes it attractive to clinicians and patients alike. Further, OX is purported to have a much greater anabolic potential than T, with fewer of the androgenic effects.
    Great study...it clearly shows that greater results can be had from Testosterone than from Anavar ...oh...wait...didn't you read all of it? Especially the part that said a single 200mg shot of Testosterone increased protein synthesis 200%, while Anavar increased it 44%? Here's the part I'm talking about:


    "A recent study from our laboratorydemonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences. "


    I don't think this study really supports any arguments you've made...clearly, you gain more weight from testosterone when compared with anavar, and the researchers even noted this in their study...not to mention the fact that protein synthesis is 200% greater with test, and only 44% greater with anavar. Still don't think you need test in every cycle? I'll take the 200% over the 44% every time...

    Look...anavar is a nice little drug...but the researchers have also noted in that study that, when you use anavar:

    "Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T
    "

    Sounds fun...being on a cycle with a cock-shrinking testosterone level of 98....and not taking any injectable testosterone to combat all of the sexual and mental sides that will follow...low testosterone levels can cause lethargy, depression, impotence, and a whole lot of other side effects....

    And please don't say that the sexual sides don't matter, or that you "get mad bitchez yo" ...or whatever...

    Honestly, you aren't proving your case for not needing test in every cycle...the study has clearly proven the opposite.

  8. #8
    TheMindOfRoss is offline Banned
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    Bottom Line

    Newbies, and ALL OF US for that matter--must understand what causes supression and the different KINDS of supression.

    Based on knowledge of these anabolics, one can more readily avoid side effects.

  9. #9
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    Quote Originally Posted by hooker
    Great study...it clearly shows that greater results can be had from Testosterone than from Anavar ...oh...wait...didn't you read all of it? Especially the part that said a single 200mg shot of Testosterone increased protein synthesis 200%, while Anavar increased it 28%? Here's the part I'm talking about:


    "A recent study from our laboratorydemonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences. "

    I don't think this study really supports any arguments you've made...clearly, you gain more weight from testosterone when compared with anavar, and the researchers even noted this in their study...not to mention the fact that protein synthesis is 200% greater with test, and only 44% greater with anavar. Still don't think you need test in every cycle? I'll take the 200% over the 44% every time...

    Look...anavar is a nice little drug...but the researchers have also noted in that study that, when you use anavar:

    "Serum free T concentrations were within normal physiological range on days 0, 3, and 5. However, by day 5, serum free T concentrations were significantly reduced (98 ± 10 pg/mL; P < 0.001) below day 0 (121 ± 12 pg/mL) and day 3 (126 ± 9 pg/mL) values. Hence, the total androgen concentration (T + OX) was reduced in parallel to the reduction in T (Fig. 3)."

    Sounds fun...being on a cycle with a cock-shrinking testosterone level of 98....and not taking any injectable testosterone to combat all of the sexual and mental sides that will follow...low testosterone levels can cause lethargy, depression, impotence, and a whole lot of other side effects....

    And please don't say that the sexual sides don't matter, or that you "get mad bitchez yo" ...or whatever...

    Honestly, you aren't proving your case for not needing test in every cycle...the study has clearly proven the opposite.
    The DEGREE of SUPRESSION NOTED..." (126 ± 9 pg/mL)" is NOTHING--AND THAT IS ON DAY three! DO YOU KNOW what the MEAN is?

    it does NOT mention however how ONE single DOSE of 100mg TESTOSTERONE in water (SUSPENSION) Reduced plasma T conentrations to NEAR ZILCH in DAYS!

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    "A recent study from our laboratorydemonstrated that 5 days after a single im injection of TE (200 mg), FSR and model-derived protein synthesis increased 2-fold, with no change in FBR. Further, in agreement with the present findings, Ferrando et al. (7) demonstrated an increased utilization of intracellular amino acids by showing a strong relationship between protein breakdown and protein synthesis. Although our kinetic data strongly support these findings, the magnitude of the synthetic response with OX was not as great as that with TE. With OX, we found 44% and 28% increases in FSR and model-derived protein synthesis (FO,M), respectively. Several important factors may account for these differences.

    OBVIOUSLY TESTOSTERONE causes GRATER PROTEIN SYNTHESIS--but ALSO greater SUPRESSION! OXANDROLONE can be GIVEN to WOMEN and CHILDREN!

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    Quote Originally Posted by TheMindOfRoss
    OXANDROLONE can be GIVEN to WOMEN and CHILDREN!
    Which is good news for you, I suppose.

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    yo

    Quote Originally Posted by hooker
    Which is good news for you, I suppose.



    I like you ....

  13. #13
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    Quote Originally Posted by hooker
    Which is good news for you, I suppose.

    so true

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    I think its pretty comon knowledge here that any external sex hormones will interrupt the negative feedback loop of the HPTA

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    Quote Originally Posted by TheMindOfRoss
    The DEGREE of SUPRESSION NOTED..." (126 ± 9 pg/mL)" is NOTHING--AND THAT IS ON DAY three! DO YOU KNOW what the MEAN is?


    Actually, quoting the authors of that study, next to Figure 3:

    "T decreased significantly from days 0 and 3 to day 5"

    it does NOT mention however how ONE single DOSE of 100mg TESTOSTERONE in water (SUSPENSION) Reduced plasma T conentrations to NEAR ZILCH in DAYS!
    Then post that study, please. Injecting testosterone lowers the level of testosterone in your blood? Thats news to me...because in every study I'cve ever seen, it raises it...

    Do you mean to say endogenous testosterone production, not plasma testosterone levels ? That would make more sense...

    Then again, making sense is not really your strong point...

    So far you are posting studies showing that anavar can build some muscle...and then a little bedtime story about suppression in your first post, which is pretty absurd in itself. And I am failing to see how any of what you have posted provides support for your contention that testosterone should not be included in every cycle.

    Really, AND STOP USING CAPS ALL THE TIME. It's annoying...

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    plasma

    NOT SERUM T LEVELS.....and also, I am trying desperately to find the study. It is commom knowledge. If you look at the steroid profiles on another TWO different boards, they have a Chart as follows

    Convert to Estrogen:
    Convert to DHT:
    Raises HDL
    Liver Toxic
    Effect on HPTA:


    And each steroid is rated....

    ALL testosterones rated "Severe or Extreme" for the HPTA, while most other anabolics(EQ,PRIMO,Winny,oxandrolone, dianabol ) were noted as either DOSE AND CYCLE LENGTH DEPENDENT, or simply a "yes".

    Test is HARSH to the HPTA--it is however GREAT FOR BULKING!

  17. #17
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    bump to NewB

    ALL NEWBS...understand this stuff...

  18. #18
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    Quote Originally Posted by TheMindOfRoss
    NOT SERUM T LEVELS.....and also, I am trying desperately to find the study. It is commom knowledge. If you look at the steroid profiles on another TWO different boards, they have a Chart as follows

    Convert to Estrogen:
    Convert to DHT:
    Raises HDL
    Liver Toxic
    Effect on HPTA:


    And each steroid is rated....

    ALL testosterones rated "Severe or Extreme" for the HPTA, while most other anabolics(EQ,PRIMO,Winny,oxandrolone, dianabol ) were noted as either DOSE AND CYCLE LENGTH DEPENDENT, or simply a "yes".

    Test is HARSH to the HPTA--it is however GREAT FOR BULKING!

    bro, testosterone is SUPPOSED to shut you down........it is the BEST for mass and strength........its why you are a man.......it is not only crucial for maintaining and adding muscle mass, and sexual function, but also for healthy function......therefore it is important to add to every cycle to ensure your test levels are not lowered (yes, they're lowered from var only cycles)

    yes your endogenous is shut down (it is supposed to be), but it will come back with proper PCT)

    testosterone is cheap, effective, and if anyone gets sides, they can be easily controlled.......stick with your var, primo, eq, dbol cycles and gain your few pounds.......not to mention have the test levels of an older man.......

    btw, test is great for cutting as well..........

  19. #19
    pitbull27's Avatar
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    Quote Originally Posted by wolfyEVH
    btw, test is great for cutting as well..........
    Good point!

  20. #20
    TheMindOfRoss is offline Banned
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    Quote Originally Posted by wolfyEVH
    bro, testosterone is SUPPOSED to shut you down........it is the BEST for mass and strength........its why you are a man.......it is not only crucial for maintaining and adding muscle mass, and sexual function, but also for healthy function......therefore it is important to add to every cycle to ensure your test levels are not lowered (yes, they're lowered from var only cycles)

    yes your endogenous is shut down (it is supposed to be), but it will come back with proper PCT)

    testosterone is cheap, effective, and if anyone gets sides, they can be easily controlled.......stick with your var, primo, eq, dbol cycles and gain your few pounds.......not to mention have the test levels of an older man.......

    btw, test is great for cutting as well..........

    It is crucial to ALWAYS have NORMAL amounts of TEST--not SUPRAPHYSIOLOGICAL levels of test. Because NO--you are not SHUTDOWN when you are on a var cycle--you are supressed. So to "throw the baby out with the water", is absurd. Just because your test levels are REDUCED, doesn't mean we might as well just SHUT THEM DOWN?!?! NO WAY!!

  21. #21
    TheMindOfRoss is offline Banned
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    well..

    WELL--for those juiceheads who do 16week+ cycles and are used to having NO libido--it doesn't matter I guess. but for those of us who are still healthy--Test is not the way to go-not ALWAYS.

  22. #22
    j martini is offline Member
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    Testosterone is king.

    Anavar and primo or fine, if you are looking for a more athletic muscular body, but test will truly turn you into a beast. It is also much cheaper.

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    Quote Originally Posted by TheMindOfRoss
    NOT SERUM T LEVELS.....and also, I am trying desperately to find the study. It is commom knowledge. If you look at the steroid profiles on another TWO different boards, they have a Chart as follows
    !
    I was talking about the level of test in your body...not intratesticular test, or whatever you seem to like talking about as if it's relevant. When you shoot test, you have more test floating around in your body, but at some point none of it is natural.

    By the way...concerning profiles...

    I don't look at profiles from other boards. This board has the best profiles on the 'net. Bar none. End of story.

    If you are talking about 'ology, they simply took that chart you seem fond of from Chemical Muscle Enhancement, and then pasted it over the steroid profiles from Anabolics2000.

  24. #24
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    omg ross stop it, it s getting absurd

  25. #25
    UK CHRIS is offline Associate Member
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    If he posts with any more caps im gonna shoot my computer screen.......give it up MIND...OF...ROSS!!!!!!!!!

  26. #26
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    Quote Originally Posted by hooker
    I was talking about the level of test in your body...not intratesticular test, or whatever you seem to like talking about as if it's relevant. When you shoot test, you have more test floating around in your body, but at some point none of it is natural.

    By the way...concerning profiles...

    I don't look at profiles from other boards. This board has the best profiles on the 'net. Bar none. End of story.

    If you are talking about 'ology, they simply took that chart you seem fond of from Chemical Muscle Enhancement, and then pasted it over the steroid profiles from Anabolics2000.
    I wonder who the author is of those profiles......

  27. #27
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    Quote Originally Posted by ***xxx***
    omg ross stop it, it s getting absurd
    I really wish people would just start ignoring Ross

  28. #28
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    Quote Originally Posted by longhorn814
    I really wish people would just start ignoring Ross
    Ditto

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