I have been reading a lot about test taper at the ending of a cycle as a smoother and better way to keep your gains from the cycle. Also, including some use of clomid and nolva to help the transition. I like know peoples experiences and opinions about this. thanks
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Test Taper
- Thread starter Chim Chim
- Start date
- Joined
- Mar 16, 2007
- Messages
- 25,912
It really doesnt help all that much. That's if youre using long esters like enanthate. Now if youre using short esters like prop then you would want to taper in my opinion. Long esters taper naturally on their own as the half life is so long.
- Joined
- Oct 18, 2007
- Messages
- 11
This is actually quite untrue. Even though it is a long ester, the blood levels will not be stable during the decline of the ester. I suggest you head over to t-nation, and read the threads provided from Prisoner22. This is the only site I have come across where people quit a cycle cold turkey, and rely on nolva or clomid to get the hpta back up and running. During this time, they lose too much muscle while their natural test struggles to get going. Why not taper, use a stasis period where the levels are just above that of your natural test production, then taper down so there is a smooth transition where your body now kicks the hpta into gear to provide the proper proportion of estrogen and test in the body. This protocol has worked for so many without the crash and depression of coming down from a cycle, and I suggest you give it a try in your next cycle as you will never return from your "traditional" pct.
Craig
- Joined
- Feb 8, 2007
- Messages
- 744
This is so wrong....
First of all look into pharmacokinetics of long estered test. Do you really understand how it works? Say you had an injection of test on monday of week 12 - lets say 1000 mg for the sake of simplicity. After 1 half life has passed ( cant recall exactly what it was for enanthate - lets say 7 days, the exact number doesnt really matter) - you will have 500 mg in the system. In another 7 days, 250 mg, then 125 etc. IF THIS IS NOT A SMOOTH TAPER I DONT KNOW WHAT IS!!! And it tapers down over a period of WEEKS, this is as long and as smooth as you ever are going to get!!!
Lets get into your another point.
HPTA will not recover until all exogenous test in your system is gone!!! It has no need to recover otherwise, your body will sense normal or above normal test and E2 levels, in this case it has NO REASON to be producing its own hormones!!!!
It doesnt matter if you taper or not, you need to be completely clean for HPTA recovery to begin!!!
Also low test levels are not the reason for losing gains off cycle!!! Its increased cortisol levels!! Which your body will produce as long as it senses increased androgen levels, understand this!
First of all look into pharmacokinetics of long estered test. Do you really understand how it works? Say you had an injection of test on monday of week 12 - lets say 1000 mg for the sake of simplicity. After 1 half life has passed ( cant recall exactly what it was for enanthate - lets say 7 days, the exact number doesnt really matter) - you will have 500 mg in the system. In another 7 days, 250 mg, then 125 etc. IF THIS IS NOT A SMOOTH TAPER I DONT KNOW WHAT IS!!! And it tapers down over a period of WEEKS, this is as long and as smooth as you ever are going to get!!!
Lets get into your another point.
HPTA will not recover until all exogenous test in your system is gone!!! It has no need to recover otherwise, your body will sense normal or above normal test and E2 levels, in this case it has NO REASON to be producing its own hormones!!!!
It doesnt matter if you taper or not, you need to be completely clean for HPTA recovery to begin!!!
Also low test levels are not the reason for losing gains off cycle!!! Its increased cortisol levels!! Which your body will produce as long as it senses increased androgen levels, understand this!
- Joined
- Jun 17, 2006
- Messages
- 252
tapering works for me. i take it down to 250 a week for a few weeks until my weight stabilizes. works best if you switch to a PH oral like epistane or halodrl 50 for a few weeks while your final test shot clears and cortisol levels stabilize. this is the key, otherwise coming off a androgen like test leaves cortisol levels raging. using a oral anabolic compound during this time seems to work good. adding in hcg and igf lr3 with the igf overlapping ino pct is the best.
don't knock it till you try it!
note: the one time i came off cold turkey from 750 mg a week was brutal. felt depressed and shrunk at a unbeliviable rate(13 pounds) no matter the food intake. this lead me research cortisol and its effects post cycle. doing the above will limit your expousure to high cortisol levels and give you a chance to mentally adjust to lower levels of hormones.
don't knock it till you try it!
note: the one time i came off cold turkey from 750 mg a week was brutal. felt depressed and shrunk at a unbeliviable rate(13 pounds) no matter the food intake. this lead me research cortisol and its effects post cycle. doing the above will limit your expousure to high cortisol levels and give you a chance to mentally adjust to lower levels of hormones.
Last edited:
- Joined
- Oct 31, 2007
- Messages
- 32
Rather than using a TAPER, where you will still essentially transition from a state of HPTA shutdown directly into PCT, I suggest using a "Finisher"...
The FINISHER: A FAST-acting steroid MUST BE UTILIZED at the end of your cycle's duration! You MUST remain ANABOLIC right up until post cycle therapy! If you FAIL to use a fast-acting steroid such as testosterone propionate, Winstrol or Oxandrolone during your FINAL weeks while your long-esterfied steroids leave your system, you will LOSE GAINS BEFORE YOU EVEN BEGIN post cycle therapy. This is one of the BIGGEST mistakes people make. Test E will not leave your system for at LEAST 3 weeks after your FINAL SHOT. Therefore, you MUST remain anabolic during these 3 weeks when your adrogen levels PLUMMET!
-Ross
The FINISHER: A FAST-acting steroid MUST BE UTILIZED at the end of your cycle's duration! You MUST remain ANABOLIC right up until post cycle therapy! If you FAIL to use a fast-acting steroid such as testosterone propionate, Winstrol or Oxandrolone during your FINAL weeks while your long-esterfied steroids leave your system, you will LOSE GAINS BEFORE YOU EVEN BEGIN post cycle therapy. This is one of the BIGGEST mistakes people make. Test E will not leave your system for at LEAST 3 weeks after your FINAL SHOT. Therefore, you MUST remain anabolic during these 3 weeks when your adrogen levels PLUMMET!
-Ross
- Joined
- Oct 18, 2007
- Messages
- 11
We can certainly argue this until we are both blue in the face, low test levels not responsible for losing gains off cycle? Is that some sort of joke? I ask you to try the taper, read about it and try it......sometimes talking about the science behind certain protocols isn't always the answer, I suggest you try a proper taper and then come back here with your testimonial. EVERY person I have ever heard using a proper taper would NEVER go back to a standard cold turkey pct.
Craig
- Joined
- Oct 18, 2007
- Messages
- 11
- Joined
- Oct 18, 2007
- Messages
- 11
From Prisoner22, researched based taper
Testicular atrophy is not something you need to be afraid of. It is simply what any muscle, gland or node appears like when it is not at work.
When the testes are not being activated by LH secretion from your pituitary to manufacture sperm, their metabolic demands decrease, and with that blood supply decreases as well. Blood supply increases or decreases to any area of the body via vasodilatation, which is triggered by an increase in acidosis - the by-product of tissue metabolism. You can see this quit evidently in your muscles when you train arms you get a pump and your arms can increase in diameter sometimes as much as 1/2 inch to a full inch.
Lymph nodes increase in size during times of infection - same process - an increase in tissue metabolism means greater blood flow needs, which causes increase in size, and temperature - due both to increased blood flow and metabolism.
Atrophy has nothing to do with tissue down grade or tissue remodelling. So don't have fear that you are doing damage to your testicles while you are on steroids.
Actually by not subjecting them to any LH or minimal amounts you will cause the leydig receptors to actually be MORE sensitive to your own natural secretion of LH from the pituitary, so once you taper off, initially your test levels should be HIGHER for a bit until your body regulates itself and returns to homeostasis.
As for using hcg, it will only work for the weeks you use it during the long cycle, and after that for a long period of time your testicles will return to being as small or even smaller. Receptor mediated drugs like HCG over time, create what is commonly know as 'tolerance'. Over time the dose of the drug will have to be increased to creat the same effect. Now this rule is INARGUABLE! it's just a fact of pharmacology. And is the reason why not to use hcg, as your ledig receptors will be LESS sensitive to your own natural secretion of LH when you come off, and you can imagine that this will have the opposite effect of what was stated in the above paragraph.
So you see that is why it's not that productive at anytime to use HCG.
Now to the research supporting using testosterone to taper off with:
Studies of using testosterone for a male contraceptive have shown that it does not cause azoospermia in all men and definitely not at lower dosages (below 100mg test E per week) (Masumoto, 1990) (Armory, et al., 2001). That is the reason test E has never been used for a contraceptive. The fact is that even while you are on cycle your body is still active to a certain degree secreting LH. Depending on what steroid(s) you are using i.e. the degree of androgenicity/ how strongly a steroid binds to the AR and the ease in which a compound is aromatised will govern to what degree your hpta is still active (Winters,et al., 1979).
Studies have actually proved this, where using 50mg of test enanthate on a weekly basis in normal men only lowered FSH and LH secretion by 50% when compared to the placebo group, and larger doses of 100mg and 300mg per week though found to be suppressive, were equally inconsistent in causing azoospermia (Masumoto, 1990) (Armory, et al., 2001). Doses of 25mg of testosterone enanthate had no effect on FSH or LH levels or sperm production compared with placebo (Masumoto, 1990).
A good example of this that many of you have probably found is if you are on cycle using lighter compounds such as Primo, Anavar, smaller amounts of Test, Equipoise, Winstrol, Tbol, Dbol, e.t.c. your testicles may not be in a fully atrophied state, however, if you switch your drugs to nandrolone, or trenbolone (which bind strongly to the AR), you will see further shrinkage in the testes. This anecdotal evidence clearly backs the above findings: Some steroids are more suppressive and cause greater shutdown! That of course is why I recommend waiting six weeks at a static 100mg of test E per week, to clear these steroids and their derivatives from your body before gradually decreasing the testosterone dose.
Further, there is evidence to show that using an anti-E concurrently with 100 mg of test E per week, so that E is prevented from binding with the receptors in the Hypothalamus prevents any shutdown of sperm production at all (Naftolin, et al., 1973)(Winters, et al., 1979). Highly anabolic agents such as halo, e.t.c at these low doses where shown to do similarly without even the use of an anti E, as these drugs do not aromatize (Winters, et al., 1979).
So, if you want to regain testicular size during a cycle, simply plan in your cycle to remove the highly androgenic compounds from your body (i.e. compounds that aromatise well and bind well to the AR), switching to compounds that have a higher anabolic ratio and concurrently using clomid, and you will ultimately improve the testicular size.
Absolutely no HCG is needed to accomplish this!
So anyways to wrap up, as I said before, the hpta is not fully suppressed when using testosterone in weekly doses below 100 mg of Enathate per week, if used concurrently with an anti E. The goal is to keep estrogen in physiologically normal, or slightly lower than normal levels, or else use clomid or nolva, which antagonize the ER. By doing this you can actually stave off 100% of hpta suppression, while still using 100 mg of test Enathate a week according to the literature.
If you wait the six week static waiting period, using 100mg of Test enathate per week while allowing other non testosterone compounds you may have used during your cycle to clear- (which I might add is like a natural taper - allowing your body to slowly come down from being on say greater than 1 gram of AAS per week) and then you begin to taper your dose from 100 mg per week using an anti E concurrently to ensure the hpta is capable of being active....
Each week as you continue to taper down your dose of test, the amount of FSH/LH secreted in your pituitary will increase, and the amount of natural test will increase as well. As LH increases, Sperm production increases, which increases the metabolic demands of the testes, and blood flow then dramatically increases to the area in response to metabolic demands causing hypertrophy - and usually some discomfort - actually some have had to use ice to the area to relieve the discomfort!
Tapering off your anti-E:
As you get down to the 50-25mg per week range you should be tapering off the anti-E as it will no longer be needed to keep your hpta active according to the literature. This is necessary to do on another front, as you need to up-regulate the ER so that it isn't super sensitive to small amounts of estrogen when you finally go off causing late-onset gyno, and even complete shut down... Chronic use of anti-E's causes decreases in estrogen exposure, and just like any drug, if you don't use it for a while, your body becomes more sensitive to it's effects. This means you need to slowly reacclimatize your ER to normal amounts of estrogen aromatisation. You accomplish this by tapering your anti-E so that you should be completely off it by the week you are using only 25mg, which research shows causes absolutely no hpta suppression whatsoever.
So anyways, by the end of the taper you can see now how the testes will have had plenty of time to increase in size. If you didn't use hcg, you can also see how the testes would have been almost hyper-responsive to your own natural LH production when it actually 'kicked into gear'.
And of course the six week waiting period on 100mg of test E is important, as it doesn't matter what pct method you use, if you still have levels of AAS in your system and their by-products, it doesn't matter what you do, you can't recover yet until they are cleared.
So basically the taper does the following:
-It gives your body time to adjust from being exposed to a lot of hormones to being just on normal physiological amounts vs the cold turkey approach
-It allows non-testosterone AAS to clear your body, while you still maintain your size and your libido and workout intensity doesn't have to change
-It allows 'lag-time', for the testes to respond, and your body to adjust back to normal amounts of testosterone.
-At no time does the level of testosterone in your body ever fall bellow physiological norms.
-At no time should you expect to lose your libido
-Best of all you can count the entire taper period as being 'off steroids' as technically you are in the normal physiological range of blood testosterone levels for the entire time you are doing the six week taper. (not the six week waiting period).
Therefore you can return to another cycle in six-week time- and expect good gains.
.
References
Armory, J., Anawalt, B., Bremner, W., Matsumoto, A., (2001) Daily Testosterone and Gonadotropin Levels are Simmilar in Azoospermic and Nonazoospermic Normal Men Administered Weekly Testosterone: Implications for Male Contraceptive Development. Journal of Andrology, 22(6). 1053-1060
Matsumoto, A., (1990) Effects of chronic Testosterone Administration in Normal Men: Safety and Efficacy of High Dosage Testosterone and Parallel Dose-Dependant Suppression of Luteinizing Hormone, Follicle Stimulating Hormone, and Sperm Production*. Journal of Clinical Endocrinology and Metabolism, 70(1). 282-287
Naftolin, F., Judd, H., Yen, S., (1973) Pulsatile Patterns of Gonadotropins and Testosterone in Man: The Effects of Clomiphene With and Without Testosterone. Journal of Clincal Endocrinology and Metabolism, (36)1. 285-
Winters, S., Janick, J., Loriaux, L., Sherrins, J., (1979) Studies of Sex Steroids in the Feedback Control of Gonadotropin Concentrations in Men. II. Use of Estrogen Antagonist Clomiphene Citrate*. Journal of Clinical Endocrinology and Metabolism, 48(1). 222-234
Testicular atrophy is not something you need to be afraid of. It is simply what any muscle, gland or node appears like when it is not at work.
When the testes are not being activated by LH secretion from your pituitary to manufacture sperm, their metabolic demands decrease, and with that blood supply decreases as well. Blood supply increases or decreases to any area of the body via vasodilatation, which is triggered by an increase in acidosis - the by-product of tissue metabolism. You can see this quit evidently in your muscles when you train arms you get a pump and your arms can increase in diameter sometimes as much as 1/2 inch to a full inch.
Lymph nodes increase in size during times of infection - same process - an increase in tissue metabolism means greater blood flow needs, which causes increase in size, and temperature - due both to increased blood flow and metabolism.
Atrophy has nothing to do with tissue down grade or tissue remodelling. So don't have fear that you are doing damage to your testicles while you are on steroids.
Actually by not subjecting them to any LH or minimal amounts you will cause the leydig receptors to actually be MORE sensitive to your own natural secretion of LH from the pituitary, so once you taper off, initially your test levels should be HIGHER for a bit until your body regulates itself and returns to homeostasis.
As for using hcg, it will only work for the weeks you use it during the long cycle, and after that for a long period of time your testicles will return to being as small or even smaller. Receptor mediated drugs like HCG over time, create what is commonly know as 'tolerance'. Over time the dose of the drug will have to be increased to creat the same effect. Now this rule is INARGUABLE! it's just a fact of pharmacology. And is the reason why not to use hcg, as your ledig receptors will be LESS sensitive to your own natural secretion of LH when you come off, and you can imagine that this will have the opposite effect of what was stated in the above paragraph.
So you see that is why it's not that productive at anytime to use HCG.
Now to the research supporting using testosterone to taper off with:
Studies of using testosterone for a male contraceptive have shown that it does not cause azoospermia in all men and definitely not at lower dosages (below 100mg test E per week) (Masumoto, 1990) (Armory, et al., 2001). That is the reason test E has never been used for a contraceptive. The fact is that even while you are on cycle your body is still active to a certain degree secreting LH. Depending on what steroid(s) you are using i.e. the degree of androgenicity/ how strongly a steroid binds to the AR and the ease in which a compound is aromatised will govern to what degree your hpta is still active (Winters,et al., 1979).
Studies have actually proved this, where using 50mg of test enanthate on a weekly basis in normal men only lowered FSH and LH secretion by 50% when compared to the placebo group, and larger doses of 100mg and 300mg per week though found to be suppressive, were equally inconsistent in causing azoospermia (Masumoto, 1990) (Armory, et al., 2001). Doses of 25mg of testosterone enanthate had no effect on FSH or LH levels or sperm production compared with placebo (Masumoto, 1990).
A good example of this that many of you have probably found is if you are on cycle using lighter compounds such as Primo, Anavar, smaller amounts of Test, Equipoise, Winstrol, Tbol, Dbol, e.t.c. your testicles may not be in a fully atrophied state, however, if you switch your drugs to nandrolone, or trenbolone (which bind strongly to the AR), you will see further shrinkage in the testes. This anecdotal evidence clearly backs the above findings: Some steroids are more suppressive and cause greater shutdown! That of course is why I recommend waiting six weeks at a static 100mg of test E per week, to clear these steroids and their derivatives from your body before gradually decreasing the testosterone dose.
Further, there is evidence to show that using an anti-E concurrently with 100 mg of test E per week, so that E is prevented from binding with the receptors in the Hypothalamus prevents any shutdown of sperm production at all (Naftolin, et al., 1973)(Winters, et al., 1979). Highly anabolic agents such as halo, e.t.c at these low doses where shown to do similarly without even the use of an anti E, as these drugs do not aromatize (Winters, et al., 1979).
So, if you want to regain testicular size during a cycle, simply plan in your cycle to remove the highly androgenic compounds from your body (i.e. compounds that aromatise well and bind well to the AR), switching to compounds that have a higher anabolic ratio and concurrently using clomid, and you will ultimately improve the testicular size.
Absolutely no HCG is needed to accomplish this!
So anyways to wrap up, as I said before, the hpta is not fully suppressed when using testosterone in weekly doses below 100 mg of Enathate per week, if used concurrently with an anti E. The goal is to keep estrogen in physiologically normal, or slightly lower than normal levels, or else use clomid or nolva, which antagonize the ER. By doing this you can actually stave off 100% of hpta suppression, while still using 100 mg of test Enathate a week according to the literature.
If you wait the six week static waiting period, using 100mg of Test enathate per week while allowing other non testosterone compounds you may have used during your cycle to clear- (which I might add is like a natural taper - allowing your body to slowly come down from being on say greater than 1 gram of AAS per week) and then you begin to taper your dose from 100 mg per week using an anti E concurrently to ensure the hpta is capable of being active....
Each week as you continue to taper down your dose of test, the amount of FSH/LH secreted in your pituitary will increase, and the amount of natural test will increase as well. As LH increases, Sperm production increases, which increases the metabolic demands of the testes, and blood flow then dramatically increases to the area in response to metabolic demands causing hypertrophy - and usually some discomfort - actually some have had to use ice to the area to relieve the discomfort!
Tapering off your anti-E:
As you get down to the 50-25mg per week range you should be tapering off the anti-E as it will no longer be needed to keep your hpta active according to the literature. This is necessary to do on another front, as you need to up-regulate the ER so that it isn't super sensitive to small amounts of estrogen when you finally go off causing late-onset gyno, and even complete shut down... Chronic use of anti-E's causes decreases in estrogen exposure, and just like any drug, if you don't use it for a while, your body becomes more sensitive to it's effects. This means you need to slowly reacclimatize your ER to normal amounts of estrogen aromatisation. You accomplish this by tapering your anti-E so that you should be completely off it by the week you are using only 25mg, which research shows causes absolutely no hpta suppression whatsoever.
So anyways, by the end of the taper you can see now how the testes will have had plenty of time to increase in size. If you didn't use hcg, you can also see how the testes would have been almost hyper-responsive to your own natural LH production when it actually 'kicked into gear'.
And of course the six week waiting period on 100mg of test E is important, as it doesn't matter what pct method you use, if you still have levels of AAS in your system and their by-products, it doesn't matter what you do, you can't recover yet until they are cleared.
So basically the taper does the following:
-It gives your body time to adjust from being exposed to a lot of hormones to being just on normal physiological amounts vs the cold turkey approach
-It allows non-testosterone AAS to clear your body, while you still maintain your size and your libido and workout intensity doesn't have to change
-It allows 'lag-time', for the testes to respond, and your body to adjust back to normal amounts of testosterone.
-At no time does the level of testosterone in your body ever fall bellow physiological norms.
-At no time should you expect to lose your libido
-Best of all you can count the entire taper period as being 'off steroids' as technically you are in the normal physiological range of blood testosterone levels for the entire time you are doing the six week taper. (not the six week waiting period).
Therefore you can return to another cycle in six-week time- and expect good gains.
.
References
Armory, J., Anawalt, B., Bremner, W., Matsumoto, A., (2001) Daily Testosterone and Gonadotropin Levels are Simmilar in Azoospermic and Nonazoospermic Normal Men Administered Weekly Testosterone: Implications for Male Contraceptive Development. Journal of Andrology, 22(6). 1053-1060
Matsumoto, A., (1990) Effects of chronic Testosterone Administration in Normal Men: Safety and Efficacy of High Dosage Testosterone and Parallel Dose-Dependant Suppression of Luteinizing Hormone, Follicle Stimulating Hormone, and Sperm Production*. Journal of Clinical Endocrinology and Metabolism, 70(1). 282-287
Naftolin, F., Judd, H., Yen, S., (1973) Pulsatile Patterns of Gonadotropins and Testosterone in Man: The Effects of Clomiphene With and Without Testosterone. Journal of Clincal Endocrinology and Metabolism, (36)1. 285-
Winters, S., Janick, J., Loriaux, L., Sherrins, J., (1979) Studies of Sex Steroids in the Feedback Control of Gonadotropin Concentrations in Men. II. Use of Estrogen Antagonist Clomiphene Citrate*. Journal of Clinical Endocrinology and Metabolism, 48(1). 222-234
- Joined
- Oct 31, 2007
- Messages
- 32
Great post Jcraig!!
May I add:
**How To AVOID HPTA SHUTDOWN!**
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
The Hypothalamus has Androgen, Estrogen, and Progesterone receptors.
Each and EVERY anabolic steroid affects these receptors DIFFERENTLY.
Some steroids affect ALL receptors, while some only affect ONE type of receptor, while others have very little effect on ANY of these receptors.
UNDERSTANDING WHICH steroids affect which receptors, and to WHAT DEGREE, will FULLY enable the steroid user to COMPLETELY and systematically AVOID HPTA SHUTDOWN!
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
Steroids that cause an OVERSATURATION(too many receptors activated) of these various hormone receptors, WILL CAUSE SHUTDOWN.
Steroids that DO NOT CAUSE an OVERSATURATION of ANY of these various hormone receptors, will NOT cause SHUTDOWN!
The Following drugs either DIRECTLY or INDIRECTLY activate ESTROGEN receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
The Following drugs either DIRECTLY or INDIRECTLY activate PROGESTERONE receptors, to varying degrees:
Nandrolone
Trenbolone
Oxymetholone
The Following drugs activate Androgen receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
Trenbolone
Halotestin
Oxandrolone
Stanzolol
Chlorodehydromethltestosterone
Methyltestosterone
Methenolone...
(ALL AAS*)
As we can see, the steroids that cause HPTA SHUTDOWN either OVERSATURATE ONE SPECIFIC receptor, or they activate too many TOTAL receptors(Androgen/Estrogen/Progesterone)
For instance, Trenbolone causes HPTA SHUTDOWN because it OVERSATURATES BOTH, the ANDROGEN and the PROGESTERONE receptors.
Testosterone causes SHUTDOWN because it converts to ESTROGEN and DHT, therefore, it oversaturates the Androgen/Estrogen receptors.
As we can ALSO SEE, the steroids that DO NOT cause SHUTDOWN of the HPTA, do NOT oversaturate ANY of the different hormone receptors, and thus, do NOT cause SHUTDOWN.
Methenolone(Primobolan) does not possess ANY Estrogenic or Progestational ACTIVITY WHATSOEVER. It does, by virtue of being an anabolic steroid, posses a SMALL Androgenic component. Because it lacks ANY ESTROGENIC/PROGESTATIONAL component, and it lacks a strong Androgenic component, it WILL NOT CAUSE SHUTDOWN!
Oxandrolone(Anavar) posseses NO Estrogenic/Progestational component either. AND, it also lacks a strong androgenic component. Thus, Anavar will NOT cause shutdown.
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
*It must also be noted, that ANY steroid in LARGE enough DOSAGES for long enough DURATIONS, can cause SHUTDOWN of the HPTA.
NOT ALL ANDROGENS CAUSE SHUTDOWN*
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)
Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
-------------------------------------------------------------------------
Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.
We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS
[R]
May I add:
**How To AVOID HPTA SHUTDOWN!**
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
The Hypothalamus has Androgen, Estrogen, and Progesterone receptors.
Each and EVERY anabolic steroid affects these receptors DIFFERENTLY.
Some steroids affect ALL receptors, while some only affect ONE type of receptor, while others have very little effect on ANY of these receptors.
UNDERSTANDING WHICH steroids affect which receptors, and to WHAT DEGREE, will FULLY enable the steroid user to COMPLETELY and systematically AVOID HPTA SHUTDOWN!
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
Steroids that cause an OVERSATURATION(too many receptors activated) of these various hormone receptors, WILL CAUSE SHUTDOWN.
Steroids that DO NOT CAUSE an OVERSATURATION of ANY of these various hormone receptors, will NOT cause SHUTDOWN!
The Following drugs either DIRECTLY or INDIRECTLY activate ESTROGEN receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
The Following drugs either DIRECTLY or INDIRECTLY activate PROGESTERONE receptors, to varying degrees:
Nandrolone
Trenbolone
Oxymetholone
The Following drugs activate Androgen receptors, to varying degrees:
Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
Trenbolone
Halotestin
Oxandrolone
Stanzolol
Chlorodehydromethltestosterone
Methyltestosterone
Methenolone...
(ALL AAS*)
As we can see, the steroids that cause HPTA SHUTDOWN either OVERSATURATE ONE SPECIFIC receptor, or they activate too many TOTAL receptors(Androgen/Estrogen/Progesterone)
For instance, Trenbolone causes HPTA SHUTDOWN because it OVERSATURATES BOTH, the ANDROGEN and the PROGESTERONE receptors.
Testosterone causes SHUTDOWN because it converts to ESTROGEN and DHT, therefore, it oversaturates the Androgen/Estrogen receptors.
As we can ALSO SEE, the steroids that DO NOT cause SHUTDOWN of the HPTA, do NOT oversaturate ANY of the different hormone receptors, and thus, do NOT cause SHUTDOWN.
Methenolone(Primobolan) does not possess ANY Estrogenic or Progestational ACTIVITY WHATSOEVER. It does, by virtue of being an anabolic steroid, posses a SMALL Androgenic component. Because it lacks ANY ESTROGENIC/PROGESTATIONAL component, and it lacks a strong Androgenic component, it WILL NOT CAUSE SHUTDOWN!
Oxandrolone(Anavar) posseses NO Estrogenic/Progestational component either. AND, it also lacks a strong androgenic component. Thus, Anavar will NOT cause shutdown.
By understanding WHICH steroids cause SHUTDOWN and which steroids do NOT, we can formulate a perfect EXTENDED CYCLE.
*It must also be noted, that ANY steroid in LARGE enough DOSAGES for long enough DURATIONS, can cause SHUTDOWN of the HPTA.
NOT ALL ANDROGENS CAUSE SHUTDOWN*
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)
Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
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Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.
We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS
[R]
- Joined
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This has been my experience exactly. If you keep pumping in more exogenous test you will continue to suppress your own endogenous output. All tapering did was put off my pct that much longer, and in the end you need a longer pct to recover.
Last edited:
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Many have a lot of luck running it that way. It looked good hypothetically and tested out to be just as good. Doing short esters for only 2 weeks though, perhaps the 3 weeks is better.
Last edited:
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The point is to slowly taper the exogenous test. Testosterone is testosterone, your body cannot tell the difference if it is injected or producing it naturally. Based on how much test is currently in the body, the hpta reacts to keep the balance. You certainly would not be puting off pct any longer if your are injecting below maintanace level of your natural test, and therefor creating an environment where the body will begin producing its own.
Craig
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This is not true. I have seen something on 2 week oral cycles causing a rebound of test to higher than normal but this is not true of any extended cycle. It is lutenizing hormone that recovers quickly after a cycle, to above normal levels! The reason it may take a long time to recover is that the testes are not responsive after a cycle.
You can read more about this if you read Dr Chrisler's (SWALE) posts on various boards.
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Actually, the testes are very responsive after a cycle, especially when subjected to LH which they have not seen for an extended period of time. The problem is the state of atrophy the testes have been subject too, which takes time for them to recover. Many people including myself feel like I have been "kicked in the junk" so to speak for a few days while the boys get back to a normal size.
Craig
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- Nov 9, 2003
- Messages
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I have found threw experimentation what works best for me is to end my cycles with short ester, prop in my case. I end all test cycles with two weeks of test prop. It seems to make the transition faster and less painful, loosing minimum gains. With this protocol you start pct right after last inject, no two week wait like with long ester.
Jig
Jig
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