Not trying to start a fight with P22 or any of the taper guys, as I stated I am giving it a shot just as P22 laid it out, only exception is I am running a 100 MG for 4 weeks instead of 6 because I ran Primo for the last 3 weeks of my cycle and by the time the taper started I had been off Deca for 7 weeks or so.
Anti Taper Information
Two things need to be understood.
Testicular sensitivity will degrade from both too much activity and insufficient activity. It is important to maintain the balance. Steroid use will cause insufficient activity and will cause the testes to become desensitized to the effects of LH. (about 90% reduction in sensitivity after 16 weeks of steroid use, despite what the author says) (1-6)
If an individual becomes desensitized, normal physiological levels of LH or FSH will not be enough to stimulate normal production again. A super-physiological dose would be required to ï¿½??shockï¿½?? the testes back into normal production. Puberty would be a good comparative example.
The best PCT in the world involves duplicating the hormonal milieu of puberty (Very high LH/FSH, GH, IGF-1, TGF, ect) Puberty does not happen with a trickle of LH and FSH ï¿½?? it is a complete gonadotropin/hormonal bombardment.
Now, there are quite a few things wrong in that article. [It would take hours to refute every wrong assumption] For simplicity sake, here is the sentence with the biggest problem that shows rudimentary HPTA knowledge on the authors behalf -
ï¿½??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.ï¿½??
Firstly, you donï¿½??t need to taper to bring back LH/FSH levels. They will automatically return to normal levels within weeks of cessation from AAS use and will come back even faster if you use anti-estrogens such as arimidex, letrozol, clomid, nolva, ect. Regaining normal LH/FSH is not the problem with recovering from AAS. The problem lies in sensitivity, as in, the testicular response to LH/FSH
In the study referenced below, a group of men were administered steroids for 16 weeks. After the steroid use they were administered 4500iu of hCG to test the response in T production. The result was that the hCG increased testosterone to only 1/3 of the pre-steroid values.
This suggests that the leydigs where dramatically less responsive to hCG/LH stimulation because of the 16 week deprivation of LH.
[FYI, in a healthy individual a 4500iu hCG shot would more than double testosterone]
So, the problem with tapering is that even if LH began to trickle from the pituitary on a lesser steroid dose, it would be a fraction of what is normally produced, and would be far less than what would be required to ï¿½??shockï¿½?? the testes into T production.
The purpose of on cycle hCG [as the author managed to construe] is to keep the testes functioning normally during a cycle when a sufficient LH/FSH signal is absent. Again, this is about balance, and too much hCG can desensitize, but the right dose will prevent desensitization. I often suggest 200-250iu 2x a week as the ideal dose during a cycle.
Whatï¿½??s worse about this authors protocol is that guys are now extending their once 8 week cycle to a 14 week cycle in belief that they are actually recovering in those last 6 weeks on a lower dose of steroid. The fact is, they arnt producing an ounce of their own testosterone, and are only further decreasing their testicular sensitivity to LH. (thus making PCT even harder in the future)
Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)
Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 - 2602.
Luteinizing hormone on Leydig cell structure and function.
Histol Histopathol 12:869ï¿½??882 (1997)
Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
SM Mendis-Handagama, PA Watkins, SJ Gelber, and TJ Scallen
Endocrinology, Dec 1992; 131: 2839.
Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, Mendis-Handagama SMLC, Zirkin BR, Ewing LL.
Endocrinology 1988; 123:2906ï¿½??2915.
6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 - 1111.
Here is the original taper thread…
Tapering: research based
I thought I would post this here for all to read, as I have been promising to drop a reasearched based article written by me , and most are familiar with the testosterone tapering protocol I use from other threads. Enjoy the read!
Tapering: research based
P22 -What about testicular atrophy? I think that is the biggest concern (at least MY biggest concern) when going on long, heavy cycles. I am not that concerned with fertility issues, just the physiological aspects of seeing my testicles in an unhealthy state.
What if one chose to self-administer testosterone therapy with heavy and light doses for a long period of time? How do you avoid increasingly shrunken balls?
Is your stance that we can achieve 100% HPTA recovery with restored testicle size from the test taper? Wouldn’t this recovery rate depend on age (i.e. the older you are, the slower the recovery and possibly decreased testicle size)?? Do you think that NO ONE at any age should use HCG, even for intermittent use during the cycle?
And I ask all of this respectfully because I would like your thoughts on the topic.
Good question. 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.
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