T Nation

P-22 Test Tapering 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


lattimus wrote:
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

Test Tapering for PCT
First Cycle - 27 Years Old

Thanks for putting this together P22.


Very informative. Thanks for the lesson.


Very good read. When I get these nagging injuries cured for good, I plan to get on the sauce and will follow your protocol. It may still be a while but the day will come. Then I'll be like "BOOM! take a look at this hunk of mass..."


Excellent work. Very promising



A couple of questions and comments. Again I am not seeking an argument or to start a pissing match just seeking information

In the first study you cite which is based on TE as a male contraceptive, the subjects that are referenced were never given more than 25, 50 MGS of TE if I am reading it right. The subjects that were receiving 100 or 300 MG TE appear to be suppressed. It seems like it would be more supportive if the subjects were given supraphysiologic doses of TE, then used the lower dose and then were assessed. Maybe I am reading it wrong, but the higher dose TE subjects were shut down?

Here is the key phrase In the 100-mg and 300-mg TE groups, mean monthly fluoroimmunoreactive FSH and LH levels were suppressed by 86%-97%, bioactive FSH and LH levels by 62%-80%, and roughly half the subjects became azoospermic.

It appears the 2nd references the same study as the first. Here is the key phrase to me.
In normal men, chronic testosterone (T) administration results in negative feedback suppression of gonadotropin and sperm production. However, azoospermia is achieved in only 50-70% of men treated with high dosages of T. So are 50-70% of men shut down with high dosage or most are and some are not. So I guess the only way to find out where a AAS user would fall is to try the taper method after a heavy cycle. If your lose muscle, get depressed, feel lethargic 6 months later, maybe you should try a conventional PCT or just go back on,?

In the 3rd abstract if this is the one you were referencing from pubmed, it takes eugonadal men and administers clomid and we see that 6 weeks later test levels are up. Clomid is an anti-cancer/fertility drug as are most of the AIs. You asked someone to explain to you why anyone would want to take fertility or anti cancer drugs like pergonal or Lupron, I guess because they raise test levels and increase sperm levels like Clomid and Tamoxifen, one anti-cancer and one a dual use fertility drug for males and females. If this is not the one you were referencing could you post the abstract.

I could not get the fourth reference to come up. It was probably me. Can you post that as well?

Daily testosterone and gonadotropin levels are similar in azoospermic and nonazoospermic normal men administered weekly testosterone: implications for male contraceptive development
J. K. Amory, B. D. Anawalt, W. J. Bremner and A. M. Matsumoto
Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System and Department of Medicine, University of Washington School of Medicine, Seattle, USA. jamory@u.washington.edu
Weekly intramuscular administration of testosterone esters such as testosterone enanthate (TE) suppresses gonadotropins and spermatogenesis and has been studied as a male contraceptive. For unknown reasons, however, some men fail to achieve azoospermia with such regimens. We hypothesized that either 1) daily circulating serum fluoroimmunoreactive gonadotropins were higher or testosterone levels were lower during the weekly injection interval, or 2) monthly circulating bioactive gonadotropin levels were higher in nonazoospermic men. We therefore analyzed daily testosterone and fluoroimmunoreactive gonadotropin levels as well as pooled monthly bioactive and fluoroimmunoreactive gonadotropin levels in normal men receiving chronic TE injections and correlated these levels with sperm production. After a 3-month control period, 51 normal men were randomly assigned to receive intramuscular TE at 25 mg (n = 10), 50 mg (n = 9), 100 mg (n = 10), 300 mg (n = 10), or placebo (n = 12) weekly for 6 months. After 5 months of testosterone administration, morning testosterone and fluoroimmunoreactive follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were measured daily for a 1-week period between TE injections. In addition, fluoroimmunoreactive and bioactive FSH and LH levels were measured in pooled monthly blood samples drawn just before the next TE injection. In the 100-mg and 300-mg TE groups, mean monthly fluoroimmunoreactive FSH and LH levels were suppressed by 86%-97%, bioactive FSH and LH levels by 62%-80%, and roughly half the subjects became azoospermic. In the 1-week period of month 6, daily testosterone levels between TE injections were within the normal range in men receiving placebo, or 25 or 50 mg of weekly TE, but were significantly elevated in men receiving 100 or 300 mg of weekly TE. At no point during treatment, however, were there significant differences in daily testosterone or fluoroimmunoreactive gonadotropin levels, or monthly bioactive gonadotropin levels between men achieving azoospermia and those with persistent spermatogenesis. This study, therefore, demonstrates that neither monthly nor daily differences in serum testosterone, or fluoroimmunoreactive or bioactive gonadotropins explain why some men fail to completely suppress their sperm counts to zero with weekly TE administration. Innate differences in the testicle's ability to maintain spermatogenesis in a low-gonadotropin environment may explain persistent spermatogenesis in some men treated with androgen-based contraceptive regimens.

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

Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production
AM Matsumoto
Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington 98108.
In normal men, chronic testosterone (T) administration results in negative feedback suppression of gonadotropin and sperm production. However, azoospermia is achieved in only 50-70% of men treated with high dosages of T. Furthermore, the relative sensitivity of LH and FSH secretion to chronic administration of more physiological dosages of T is unclear. We determined whether a T dosage higher than those previously given would be more or less effective in suppressing spermatogenesis and whether, within the physiological range, T would exert a more selective effect on LH than on FSH secretion. After a 4- to 6-month control period, 51 normal men were randomly assigned to treatment groups (n = 9-12/group) receiving either sesame oil (1 mL) or T enanthate (25, 50, 100, or 300 mg, im) weekly for 6 months. Monthly LH and FSH levels by RIA and twice monthly sperm counts were determined. During treatment, T levels were measured daily between two weekly injections. Chronic T administration in physiological to moderately supraphysiological dosages resulted in parallel dose- dependent suppression of LH, FSH, and sperm production. T enanthate (50 mg/week) suppressed LH and FSH levels and sperm counts to 50% of those in placebo-treated men (ED50). T enanthate (300 mg/week), was no more effective than 100 mg/week in suppressing LH, FSH, and sperm production. Serum T levels in men who received 100 and 300 mg/week T enanthate were 1.5- and 3-fold higher than those in placebo-treated men, respectively. Except for mild truncal acne, weight gain, and increases in hematocrit, we detected no significant adverse health effects of chronic high dosage T administration. We conclude that 1) LH and FSH secretion are equally sensitive to the long term negative feedback effects of T administration; 2) sperm production is suppressed in parallel with the LH and FSH reductions induced by chronic T administration; and 3) even at the clearly supraphysiological dosage of 300 mg/week, T enanthate does not reliably induce azoospermia in normal men. However, there was also no evidence of a stimulatory effect of this T dosage on spermatogenesis. Furthermore, we found no evidence of major adverse health effects of T administered chronically even at the highest dosage.

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-

Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism.

Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, Goluboff E.

Department of Urology, NY Presbyterian Medical Center, New York, NY, USA.

AIM: Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio. METHODS: Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed. RESULTS: The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 +/- 39.8 ng/dL and 32.3 +/- 10.9, respectively. By the first follow-up visit (4-6 weeks), the mean testosterone level rose to 610.0 +/- 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients. CONCLUSIONS: Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estradiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway.


Yes for the most part anything over 100mg seemed to cause shutdown in most subjets.

I don't folow this? The studies show a stepped progression of degree's of suppression according to how much test Enantate is being given on a weekly basis. What you have to read into this is that the negative feedback loop works both ways. - I you go from 100mg per week of AAS use to 50mg per week of AAS use, you should expect to be only 50% suppressed - meaning your testes are producing near 50% of the testosterone in you body at the moment if you are following my protocol. There is absolutely no reason as I have said if you were eugonadic before going on why you shouldn't return to the same state following the taper. If you arn't eugonadic then you can take this research a step further - adding 25 mg per week of test E won't cause any suppression but may just be the extra little amout you need.


I'm just wondering why T-Nation hasn't offered you a job.

I may not agree with you 100% but at least you present your case in a very intelligent and respectful manner - something that has been sorely missing for the last 6 months, or so.


You stated that this was for long and heavy cycles, but what are your thoughts on shorter cycles? Are "conventional" PCT methods adequate with them or do you recommend a similar tapering strategy there as well?


I depends on what esters you are using. If you use the Decanoate ester i.e. nandrolone, it is best if you use this method to come off, as you will need the six week waiting period.

as for the taper itself after the six week waiting period, the length of how long you want to taper for is completely up to you.
Just keep in mind that you are doning absolutely no harm to your hpta by stringing it out further, to ensure the easieset come-down possible.


This is surely a very interesting read :slightly_smiling:



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I also wonder why T-Nation doesn't hire you as well or at least ask you to write an article or two for the masses. Not only is it quite evident that you are quite knowledgeable in this field, you are also one who has direct experience with the information you write.

When I finally do embark on another traditional cycle (I'm still in the middle of some other exotic protocols now, and don't want to mess up my evaluation process) I plan on using the tapering protocol for PCT. I just makes logical sense to me and appeals to my understanding and formal professional training of how "systems", especially feedback control systems, work.


So even when you are at 50mgs of test/ week, you're not allowing full recovery. We can agree that when you have 50mgs of test injected, you get to keep half of your LH and FSH, right? Ok...soooo...

From skimming this post, there is no clear evidence presented which shows that when you are already 100% suppressed, you'll even begin to recover while you are using this dose.

Look at it this way (rewording of what's been said by P22):

50mgs of testosterone will allow you to keep 50% of your LH and FSH levels.
Right? Lets agree that his study strongly suggests the validity of that statement.

Ok, now lets apply that to a taper:

Since you are starting fully suppressed and therefore have no LH or FSH to speak of, you can keep your 50% of it by using 50mgs of Test. 50% of nothing is still nothing. 50% recovery of nothing is still nothing. Thus HPTA recovery will probably be nothing.

Thinking otherwise is like having a bank account with no money in it, and trying to earn interest! Yeah, just because the bank promises 4% interest, doesn't mean you get it if there's no money to start with in your account.

As you're tapering down, by his admission, you are fully suppressed until you reach the 50mg/week dose, at which point you retain 50% of your LH and FSH. Which in this case is nothing. You've kept 50% of the HPTA you started with, as per the study. You've kept nothing, also. Remember, the 50mgs doesn't RAISE your test to 50% of baseline...it LOWERS them by 50%. And you already have nothing in that bank.

In addition, why would this taper be more worthwhile than letting the natural half-life of TE just taper itself down?

Well researched, and a good effort- but invalid. The leap from "50mgs of TE lowers LH/FSH to 50%" to "50 mgs of TE will increase your LH/FSH by 50%" is being attempted here.

But it doesn't even matter, because a Billion percent of nothing is still nothing...and even if you can keep 50% of your HPTA running while shooting 50mgs of TE....that's not going to help you at all, because 50% of your non-functioning HPTA- is still zero.

If anyone is interested, this protocol, dose for dose and week for week- is the exact one Duchaine outlined in the original "Underground Steroid Handbook."


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How long does the HTPA take to recover by itself after being completly suppressed (by a normal cycle)?


I see what you are saying...but
And therefore the lag time of Testosterone Enanthate's natural taper...can be disproportionately altered by injecting Testosterone Enanthate? Just in smaller doses? If it's a proportionate lag time, then you're left with the same problem, aren't you?

The Lag time will be the lag time, if there even is one that's noteworthy...and I'm not convinced that there is. You're still injecting the same drug, just in smaller doses, and the lag time would be proportionately the same.

But the bigger issue, and real problem with this protocol, is the much larger issue I raised above.


In yo face nurse boy !!!


E-thuggin' it yo!


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