Understanding Post Cycle “T” Recovery
by William Llewellyn

O.K. You have been on an awesome 4-month cycle of Sustanon and Dianabol. You’ve gained a massive 20 lbs, and are extremely pleased with your results. You can’t stop looking in the mirror. But there is a problem now starting to eat away at you. You are going to run out of steroids very soon (you know you need a break anyway), and your testicles are the size of raisins. Your body is producing less testosterone than a 9-year-old girl, and you are scrambling to figure out what to do to avoid a nasty post-cycle crash that could potentially strip away some of your hard-earned muscle. The opinions on how to restore endogenous testosterone production post-cycle seem to be different everywhere you look. What option is best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right post-cycle program can be quite confusing. In this article I would therefore like to discuss the role of anti-estrogens and HCG during this delicate window of time, while detailing an effective strategy for their use.

The Axis

The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body’s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

Testicular Desensitization

Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.

Post-Cycle LH Levels

Post Cycle Testosterone Levels

Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.

The Role of Anti-estrogens

It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.

HCG

So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.

Finalizing the Program

An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added (my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.

Sample Post-cycle Plan:

Week
Amount

Week 3:
5000IU HCG total + 20mg Nolvadex daily

Week 4:
5000IU HCG total + 20mg Nolvadex daily

Week 5:
2500IU HCG total + 20mg Nolvadex daily

Week 6:
20mg Nolvadex daily

Week 7:
20mg Nolvadex daily

Week 8:
20mg Nolvadex daily

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Chris
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Clomid, Nolvadex and Testosterone Stimulation
by William Llewellyn

Introduction

I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.

Clomid and Nolvadex

I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.

Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.

Pituitary Sensitivity to GnRH

But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.

The Estrogen Clomid

The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".

Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.

Conclusion

To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.

Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.

In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.

References:

1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45

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Chris
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How To Cycle Off From Steroids...
by Pat Arnold

Introduction

Heavy steroid using athletes, particularly weight lifters, bodybuilders, football players, hockey players, shotputters etc., are subject to many adverse consequences from continuous steroid use without a break. Adverse cardiovascular effects, liver stress, HPTA downregulation, excessive virilization (women) and psychological disturbances or dependency, are some of the major problems that may develop in these individuals. Additionally, users may develop a tolerance for anabolic steroids that can only be overcome by increasing the dosage or by ceasing the use altogether. The latter, of course, is a much healthier course of action than the former.

Coming off of steroids, particularly long-term usage, is certainly not easily done without considerable loss of muscle mass. Additionally, there can be psychological effects that include depression and loss of motivation. For many athletes, especially those with schedules that do not allow prolonged periods away from competition completely coming off of steroids is not considered an option. However, if these athletes knew how to take the right approach they just might be able to cycle off and have a good chance at maintaining much of their physical condition. This could enable them to increase their ultimate potential in their sports as well as their longevity in the competitive arena.

The Strategy
The off cycle regimen must consist of proper drug, nutritional, and training protocols. The primary goals to achieve are the following:

Minimization of protein catabolism

Maintenance of muscle glycogen levels

Maintenance of high-normal red blood cell levels

Minimization of fat deposition

Avoidance of injury, or injury aggravation

Maintenance of healthy attitude and psychological state

Drugs
This is an off steroids cycle and most certainly not an off drugs cycle. In fact, the proper use of non-steroidal drugs is the mainstay of this program and is vital to its success. I will describe the drugs to be used, why they are used, and how they should be used.

Growth Hormone

GH is probably the single most important drug to maintain muscle mass and bodyweight off of steroids. While GH is not known to be great for anabolic effects, it is very effective for anti-catabolism. Anti-catabolism, or minimization of muscle mass loss, is after all what we are most interested in here. GH has an overall anti-proteolytic effect on the body and shifts the body’s metabolism away from the utilization of amino acids and glucose for energy, and towards the use of fat. The end result will be a protective effect upon muscle protein and glycogen, and a mobilizing effect upon body fat.

Many bodybuilders have discovered how wonderful GH, at the proper dosages, is in maintaining their muscle mass off of steroids. Former IFBB pro Gary Strydom once commented that he didn’t care if the IFBB tested for steroids, as long as they didn’t test for GH.

Notice how I said “at the proper dosages”. That’s right, small dosages just won’t cut it. For most people a minimum of 4 i.u. a day is required to impart a proper metabolic response in the body. Some may go as high as 18 i.u. a day but at this levels many problems can occur (i.e. edema, nerve impingement).

There probably is no great advantage to taking GH more than once a day, though some may inject twice a day. GH primarily works through its conversion to IGF-1 and the half-life of IGF-1 in the body is plenty long (8-16 hours). So once a day administration will be good enough to maintain pretty constant levels of IGF-1 in the blood. Furthermore, evidence is also mounting that GH breaks down to certain active peptide fragments with specific biological functions (i.e. lipolysis) and that these have prolonged half lives. Therefore, the active lifetime of the intact GH molecule itself in the blood might be pretty irrelevant.

GH is not cheap through most channels. However, good GH can be obtained from Asia at a fraction of the cost (10 – 20%) that it is available elsewhere.

I think I should also mention now that there is a big misconception amongst people as to what the shelf life of GH is, and that most people grossly underestimate it. The Journal of Chemical Technology states that freeze dried GH products (unreconstituted) are quite stable under refrigerated conditions, and a 24-month shelf-life is typical at this temperature. Also, although solutions of GH at neutral pH readily deamidate (lose ammonia group from end of molecule), and storage of the reconstituted product is limited to a few weeks under refrigerated conditions, biological activity is relatively unaffected even after prolonged storage. So the stuff really stays pretty active in the ‘frig for a considerable time. By the way, reconstituted solutions of GH should NEVER be frozen (this will be the death of it).

Lis-Pro Insulin (Humalog®)

The use of insulin provides a couple of very important functions in the off steroid period. First of all, it helps preserve glycogen storage in the muscle. Steroids are very good at stimulating glycogen storage and this property likely plays an integral part in their performance enhancing benefits. Going off of steroids leads to a reversal of this and the result is muscular weakness, fatigue, and loss of size and bodyweight. The proper use of insulin can help minimize this.

Furthermore, insulin can help to minimize protein breakdown through its anti-proteolytic effects. Insulin is quite potent in regards to its protective effect on muscle protein, unfortunately it also is very potent in regards to its protective effect on maintaining body fat. Insulin therefore has to be used in the proper fashion to maximize the former, and minimize the latter.

The proper usage of insulin requires the fast acting insulin analog known as Lis-Pro insulin, or Humalog®. This altered insulin product is available only by prescription. It differs from other insulin in that it is absorbed quickly into the body after subcutaneous injection. The average time to peak blood levels is 90 minutes and generally it is out of your system in 3 to 4 hours.

Humalog® is to be taken immediately after training. The physiology of the body after intense training is such that the benefits of insulin can be maximized, while drawbacks are minimized. Muscle insulin sensitivity as well as insulin independent glucose uptake will peak in the 2-3 hours or so after training. In this time, insulin will preferentially stimulate glucose uptake and glycogen synthesis in muscle over fat. Additionally, high insulin levels at this time will help to counteract the catabolic state that exists in muscles right after they have been damaged by training. A discernible improvement in training recovery (less soreness and injury pain) is often noticed by individuals who utilize this technique.

Humalog® administration must be followed by intake of simple carbohydrates and protein within 20 minutes. A general rule is one unit of Humalog® per ten kilograms bodyweight, and ten grams of carbs and ten grams of protein per unit of Humalog®. That sounds like a lot of carbs and protein but it must be ingested. Whey protein is best, and glucose or maltodextrin can be used for the carbs. 5 grams of creatine can also be added as well as well as 5-10 grams of glutamine.

Erythropoietin (EPO)

Erythropoietin (EPO) is a protein hormone secreted by the kidneys and liver that stimulates red blood cell production (erythropoiesis). Red blood cells carry oxygen to the tissues of the body and so obviously are vital to maximal health and athletic performance.

When people take anabolic steroids, particularly some oral ones such as Anadrol®, erythropoiesis is stimulated. The result is an increase in the proportion of blood cells in the blood, also known as the hematocrit. This increase in the hematocrit is partially responsible for the energizing and recovery benefits of steroids. It may also contribute to the blood volume and vascularizing effects of anabolics.

When you go off anabolics, the increase in hematocrit gradually subsides and you return to pre-cycle lower levels (or below). This effect will take its toll on your physical condition and ability to train at high intensity. Therefore, administration of exogenous EPO can have obvious benefits in the steroid withdrawing athlete.

In addition to its effect in increasing hematocrit, there is some evidence that EPO has direct anabolic effects. It has been shown in rat studies to substantially increase weight gain and injury repair after surgery. Furthermore, EPO receptors are present on myoblasts (immature muscle cell progenitors) and may have a potential in muscle development and repair.

EPO is sold in recombinant form (rhEPO) for injection. One popular form is called Epogen®, and it is made for subcutaneous usage. A safe or starting dosage is usually 20 i.u. per kilogram bodyweight, 3 times/week. After two or three weeks, a maintanence dose of 20 iu/kg BW can be taken once a week. One should wait about two weeks after ceasing steroids to commence EPO therapy to avoid any excessive increases in hematocrit which can be quite dangerous. It is also very advisable to have periodic blood tests that include a hematocrit assay while taking EPO just to be safe. Interestingly, I think that this test is automatically done for free everytime you donate blood, and all you need to do is ask the nurse what your hematocrit is reading (just out of curiosity of course).

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Chris
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PCT - Start Times

Below you'll find starting times for your PCT based on the active life of each compound. The active life is the duration of time it takes for the exogenous hormone to be absorbed, utilized, and expelled; no longer being bioavailable. Keep in mind that active life is an approximation which is dependant on dose, ester, as well as the individuals metabolization of the compound ; but for the moderate user, these are as close to precise as you'll find.

Anadrol/Anapolan: 24 hours after last administration
Deca: 21 days after last injection
Dianabol: 24 hours after last administration
Equipoise: 21 days after last injection
Fina: 3 days after last injection
Primobolan depot: 14 days after last injection
Sustanon: 18 days after last injection
Testosterone Cypionate: 18 days after last injection
Testosterone Enanthate: 14 days after last injection
Testosterone Propionate: 3 days after last injection
Testosterone Suspension: 24 hours after last administration
Winstrol: 24 hours after last administration

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Chris
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Inhibitioan and Recovery of Natural Testosterone Production

by Bill Roberts

One of the most significant side effects of anabolic/androgenic steroid (AAS) use is inhibition of natural testosterone production. There is no way to entirely avoid the problem, but there are ways to minimize the problem and recover natural testosterone levels reasonably quickly after a cycle. In this article, we will look at the problem of inhibition, its causes, and the best solutions currently known.


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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.
Inhibitioan and Recovery of Natural Testosterone Production Continued

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.

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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Chris
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