Recovery of Natural Testosterone Shut Down.

One of the most significant side effects of anabolic steroids 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.

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 where used 50 mg/day of Trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, and 50 mg/day Clomid as an estrogen receptor blocker.  Estrogen levels remained in the normal range. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct.  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. 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 ) manipulation of these would not seem useful in bodybuilding.

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.

Inhibition From Anabolic Steroids 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 anabolic steroids 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 anabolic steroids 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 anabolic steroids 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 anabolic steroids 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.

Drugs of Use With Regard to Inhibition

Arimidex:  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 anabolic steroids: 

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.

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 anabolic steroids 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 anabolic steroids being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful

Human Growth Hormone and Testosterone Therapy for Heart Failure

Human Growth Hormone (HGH) and testosterone supplementation have shown promising effects in patients with heart failure despite numerous small, short-term clinical trials showing mixed results. Selected patients may benefit from supplementation in addition to conventional therapy, in particular patients with documented hormonal deficiency (below or in the low-normal range). Patients with suspected HGH resistance may warrant pretreatment screening prior to supplementation to adjust dosing and possible direct IGF-1 administration in addition to HGH. However, from our knowledge, there are no direct studies with both HGH and IGF-1 supplementation in  heart failure, thus recommendations cannot be made regarding this dual therapeutic approach.

Minimal data exist for combined therapy of HGH and testosterone in the setting of heart failure. The studies using combined HGH and testosterone supplementation were mostly conducted in older men with testosterone and IGF-1 in lower ranges of normal. One study showed promising effects on the improvement of body composition and muscle performance,  while another study found no change in function, mood and body composition. However, the latter study observed improvements in balance and muscle IGF-1 gene expression. Future studies investigating combined HGH and testosterone therapy in patients with heart failure would be warranted in order to assess possible synergistic effects, which may be advantageous over monotherapy.

Testosterone treatment has been shown to exert beneficial effects in both men and women with heart failure with few adverse effects. In our patients with advanced heart failure and other comorbid conditions, we routinely screen for and treat testosterone deficiency. Approximately 20–30% of our heart failure patients, those with ventricular assist devices and patients with postorthotopic heart transplantation status, have received supplemental testosterone at some point. Anecdotally, the patients have improved nutritional status as well as improved functionality and sense of well being. Although our patients appear to show some clinical improvement with testosterone therapy, we currently do not have conclusive data to recommend testosterone therapy in heart failure patients. Despite the promising role of hormonal supplementation in Heart Failure, larger, long-term, randomized clinical trials are warranted to further assess efficacy and safety of manipulation of the hormonal imbalance in patients with chronic Heart Failure.

Patients with heart failure are often observed to have hormonal dysregulation. HGH/IGF-1 axis derangement and testosterone deficiency have been an area of great interest as an adjunctive therapy in patients with advanced heart failure. While early studies show that HGH supplementation in patients with heart failure enhances cardiac function resulting in improvement in clinical symptoms, subsequent studies did not demonstrate significant improvements in cardiac morphology, performance or clinical status. However, the studies have been small with relatively short study duration. Of note, the inconsistent data may be linked to HGH resistance in patients and this may affect the biochemical response to HGH therapy. Patients with HGH resistance were observed to have lower levels of IGF-1, thus combination therapy of both HGH and IGF-1 may be beneficial. Coadministration of HGH and IGF-1 in patients with heart failure have not been fully investigated, thus the efficacy and safety of this therapeutic approach remains uncertain.

The majority of adverse effects observed in patients on long-term HGH replacement therapy include edema, insulin resistance, arthralgia and myalgia. These adverse effects were often related to higher dosing; therefore, appropriate dosing will have to be addressed to minimize adverse effects but maximize beneficial outcomes. Because there are inconsistent data on efficacy and lack of long-term assessment on safety – large randomized clinical trials are needed to fully evaluate these issues before starting patients on HGH-replacement therapy.

Similarly, testosterone therapy in patients with heart failure shows improvement in functional status and prognosis. Multiple studies observe improvements in parameters such as LV performance, incremental shuttle walk test and mean peak oxygen consumption. The adverse effects of testosterone therapy have been associated with exacerbation of prostate cancer, atherosclerosis, unfavorable lipid profiles and polycythemia. These adverse effects were mainly observed when testosterone was administered at supraphysiological levels. Despite the positive benefits of testosterone replacement, the long-term efficacy and safety remains unclear and will need to be addressed prior to committing a patient to long-term therapy.

HGH and testosterone therapy have shown promising benefits in patients with heart failure. At present, many institutions, including our own, are actively participating in trials to reproduce the data observed in earlier studies. As more data are available and large clinical studies show consistent benefits with minimal adverse effects, hormonal supplementation may become an integral agent in the treatment of heart failure. If the benefits and safety are clearly established, patients may be prescreened for low levels of HGH and testosterone early on in their course of disease. This strategy may lead to earlier initiation of hormone therapy with hopes of improving functional status and quality of life.

Anabolic Steroids & Hair Loss – Available Treatment Options

When it comes to the subject of hair loss, you will find strong opinions on both sides of the fence. For some, it is simply a natural part of life; not something to be feared or despised. Being met with acceptance, these individuals fret little over the state of their hairline, opting to take a razor to their heads rather than invest in potentially costly treatments designed to spare this cranial covering. For others, hair loss can have a profound impact on the emotional well being of the individual, causing anxiety and negatively affecting one’s self-perception and quality of life.

While hair loss is genetically dependent, the use of anabolic steroids can dramatically accelerate the rate at which hair loss takes place, causing the user to begin the balding process 5, 10, or even 20 years sooner than would have occurred under natural circumstances.

A misconception exists that only certain steroids can exacerbate hair loss; particularly those with either a strong androgenic component or which convert to DHT. This is untrue. There is no doubt that certain anabolic steroids are more problematic than others, but the reality is that any anabolic steroids can hasten the rate at which hair is shed, even those with the best track records of success, such as Anavar or Turinabol. While personal response will play the largest role in determining how one responds to the various anabolic steroids, it should be understood up-front that all anabolic steroids share this potential trait.

Still, we are not completely at the mercy of these drugs. We have at our disposal a variety of treatments/procedures capable of stopping or even reversing this undesirable side effect. How one reacts to these can vary considerably, as results are dependent on drug/supplement type, personal response to the treatment employed, and whether or not the root cause is being properly addressed. However, prior to engaging in any hair loss program, one should first determine the exact cause(s), as this can eliminate wasted time and money. To this end, setting up an appointment with an endocrinologist who specializes in this area is a must, as bloodwork is necessary in order to verify the origin of hair loss, thereby pointing one in the correct direction.

The most commonly used products in this category is Finasteride, which belong to the category of drugs known as 5-AR inhibitors. By directly decreasing the conversion of testosterone to DHT, these products reduce the amount of DHT available to androgen receptors in the scalp, thereby slowing or even halting DHT-induced hair loss. For those steroid users who rely on testosterone to increase muscle mass, 5-AR inhibitors are the most effective form of hair loss prevention available.

However, one should be aware that these drugs have side effects when consumed orally. Orally ingested 5-AR’s are systematic in nature, affecting DHT production throughout the entire body. This can have multiple unwanted side effects, such as a decrease in libido, reduced strength, and a weakened alpha-male mind-set. For this reason topical preparations are gaining in popularity, as their subdermal delivery systems allow the drug to bypass the circulatory system and directly enter the hair follicle where they are wanted.

As effective as these drugs can be for preventing DHT-induced hair loss, they offer no protection from the hair-shedding effects of other anabolic steroids. In order to prevent/reduce hair loss from other steroids, one must turn to anti-androgenic preparations which prevent anabolic steroids from binding to the AR, such as spirinolactone. Most bodybuilders will recognize spirinolactone as a potassium-sparring diuretic most commonly used to dry-out before going onstage, but of particular relevance to this discussion is its ability to bind to the AR, effectively preventing other androgens from attaching to the androgen receptor and exerting their deleterious effects on the hairline. It should also be mentioned that Spirinolactone possesses mild 5-AR inhibiting effects of its own, although certainly not as potent as Finasteride. Available in both oral and topical form, most choose to use the topical version due to its diminished propensity to cause systematic side effects.

Other drugs/supplements which fall into this same category of anti-androgens include metformin, various types of DHT inhibiting shampoos While the active ingredients and delivery methods of these products may vary, their mechanisms of action are identical, in that they either reduce DHT conversion or prevent DHT/steroids from attaching to the receptor site.

Products which speed the rate of hair growth: These products do not reverse or even stop hair loss. Rather, they supply ingredients which help your currently existing hair grow more quickly. Usually amino acid and vitamin-based, these products are most often formulated as shampoos. Higher quality versions utilize delivery systems similar to the topical anti-androgens, allowing them to penetrate the scalp and reach target tissues in concentrated form. While tablet/capsule varieties exist, orally consuming these products often prevents the active ingredients from reaching the hair follicle at sufficient dosages.

Hair fortifying/volumizing products: This category has no effect on hair loss prevention, re-growth, or the rate of hair growth. The sole purpose of these products is to strengthen the individual hair strands, while making them look thicker and healthier. This adds to the overall body, or volume of one’s hair. Basically, it “dresses up” what you already have, making it look better. There are numerous different products that fit this description, which again, are mostly in the form of shampoos.

With plenty of options available for treating hair loss, there is no need to sit back and let nature take its course. With a little bit of forethought and planning, anyone should be able to slow, stop, or even reverse this process. In almost all cases a holistic approach is best, as many of these products work synergistically to produce results superior to single product programs.

Although no one program can claim to be the most effective, certain protocols appear to provide above average results in the general population. These programs typically include an anti-androgen, a nitric oxide stimulator, anti-androgenic shampoos, and vitamin & mineral supplementation.

Keep in mind that these products take several weeks—and usually several months—just to begin working, so a long-term commitment (at least 6-12 months) is required in order to reap the desired benefits. Lastly, this is not a one and done cure. These products must be used indefinitely in order to continue experiencing these benefits. Otherwise, the hair loss process will resume all over again. While a permanent solution would be ideal, at least we have clinically and anecdotally proven products at our disposal, which will continue providing results so long as one is willing to use them over the long-haul.

Hair Loss and Bodybuilding

Everybody loses some hairs daily, for example, when combing or washing their hair, and this is a norm. But losing too much hair is a pathology and should be treated. Some start to lose hair in their twenties. The hair of others start to thin and fall out after a stress, while some people are just predisposed to hair loss and become bald gradually, as they age. Statistically men are affected by baldness much more often, than women. But what causes hair fall in men and how can it be treated?

About one of three men suffers from hair loss. Men are more predisposed to hair fall due to testosterone, the principal male sex hormone, which is normally present in a male’s body in larger amounts, than in a female’s one. In general hair fall can be caused by the following factors:

• stress,
• chemotherapy,
• pregnancy,
• overactive or malfunctioning thyroid gland,
• certain infections,
• iron deficiency,
• menopause

One of the side effects of anabolic steroids is baldness. This is due to the fact, that anabolic steroids contain this male sex hormone. As bodybuilding is associated with anabolic steroids, bodybuilders often suffer from this condition. Avoiding steroid abuse can help prevent hair loss.

No matter, what causes hair loss – stress or the intake of certain drugs, – the following procedures are proved to be effective against hair fall:

• hormone therapy,
• applying special lotions,
• hair transplantation.

The first way to treat baldness is hormone therapy. It hinders the male sex hormone affecting hair follicles and, thus, stops hair fall. It can be quite effective, if used during a long period of time. One of the disadvantages of hormone therapy is the fact, that the side effects of its long-term use are unknown. By the way, it’s not recommended to bodybuilders, as it can hinder muscle growth, which is actually the aim of every bodybuilder.

In addition to hormone therapy, there are also local solutions of the hair fall problem, such as using topical lotions containing minoxidil (Brand name: Rogaine). They are applied directly to the scalp. Such lotions improve blood circulation of the hair follicles, which slows down hair loss. There has not been carried out any studies on the interaction of lotions containing minoxidil and anabolic steroids taken intramuscularly or orally.

Today hair transplantation has become pretty popular among men wanting to stop losing their hair. It is a surgical procedure and involves the following: the hair follicles are taken from one part of the head (or the body) and are then implanted in the “problematic zones”. This procedure is very promising to give men losing hair their head of hair back. Besides, it can be used by bodybuilders, as there hasn’t been found contraindications.
Before choosing this or that method of hair loss treatment, consult a qualified doctor.