On the exit from the “cycle” of AAS and the role of gonadotropin in this process



Once on the forum of one of the sites I respect, I happened to read the following maxim. I am citing it not literally, because, speaking on the forums, many for some reason prefer to resort to vocabulary, which is usually called “obscene”, and such for such a solid publication as our magazine is, for obvious reasons, unacceptable. But the general meaning will be preserved by me intact. So, the author of this maxim wonders why clomid is so praised , and asks the question of who is spreading the obviously false information that gonadotropin (meaning human chorionic gonadotropin) does not contribute to the restoration of the functioning of the “hypothalamus-pituitary-testicles” arc (HPH) …

The answer to the second question is all modern medicine and your humble servant as well. As for Clomid, I personally have more than once explained its role in restoring the normal functioning of the HHN on the pages of our magazine, but I will not consider it a pain to repeat all this again. But I will approach the issue today a little more broadly – this time the topic will be those processes that occur in the body when you stop taking androgens, as well as drugs and techniques that allow you to reduce the negative consequences of these processes to a minimum.

A quick look at the endocrine system in men

More precisely – on the so-called “hypothalamus-pituitary-testicles” arc. Take a look at the picture.

Testosterone is produced by Leydig cells in the testes under the influence of luteinizing hormone (LH). The higher the LH level, the more testosterone Leydig cells will produce and vice versa. The luteinizing hormone is produced by the pituitary gland, and another hormone, follicle-stimulating hormone (FSH), is produced by the same gland, its task is to stimulate spermatogenesis. The main effect on the production of both LH and FSH is exerted by hypothalamic gonadotropin-releasing hormone (GnRH).

The hypothalamus “reads” information about the level of testosterone and estradiol in the blood and regulates the production of GnRH depending on this. Interestingly, both too high estradiol levels (above normal) and too low (below normal) have a negative effect on the production of GnRH.

The pituitary gland also “uses” data on the levels of testosterone and estradiol for independent, without “interference” of the hypothalamus, to regulate the secretion of LH and FSH. In fact, the HHP arc is a very complex mechanism with many independent “sensors” and adjustment mechanisms. And any complex mechanism is very easy to disable. At least for a while.

What happens in the body as a result of the use of AAS?

Actually, it all depends on what androgens and anabolic steroids were used during the “cycle”. Let’s take a look at Table 1, which shows the effect of various AAS on endogenous testosterone production.

Table 1

A drug Qualities Affecting Endogenous Testosterone Production Suppression of endogenous testosterone production
Testosterone Propensity for aromatization Strong
Nandrolone Progestogenic activity Strong
Norethandrolone Progestogenic activity Strong
Methandrostenolone Propensity for aromatization Expressed
Oxymetholone Progestogenic activity Expressed
Trenbolone Unexpressed progestogenic activity Moderate
Fluoxymesterone Light tendency to aromatize * Moderate
Boldenone Light tendency to aromatize Moderate
Oral-turinabol No Moderate
Drostanolone No Below the average
Stanozolol No Below the average
Oxandrolone No Minor
Methenolone enanthate No Practically absent
Methenolone acetate No Is absent
Ethylestrenol No Is absent

* – in dosages accepted in bodybuilding

As you can see, a number of AAS have practically no effect on the normal functioning of the HH arc, recovery after taking them occurs quite quickly and painlessly and without aids. The trouble is that such drugs ( ethylestrenol , methenolone ( primobolan ), oxandrolone , drostanolone , stanozolol ) do not give any significant weight gain, forcing you and me to seek help from more “heavy” drugs. And the use of the latter entails a whole “bouquet” of undesirable consequences. Here they are:

  1. Drop in LH levels.
    2. Increased levels of cortisol (hydrocortisone).
    3. Increase in the level of estrogen (estradiol).
    4. Increase in the level of sex hormone binding globulin (SHBG), which leads to a decrease in the level of free testosterone in the blood. It is interesting that it is the “short” AAS esters that give a sharper “surge” in the level of SHBG.
    5. Increasing the level of prolactin, otherwise called luteotropic hormone and stimulating the growth of the mammary glands and the secretion of milk, which you and I, of course, unnecessarily.

In addition, as can be seen from the table, a number of AAS have progestogenic activity, and progesterone in quantities exceeding the norm has a very negative effect on LH secretion. Nandrolone metabolites have an extremely negative effect on the restoration of endogenous testosterone production. And if we take into account the fact that an increased level of these metabolites is observed after and one and a half to two months after the end of taking nandrolone decanoate [1] ( nandrolone phenylpropionate is a somewhat more gentle drug in this regard), it is clear that it is worth removing the “deco” at least than a month before the end of the “cycle”.

In order not to guess, but to know for sure what is happening in the body, there are blood tests. I think that at least once – at the end of the “cycle” – each of us can use them within our means. You will read about what to “analyze” and how to interpret the results obtained below.

Drugs used during the exit from the “cycle”

Let’s be honest: the use of gonadotropin during the exit from the “cycle” is more a tribute to traditions than a real necessity. I confess that I myself have paid this tribute more than once and sometimes continue to do so until now (however, not only me – some doctors, who, however, are not specialists in the field of sports medicine, believe that the restoration of testosterone against the background of joint and ADEQUATE use of gonadotropin and clomid / tamoxifenis somewhat faster). But still, I am more inclined to believe that it is worth using gonadotropin only during the “cycle” of AAS, and then only by athletes who have no special problems with aromatization (although recently the aforementioned scheme for using gonadotropin, which I called ADEQUATE – it allows, if not to exclude all the side effects of this drug, then to reduce them to an absolute minimum; more about it below). Let me explain why I began to lean towards this opinion.

Gonadotropin is very similar in chemical structure to LH (and FSH). Its appearance in excess in the body is the same signal for the hypothalamus as an increased LH content in the blood – the result is the cessation (or significant reduction) of GnRH secretion. That is, gonadotropin does not allow the pituitary gland to recover LH secretion, which naturally leads to the fact that the production of endogenous testosterone will not be restored. So gonadotropin still affects the functioning of the HH arc, but not in the direction of its (functioning) NORMALIZATION, but in the direction of DISTURBANCE. The use of gonadotropin in the middle of the AAS “cycle” prevents testicular atrophy; in fact, such atrophy is certainly reversible,

And now about the aforementioned scheme for the use of gonadotropin, the one that minimizes all the negative consequences of the use of this hormone. It is usually customary to do injections of gonadotropin 2000-5000 IU (two to three injections) in 4-5 days, sometimes in a week. The scheme under consideration prescribes DAILY injections of the drug at 500-1000 IU for 7-10 days. That is, the total amount of injected gonadotropin remains practically the same, and the side effects from its use are reduced to almost zero.

Unlike gonadotropin, taking Clomid or Tamoxifen during the exit from the cycle is almost inevitable. Desirable – in conjunction with Proviron (Mesterolone) – so the desired effect will be achieved somewhat faster. Let me explain why. Both clomid and tamoxifen are estrogen receptor blockers. Blocking these receptors in the hypothalamus stimulates the latter to increase the production of GnRH, which further leads to an increase in the production of LH by the pituitary gland. This is in theory. In practice, this approach sometimes (fortunately, quite rarely) does not work, and then you have to rely only on time – sooner or later, but the normal functioning of the hypothalamus will still be restored.

The use of Proviron will lead to inhibition of aromatase, and, as a result, to a decrease in the level of estradiol in the blood, and excessive amounts of this hormone, as we recall, have a very negative effect on the production of LH by the pituitary gland. The use of Arimidex instead of Proviron will, of course, give a faster effect (already 1-2 tablets of this drug almost completely suppress the secretion of aromatase), but this effect may be excessive – for the normal functioning of the HH arc, a certain (within normal) level of estrogen is still needed blood.

In the period of exit from the cycle, in some cases, the use of bromocriptine will be justified. And what drugs will not be superfluous here are insulin and … methandrostenolone. But the use of these and some other drugs will be discussed in the next section.

Practical recommendations for getting out of the “cycle”

As I wrote above, it would be reasonable at the end of the course to conduct a blood test, determine the blood level of luteinizing hormone, estradiol, cortisol, as well as the percentage of free testosterone (according to this indicator, you can determine the level of SHBG) and compare them with the norm [2 ] – I mean, you guessed it, the male body, here they are:

table 2

Luteinizing hormone 6-23 IU / ml (average – 13.1 IU / ml)
Total estradiol (E2) 8-26 pg / ml (29-132 pM / l)
Prolactin 7-18 ng / ml
Hydrocortisone (cortisol) 60-240 μg / L (0.14-0.64 μM / L)
Free testosterone,% 1-2.7

It should be said that measurements should be taken in the morning hours, the levels of a number of hormones in the blood in the morning and in the evening can differ significantly (the level of hydrocortisone, for example, decreases by 50% in the evening).

Now we are armed with knowledge and can choose which of the following tasks need to be solved (it is desirable to solve them simultaneously):

Suppression of cortisol activity

From my point of view, this is task number 1. In order not to let the “destructive hormone” take its own, you need to:

1.Maintain protein intake at an appropriate level, its amount in the diet should not fall below 3 g per kilogram of dry weight;
2. to maintain at a sufficiently high level the total caloric content of the diet;
3. to reduce the total volume and intensity of training, it is advisable to adhere to a scheme with high weights, low repetitions, a small number of sets per muscle group and sufficiently long breaks between sets;
4. completely eliminate aerobic exercise;
5. avoid stress and lack of sleep – they, like nothing else, increase the level of cortisol in the body;
6. take at least 10-20 g of glutamine per day.

But this, of course, is not all, one cannot do without the intervention of the “achievements of the pharmaceutical industry”. We need anti-catabolics, and the best known is methandrostenolone . “Well, yes,” you say, “but methandrostenolone very well suppresses the production of endogenous testosterone, and besides, it has a tendency to aromatization!” It’s like that. But if you take the drug in the morning (the last dose is no later than 1 pm), then these negative moments can be practically avoided (although the recovery period, of course, will be somewhat delayed).

Another powerful anti-catabolic agent is insulin; I generally think that it is very difficult, if not impossible, to do without this hormone during the recovery period. Insulin can be taken according to any of the known schemes, but the best during this period will be a daily intake, which is best divided into two injections – morning and mid-day.

Finally, DHEA. Dehydroepiandrosterone, quite useless if your age has not passed the sacramental mark of 45 years, turned out to be a good anti-catabolic. True, it is necessary to take it to provide an anti-catabolic effect in “horse” doses – 150 mg each morning and evening.

All of the above drugs block cortisol receptors. In order to lower the level of this hormone, phosphatidylserine is needed. Regular use of this drug in an amount of 800-1200 mg per day lowers cortisol levels by 30-45%. In addition to phosphatidylserine, 2-5 g of vitamin C can be taken after training.

Ensuring a normal training process

It is not always possible to find motivation for training after stopping the use of AAS due to depression. Will help here … all the same insulin. This drug, as it were, “stabilizes” the psyche, makes a person more calm and balanced.

Insulin, on the other hand, is responsible for the faster accumulation of glycogen in the muscles, which allows for normal recovery after training. Creatine is also useful during the recovery period – it will to some extent help maintain strength and muscle volume.

Normalizing estradiol levels

Here it is better to act in two directions at once – to block estrogen receptors and to reduce the level of the aromatase enzyme in peripheral tissues. Both clomid (clomiphene citrate) and tamoxifen will cope with the first task equally well; to solve the second, it is best to resort to the help of proviron (mesterolone). We have already written about the dosages of all these drugs.

Normalization of prolactin levels

The synthesis of prolactin is better than other drugs to suppress bromocriptine. He is also able to slightly increase the secretion of growth hormone (although in patients with acromegaly, bromocriptine just reduces the synthesis of growth hormone) and leptin – the so-called hormone of satiety, and at the same time significantly increase libido. Both the first and the last features are inherent in the drug due to the fact that it is a specific agonist of dopamine receptors (mainly type D 2 ). And in the aggregate, everything gives, moreover, a good fat burning effect.

Bromocriptine also has one more useful effect – the drug allows you to fight the development of gynecomastia that has arisen during the use of drugs with pronounced progestogenic activity.

The half-life of bromocriptine is 12 hours. Based on this, one can recommend taking one 2.5-milligram tablet of the drug in the morning and in the evening. To enhance the effect of the drug during the first two weeks, you can add a daily intake – also one tablet.

Restoring endogenous testosterone production

Again, Clomid and Tamoxifen are the best at this task (in the long term). We have already written about the advantages and disadvantages of both drugs (see the article ” Tamoxifen against Clomid “), so the final choice is yours. I will only repeat that the use of 20 mg of tamoxifen per day for just 10 days led to an increase in endogenous testosterone levels by 42%; the same result was achieved when 150 mg of clomid were used daily over the same period of time. Tamoxifen increases the sensitivity of the pituitary gland to GnRH, prolonging its administration for up to 6 weeks led to an increase in LH levels by 72%, and testosterone levels by 83% compared to baseline!

Among the disadvantages of drugs, it is worth noting the fact that clomid increases the level of SHBG, and tamoxifen inhibits the production of IGF-1 by the body. What is better and what is worse is up to you.

From other means, tribulus terrestris and such a trace element as zinc (preferably included in the ZMA complex ) in the amount of 100 mg per day will help very much in restoring the level of endogenous testosterone .

Decrease in SHBG levels

It is also far from the least important task. Obviously, it is with the increased level of SHBG that the decrease in the effectiveness of AAS (especially testosterone) is associated towards the end of the “cycle”. And given the fact that the increased level of SHBG in the blood lasts long enough, it can be assumed that without taking appropriate measures, the next “cycle” of AAS will be less effective than the previous one due to the lower amount of free testosterone.

What drugs help to reduce SHBG levels? First of all, this is incomparable insulin – you see, and this hormone is very useful here. Further – Proviron, it has been absolutely reliably proven that Mesterolone is able to increase the amount of free testosterone in the blood by attaching to globulin that binds sex hormones, and thus reducing the activity of the latter.

Oral stanozolol. According to a 1989 study, stanozolol lowers the level of sex hormone binding globulin (SHBG) in the blood by 50%. So this drug can be used in between “cycles” instead of methandrostenolone. However, the same “methane” also has (at least in theory) the ability to slightly lower the level of SHBG, but this feature of the drug is not yet proven.

So, we examined all the tasks we face, and saw that they can be solved without resorting to the help of gonadotropin. So let’s leave this undoubtedly very necessary drug for use within the “cycle”, and entrust recovery issues to other means – the same clomid and tamoxifen, for example.

The hypothalamus “reads” information about the level of testosterone and estradiol in the blood and regulates the production of GnRH depending on this. Interestingly, both too high estradiol levels (above normal) and too low (below normal) have a negative effect on the production of GnRH.

Nandrolone metabolites have an extremely negative effect on the restoration of endogenous testosterone production. And if we take into account the fact that an increased level of these metabolites is observed after and one and a half to two months after the end of taking nandrolone decanoate (nandrolone phenylpropionate is a somewhat more gentle drug in this regard), it is clear that it is worth removing the “deco” no less than for a month before the end of the “cycle”.

Gonadotropin is very similar in chemical structure to LH (and FSH). Its appearance in excess in the body is the same signal for the hypothalamus as an increased LH content in the blood – the result is the cessation (or significant reduction) of GnRH secretion.

Another powerful anti-catabolic agent is insulin; I generally think that it is very difficult, if not impossible, to do without this hormone during the recovery period. Insulin can be taken according to any of the known schemes, but the best during this period will be a daily intake, which is best divided into two injections – morning and mid-day.

Obviously, it is with the increased level of SHBG that the decrease in the effectiveness of AAS (especially testosterone) is associated towards the end of the “cycle”. And given the fact that the increased level of SHBG in the blood lasts long enough, it can be assumed that without taking appropriate measures, the next “cycle” of AAS will be less effective than the previous one due to the lower amount of free testosterone.

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