Post Cycle Therapy

By Author: Angelica
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Today it is a very different story in which the scientific and medical understanding of the use of anabolic steroids has grown exponentially since the old days of bodybuilding and the use of anabolic steroids in athletics. Thanks to numerous developments of active ingredients for hormone restoration after taking anabolic steroids and the increasing scientific and medical knowledge, taking anabolic steroids and the associated disorders of the endocrine system has become much safer than ever before. With the right knowledge of how to properly and efficiently restore HPTA and the body's hormonal system through post-cycle therapy (PCT), people can not only emerge from their anabolic steroid cycles,

After using exogenous anabolic steroids, the majority of users will experience what is referred to as a "hormonal crash" or "post-cycle crash". This is an endogenous environment in which important hormones are important for maintaining the newly formed muscle mass that has been suppressed or shut down. The key hormones in question are LH (luteinizing hormone), FSH (follicle-stimulating hormone) and then (and most importantly) testosterone. ...
... LH and FSH are known as gonadotropins. These are hormones that signal the gonads (testes) to start or increase the production and secretion of testosterone. In addition to low levels of these hormones, the overall balance of total hormones is essentially disturbed, causing testosterone levels to be low and most (depending on many factors), Estrogen levels and cortisol levels are higher (a steroid hormone that destroys muscle tissue) will be at normal levels. If the testosterone level is low and the cortisol level is in the normal (or high) range, cortisol now becomes a threat to the newly created muscle that was formed during the recent steroid cycle (testosterone properly suppresses and counteracts cortisol's catabolic effects on muscle tissue) . SHBG (sex hormone-binding globulin) is also a problem here, which is a protein that binds to sex hormones (testosterone) and makes them inactive, essentially handcuffing them and preventing them from working.

Normally, the human body restores this hormone imbalance and restores its endogenous testosterone level over time. However, studies have shown that this happens over a period of 1 to 4 months without the action of testosterone-stimulating active ingredients. Obviously, this is enough time for the hormonal imbalance to devastate the body and cause everyone to lose most or all of the new muscle gained during that time. Therefore, all users of anabolic steroids should strive for the fastest possible hormone recovery, which is supported and promoted through the correct use of a testosterone stimulating compounds. In addition, trying to allow the body to recover on its own represents a very high probability of long-term endocrine damage to HPTA over time, causing the individual to develop hypogonadism induced by anabolic steroids (the inability to produce the correct testosterone levels for the drug) for the rest of their lives). It is therefore of the utmost importance that a proper onePost-cycle therapy This involves using multiple recovery connections to not only bring HPTA function back to normal as quickly as possible but also to avoid any permanent damage that takes precedence over preserving recently gained muscle mass to have.

Which post cycle therapy protocol is to be used?
There are many different types of PCT protocols that have been developed over the years, and at first glance, everyone will be extremely confused as to how many different opinions exist among the anabolic steroids that the community uses and how many different ones established PCT protocols are in existence. This article presents the best possible and most efficient post-cycle therapy protocol based on valid scientific data and logical considerations. This article will also dispel various myths related to PCT and outline which PCT protocols should not be followed due to recent advanced developments, as well as newer better scientific and medical knowledge about them, how an appropriate post-cycle therapy protocol should work. At this point in time, there are still very outdated - and consequently ineffective - PCT protocols that are still used by many users of anabolic steroids, and this poses a serious danger, not only to the person who unknowingly is outdated Post cycle therapy program used but also for people who observe, learn and collect ideas from that person.

Without a proper understanding of what is going on in the endocrine system during these crucial weeks, and without understanding what connections to use, what each connection does, and how to use them correctly, serious problems can arise.

The HPTA: how it works
The HPTA is the hypothalamic-pituitary-testicular axis, an axis of interconnected endocrine glands in the body that deal with and control testosterone production.

A HPTA diagram is shown above. The HPTA regulates how much testosterone is produced at a given time and how much testosterone circulates in the body. Each individual is essentially programmed through their genetics (DNA) on how much maximum testosterone they will produce, and this is the most important determining factor. There are other factors that determine how much testosterone a person will produce, and these include age, diet, body composition, lifestyle, and physical activity. All of these factors play a role in how much testosterone a person will produce overall.

The HPTA works under the so-called negative feedback loop, whereby the body reduces its production and secretion of testosterone if too much testosterone circulates in the body, and also adapt if too little testosterone is detected. This detection and adjustment, known as a negative feedback loop, is controlled by the hypothalamus, which is essentially the main gland for all endocrine and hormonal functions in the body. The negative feedback loop is ultimately the body's attempt to maintain hormonal homeostasis, which involves regulating a system (in this case, the body's internal systems) to maintain stable and consistently favorable conditions. All endocrine glands work in one way or another and to different degrees through the negative feedback loop. In the case of post-cycle therapy The main problem lies in the negative feedback loop of the HPTA.

Within the HPTA, the concern during PCT is the restoration and regulation of the following 5 hormones for homeostasis:

- GnRH (gonadotropin-releasing hormone)
- LH (luteinizing hormone)
- FSH (follicle-stimulating hormone)
- testosterone

The HPTA starts with the first axis point, the hypothalamus, which recognizes that the human body has to produce more testosterone and releases different amounts of GnRH. GnRH is a hormone that signals the next axis point, the pituitary, to start producing and releasing two important gonadotropins: LH and FSH. LH and FSH are two hormones that work to signal the point on the third axis, the testes, and to start the production and secretion of testosterone. This is the final stage of testosterone production in the HPTA.

There are two primary hormonal factors that are used to inhibit, reduce, suppress, or stop testosterone production in the HPTA:

- Excess testosterone - Excess estrogen

Although there are other hormones that work to inhibit and suppress HPTA function (like progestins and prolactin), these are the two primary conditional hormones that are of concern. If the hypothalamus detects too high levels of testosterone and / or estrogen in the body (either through the use of exogenous androgens in an anabolic steroid cycle or otherwise), the hypothalamus tries to restore balance by doing essentially the opposite of that what was previously described. The hypothalamus reduces or stops the production of GnRH, which stops the production of LH and FSH, which ultimately reduces or stops the production of testosterone. As long as the ideal hormonal environment of the hypothalamus is not restored, The production of the various signaling hormones within the HPTA does not begin, and it will often take months for the body to do this alone without the intervention of testosterone stimulants. The reason why the recovery of the HPTA naturally takes so long should be very clear due to the described functioning of the HPTA.

This basic understanding of the mechanisms of HPTA and the negative feedback loop described above is essential to understand how and why a proper PCT needs to be developed and used after an anabolic steroid cycle.

Decisive factors in restoring HPTA
When using anabolic steroids, there are several key factors that determine how difficult it is for a person to restore their HPTA and endogenous testosterone function during PCT. These are the following factors, which are not important in any particular order:

1. Individual answer
2. Type of anabolic steroid used
3. Cycle duration (degree of testicular desensitization)

1. Individual response: Every individual reacts to a chemical, compound, anabolic steroid, food or drug in different ways. While some people may not experience HPTA suppression or shutdown at all, others may experience severe HPTA suppression and shutdown to the extent that they may take significantly longer periods of time to ensure full recovery than most others. Like everything else, this is a spectrum in which there are the very “happy” people who recover very quickly and easily at one end of the spectrum and the “unhappy” people who have a hard time recovering after the cycle can. In between is the average.

2. Type of anabolic steroids used (the anabolic steroids used): All anabolic steroids have HPTA suppression or shut down by the negative feedback loop mechanisms, and there are no exceptions to this. Various anabolic steroids are known to be mildly suppressive, while others are known to be strongly suppressive. It all depends on several reasons, many of which are not discussed here. In any case, no matter how mild or hard an anabolic steroid exerts HPTA suppression, all anabolic steroids when used for typical cycle lengths of weeks at a time, will eventually result in the HPTA shutting down or at least strongly suppressing their hormonal signaling processes.

3. Cycle time (degree of desensitization of the testes): this is possibly the most important and influential factor. As anabolic steroids continue to be used, the majority of testicular Leydig cells remain dormant and inactive, and the longer these interstitial cells remain dormant and inactive, the greater the difficulty of essentially getting these cells onto the React stimulus from LH and FSH again. Studies have found that the problem of restoring Leydig cells after using anabolic steroids is not due to a deficiency in LH, but to the desensitization of Leydig cells to LH. In a study in which male test subjects were given exogenous testosterone for 21 weeks, LH levels were suppressed shortly after the start of administration. At the end of the 21-week period, however, it was observed that LH levels rose within 3 weeks once exogenous testosterone administration ceased, but testosterone levels did not arise until many weeks later in most subjects.

The three primary testosterone stimulants for HPTA recovery during PCT
Before you look at the three different types of testosterone stimulating substances for hormone recovery during post-cycle therapy, it is very important for individuals to understand that the use of a single compound with the exception of one or two selected substances for the Hormone restoration is inadequate during PCT. Ideally, all post-cycle therapy programs should be a multi-component PCT program that contains several different compounds that work together to achieve the most effective and fastest possible HPTA recovery after an anabolic steroid cycle.

The three categories of connections are (in order of importance):

1. SERMs (Selective Estrogen Receptor Modulators)
2. Aromatase Inhibitors
3. HCG (Human Chorionic Gonadotropin)

SERMs: The active substance classes in the SERM category include: Nolvadex (tamoxifen citrate), Clomid (clomiphene citrate), Raloxifene and Fareston (toremifene citrate). The nature of a SERM is that it shows the mixed effects of estrogen agonists and estrogen antagonists on the body. This means that while a SERM can block the effects of estrogen at the cellular level in certain tissues, it can increase the effects of estrogen in other areas of the body. These can be both positive and negative effects. For example, Nolvadex shows estrogenic agonistic effects in the liver, which have a positive effect in every respect, since their effects lead to a positive change in the cholesterol profiles (which is desired by many). All SERMs act to varying degrees as estrogen antagonists in this area to mitigate the effects of estrogen on breast tissue and to reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. to mitigate the effects of estrogen on breast tissue and reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. to mitigate the effects of estrogen on breast tissue and reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs.

Aromatase inhibitors: These are compounds such as Aromasin (exemestane), Arimidex (Anastrozole) and Letrozole (Femara). Instead of blocking the activity of estrogen at the cellular level in different tissues, aromatase inhibitors (AIs) serve to lower the total circulating level of estrogen in the body by inhibiting the aromatase enzyme, which is the enzyme responsible for converting androgens to estrogen is. Converting androgens to estrogen results in an excess of estrogen, which, as explained earlier in this article, triggers the negative feedback loop that leads to the suppression of testosterone production. By reducing the total amount of circulating blood plasma estrogen, the negative feedback loop is activated in a positive way and LH and FSH are released, to produce and secrete more testosterone. This is largely due to the hypothalamus, which detects that estrogen levels are in the bloodstream also low and will try to increase testosterone levels in the bloodstream so that part of the excreted testosterone is able to be flavored in estrogen to restore hormonal balance. The other meaning of aromatase inhibitors is the ability to mitigate the estrogenic effects of HCG, which will be explained shortly. However, it is important to note that the majority of aromatase inhibitors do not match SERMs such as Nolvadex very well and that very specific decisions regarding the use of AI should be made PCT.

HCG: Human chorionic gonadotropin is mostly synthetic LH. It is a protein hormone that is produced in large quantities by pregnant women and contains a protein subunit that is 100% identical to LH. Therefore, when administered to men, it mimics the effects of LH in target tissues such as the testicles. The result is an increase in testosterone production by stimulating Leydig cells with HCG. HCG should never be used alone because its nature as a gonadotropin itself triggers a negative feedback loop, causing the pituitary gland to stop producing LH after using HCG until the use of HCG is discontinued. Therefore, HCG must be used together with a SERM and especially an aromatase inhibitor, since HCG has been shown to increase aromatase activity in the testes,

Put everything together
Readers may be wondering which compounds to choose from the three categories listed and how to use them correctly. The answer is to understand the characteristics of everyone and to use these characteristics efficiently and appropriately.

HCG
The first item to be examined is HCG. The majority of anabolic steroid users from the 1960s - mid-1980s did not even use compounds for hormone recovery purposes, and the term PCT did not even exist at that time. As the use of HCG became more popular (around 1980), it was the only compound used. Since then, medical and scientific understanding of such things has increased exponentially, and there should be no reason for an informed and properly trained person to use HCG for PCT alone. In connection with one of the other two connection categories (AI and SERM), the dynamics change considerably.

It has previously been mentioned that much of the difficulty in obtaining HPTA after an anabolic steroid cycle is the result of the desensitization of Leydig cells. HCG is essentially an analog of LH, and the testes after a long cycle of anabolic steroids would be as insensitive to HCG as to LH. However, the human body itself produces LH levels that are far too inefficient for proper and rapid testosterone production. The body's own increase in LH and FSH after an anabolic steroid cycle is also not a rapid climax, but a very slow and steady increase, as can be seen from the aforementioned study, in which it only started after 3 weeks to reach the LH values ​​normal physiological measurements after discontinuation of exogenous testosterone.

HCG, which is used in a dose of 100 - 1,500 IU every 2 days in the first 1-2 weeks of PCT in a specific way, enables the patient to supply the testicles with a high dose to give them a “shock” - To give effect and maintain this shock effect on the Leydig cells of the testicles for a longer period of the first 1-2 weeks after the cycle therapy. Indeed, studies have shown the incredible effectiveness of HCG for this purpose, and it is even clinically suggested to use HCG to treat hypogonadism induced by anabolic steroids. After this consideration, the other two compounds (the SERM and the AI) should be used as supporting compounds for the use of HCG in this period of 1 to 2 weeks,

Despite the good news regarding HCG's ability to support hormone recovery, two questions remain to be resolved:

- The fact that HCG causes an increased production of aromatase, which leads to increased estrogen levels.
- After stopping HCG, the body has only a very low endogenous LH and FSH production due to the exogenous administration of HCG.

Aromatase inhibitor: Aromasin (exemestane) above all
The first of the two remaining problems that need to be addressed is that HCG triggers an increase in testicular aromatase expression and an increase in estrogen in the body. It should also be noted that there is an increase in the level of progesterone in the testicles. Of course, an increase in estrogen during PCT is undesirable, since it has already been explained that estrogen triggers the suppression of endogenous testosterone production, and there is no doubt that everyone wants to have estrogenic side effects during PCT.

Therefore, there is an option to include an aromatase inhibitor. However, there is a major problem with the other two of the three main aromatase inhibitors (Arimidex and Letrozole). The problem is the fact that Arimidex and Letrozole have direct negative interactions with Nolvadex in a PCT program involving the use of SERMs like Nolvadex and Clomid, which are known to be absolutely essential components of a PCT program. The problem here is that Arimidex (or Letrozole) and Nolvadex both work directly against each other. One study showed that Nolvadex, when used with Arimidex, reduces the blood plasma level of Arimidex (as well as letrozole, another commonly used aromatase inhibitor). The conclusion here is that using Arimidex or Letrozole with Nolvadex together is a very bad idea and can be counterproductive when used together in a PCT protocol. Aromasin completely bypasses this problem because it has been proven that there are no interactions with Nolvadex, unlike the other two aromatase inhibitors mentioned above. In one study, Aromasin did not show such reduced efficacy or decreased blood plasma levels when using Nolvadex.

The other advantage of choosing Aromasin over all other AIs is that Aromasin has been shown in several studies to have a far less negative effect on cholesterol profiles than other aromatase inhibitors that used Aromasin for 24 weeks in a particular study in cancer patients Exemestane administration did not affect cholesterol profiles, and some other studies have also shown that using Aromasin has no effect on cholesterol profiles, although there have been some studies that have shown negative effects on cholesterol profiles due to the use of Aromasin, it is apparent that there is no significant or negative effect of Aromasin on cholesterol than other aromatase inhibitors.

In addition to these benefits of Aromasin, it is very clear that Aromasin is able to increase testosterone levels in men, as studies have shown. For example, in a particularly noteworthy study, 12 healthy young male volunteers were selected who were randomly given aroma doses of 25 mg and 50 mg over a period of 10 days and who not only had significant estrogen suppression (38%) but also testosterone levels It was observed that the test subjects gained an incredible 60%.

According to this information, Aromasin would be the best possible aromatase inhibitor of choice to counteract the increased aromatase activity caused by HCG. Therefore, Aromasin would be used at a full daily dose of 25 mg and only if HCG was used. As soon as HCG is discontinued, Aromasin should also be discontinued.

The only issue that needs to be addressed now is to stimulate and maintain proper endogenous LH release to drive recovery until the body can become self-sufficient.

SERMs: Nolvadex and Clomid
The question is often asked among the anabolic steroids that the community uses: Clomid or Nolvadex? Which one for PCT?

Zuallererst ist die bestmögliche Zugabe zu HCG in einem PCT-Protokoll Nolvadex (Tamoxifen Citrate), da Studien gezeigt haben, dass HCG und Nolvadex zusammen einen bemerkenswerten synergistischen Effekt in Bezug auf die Stimulierung der endogenen Testosteronproduktion gezeigt haben und Nolvadex tatsächlich arbeiten, um den Desensibilisierungseffekt auf die Leydig-Zellen der Hoden zu blockieren, der durch hohe Dosen von HCG verursacht wird. Dies ist sehr wichtig, da eine zu geringe LH-Sekretion über längere Zeiträume eine Desensibilisierung der Gonadotropine bewirken kann, eine zu starke Gonadotropinstimulation (in Form von HCG oder auf andere Weise) ebenfalls eine Desensibilisierungswirkung hervorruft.

Second, mg for mg, Nolvadex is far more effective than Clomid in stimulating endogenous testosterone production and a cheaper choice than Clomid itself. Studies have shown that 150 mg Clomid (Clomiphene Citrate) administered daily reduced endogenous testosterone levels of 10 healthy men increased approximately 150%, while 20 mg Nolvadex (Tamoxifen Citrate) increased endogenous testosterone levels by the same amount daily. It is very obvious here that Clomid is very effective for this purpose, but Nolvadex appears to be a cheaper choice since it is more effective than Clomid compared to mg for mg. The advantages of Nolvadex compared to Clomid do not end here - although Clomid shows estrogen antagonist effects on the pituitary gland like Nolvadex, however, shows estrogen agonist effects there too. This means that Clomid actually acts to varying degrees as a pituitary estrogen, triggers the negative feedback loop, and reduces testosterone-stimulating gonadotropin (LH and FSH) emissions. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it.

When it comes to dosing Nolvadex, the standard dose for PCT and to stimulate the release of GnRH (Gonadotropin-Releasing Hormone), LH, FSH and ultimately testosterone is the same as a simple Nolvadex dose of 20-40 mg daily. In all studies with Nolvadex doses to stimulate endogenous testosterone production, only 20 to 40 mg Nolvadex were used per day, and it was actually shown that doubling the dose to 40 mg or more did not produce a significant difference in endogenous testosterone secretion. The only reason why many choose to use Nolvadex 40 mg daily for the first 1-2 weeks of a PCT program is to achieve optimal peak plasma levels faster to ensure faster HPTA recovery.

The final layout
The ideal post-cycle therapy protocol should then be as follows:

4 - 6 weeks total PCT time (depending on the individual's ability to recover )
Week 1 - 2:
- HCG at 1000iu / E2D
- Aromasin (exemestane) at 25 mg / day
- Nolvadex (tamoxifen citrate) at 40 mg / day
week 2 - 6:
- Nolvadex (tamoxifen citrate) at 20 mg / day

Additional optional components (vitamins / supplements / compounds) to support PCT

Apart from the main components that are being discussed, there are various other components that are largely optional but are still very effective for hormonal restoration of HPTA during the weeks after cycle therapy.

Vitamin D (Cholecalciferol): There is ample evidence backed by studies that the legalization of Vitamin D (Cholecalciferol) has a significant effect on increasing testosterone levels in men and also has a significant ability to suppress SHBG levels in the body. Indeed, one of the best PCT supplements is vitamin D. There are a plethora of clinical studies showing that low levels of vitamin D correspond to low endogenous testosterone production (especially in the winter months for obvious reasons). In a study carried out in Austria, in which around 200 subjects were involved in a group with 3332iu vitamin D and a placebo group daily, the results showed that those men with sufficient vitamin D levels had significantly higher testosterone levels and significantly lower SHBG levels when compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. if compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. if compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D.