Criticisms of all of 4chloro’s threads are appreciated, and are the reason I post in first place.
Post Cycle Therapy:
There are two main ways people cycle Anabolic Steroids, using a PCT or "blast and cruise".
Blasting and Cruising:
This is the method of running a low dose of 100-250mg of Testosterone along with hCG year round and doing "blasts" consisting of 4-20 week periods where higher dosages of gear is used before dropping back down to the "cruise" to let the body recover.
It is also not unheard of for people to run 500 to 1000mg of testosterone along with hCG and GH year round for many years on end. This won't give you any awards in the health department, but so long as you keep hematocrit under control (baby aspirin and double plate donates) cigarettes would likely kill (or at least give you problems) sooner.
Recovery of Natural Testosterone:
By far the most popular method of cycling is to cycle "on" and "off" by running Steroids for a period of weeks before attempting to *maybe* regain endogenous testosterone production.
Steroids are another demonstration of the body’s extraordinary ability to adapt to any situation in an attempt to regain homeostasis. When exogenous androgens are administered, the body will reduce it's own production of testosterone. Most of the time this is complete suppression, however this can depend on dosage and cycle length. 50mg of Turanabol will likely not completely shut down endogenous production, nor will Proviron and other mild non-estrogenic DHT derivatives, however if taken for long enough, full suppression will occur.
Your body does this through the "negative feed-back loop", which is an important neuroendocrine regulatory system. In the male body this is primarily moderated by estrogen, as it is 200x more suppressive than testosterone or DHT on a molar basis. The feedback loop is a mechanism of the "hypothalamic pituitary testicular axis" commonly referred to as the "HPTA" it involves the all of the mechanisms associated with Testosterone Production.
Let's first look at the basic mechanism of Testosterone production in the Male body.
Testosterone Production:
Everything starts in the Hypothalamus, which releases "Gonadotropin-releasing hormone" (GnRH), GnRH is a tropic peptide neurohormone. The opioid receptors are directly involved with the production of GnRH, taking exogenous opiates will retard GnRH release, whilst opioid receptor antagonists will cause a release of GnRH. b-Endorphin -which binds to the u-opioid receptor- is the primary culprit in binding to the GnRH secretory neurons in the hypothalamus to inhibit GnRH release. These peptide hormones are likely released as the result of ER and AR receptor binding in a different part of the brain, rather than direct interaction with the GnRH neurons. Endogenous Opioid Peptides are responsive to Androgens and Estrogens, whereas the GnRH neurons are not, but instead are responsive to the Endogenous Opioid peptides.
GnRH binds to the Anterior Pituitary gland, stimulating a release of Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH).
LH and FSH work synergistically to stimulate Leydig Cell production of Testosterone in the Testes. LH is primarily responsible for Leydig Cell stimulation while FSH primarily stimulates the Sertoli Cells and "stimulates primary spermatocytes to undergo the first division of meiosis, to form secondary spermatocytes". FSH also increases androgen binding in the Testes, which is essential for the initiation of Spermatogenesis. FSH indirectly enhances Testicular LH sensitivity. Although FSH is primarily responsible for Sperm production, the intratesticular testosterone released by the Leydig Cells in response to LH is necessary for spermatogensis to occur, as well as proper erectile function.
Testosterone is synthesized from numerous enzymatic reactions starting with Cholesterol's conversion to pregnenolone:
http://en.wikipedia.org/wiki/File:Steroidogenesis.svg
Greater than 95% of a Male's testosterone is produced by the Testes, however small amounts can be converted in the body through Adrenal hormones. The Testes are also responsible for the production of Pregnenolone, which is an important precursor to many intermediate steroid hormones within the body and the brain. Most people on cycle without the use of hCG will find their DHEA and Pregnenolone levels low and ACTH high. Steroids and Prostaglandins interact with Steroid and Prostaglandin specific receptors in the presynaptic region of brain neurons, controlling ion flow/concentration in their own ways similar to other neuromodulators (monoamines, catecholamines etc), thus playing a role in brain function.
Even slight testicular atrophy is indicative of complete -or near complete- HTPA suppression. The Leydig Cells are so small that the Testes must achieve their full size in order for proper functioning. The Sertoli Cells make up the vast majority of testicular volume.
To review:
------------------------------------------------------------------------------------------------------------------------------------
Lack of Endogenous Opioid receptor activation -----> GnRH from Hypothalamus ---------> LH and FSH release from Anterior Pituitary --------> LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes ---------> increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
Oestrogens act to not only suppress GnRH release, they also down-regulate the GnRH receptors in the Pituitary. Hence this is the reason Oestrogens (Prolactin, Estradiol, progesterone etc) are the primary target in a typical PCT where estrogenic activity is blocked at the pituitary.
From all this information we can gather a few things we need to have in order for complete HPTA function:
- Non-atrophied Testes
- Little to no estrogenic GnRH receptor down-regulation
- Controlled levels of Oestrogens
- GnRH release
- LH and FSH release
These inferences can be used to construct an ideal PCT, at least with the resources we have largely available to us.
Step 1: Control estradiol and Prolactin on cycle. This can be done using DHT and or an Aromatase inhibitor as well as Mirapex (pramipexole hcl)
Step 2: Maintain Testicular function on cycle with the use of hCG. 250 IU's biweekly will be sufficient in most cases.
Step 3: After your cycle is complete continue the use of an Aromatase inhibitor and or Mirapex until the steroid clears (~21 days for undecanoate, ~14 days Enanthate, ~3-5 days propionate and acetate esters, 24hours for orals)
Step 4: Initiate a sensible PCT protocol. I recommend the following:
Week 1: 500 IU's hCG daily
Weeks 1-4: 25mg Aromasin 2x per week
Weeks 1-6: 250mcg Pramipexole hcl 3x a day
Weeks 1-6: 3-5g D-aspartic acid
AFTER the hCG clears, so on day 10 of PCT, Inject 100mcg of Triptorellin acetate
Tapering:
Aromasin
Weeks 5-6: 25mg Aromasin once a week
Weeks 7-8: 12.5mg Aromasin once a week
Pramipexole hcl
Weeks 7-10: .25mg 2x a day
Weeks 10-12: .125mg 2x a day
Weeks 12-14: .125mg before bed
Neglecting to taper off these medications can lead to a rebound of systems, and in the case of Mirapex, dopamine withdrawal.
A simple cycle that takes care of all the basics outlined above would be the following:
Weeks 1-12: 500mg Testosterone Enanthate
Weeks 1-12: 500 IU's hCG
Weeks 1-12: 50-100mg Proviron (daily) or 350-500mg Masteron a week.
Weeks 12-14: 25mg Aromasin 3x a week
Week 13: 500 IU's hCG daily
Weeks 14-20: PCT (as outlined above) Note that if you are following this cycle, the hCG is used while the ester is still clearing so that you can save a week on your recovery.
Analysis:
The PCT outlined above acts to restore HPTA functioning in several ways.
------------------------------------------------------------------------------------------------------------------------------------
Lack of Endogenous Opioid receptor activation -----> GnRH from Hypothalamus ---------> LH and FSH release from Anterior Pituitary --------> LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes ---------> increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until Homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
When the basic version of the feedback loop is viewed it can be seen where each piece of the above PCT comes into play. Starting with the Testes we can work backwards through the feed back loop (if this seems repetitive, that's the point):
- hCG is used on cycle and during PCT to maintain the normal functioning of the Leydig Cells (and to a lesser degree the Sertoli Cells).
When the testes atrophy, LH sensitivity is greatly reduced, and the body will pump out large amounts of LH until the feedback loop inhibits its release. When the Leydig Cells have atrophied and steroid concentrations are low, your body will release growth factors that will cause the atrophied cells to grow back again independent of LH. Meaning that there are intermediary growth factors that will restore cell size WITHOUT the presence of LH. Before the body even tries to stimulate testosterone production, it attempts to restore testicular functioning. This is precisely why hCG is necessary on cycle, as it stops the testes from atrophying in the first place. Your body will only release the growth factors to restore testicular size when the feedback loop is non-interrupted, hence the reason they shrink on cycle. hCG can stimulate testicular growth on cycle while your neuroendocrine system is suppressed.
- DHT and or Aromasin are used on cycle to prevent estrogenic side effects, as well as to reduce Oestrogen related GnRH receptor down-regulation. Off cycle Aromasin is used to keep estrogen levels low to stimulate GnRH release, as estrogen is far more suppressive than testosterone. Lowering the amount of Estrogen that can bind to the Hypothalamus will conversely increase GnRH release as the body attempts to reach homeostasis, as the primary method of estrogen production in males is the aromatisation of Testosterone to Estradiol. Thus testosterone levels are raised, until equilibrium is once again reached.
- Pramipexole is used to reduce levels of Prolactin. Prolactin is a peptide hormone that is secreted by the hypothalamus; Prolactin is regulated by the dopamine-2 receptors on lactotrophs, Dopamine binding to these receptors causes inhibition of prolactin secretion. Serotonin in certain parts of the brain will reduce dopamine-2 receptor binding thus increasing prolactin, this is the very reason why SSRI's can raise prolactin to a large degree. Conversely, Mirapex is a D-2 receptor agonist (as well as an agonist at a host of other D receptors). Not only is Prolactin is suppressive to GnRH release; it also has very deleterious effects on sexual desire and performance. Mirapex will also raise the amount of Growth Hormone secreted by the pituitary, which is useful for a large number of reasons post cycle, including sexual function and testicular function.
- Triptorellin is essentially a longer acting form of GnRH, it is also known as GnRH Acetate. In high doses it is used to essentially chemically castrate a male by overloading the GnRH receptors to such a large degree that permanent down-regulation occurs. However, the dose utilized for this PCT is significantly smaller (100mcg as opposed to 4.5mg). Looking at the above chart, GnRH, next to the endogenous opioid receptors, is the first step in the feedback loop chain. Over the course of the weeks you’ve been on cycle, GnRH release has been at zero, which theoretically would cause down-regulation in this area, meaning GnRH release is less responsive to stimulus post cycle. Injecting this exogenous GnRH floods your body with a large amount of GnRH to help get the entire cycle going again full swing. Small case studies have shown its efficacy even in cases of long-term steroid use. Triptorellin is so useful in this case because we already have everything else in place for the body to be responsive to GnRH in the first place.
There are several theories on why Triptorellin should (or shouldn’t) produce a lasting increase/normalization of LH and FSH which is a discussion for another thread, but one could infer that because it is essentially “reintroducing” your HPTA to homeostasis that receptors become responsive to GnRH once again to adapt to the large (but not too large) dose of GnRH. Physiologically the body will tend to atrophy/down-regulate anything that it is not in use or not needed, and compensate for a situation where it is needed. Take steroids for example, when a large amount of testosterone is introduced, the body will adapt by increasing the amount of androgen receptors it produces, whereas with lower levels of testosterone it will decrease cellular production of AR’s. The same can also be seen with testicular atrophy on cycle, and the return of testicular size off cycle. However too much of something (not with steroids as the body has a saturation point) toxicity will occur and these systems can be damaged, such as the immense flood of serotonin from MDMA ingestion, which can cause serotonin nerve damage.
In short:
hCG: to restore/maintain the body’s ability to physically create steroids, by preventing Sertoli and Leydig cell down regulation AKA testicular atrophy.
Aromasin and or DHT: ON cycle to help maintain the body’s response to GnRH. OFF cycle (aromasin only) to reduce estrogen’s inhibitory effect on GnRH release, thereby increasing GnRH (and LH) release through the negative feedback loop and preventing side effects from possible estrogen level spikes post cycle.
Pramipexole: To reduce prolactin thereby increasing testosterone due to prolactin’s ability to suppress GnRH release, as well as reducing the negative effects of estrogen. Also helps with sexual function, muscle preservation, sleep, wellbeing, motor skills, restoration of testicular function and all over positives of increased endogenous GH.
Triptorellin: To restore homeostasis by activating GnRH receptors, potentially the most important part of the feedback loop, thereby possibly normalizing GnRH receptor density.
To label the loop we could put each of the drugs used as where it stands in the process:
------------------------------------------------------------------------------------------------------------------------------------
0Lack of Endogenous Opioid receptor activation -----> 1GnRH from Hypothalamus ---------> 2LH and FSH release from Anterior Pituitary --------> 3LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes --------->4 increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until Homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
1: Triptorellin OFF cycle and Aromasin and or DHT ON cycle
2: Aromasin OFF cycle
3: hCG both on and off cycle
4: Pramipexole, as it effects all of these systems in a favorable way
0: Is listed, however, due to the relative unavailability and side effects of opioid antagonists naltrexone, Nalexone etc. are not used in this PCT. However Mirapex will help regulate this system favorably.
Post Cycle Therapy:
There are two main ways people cycle Anabolic Steroids, using a PCT or "blast and cruise".
Blasting and Cruising:
This is the method of running a low dose of 100-250mg of Testosterone along with hCG year round and doing "blasts" consisting of 4-20 week periods where higher dosages of gear is used before dropping back down to the "cruise" to let the body recover.
It is also not unheard of for people to run 500 to 1000mg of testosterone along with hCG and GH year round for many years on end. This won't give you any awards in the health department, but so long as you keep hematocrit under control (baby aspirin and double plate donates) cigarettes would likely kill (or at least give you problems) sooner.
Recovery of Natural Testosterone:
By far the most popular method of cycling is to cycle "on" and "off" by running Steroids for a period of weeks before attempting to *maybe* regain endogenous testosterone production.
Steroids are another demonstration of the body’s extraordinary ability to adapt to any situation in an attempt to regain homeostasis. When exogenous androgens are administered, the body will reduce it's own production of testosterone. Most of the time this is complete suppression, however this can depend on dosage and cycle length. 50mg of Turanabol will likely not completely shut down endogenous production, nor will Proviron and other mild non-estrogenic DHT derivatives, however if taken for long enough, full suppression will occur.
Your body does this through the "negative feed-back loop", which is an important neuroendocrine regulatory system. In the male body this is primarily moderated by estrogen, as it is 200x more suppressive than testosterone or DHT on a molar basis. The feedback loop is a mechanism of the "hypothalamic pituitary testicular axis" commonly referred to as the "HPTA" it involves the all of the mechanisms associated with Testosterone Production.
Let's first look at the basic mechanism of Testosterone production in the Male body.
Testosterone Production:
Everything starts in the Hypothalamus, which releases "Gonadotropin-releasing hormone" (GnRH), GnRH is a tropic peptide neurohormone. The opioid receptors are directly involved with the production of GnRH, taking exogenous opiates will retard GnRH release, whilst opioid receptor antagonists will cause a release of GnRH. b-Endorphin -which binds to the u-opioid receptor- is the primary culprit in binding to the GnRH secretory neurons in the hypothalamus to inhibit GnRH release. These peptide hormones are likely released as the result of ER and AR receptor binding in a different part of the brain, rather than direct interaction with the GnRH neurons. Endogenous Opioid Peptides are responsive to Androgens and Estrogens, whereas the GnRH neurons are not, but instead are responsive to the Endogenous Opioid peptides.
GnRH binds to the Anterior Pituitary gland, stimulating a release of Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH).
LH and FSH work synergistically to stimulate Leydig Cell production of Testosterone in the Testes. LH is primarily responsible for Leydig Cell stimulation while FSH primarily stimulates the Sertoli Cells and "stimulates primary spermatocytes to undergo the first division of meiosis, to form secondary spermatocytes". FSH also increases androgen binding in the Testes, which is essential for the initiation of Spermatogenesis. FSH indirectly enhances Testicular LH sensitivity. Although FSH is primarily responsible for Sperm production, the intratesticular testosterone released by the Leydig Cells in response to LH is necessary for spermatogensis to occur, as well as proper erectile function.
Testosterone is synthesized from numerous enzymatic reactions starting with Cholesterol's conversion to pregnenolone:
http://en.wikipedia.org/wiki/File:Steroidogenesis.svg
Greater than 95% of a Male's testosterone is produced by the Testes, however small amounts can be converted in the body through Adrenal hormones. The Testes are also responsible for the production of Pregnenolone, which is an important precursor to many intermediate steroid hormones within the body and the brain. Most people on cycle without the use of hCG will find their DHEA and Pregnenolone levels low and ACTH high. Steroids and Prostaglandins interact with Steroid and Prostaglandin specific receptors in the presynaptic region of brain neurons, controlling ion flow/concentration in their own ways similar to other neuromodulators (monoamines, catecholamines etc), thus playing a role in brain function.
Even slight testicular atrophy is indicative of complete -or near complete- HTPA suppression. The Leydig Cells are so small that the Testes must achieve their full size in order for proper functioning. The Sertoli Cells make up the vast majority of testicular volume.
To review:
------------------------------------------------------------------------------------------------------------------------------------
Lack of Endogenous Opioid receptor activation -----> GnRH from Hypothalamus ---------> LH and FSH release from Anterior Pituitary --------> LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes ---------> increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
Oestrogens act to not only suppress GnRH release, they also down-regulate the GnRH receptors in the Pituitary. Hence this is the reason Oestrogens (Prolactin, Estradiol, progesterone etc) are the primary target in a typical PCT where estrogenic activity is blocked at the pituitary.
From all this information we can gather a few things we need to have in order for complete HPTA function:
- Non-atrophied Testes
- Little to no estrogenic GnRH receptor down-regulation
- Controlled levels of Oestrogens
- GnRH release
- LH and FSH release
These inferences can be used to construct an ideal PCT, at least with the resources we have largely available to us.
Step 1: Control estradiol and Prolactin on cycle. This can be done using DHT and or an Aromatase inhibitor as well as Mirapex (pramipexole hcl)
Step 2: Maintain Testicular function on cycle with the use of hCG. 250 IU's biweekly will be sufficient in most cases.
Step 3: After your cycle is complete continue the use of an Aromatase inhibitor and or Mirapex until the steroid clears (~21 days for undecanoate, ~14 days Enanthate, ~3-5 days propionate and acetate esters, 24hours for orals)
Step 4: Initiate a sensible PCT protocol. I recommend the following:
Week 1: 500 IU's hCG daily
Weeks 1-4: 25mg Aromasin 2x per week
Weeks 1-6: 250mcg Pramipexole hcl 3x a day
Weeks 1-6: 3-5g D-aspartic acid
AFTER the hCG clears, so on day 10 of PCT, Inject 100mcg of Triptorellin acetate
Tapering:
Aromasin
Weeks 5-6: 25mg Aromasin once a week
Weeks 7-8: 12.5mg Aromasin once a week
Pramipexole hcl
Weeks 7-10: .25mg 2x a day
Weeks 10-12: .125mg 2x a day
Weeks 12-14: .125mg before bed
Neglecting to taper off these medications can lead to a rebound of systems, and in the case of Mirapex, dopamine withdrawal.
A simple cycle that takes care of all the basics outlined above would be the following:
Weeks 1-12: 500mg Testosterone Enanthate
Weeks 1-12: 500 IU's hCG
Weeks 1-12: 50-100mg Proviron (daily) or 350-500mg Masteron a week.
Weeks 12-14: 25mg Aromasin 3x a week
Week 13: 500 IU's hCG daily
Weeks 14-20: PCT (as outlined above) Note that if you are following this cycle, the hCG is used while the ester is still clearing so that you can save a week on your recovery.
Analysis:
The PCT outlined above acts to restore HPTA functioning in several ways.
------------------------------------------------------------------------------------------------------------------------------------
Lack of Endogenous Opioid receptor activation -----> GnRH from Hypothalamus ---------> LH and FSH release from Anterior Pituitary --------> LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes ---------> increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until Homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
When the basic version of the feedback loop is viewed it can be seen where each piece of the above PCT comes into play. Starting with the Testes we can work backwards through the feed back loop (if this seems repetitive, that's the point):
- hCG is used on cycle and during PCT to maintain the normal functioning of the Leydig Cells (and to a lesser degree the Sertoli Cells).
When the testes atrophy, LH sensitivity is greatly reduced, and the body will pump out large amounts of LH until the feedback loop inhibits its release. When the Leydig Cells have atrophied and steroid concentrations are low, your body will release growth factors that will cause the atrophied cells to grow back again independent of LH. Meaning that there are intermediary growth factors that will restore cell size WITHOUT the presence of LH. Before the body even tries to stimulate testosterone production, it attempts to restore testicular functioning. This is precisely why hCG is necessary on cycle, as it stops the testes from atrophying in the first place. Your body will only release the growth factors to restore testicular size when the feedback loop is non-interrupted, hence the reason they shrink on cycle. hCG can stimulate testicular growth on cycle while your neuroendocrine system is suppressed.
- DHT and or Aromasin are used on cycle to prevent estrogenic side effects, as well as to reduce Oestrogen related GnRH receptor down-regulation. Off cycle Aromasin is used to keep estrogen levels low to stimulate GnRH release, as estrogen is far more suppressive than testosterone. Lowering the amount of Estrogen that can bind to the Hypothalamus will conversely increase GnRH release as the body attempts to reach homeostasis, as the primary method of estrogen production in males is the aromatisation of Testosterone to Estradiol. Thus testosterone levels are raised, until equilibrium is once again reached.
- Pramipexole is used to reduce levels of Prolactin. Prolactin is a peptide hormone that is secreted by the hypothalamus; Prolactin is regulated by the dopamine-2 receptors on lactotrophs, Dopamine binding to these receptors causes inhibition of prolactin secretion. Serotonin in certain parts of the brain will reduce dopamine-2 receptor binding thus increasing prolactin, this is the very reason why SSRI's can raise prolactin to a large degree. Conversely, Mirapex is a D-2 receptor agonist (as well as an agonist at a host of other D receptors). Not only is Prolactin is suppressive to GnRH release; it also has very deleterious effects on sexual desire and performance. Mirapex will also raise the amount of Growth Hormone secreted by the pituitary, which is useful for a large number of reasons post cycle, including sexual function and testicular function.
- Triptorellin is essentially a longer acting form of GnRH, it is also known as GnRH Acetate. In high doses it is used to essentially chemically castrate a male by overloading the GnRH receptors to such a large degree that permanent down-regulation occurs. However, the dose utilized for this PCT is significantly smaller (100mcg as opposed to 4.5mg). Looking at the above chart, GnRH, next to the endogenous opioid receptors, is the first step in the feedback loop chain. Over the course of the weeks you’ve been on cycle, GnRH release has been at zero, which theoretically would cause down-regulation in this area, meaning GnRH release is less responsive to stimulus post cycle. Injecting this exogenous GnRH floods your body with a large amount of GnRH to help get the entire cycle going again full swing. Small case studies have shown its efficacy even in cases of long-term steroid use. Triptorellin is so useful in this case because we already have everything else in place for the body to be responsive to GnRH in the first place.
There are several theories on why Triptorellin should (or shouldn’t) produce a lasting increase/normalization of LH and FSH which is a discussion for another thread, but one could infer that because it is essentially “reintroducing” your HPTA to homeostasis that receptors become responsive to GnRH once again to adapt to the large (but not too large) dose of GnRH. Physiologically the body will tend to atrophy/down-regulate anything that it is not in use or not needed, and compensate for a situation where it is needed. Take steroids for example, when a large amount of testosterone is introduced, the body will adapt by increasing the amount of androgen receptors it produces, whereas with lower levels of testosterone it will decrease cellular production of AR’s. The same can also be seen with testicular atrophy on cycle, and the return of testicular size off cycle. However too much of something (not with steroids as the body has a saturation point) toxicity will occur and these systems can be damaged, such as the immense flood of serotonin from MDMA ingestion, which can cause serotonin nerve damage.
In short:
hCG: to restore/maintain the body’s ability to physically create steroids, by preventing Sertoli and Leydig cell down regulation AKA testicular atrophy.
Aromasin and or DHT: ON cycle to help maintain the body’s response to GnRH. OFF cycle (aromasin only) to reduce estrogen’s inhibitory effect on GnRH release, thereby increasing GnRH (and LH) release through the negative feedback loop and preventing side effects from possible estrogen level spikes post cycle.
Pramipexole: To reduce prolactin thereby increasing testosterone due to prolactin’s ability to suppress GnRH release, as well as reducing the negative effects of estrogen. Also helps with sexual function, muscle preservation, sleep, wellbeing, motor skills, restoration of testicular function and all over positives of increased endogenous GH.
Triptorellin: To restore homeostasis by activating GnRH receptors, potentially the most important part of the feedback loop, thereby possibly normalizing GnRH receptor density.
To label the loop we could put each of the drugs used as where it stands in the process:
------------------------------------------------------------------------------------------------------------------------------------
0Lack of Endogenous Opioid receptor activation -----> 1GnRH from Hypothalamus ---------> 2LH and FSH release from Anterior Pituitary --------> 3LH and FSH stimulate Spermatogenesis and Steroid synthesis from Cholesterol in the Testes --------->4 increased levels of Endogenous Steroids ----------> Endogenous Opioid receptor activation ---------> Reduced GnRH response --------> and so on the loop continues until Homeostasis is reached.
------------------------------------------------------------------------------------------------------------------------------------
1: Triptorellin OFF cycle and Aromasin and or DHT ON cycle
2: Aromasin OFF cycle
3: hCG both on and off cycle
4: Pramipexole, as it effects all of these systems in a favorable way
0: Is listed, however, due to the relative unavailability and side effects of opioid antagonists naltrexone, Nalexone etc. are not used in this PCT. However Mirapex will help regulate this system favorably.
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