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Old 12-30-2008, 12:45 AM   #2

bubbafrombama

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DefaultHCG and PCT recovery protocols.
Please read the entire thread I copied below. It is very important not to akolip read the first two posts below only, as post #3 and #4 are from Dr. Swale (HRT specialist), and he completely contradicts post #1 and William Llewellyn's post #2.
http://www.uk-muscle.co.uk/steroid-t...protocols.html
Post #1:

Quote:

Below are a few articles I came across so I thought I would copy and paste them. They seem to have the same flavor but contradict each other to some degree.
I have no idea who the authors are other than what the poster suggests.
post cycle therpy
--------------------------------------------------------------------------------
Here is one way;
Hypogonadotropic Hypogonadism:
Pulsatile secretion of gonadotropin releasing hormone (GnRH) from the hypothalamus is required for both the initiation and maintenance of the reproductive axis in the human. Pulsatile GnRH stimulates the biosynthesis of luteinizing hormone (LH) and follicle stimulating hormone (FSH) that in turn initiates endogenous testosterone production and spermatogenesis as well as systemic testosterone secretion and virilization. Failure of this episodic GnRH secretion or disruption of gonadotropin secretion results in the clinical syndrome of hypogonadotropic hypogonadism (HH).
The usage of anabolic androgenic steroids (AAS) may result in a functional form of HH known as Secondary Acquired Hypogonadotropic Hypogonadism and is diagnosed in the setting of a low testosterone level and sperm count in association with low or inappropriately normal serum LH and FSH concentrations.
In order to avoid any unnecessary confusion, it is important to understand what the actions of Gonadatropin therapy and Selective Estrogen Receptor Modulators are as well as how they differ from each other and more specifically, during post cycle recovery (PCT).
Gonadotropin Therapy:
There is nothing more effective than Human Chorionic Gonadotropin (HCG). The action of HCG is identical to that of pituitary LH. This takes place independently and is not affected by exogenous hormones and/or preexisting HPTA suppression. Therefore, it directly stimulates a dramatic increase in endogenous testosterone production, spermatogenesis and testicular volume. The primary goal during the first few weeks of PCT is to quickly restore testicular volume and function. Also, the dramatic increase in testosterone production is necessary to avoid and/or minimize the unfavorable "crash" effect. In the majority of individuals with larger testes at baseline, HCG alone is sufficient in restoring endogenous testosterone production as well at the induction of spermatogenesis which is most likely a result of residual FSH secretion. Once there is a plateau in the response to HCG, treatment with an FSH preparation such as human menopausal gonadotropin (HMG) or recombinant follicle stimulating hormone (rFSH) should be added in combination to HCG.
The addition of an FSH preparation is rarely required and is best suited for severe cases of HH. FSH preparations are not readily available to most individuals. Therefore, there is no need to go into details with respect to its application at this time.
HCG is administered by subcutaneous (SC) or intramuscular (IM) injection. The average (3ml 22-25G x ⅝-1½”) syringe is adequate for IM injections but insulin syringes (½-1ml 28-30G x ½-1”) are recommended for SC injections. In regards to effectiveness, there should be no discernable difference between either of the techniques. The individual should opt for the most comfortable and/or convenient form of administration.
The following is a description of the available preparations by Serono:
HCG ampoules are supplied in 500, 1,000, 2,000, 5,000 and 10,000 IU preparations accompanied by 1 ml of sterile dilluent. It should be stored at a controlled room temperature (15-30 degrees C or 59-86 degrees F) and should be used immediately after reconstitution.
HCG multidose vials are supplied in 2,000, 5,000 and 10,000 IU preparations accompanied by 10 ml of bacteriostatic water. It should be stored at a controlled room temperature (15-30 degrees C or 59-86 degrees F), refrigerated (2-8 degrees C or 36-46 degrees F) after reconstitution and used within 30 days.
Other manufacturers are available and preparations may vary.
The terms international units (IUs) can occasionally cause confusion when reconstituting and measuring HCG. The actual process is quite elementary and the concentration per ml (cc) is dependant on the concentration of the lyophilized powder and the volume of dilluent used for reconstitution. For example, if you dilute 5,000 IUs HCG with 5ml (cc) solvent, the end result is 1,000 IUs per ml (cc). Divide the same 5,000 IUs with 10 ml (cc) and the end result is 500 IUs per ml (cc).
Bacteriostatic water should always be utilized during reconstitution when long term (30 day) storage and multi dose administration are required.
Selective Estrogen Receptor Modulators:
Selective estrogen receptor modulators (SERMs) such as Clomiphine (Clomid) and Tamoxifen (Nolvadex) increase pituitary LH secretion in secondary manner by blocking estrogen negative feedback on the HPTA. On average, this is not strong enough by itself to counteract the severe imbalance of the androgen:estrogen ratio that is encountered post cycle, especially in the presence of testicular atrophy. Therefore, SERMs are used during PCT primarily as an anti estrogen and to continue the stimulation of pituitary LH after HCG has been discontinued.
Nolvadex is widely available in 10 mg or 20 mg tablet preparations and Clomid is available in 50 mg tablet preparations.
Before Beginning PCT:
It is highly recommended to establish baseline blood values before beginning a cycle. The same principle applies to establishing post cycle blood values, which are necessary for evaluating recovery. Post cycle blood work should be obtained approximately 4 weeks after the cessation of PCT in order to determine accurate readings. Additional blood work should be performed when applicable and/or required.
The following are Fasting blood values:
Hormone
1. Cortisol, Total
2. Estradiol, Extraction
3. Prolactin
4. LH
5. FSH
6. T3, Free
7. T4, Free
8. TSH
9. Testosterone, Total, Free and Weakly Bound
10. Hemoglobin A1C
11. Fasting Insulin
12. Somatomedian C (optional)
Cardiovascular
13. CBC
14. Comprehensive Metabolic Panel
15. Lipid Panel
Other
16. GGT Important Liver Value not included in Comp Metabolic Panel
When to begin PCT:
On average, begin PCT approximately 5-10 days after your last injection regardless of longer acting esters. Begin PCT 1-3 days after your last injection and/or intake when using short acting esters.
Keep in mind, pituitary LH secretion automatically increases as the hormones diminish from your system. The elevated androgen levels are from an exogenous source and your endogenous production is suppressed. Therefore, waiting for the exogenous androgens to completely clear from your system, ultimately results in lower total concentrations of androgens in your system when beginning PCT. This leads to an unfavorable andgrogen:estrogen ratio and the well known “crash” effect.
As previously mentioned, the actions of HCG take place independently and is not affected by exogenous hormones and/or preexisting HPTA suppression. There are no contradictions with respect to the effectiveness of HCG usage while exogenous hormones are present in your system.
PCT Protocol(s):
1.) 1,000 IUs HCG 3x/wk (mon/wed/fri) in combination with 20 mgs Nolvadex ED for the first 3 weeks. After, discontinue HCG and continue with 20 mgs Nolvadex ED for an additional 3 weeks.
2.) 1,000 IUs HCG 3x/wk (mon/wed/fri) in combination with 20 mgs Nolvadex ED and 50 mgs Clomid ED for the first 3 weeks. After, discontinue HCG and continue with 20 mgs Nolvadex ED and 50 mgs Clomid ED for an additional 3 weeks.
3.) 1,500 IUs HCG 3x/wk (mon/wed/fri) in combination with 20 mgs Nolvadex ED for the first 3 weeks. After, discontinue HCG and continue 20 mgs Nolvadex ED for an additional 3 weeks.
4.) 1,500 IUs HCG 3x/wk (mon/wed/fri) in combination with 100 mgs Clomid ED and 20 mgs Nolvadex ED for the first 3 weeks. After, discontinue HCG and continue with 50 mgs Clomid ED and 20 mgs Nolvadex ED for an additional 3 weeks.
Option one can be considered as a standard PCT protocol. This should apply to all basic cycles. Option 2 is generally the same as option one except for the addition of Clomid which is added as a supporting recovery aid. Option three and four incorporate a higher HCG dosage and have a relationship similar to options one and two in the sense that Clomid is incorporated in the latter as a supporting recovery aid.
The majority of my experience is with intermediate to advanced athletes whom have completed multiple cycles with higher dosages. Therefore, based upon previous blood work results and considering the common or convenient preparations available, we have established that 1,500 IUs 3x/wk (mon/wed/fri) to be the optimal HCG dosage to begin with. The Nolvadex dosage remains unchanged however Clomid is utilized throughout the entire PCT at 100 mgs ED during the first 3 weeks and 50 mgs ED for the last 3 weeks.
HCG During Cycle:
HCG in combination with Nolvadex can and should be used during prolonged (12+/wks) and high dosage (1,000+mgs/wk) cycles. In this case, 500-1,000 IUs HCG ED in combination with 20 mgs Nolvadex ED for 7-10 days consecutively is administered mid cycle or intermittently (every 6-8 weeks) during the cycle.
Maintaining testicular volume during cycle does in fact improve recovery when compared to atrophied testes when beginning PCT. This solution addresses both testicular atrophy and prevention of Leydig cell desensitization (discussed next) associated with HCG usage.
Leydig Cell Desensitization:
Leydig cell desensitization does in fact occur to some degree with prolonged or high dose HCG usage. Using it continuously during a cycle could possibly cause the LH receptor to desensitize which in turn would ultimately render the PCT to be either less effective or possibly useless. This seems counterproductive. HCG will not be needed on cycles where the proper ancillaries are used and where the dosages/durations are realistic.
The previous summary was a general statement. The reality and good news is that Leydig cell desensitization due to HCG usage is blocked and/or minimized by Nolvadex. This occurs by suppressing HCG's ability to inhibit the conversion of 17 alpha hydroxyprogesterone to testosterone.
Additional Factors That Influence Recovery:
Factors that may complicate and/or delay recovery are elevated levels of estrogen and prolactin. Both of these hormones, when elevated, exert negative feedback on the HPTA. Estrogen and its side effects can be controlled by using an aromatase inhibitor such as Aromasin, Femara and Arimidex during cycles including aromatizing AAS. Prolactin and its side effects can be controlled by using an anti Prolactin such as Cabergoline (Dostinex) or Bromocriptine (Parodel) during cycles containing nandrolones. If these measures have not been addressed during the cycle, they will more than likely need to be addressed during PCT. In this scenario, the objective is to lower these hormones to acceptable levels in order to avoid the complications and/or delay in recovery. Blood work is imperative in evaluating the effectiveness of therapy. This will provide a clear and concise answer in regards to the adjustment of dosages and continuation of medication if necessary.
There are numerous studies which support and refute the association of nandrolones and prolactin. However, based on first hand experience and blood work results, there are far more individuals today whom can testify that the usage of nandrolones can attribute to an increase in prolactin concentrations. In addition, many individuals have reported elevated prolactin levels during cycles which do not contain nandrolones. The common factor within these cases is supraphysiological levels of estrogen. Estrogens act directly at the pituitary level by causing the stimulation of lactotrophs which in turn enhances prolactin secretion. This is another reason why estrogen management in the form of an aromatase inhibitor should be included with cycles containing aromatizing AAS. Although not absolutely necessary and considering the necessary restoration of physiological estrogen values, there is sufficient evidence which suggests that aromatase inhibitors can improve and increase recovery rates.
Unsuccessful PCT:
In some cases the aforementioned post cycle therapy protocols as well as those which are not mentioned may be unsuccessful in the restoration of homeostasis. This should not warrant immediate concern. Many endocrinologists have concluded that the only form of treatment in this particular scenario is hormone replacement therapy (HRT).
This is far from the truth. The reason many endocrinologists have come to this conclusion is due to the fact that very few of them have the experience treating severe forms of secondary acquired hypogonadotropic hypogonadism. They are unfamiliar with proper protocols which include high dosage HCG administration and additional gonadotropin preparations such as HMG or rFSH. This complication puts the patient at risk for potential and unknown side effects in the eyes of the doctor. Therefore, HRT is a reasonable solution since it will quickly alleviate the majority of the uncomfortable symptoms that the patient is experiencing.
Aside from disappointing blood work results which illustrate the typical signs of an unsuccessful recovery, the key physical indicator that the treatment is unsuccessful is testicular atrophy. In this case, HCG is continued with the necessary adjustments in dosage and frequency until an increase in testicular volume has been achieved. There is no one size fits all protocol since every case varies and deserves an individualized approach. Subsequent changes will be based upon the individual’s response to each particular stage. All the variable factors involved during the recovery process need to be considered. It's far from accurate to reach the conclusion that HRT is needed if one specific recovery protocol is not successful.
Ongoing Argument(s):
Hypothetically speaking, if testicular function and volume have been maintained during cycle with HCG, SERMs are then utilized to counteract the imbalance in the androgen:estrogen ratio encountered post cycle as the exogenous androgens diminish. This results in the prevention of estrogenic side effects while increasing pituitary LH secretion which in turn increases testosterone production.
There is nothing wrong with using a commonly referred to protocol which recommends 250-500 IUs HCG 1-2x/wk to be incorporated throughout the cycle. However, a significant cause for concern in regards to this protocol relates to the cessation of HCG once the cycle has completed and from that point on, the only substances used during PCT are SERMs which consist of Nolvadex and/or Clomid. Realistically, there is absolutely no guarantee that this formula prevents testicular atrophy to the extent where the overall volume and function of the testes are in an optimal state. Unfortunately, a large majority of individuals do not realize or are not aware that Leydig cell desensitization does in fact occur with prolonged or high dosage HCG usage. Therefore, users which follow this protocol whom do not incorporate Nolvadex or an aromatase inhibitor are now susceptible to Leydig cell desensitization which may render HCG usage post cycle ineffective when and if needed.
During conservative cycles, there is substantial evidence which exists that supports the effectiveness of the HCG during cycle and SERMs only post cycle protocol, especially when proper estrogen and prolactin management has been incorporated. However, this conclusion is much more difficult to achieve on heavy or prolonged cycles. Testicular volume should be maintained to an acceptable extent but that does not necessarily result in an improved recovery as severe HTPA suppression still exists which is not immediately repairable through the usage of SERMs.
The most common argument here when incorporating HCG during PCT is that HCG itself is suppressive. This is true and one particular way this occurs is though the constant binding of HCG which disrupts the endogenous pulsatile secretion of LH. A recent study which included the usage of 250 mcgs Ovidrel (rHCG) 2x/wk for 12 weeks demonstrated that the patients resumed normal HPTA function within four weeks upon cessation, without the usage of SERMs. What’s even more interesting is that 250 mcgs rHCG is the equivalent of approximately 5,000 IUs uHCG. Therefore, putting things into perspective, a few additional weeks of suppression is nothing to be overly concerned about compared to and considering the 12 weeks of suppression incurred during the average cycle. The usage of HCG during PCT is a minimally intrusive variable where the benefits clearly exceed the associated costs.
Conclusion:
PCT should begin after the last injection and/or AAS intake. More specifically, a relative guideline to begin PCT is within 5-10 days when using long acting esters or 1-3 days when using short acting esters. This PCT protocol should consist of 1,000-1,500 IUs HCG 3x/wk (mod/wed/fri) in combination with 20 mgs Nolvadex ED and, if necessary, 50-100 mgs Clomid ED. The mid/intermittent cycle protocol of 500-1,000 IUs HCG and 20 mgs Nolvadex ED for 7 days consecutively can and should be utilized when necessary during prolonged (12+/wks) or heavy dosage (1,000+mgs/wk) cycles. In addition, blood work should be performed before beginning a cycle and after completing a cycle in order to establish baseline values and evaluate recovery, respectively.
If recovery is unsuccessful, HCG is continued with an adjustment in dosage and frequency as necessary until the increase in testicular volume and function have been achieved which is unlike the more typical, yet incorrect belief that HCG is only to be used for a short period of time. Once there is a plateau in the response to HCG, treatment with an FSH preparation such as human menopausal gonadotropin (HMG) or recombinant follicle stimulating hormone (rFSH) should be added at a starting dose of 75-150 IUs on alternate days. This continual usage is not necessary and avoidable in most cases by utilizing the mid/intermittent protocol previously mentioned, but it is much more common and less avoidable with long term (1+/yr) users, whom have not taken the suggested preventive measures, and/or improper recovery from previous cycles regardless of which protocol is chosen.
With the usage of HCG post cycle, your androgens are elevated but well below that of supraphysiological concentrations from exogenous hormones. In addition, a noteworthy difference is that the effect is through a direct stimulation of testicular production compared to the secondary nature of SERMs in conjunction in the presence of testis that are not guaranteed to be in an optimal functioning state. Upon completion, blood work will display significantly higher levels of LH, FSH and testosterone in this environment which includes HCG and SERMs during PCT versus HCG during cycle and SERMs only during PCT. This ultimately results in a more comfortable as well as tolerable recovery both physically and psychologically. In conclusion, HCG should always be included during PCT in combination with SERMs regardless of what protocol has been utilized during cycle to prevent testicular atrophy, in order to achieve an optimal recovery.
Post #2:

Quote:

Another:
Heres another way, kind of similar;
Understanding Post Cycle “T” Recovery
By William Llewellyn
O.K. You have been on an awesome 4-month cycle of Sustanon and Dianabol. You’ve gained a massive 20 lbs, and are extremely pleased with your results. You can’t stop looking in the mirror. But there is a problem now starting to eat away at you. You are going to run out of steroids very soon (you know you need a break anyway), and your testicles are the size of raisins. Your body is producing less testosterone than a 9-year-old girl, and you are scrambling to figure out what to do to avoid a nasty post-cycle crash that could potentially strip away some of your hard-earned muscle. The opinions on how to restore endogenous testosterone production post-cycle seem to be different everywhere you look. What option is best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right post-cycle program can be quite confusing. In this article I would therefore like to discuss the role of anti-estrogens and HCG during this delicate window of time, while detailing an effective strategy for their use.
The Axis
The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body’s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.
Testicular Desensitization & Post-Cycle LH Levels
Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.
Post Cycle Testosterone Levels
Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.
The Role of Anti-estrogens
It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.
HCG
So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.
Finalizing the Program
An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2), which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added ( my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.
Sample Post-cycle Plan:
Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily
In Closing
I hope this article provided a well-needed new look at the mechanisms involved in post-cycle testosterone recovery. Indeed I believe it should debunk a commonly held belief these days, as we seen now that those advocating the sole use of Clomid post cycle are sorely missing the mark. The problem goes much deeper than just getting LH levels back. In fact, we see that LH doesn’t even need much help kicking back into gear, and a drug like Clomid will do very little to help this anyway in the absence of significant estrogen levels anyway. HCG is a drug with undeniable usefulness during the post-cycle window, and many bodybuilders have been much too quick to abandon it. It is truly fundamental to an effective recovery program, and would not consider any dose or combination of anti-estrogens or aromatase inhibitors capable of doing the job without it.
Post #3:

Quote:

This is funny that I found my own article on another board and thought I have read this before.
This is in rebuttel to Jenetic's article.
Now I feel that using too little HCG will not have the desired effects to bring back testicular function after a cycle.
That article was nicely written but I do see some flaws in it.
Not picking on the article but coming from Swale's end that does allot of blood work; I have a problem with the post as it contradicts what Swale suggests for instance.
First advising the use of 1500iu of HCG is just too much.
This is a direct quote from his article on HCG. For those who do not know Dr. Swale he is a HRT Dr and probably one of the best in the world. He even teaches endocrinologists in lectures. Now that we know his background I feel he is more qualified in his field than any other poster on boards. Not only that this is his job and he looks at blood work every day.
His quote:
“It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.
All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).”
QD is every 3 days and this is just the way he writes it for some reason I don’t know but it is every 3 days.
Here is another of his Quotes from a different article.
His quote:
“I advise my AAS patients to use small amounts of HCG (250IU to 500IU) every third day, right from the beginning of the cycle. This serves to maintain testicular form and function. This is infinitely better than waiting until they have seriously atrophied. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.
Any more than 500IU of HCG per day causes too much aromatase activity. This drives up estrogen levels, unopposed by increased testosterone production. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).
If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.”
As you can see here there is direct contradiction between and I would take Swale’s advice over pretty much any others. He has used gear too so I do think he has more credibility too.
First off Jenetic suggests it is length that causes desensitizing and not amount. Swale on the other hand suggests it is amount and not length.
Let’s do the math here.
1500x 3 times a week is 4500iu for 3 weeks (21 days).
250 every 3 days is 2000iu 22 days.
Less than half was used. If he did say “(I have yet to see more than 350IU per dose required).” Why use more?
Ok the issue of nandrolones and prolactin.
I e-mailed him (Swale) on this issue directly here is his e-mail to me:
Quote:
Originally Posted by SWALE
I have never seen deca elevate PRL.
Prog inhibits the conversion to DHT. DHT opposes estrogen by several different mechanisms.
I have to get back to work now....
Ok, the PRL is abbreviated for prolactin and the Prog is abbreviated for progesterone.
I was suggesting to him about prolactin and shutdown and my supplementation of progesterone as suggested by my HRT Dr.
Now here is another E-mail I got from him on progesterone.
Quote:
Originally Posted by SWALE
If you feel better on progesterone, then do what works for you, of course. there is something else going on there, as prog enhances estrogenic effects, not inhibits same.
you might want to share with the other Bro that it makes no sense to take dostinex with tren, etc. inhibiting natural production has no benefit while supplementing a hormone's agonist. the body does that on its own, if necessary, and you risk lowering prolactin too much. this compromises immune function and also puts the LH receptors at risk.
HPTA-suppression from deca definitely is due to progestogenic effects there.
prog inhibits DHT, and that leaves estrogen to its feminizing features. simple as that.
So in my interpritation of this all, either Swale is wrong or Jenetic is wrong as niether one can be correct.
I also use small amounts of HCG myself and do notice good results using the amounts Swale suggests.
(UK-muscle article)
Post #4:

Quote:

by swale (MD / hrt specailist). originally posted at steroidology
I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.
Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).
If 250IU or 500IU on two days each week isn?t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn?t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.
The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM?s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.
I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a?bridge?. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can?t?fool? the body?it is smarter than you are.
I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground?and we don?t want that, do we?).
All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other
JC: Dr. John has updated the original paper you published. Here it is:
My New HCG Protocol Paper
This paper is about to be published in The American Academy of Anti-Aging Medicine 2004 Clinical Updates:
AN UPDATE TO THE CRISLER HCG PROTOCOL
By John Crisler, DO
In my paper?My Current Best Thoughts on How to Administer TRT for Men?, published in A4M?s 2004/5 Anti-Aging Clinical Protocols, I introduced a new protocol where small doses of Human Chorionic Gonadotrophin (HCG) are regularly added to traditional TRT (either weekly IM testosterone cypionate or daily cream/gel). The reasons and benefits of this protocol are as follows, along with a new improvement I wish to share:
Any physician who administers TRT will, within the first few months of doing so, field complaints from their patients because they are now experiencing troubling testicular atrophy. Irrespective of the numerous and abundant benefits of TRT, men never enjoy seeing their genitals shrinking! Testicular atrophy occurs because the depressed LH level, secondary to the HPTA suppression TRT induces, no longer supports them. It is well known that HCG?a Luteinizing Hormone (LH) analog?will effectively, and dramatically, restore the testicles to previous form and function. It accomplishes this due to shared moiety between the alpha subunits of both hormones.
So, that satisfies an aesthetic consideration which should not be ignored. Now let?s delve into the pharmacodynamics of the TRT medications. For those employing injectable
testosterone cypionate, the cypionate ester provides a 5-8 day half-life, depending upon the specific metabolism, activity level, and overall health of the patient. It is now well-established that appropriate TRT using IM injections must be dosed at weekly intervals, in order to avoid seating the patient on a hormonal, and emotional, roller coaster. Adding in some HCG toward the end of the weekly?cycle? compensates for the drop in serum androgen levels by the half-life of the cypionate ester. Certainly the body thrives on regularity, and supplementing the TRT with endogenous testosterone production at just the right time?without inappropriately raising androgen OR estrogen (more on that later)?approximates the excellent performance stability of transdermal testosterone delivery systems for those who, for whatever reason or reasons, prefer test cyp.
But there?s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.
It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.
In my previous report I recommended 250IU of HCG twice per week for all TRT patients, taken the day of, along with the day before, the weekly test cyp injection. After looking at countless lab printouts, listening to subjective reports from patients, and learning more about HCG, I am now shifting that regimen forward one day. In other words, my test cyp TRT patients now take their HCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).
I made this change after realizing that the previous HCG protocol was boosting serum testosterone levels too much, as the test cyp serum concentrations rise, approaching its peak at roughly the 72 hour mark. The original goal of supporting serum androgen levels with HCG had overshot its mark.
Those TRT patients who prefer a transdermal testosterone, or even testosterone pellets (although I am not in favor of same), take their HCG every third day. They needn?t concern themselves with diminishing serum androgen levels from their testosterone delivery system. These patients will, of course, notice an increase in serum androgen levels above baseline.
While HCG, as sole TRT, is still considered treatment of choice for hypogonadotrophic hypogonadism by many, my experience is that it just does not bring the same subjective benefits as pure testosterone delivery systems do?even when similar serum androgen levels are produced from comparable baseline values. However, supplementing the more?traditional? TRT of transdermal, or injected, testosterone with HCG stabilizes serum levels, prevents testicular atrophy, helps rebalance expression of other hormones, and brings reports of greatly increased sense of well-being and libido. My patients absolutely love it. As time goes on, we are coming to appreciate HCG as a much more powerful--and wonderful--hormone than previously given credit.
Copyright John Crisler, DO 2004. This article may, in its entirety or in part, be reprinted and republished without permission, provided that credit is given to its author, with copyright notice and 2. www.AllThingsMale.com clearly displayed as source. Written permission from Dr. Crisler is required for all other uses.
Last edited by bubbafrombama; 12-30-2008 at 12:56 AM.
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