Pheedno's PCT

[Da Bull]

Posted by Pheedno @ Anabolicreview


My post cycle therapy consists of a three compound administration which is designed so that there is a primary and secondary LH stimulator which both are maximizing potential early in the duration; with the primary being phased out in extended protocol. With the addition of an Aromatase Inhibitor, which makes the above possible, the individual will also endure less of an increase in Sex Hormone Binding Globulin, which allows free testosterone levels to reach base line at a much quicker pace. The individual will also see less of a problem in most cases with sexual libido as the bounding SHBG is controlled(to an extent). Below you will find my suggested bare minimum, as well as a sample of an extended protocol. Extended PCT protcol is cycle length dependant so the below is not the standard for all cycles


PCT for cycles 8-16wks:
Day 1-30- .25mg L-dex + 100mg Clomid + 20mg Nolva

Extended protocol sample for a 12+ month cycle:
Day 1-15_ .25mg L-dex + 100mg Clomid + 20mg Nolva
Day 16-45_.25mg L-dex + 75mg Clomid + 20mg Nolva
Day 46-65_.25mg L-dex + 20mg Nolva
Day 66-80_.25mg L-dex

Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur.
With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual PCT duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux
occured PC while clomid is the primary LH stimulator(Even more so in the case an AI is not used).
2. If your running a longer PCT, clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary. In the longer forms of PCT, the clomid will be phased out, leaving Nolva and L-dex

Arimidex(or L-dex)
Estrogen is the main inhibitence of restoring HPTA, and AI administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of PCT, since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis

[Da Bull]

Posted bt Pheedno @ Anaboicreview


Tamox vs Clomid

Am J Physiol 1983 Feb;240(2):E125-30

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

Adashi EY, Hsueh AJ, Bambino TH, Yen SS.

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

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Br J Pharmacol 1978 Apr;62(4):487-93

Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.

Kurl RN, Morris ID.

1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.

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the following study was not available in my library, so i wasn't able to obtain the article or abstract. it may have to be purchased, so if someone is interested, here's the title and authors of the research.

Nippon Funin Gakkai Zasshi 1978 Oct;23(4):398-404

[The hormonal dynamics picture of tamoxifen treatment cases, in comparison of clomid treatment cases]

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Cochrane Database Syst Rev 2000;(2):CD000151

Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.

Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN.

[Da Bull]

Posted by Pheedno @ Anabolicreview


Case for Clomid

J Clin Endocrinol Metab 1985 Nov;61(5):842-5

Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.

Winters SJ, Troen P.

To examine the mechanism by which endogenous estrogens inhibit gonadotropin secretion in men, blood samples were drawn every 10 min for 12 h in five men before and at the completion of 3 weeks of treatment with the estrogen antagonist clomiphene citrate (50 mg twice daily). Samples were analyzed for LH and alpha-subunit by RIA. Clomiphene produced a 3-fold rise in circulating LH levels, which was associated with a 80% increase in pulse frequency and a 70% increase in pulse amplitude. Immunoreactive alpha-subunit secretion was also pulsatile before and after clomiphene treatment. Mean alpha-levels rose 70%, together with a 39% increase in pulse frequency and a 41% increase in pulse amplitude. Circulating testosterone and estradiol levels increased 2-fold and FSH levels increased 3-fold after clomiphene treatment. Insofar as each LH and uncombined alpha-subunit pulse reflects a LHRH secretory episode, our data indicate that endogenous estrogens tonically restrain the hypothalamic release of LHRH. From these results and those of previous studies, we conclude that estrogens as well as androgens are important in the testicular feedback inhibition of the hypothalamic oscillator that governs pulsatile gonadotropin secretion.


J Androl 1991 Jul-Aug;12(4):258-63

The effects of normal aging on the response of the pituitary-gonadal axis to chronic clomiphene administration in men.

Tenover JS, Bremner WJ.

Department of Medicine, University of Washington School of Medicine, Seattle.

Serum androgens decline with age in normal men, despite normal or elevated bioactive serum gonadotropins, suggesting that primary testicular dysfunction occurs with aging. The authors further assessed the question of age-related testicular dysfunction by evaluating whether raising serum gonadotropins above the normal serum range for an extended time in healthy elderly men might result in bringing their gonadal function to a level similar to that found in young adult men. Five elderly (65 to 85 years old) and five young adult men (26 to 33 years old) were given 50 mg of clomiphene citrate (CC) twice a day for 8 weeks to stimulate gonadotropin production. During that time, testosterone (T), non-sex hormone-binding globulin bound T, and estradiol increased significantly in both age groups, while serum inhibin increased significantly only in the young adult men. The increases in serum androgens with CC administration were significantly greater in the young adult men than in the elderly men. These hormone changes occurred in the setting of serum gonadotropins that increased significantly in both age groups, although there was a tendency for the elderly men to have a smaller increase in luteinizing hormone. Despite 8 weeks of stimulation of the pituitary-gonadal axis by CC administration, the elderly men demonstrated significantly diminished testicular responses compared with the young adult men. Sertoli cell function, as determined by inhibin production, was more diminished in the elderly men than was Leydig cell function. These data strengthen the hypothesis that normal aging in men is accompanied by a decline in testicular function.


Urology 1991 Oct;38(4):317-22

Possible hypothalamic impotence. Male counterpart to hypothalamic amenorrhea?

Guay AT, Bansal S, Hodge MB.

Section of Endocrinology, Lahey Clinic Medical Center, Burlington, Massachusetts.

Twenty-one men with erectile complaints who were found to have a low level of serum testosterone without a reciprocal elevation of the serum levels of luteinizing hormone were evaluated to identify whether the defect was of hypothalamic or of pituitary origin. Patients underwent a luteinizing hormone (LH)-follicle-stimulating hormone (FSH)-releasing hormone stimulation test that showed a normal but sluggish increase in LH and FSH levels, thus ruling out a pituitary defect and suggesting a suprapituitary abnormality. This was confirmed when, in response to clomiphene, patients had a normal increase in gonadotropin and testosterone levels. Although the basal as well as clomiphene and gonadotropin releasing hormone-stimulated levels of total testosterone and gonadotropins were identical in men less than and more than fifty years old, the elevation of free testosterone levels in response to clomiphene was higher in patients younger than fifty. This suggested that although the primary abnormality found in these patients is altered secretion of gonadotropin hormone-releasing hormone from the hypothalamus, an age-related decline in the responsivity of Leydig cells to LH may make it more manifest in older patients. Elevation of testosterone levels from a subnormal to a normal range in response to clomiphene administered for seven days suggests that the defect is functional and reversible and that the drug may be useful in treatment of sexual dysfunction in this group of patients.
Nephron 1993;63(4):390-4

Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.

Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P.

Department of Nephrology, Hospital Universitario Reina Sofia, Cordoba, Spain.

The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls (C). At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the

[Da Bull]

Posted by Pheedno @ Anabolicreview

Tamoxifen

nolvadex aka tamoxifen studies:

Arch Gynecol Obstet 1993;252(3):143-7

Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.

Sterzik K, Rosenbusch B, Mogck J, Heyden M, Lichtenberger K.

Abteilung Frauenheilkunde, Geburtshilfe der Universitat, Ulm, Germany.

Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had no significant effect (P > 0.05) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), or estradiol (E2). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.


Asian J Androl 2001 Jun;3(2):115-9

Effect of intermittent treatment with tamoxifen on reproduction in male rats.

Gill-Sharma MK, Balasinor N, Parte P.

Department of Neuroendocrinology, Institute for Research in Reproduction, ICMR, Parel, Mumbai, India. dirirr@vsnl.com

AIM: To identify the antifertility effect of intermittent oral administration of tamoxifen in male rat. METHODS: Tamoxifen was administered orally at a dose of 0.4 mg x kg(-1) x d(-1) with an intermittent regime for 120 days. Treated and control rats were mated with cycling female rats on days 60, 90 and 120 of treatment. The mated males were sacrificed and the weights of reproductive organs were recorded, and the serum levels of LH, FSH, testosterone and estradiol estimated by radioimmunoassay. In the female rats, the numbers of implantation sites, corpora lutea, and numbers of normal and resorbed foetuses were recorded on d 21 of gestation. The potency, fecundity, fertility index, litter size and post-implantation loss were then calculated. RESULTS: The fecundity of male rats was completely suppressed by tamoxifen while the potency was maintained at the control level. The fertility index was significantly decreased. No viable litters were sired. Post implantation loss, indicative of non-viable embryos, was observed but was not significantly increased above the control level. The weights of the testes, epididymides, ventral prostate and seminal vesicles were significantly reduced. The blood LH and testosterone levels were significantly decreased, but not FSH and estradiol. CONCLUSION: Intermittent oral tamoxifen administration completely suppressed the fecundity of adult male rats with reserved potency.

[Da Bull]

Posted by Pheedno @ AnabolicReview


Case study showing benefit to FSH, LH, and testosterone from tamox- Notice administration duration

Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S

[see related articles]

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Affiliation
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.

Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy. PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment. RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant. CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.

[Da Bull]

Posted by Pheedno @ AnabolicReview



Study between tamox administration and placebo- attention to highlighted

Int J Androl. 1992 Feb;15(1):14-8. Related Articles, Links


Comment in:
Int J Androl. 1992 Dec;15(6):507-8.

Treatment of idiopathic oligozoospermia with tamoxifen--a randomized controlled study.

Krause W, Holland-Moritz H, Schramm P.

Department of Andrology, Philipps-Universitat, Marburg, Germany.

There is no conclusive evidence of the usefulness of tamoxifen in the treatment of idiopathic oligozoospermia (OAT-syndrome), as it has been used mostly in uncontrolled studies. We herein report on the controlled treatment of OAT-syndrome with tamoxifen versus placebo following a randomized design. Seventy-six men with sperm counts of 2-20 x 10(6) ml-1, sperm motility of 20-50%, and sperm morphology (abnormal cells) between 50 and 80% were involved in the study. Patients with varicocele, a history of testicular maldescent or genital inflammation were excluded. Thirty-nine patients received tamoxifen (30 mg daily), 37 patients placebo. There was a statistically significant increase in the mean serum testosterone level after treatment in the tamoxifen-treated group (from 4.9 +/- 1.9 to 7.9 +/- 3.6 ng ml-1) in comparison to the placebo group (5.3 +/- 2.0 and 5.6 +/- 2.0 ng ml-1). Serum FSH levels increased slightly in the tamoxifen group (from 6.8 +/- 4.1 to 7.3 +/- 4.8 mU ml-1), but this was not statistically significant in comparison to the placebo group (from 5.9 +/- 3.9 to 5.2 +/- 3.5 mU ml-1). Serum levels of LH did not show any differences between groups. The sperm count increased during treatment from 9.3 +/- 11.7 to 11.4 +/- 13.7 x 10(6) ml-1 in the tamoxifen group and from 9.1 +/- 7.1 to 9.3 +/- 8.8 x 10(6) ml-1 in the placebo group; this difference did not reach statistical significance. The percentage of motile and abnormal sperm was not different between the two treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

[Da Bull]

Posted by Pheedno @ AnabolicReview


Study on benefit of tamox-again pay attention to duration. Also notice levels were checked at 2wks-12wks, but it is not specified when increased levels of FSH, LH, and T were seen at maximized effect. Levels of T and FSH are only significant, with T at miniscuel proportions

Fertil Steril. 1983 May;39(5):700-3. Related Articles, Links


Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.

Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.

Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.

[Da Bull]

This is simply an add on to a great thread.

Got this from LawnSaver on 1morerep.

Good Article on Understanding HPTA Inhibition and Recovery from AS
The Causes of Inhibition

Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.

This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the Clomid use.

So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.

What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.

Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.


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The Hypothalamic/Pituitary/Testicular Axis (HPTA)

To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.

The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.

The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.

LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.


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Inhibition From AAS Cycles

Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:

Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.

I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.


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Drugs of Use With Regard to Inhibition

Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.

Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.



Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.

HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.