Thread: PCT help
08-31-2005, 04:03 PM #1Associate Member
- Join Date
- May 2005
hey guys im 1 week through of 300mg frontload and 100mgday clomid and 20mg a day nolva PCT. I still have no sex drive, How long till the clomid kicks in.
08-31-2005, 04:04 PM #2Originally Posted by nickm748
about 2 week's for me
09-01-2005, 02:49 AM #3
This is some good info on HCG , clomid & nolva. I copied and pasted this of course.
This observational study demonstrates the possible efficacy of HCG, clomiphene citrate, and tamoxifen citrate in returning the HPGA to normal physiological function in adult males suffering from androgen induced hypogonadotropic hypogonadism. In the case of decreased testicular function manifested by low testosterone levels , it is of primary importance to first return the normal function of the testicular cells. The initial lack of response to HCG should not immediately be a cause for the initiation of testosterone replacement therapy, as with the current accepted therapy modality by many physicians. Blood analysis confirmed that no exogenous testosterone was administered during the treatment period, as exogenous androgens would have had a suppressive effect on endogenous gonadotropin production. Therefore, because of the corresponding normal gonadotropin and testosterone values, it is accepted that gonadotropin and testicular function were normal by the conclusion of treatment. The standard treatment of HIV-related muscle wasting, AAS therapy, may involve decades of treatment and the attendant problems with any therapy of a prolonged nature. Polycythemia vera, elevated hepatic enzymes, and prolonged negative alterations in lipid profile are a few of the dangers experienced by HIV patients administered AAS for extended periods. Of greatest concern is the increasing numbers of individuals who are currently being treated with AAS to increase muscle mass either for medicinal or recreational means without attention being given to periodically returning the HPGA to normal. With roughly 4 million men in the U.S. being considered hypogonadal (Lacayo R., 2000; Sheffield-Moore et al, 1999; Shelton DL, 2000), an estimated 200,000 men are currently receiving testosterone treatment for the condition (Shelton DL, 2000). As stated earlier, AAS are being prescribed to HIV & AIDS sufferers to combat progressive muscle loss. The Centers for Disease Control and Prevention (CDC) reported an estimated 635,000+ men diagnosed with AIDS through December 2000 while an estimated 97,700 have been reported with HIV (Centers for Disease Control, vol.12, No. 2, table 5; Centers for Disease Control, vol. 12, No. 2, table 6). In 2000 alone over 31,000 men were diagnosed with the AIDS virus (Centers for Disease Control, vol. 12, No. 2, figure 3). Between hypogonadal, AIDS, & HIV males, potentially over 900,000 men are being administered AAS therapy.
Studies recently published on patients suffering from various tissuedepleting conditions and HIV affliction (Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al, 1999;1999; Van Loan et al, 1999) have not identified what should be done to restore normal endocrine status post-treatment. Considering the dosages and compounds administered in many studies, there is no question that subjects were left hypogonadal after therapy. In the cases where the periodic use of testosterone or AAS are necessary, intervention to return the HPGA to normal should be initiated as soon as possible after the cessation of the AAS. As described herein, a possible treatment modality may be the combined regimen of HCG, clomiphene citrate, and tamoxifen. Medical history has demonstrated examples of physician-induced complications resulting from treatment. Iatrogenic hyperthyroidism (Bartsch & Scheiber, 1981) and iatrogenic Cushing’s syndrome (Cihak & Beary, 1977; Kimmerle & Rolla, 1985; Smidt & Johnston, 1975; Tuel et al, 1990) are cases were administered medications or treatments provoked abnormalities in patients’ normal physiology. The administration of testosterone as a treatment for hypogonadotropic hypogonadism falls into this same category of causing endocrine related abnormalities (Bhasin et al, 1996; Marynick et al, 1979; Strawford et al, 1999; Tenover, 1992). Testosterone replacement therapy has proven to be very effective in reversing the symptoms of suppressed testosterone production, but does not treat the underlying cause of the deficiency. Positive effects of testosterone treatment; i.e. improved sex drive, improved sense of well-being, lean body mass; are all transient in light of plummeting gonadotropin levels. Upon cessation of testosterone treatment patients can expect a complete reversal of positive benefits as exogenously influenced testosterone levels metabolize and decline rapidly. Further controlled studies need to be performed showing the combined effects of HCG, clomiphene citrate, and tamoxifen in returning HPGA functioning to normal. Long-term follow-up on these patients returning to normal will be necessary to ensure permanent reversal of hypogonadotropic hypogonadal conditions. In addition, studies documenting dose-response curves for pituitary inhibition and reversal due to AAS administration are critical in determining the correct dose, duration, and form of treatment that is optimal without causing permanent damage. When the need for long-term androgen use presents, using moderately supraphysiologic doses of androgens as suggested by Strawford and colleagues (1999) coupled with post-treatment HPGA restoration as demonstrated here, may be a more effective means over high-dose protocols used to offset negative alterations in lean body mass. Unfortunately current studies have yet to adequately address a standard of patient care post-androgen therapy. Because of the negative impact of the hypogonadal state on physical and mental well- being, pharmacotherapy that restores HPGA function more rapidly than current modalities would greatly benefit men with hypogonadotropic hypogonadism.
While we believe that the treatment protocol was effective in returning normal hormonal function to these men, the lack of randomization or a control group leaves room for speculation. Although cases of spontaneous return to eugonadism with no medicinal intervention have been published, these reports documented durations anywhere from 6-18 months before normal hormone status was achieved (Gazvani et al, 1997; Wu et al, 1996). If the alternative treatment modality described herein can reverse suppressed gonadotropin production and AAS associated side effects much sooner than non-treatment, further evaluation of this therapy should continue.
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