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    Thread: pct

    1. #1
      MR.MUSCLE's Avatar
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      Default pct



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      I just took my last shot of tren today,I cant get a hold of any hcg,so all i have is liquid clomid and clen,what else could I take with these's that would be good.Thank,s
      In a race,everyone runs but only one person gets the prize.So,run the race to WIN!-1st corinthians 9:24

    2. #2
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      Default Re: pct

      Check out our advertiser.

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      Default Re: pct

      SOME USE NOLVADEX WHILE DOING PCT WITH THE CLOMID
      Disclaimer: Steroid use is illegal in a vast number of countries around the world. This is not without reason. Steroids should only be used when prescribed by your doctor and under close supervision. Steroid use is not to be taken lightly and we do not in any way endorse or approve of illegal drug use. The information is provided on the same basis as all the other information on this site, as informational/entertainment value.

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    4. #4
      MR.MUSCLE's Avatar
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      Default Re: pct

      Should i start taking the clomid right away?
      In a race,everyone runs but only one person gets the prize.So,run the race to WIN!-1st corinthians 9:24

    5. #5
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      Default Re: pct

      Quote Originally Posted by MR.MUSCLE
      Should i start taking the clomid right away?
      Start your pct when the Tren half life has surpassed. So it depends on itf it was Tren Acetate (short acting, 1-2 days?), Tren Parabolan (~7 days), or Tren Enan (~10 days)

    6. #6
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      Default Re: pct

      Do you think the clomid alone will bring the boy's back?
      In a race,everyone runs but only one person gets the prize.So,run the race to WIN!-1st corinthians 9:24

    7. #7
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      Default Re: pct

      Were you taking just tren?

    8. #8
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      Default Re: pct

      Quote Originally Posted by MR.MUSCLE
      Do you think the clomid alone will bring the boy's back?
      I would suggest both Clomid and Nolva

      The following is advice from Pheedno's pct protocol:

      *******
      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

      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.

      __________________________________________________
      _________

      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.

      ______________________________

      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).

      _______________________________

      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.
      Last edited by geesler; 07-02-2005 at 11:21 PM.

    9. #9
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      Default Re: pct

      That info is mainly regarding your HPTA and Estrogen, If you were only running tren and if gyno is your concern, Gyno from tren will be progesterone induced and you will have to get an anti prolactin or/and b6 for that. Tren converts to Progesterone rather than Estrogen.

    10. #10
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      Default Re: pct

      Im going to try that after this cycle. 100mg clomid for 7-8 days then 50mg for 22day with nolva 20mg for the total 28-30 days, and .25mg ldex. and see how it works.

    11. #11
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      Default Re: pct

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      Nice- from what I've researched/read so far that seems the best bet to cover your bases

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