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  1. #1
    scott.s is offline Junior Member
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    what pct is required and for how long!!!

    What pct would be advisable to take on a six week course of Anavar .
    at what stage,what dosage and for how long???
    Thanks guys....

  2. #2
    domeyeahaigh's Avatar
    domeyeahaigh is offline Senior Member
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    probably not much but if you really want to run somethin just run nolvadex at 20mg/day for 4 weeks, although anavar taken for 6 weeks probably will shut you down very minimally if at all.

  3. #3
    peachfuzz's Avatar
    peachfuzz is offline Anabolic Member
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    you do need a post cycle with anavar . it will shut you down. however the pct can be light as suggested above.

  4. #4
    scott.s is offline Junior Member
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    when you say shut you down are you refering to erection dysfunction ????

  5. #5
    WARMachine's Avatar
    WARMachine is offline Post Cycle Extraordinaire~GOT PCT?
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    No he is refering to your HPTA.

    And i dont buy that Anavar will shut you down after only 6 weeks at relatively small doses.

    It is always best to do a small PCT to be on the safe side though.

  6. #6
    peachfuzz's Avatar
    peachfuzz is offline Anabolic Member
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    Effect of low dose oxandrolone and testosterone treatment on the pituitary-testicular and GH axes in boys with constitutional delay of growth and puberty.

    Crowne EC, Wallace WH, Moore C, Mitchell R, Robertson WH, Holly JM, Shalet SM.

    Department of Endocrinology, Christie Hospital Trust, Manchester, UK.

    OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin , SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.

    Clin Endocrinol (Oxf). 1993 Apr;38(4):393-8.
    The effects of oxandrolone on the growth hormone and gonadal axes in boys with constitutional delay of growth and puberty.
    Malhotra A, Poon E, Tse WY, Pringle PJ, Hindmarsh PC, Brook CG.

    Endocrine Unit, Middlesex Hospital, London, UK.

    OBJECTIVE: We studied the effects of oxandrolone on serum concentrations of LH, FSH, testosterone, GH, SHBG, DHEAS, IGF-I and insulin in boys with constitutional delay of growth and puberty. DESIGN: Ten boys with constitutional delay of growth and puberty, mean age 13.8 years (range 12.4-15.5) were studied. Twenty-four-hour serum concentration profiles of GH, LH and FSH were constructed by drawing blood samples at 20-minute intervals. Three study occasions over a period of 6 months were chosen to assess hormone concentrations before, during and 6 weeks after a 3-month course of oxandrolone (2.5 mg once daily) therapy. RESULTS: Growth velocity increased during oxandrolone treatment and stayed higher after therapy (pre 3.9 +/- 0.5; on 6.3 +/- 0.8; post 6.4 +/- 0.9 cm/year (mean +/- SEM) two way ANOVA, F = 5.3, P = 0.02). Oxandrolone had androgenic effects, suppressing mean serum LH concentrations from 1.7 +/- 0.3 to 1.1 +/- 0.2 U/I and serum testosterone concentrations from 1.9 +/- 0.6 to 0.8 +/- 0.1 nmol/l. SHBG concentrations were also reduced from 130.9 +/- 14.6 to 30.7 +/- 7.3 nmol/l. Serum GH concentration fell slightly from 5.9 +/- 0.6 to 4.8 +/- 0.5 mU/l. After cessation of treatment, there was a significant 'rebound' in mean 24-hour serum LH (2.6 U/l +/- 0.4) and testosterone concentrations (3.2 +/- 0.9 nmol/l) but no change in serum GH concentrations. SHBG values also rose but not to the same extent as those observed before therapy (82.0 +/- 8.4 nmol/l). There were no statistically significant differences in serum concentrations of FSH, DHEAS, IGF-I and insulin over the study period. In a stepwise multiple regression analysis of factors that might influence the growth rate observed, the 24-hour mean serum testosterone concentration and the treatment (on or off) with oxandrolone were the main influences. The relationship was described by the equation Height velocity = 0.69 (24-hour mean serum testosterone concentration)+1.70 (treatment regimen)+3.37 (adjusted R2 = 0.35, F = 8.39, P = 0.001). CONCLUSIONS: Oxandrolone has an androgenic action as shown by changes in serum LH, testosterone and SHBG concentrations and by the lack of effect on FSH. No effect of oxandrolone on the GH axis was documented. We suggest that the growth promoting effects of oxandrolone are related in part to the mild androgenic effects of the steroid and the growth acceleration following oxandrolone withdrawal may reflect increasing total serum testosterone concentrations and decreasing levels of SHBG and progress in puberty.

    PMID: 8319371 [PubMed - indexed for MEDLINE]


    another....http://jcem.endojournals.org/cgi/content/full/84/8/2705

  7. #7
    WARMachine's Avatar
    WARMachine is offline Post Cycle Extraordinaire~GOT PCT?
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    Ok so it does shut you down, though not completely. Even in small doses.

    Though ive gotta tell you, ive ran Test based cycles, and Var only, and the shutdown with Var is next to nothing imo.

    Advising the use of a PCT for saftey's sake seems to be the best advice possible.

    Thanks for the read Peachy!

  8. #8
    peachfuzz's Avatar
    peachfuzz is offline Anabolic Member
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    no problemo. and i agree var is alot easier to recover from then most.

  9. #9
    Swifto's Avatar
    Swifto is offline Banned- Scammer!
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    Quote Originally Posted by WARMachine View Post
    Ok so it does shut you down, though not completely. Even in small doses.
    Though ive gotta tell you, ive ran Test based cycles, and Var only, and the shutdown with Var is next to nothing imo.

    Advising the use of a PCT for saftey's sake seems to be the best advice possible.

    Thanks for the read Peachy!
    Your HPTA is either shutdown (not producing ganadotropins) or inhibited (producing less ganadotropins).

    Different AS will cause different effects to the HPTA.

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