Anavar alone should not shut you down regardless of what they say. However test would make it a million times better and I have no idea why you are getting sides from just 25Mg of anavar..
he never said how much he is taking or for how long he plans too, i believe the board does show that anavar use for the period we call a cycle will suppress natural test production to some degree*, that part should not be disputed its just to what extent does it impact a person and in what stage of life they are in.
now dont run off and tell everyone to use orals only lol
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]
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