deify said:
Anavar is the only roid that truly doesn't affect the HPTA and is the only one I would use to run a solid bridge between cycles.
I don't know where that myth comes from, but Anavar (Oxandrolone) inhibts the HPTA even at 2.5mg ed and will shut you down completly at higher doses, both in the rat (see study 1 below) and in humans (see study 2):
Acta Endocrinol (Copenh) 1992 Feb;126(2):173-8
The effects of an anabolic steroid (oxandrolone) on reproductive development in the male rat.
Grokett BH, Ahmad N, Warren DW.
Department of Exercise Science, University of Southern California, Los Angeles 90033.
Oxandrolone is a 5 alpha-reduced anabolic steroid that is administered for the treatment of short stature disease in children. It is a commonly used substance beginning as early as prepuberty by some individuals who are seeking to enhance athletic performance or personal appearance. Because of the lack of data on the effects of anabolic steroids on the reproductive system, we have
examined the effects of oxandrolone treatment on reproductive development in male rats with treatment beginning two days after weaning. Male, Sprague-Dawley rats (N = 12) received a daily subcutaneous injection of oxandrolone (32.7 mumol.kg-1.day-1) and the control group (N = 12) received vehicle only (dimethyl sulfoxide). Treatment began at age 23 days and continued to 60 days of age. The weights of the testes, prostate glands, and seminal vesicles in the treatment group were 69%, 50% and 29% below control levels, respectively and were all significantly decreased (p less than 0.01).
Testicular testosterone production in a 3-h incubation was inhibited in the treated animals to 1.3% of control values (p less than 0.001). Serum FSH (11.7% of control) and LH (undetectable) in the treated animals were both significantly less than controls. Histological findings indicated an arrest of advanced spermatids and a severe depletion of Leydig cells in the interstitial compartment.
It was concluded that treatment of immature male rats with oxandrolone results in effects on the adult male reproductive system which are profound and occur at several levels. The most likely affected sites are the hypothalamus, pituitary gland, and the Leydig cells.
Clin Endocrinol (Oxf) 1993 Apr;38(4):393-8 Related Articles, Links
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[/u] +/- 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.