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Anavar and the HPTA
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I don't have any specific studies on hand but I think I can give you what you want to know. One of Anavar's toted bonuses is that it does not shut down HPTA, however this depends on it's usage. The half-life of Oxandrolone is 8 hours so if you were to take 1 dose in the morning it would be mostly gone by that night. If you were to break up doses throughout the day you would have Oxandrolone in your system throughout the day/night and over the course of a few weeks it could possibly shutdown the HPTA. Bill Roberts suggests the once in the morning dosage because by the time you are going to bed for the night your levels will be very low and by the time morning comes you should have zero in your system. This gives your body a break and allows your HPTA levels to stay high.
Stick to a single morning dose and you should be fine. Also don't stay on the cycle for an extended time. The longer you stay on the cycle the greater chance you will eventually effect HPTA levels. 6-8 weeks of a morning only dosage shouldn't effect you.
Stick to a single morning dose and you should be fine. Also don't stay on the cycle for an extended time. The longer you stay on the cycle the greater chance you will eventually effect HPTA levels. 6-8 weeks of a morning only dosage shouldn't effect you.
It does not shut down but it does inhibit your HPTA.
1: Clin Endocrinol (Oxf) 1997 Feb;46(2):209-16 Related Articles, Books, LinkOut
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.
Publication Types:
Clinical trial
Randomized controlled trial
__________________________________________________________________________
J Pediatr 1979 Apr;94(4):657-62 Related Articles, Books, LinkOut
The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys with constitutionally delayed growth.
Hopwood NJ, Kelch RP, Zipf WB, Hernandez RJ.
Serial concentrations of basal serum LH, FSH, testosterone, and LH and FSH responses to intravenous gonadotropin-releasing hormone were measured before and during six months of administration of fluoxymesterone or oxandrolone in 14 boys with constitutionally delayed growth and adolescence, in order to assess the effects of these androgens on maturation of the hypothalamic-pituitary-gonadal axis. Before therapy all boys had normal hormonal responses based on bone age. At the end of six months therapy 10 of the 14 boys had lower LH responses (34 to 89% reduction) to GnRH without consistent changes in FSH responses. With both androgens, there there was significant suppression of both basal serum FSH and testosterone. Eleven boys were restudied six months after completion of therapy; basal serum LH, FSH, and testosterone and responses to GnRH were equal to or greater than pretreatment levels, indicating recovery or progressive maturation of the HPGA. All boys had increased growth velocity and imporved weight gain without excessive bone age advancement; all had improved psychosocial adjustment.
______________________________________________________________________________
1: Clin Endocrinol (Oxf) 1993 Apr;38(4):393-8 Related Articles, Books, LinkOut
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.
1: Clin Endocrinol (Oxf) 1997 Feb;46(2):209-16 Related Articles, Books, LinkOut
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.
Publication Types:
Clinical trial
Randomized controlled trial
__________________________________________________________________________
J Pediatr 1979 Apr;94(4):657-62 Related Articles, Books, LinkOut
The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys with constitutionally delayed growth.
Hopwood NJ, Kelch RP, Zipf WB, Hernandez RJ.
Serial concentrations of basal serum LH, FSH, testosterone, and LH and FSH responses to intravenous gonadotropin-releasing hormone were measured before and during six months of administration of fluoxymesterone or oxandrolone in 14 boys with constitutionally delayed growth and adolescence, in order to assess the effects of these androgens on maturation of the hypothalamic-pituitary-gonadal axis. Before therapy all boys had normal hormonal responses based on bone age. At the end of six months therapy 10 of the 14 boys had lower LH responses (34 to 89% reduction) to GnRH without consistent changes in FSH responses. With both androgens, there there was significant suppression of both basal serum FSH and testosterone. Eleven boys were restudied six months after completion of therapy; basal serum LH, FSH, and testosterone and responses to GnRH were equal to or greater than pretreatment levels, indicating recovery or progressive maturation of the HPGA. All boys had increased growth velocity and imporved weight gain without excessive bone age advancement; all had improved psychosocial adjustment.
______________________________________________________________________________
1: Clin Endocrinol (Oxf) 1993 Apr;38(4):393-8 Related Articles, Books, LinkOut
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.
