Malak said:
I am interested in hearing more about this...Does it shut you down???
"shutdown" is almost never 100%; maybe with 1g+ of test per week LH secretion will go down to nondetectable levels, but with the average cycle your testes will produce some testosterone throughout.
Only nandrolone is particularly harsh because it not only suppresses LH but also desensitizes the testes to LH.
i could not find a single study on ox's effects on adults but only on boys with growth deficiency. Ox did suppress LH at minuscule doses (as low as 2.5mg ed) but the suppression did not last the whole course; after a couple of months it rebounded even while still taking Ox. But keep in mind these boys already had a malfunctioning endocrine system.
But even with all the hoopla about Ox don't forget that is as liver toxic as any other 17aa roid. AIDS patients got problems with 20mg ed (they are running it for life without a break though)
Clin Endocrinol (Oxf) 1997 Feb;46(2):209-16
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.