Nighthawkk said:
I heard that too actually, and all that talk of leydig desensitization had me worried. Though I read an article about the duration and doses HCG is prescribed to males with either puberty issues or hypergonadotropism (sp?) and the doses were higher and for logner durations.
So if I'm running 1500iu every 4-5 days, would 20mg nolv daily be enough as I'm also on Enanth?
ARTICLE BY NANDI 12
cutting edge
tamoxifen Blocks HCG Induced Leydig Cell Desensitization
HCG induced testicular desensitization seems to be a hot topic. There are a number of studies showing that concomitant use of nolvadex ameliorates this. The first abstract suggests that HCG at least partially blocks the conversion of 17 alpha-hydroxyprogesterone (17 OHP), a testosterone precursor, to testosterone. This effect is suppressed by nolvadex.
The second abstract seems to indicate that estrogen may not be the only culprit, since nolvadex plus HCG does not increase T levels any more than HCG alone, even though the combination reduces desensitization.
Since we are trying to avoid this desensitization so when we quit the HCG our testes respond to our endogenous LH, it makes sense to always use nolvadex with HCG to at least help the problem, if not solve it completely.
J Clin Endocrinol Metab 1980 Nov;51(5):1026-9
tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.
Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg PW.
Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01). Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.
Andrologia 1991 Mar-Apr;23(2):109-14
Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.
Levalle OA, Suescun MO, Fiszlejder L, Aszpis S, Charreau E, Guitelman A, Calandra R.
Division Endocrinologia, Hospital Carlos Durand, Instituto de Biologia y Medicina Experimental, Buenos Aires, Argentina.
The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.
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