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The use of nolvadex may require gh or peptides at least

plang

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Stolen from another board......

Tamoxifen Attenuates Pulsatile Growth Hormone Secretion: Mediation in Part by Somatostatin, Gloria Shaffer Tannenbaumt, Wendy Gurd, Martine Lapointe, And Michael Pollak, Endocrinology 130:3395-3401,1992

ABSTRACT

Tamoxifen, a partial competitive antagonist to the estrogen receptor, is a potent inhibitor of the proliferation of experimental mammary carcinoma in the rat and is widely used clinically in the treatment of breast cancer. Blockade of estrogen receptors present on neoplastic cells represents the classic mechanism of action of tamoxifen, but the drug has a variety of other actions that may contribute to its antiproliferative properties. While it is recognized that estrogens play an important role in modulating pulsatile GH release, the effect of antagonists to sex steroid receptors on GH secretory dynamics has not previously been described. In the present study we examined the effect of tamoxifen on pulsatile GH secretion in free-moving adult male and female rats.

The drug, when administered in a manner previously shown to be associated with antineoplastic activity, caused a marked suppression of the amplitude of spontaneous GH secretory bursts and significantly reduced mean 6-h plasma GH levels in both sexes compared to those in their respective peanut oil-injected controls. Inhibition of spontaneous GH pulses persisted for up to 7 weeks after tamoxifen administration in both sexes. Immunoneutralization of endogenous somatostatin in tamoxifen-treated male rats completely restored both GH pulse amplitude (121.6 + 9.5 us. 62.5 + 13.5 rig/ml in tamoxifen-treated rats given normal sheep serum; P < 0.02) and mean 6-h plasma GH levels (53.3 + 6.6 us. 17.9 + 3.6 rig/ml in normal sheep serum-treated rats; P < 0.01) to levels observed in our peanut oil-injected controls.

These results demonstrate that 1) tamoxifen has potent inhibitory effects on pulsatile GH secretion; and 2) the blunting of GH pulse amplitude by tamoxifen is mediated at least in part by increased release of endogenous somatostatin. These findings motivate further investigation of the clinical significance of tamoxifen-induced suppression of GH secretion in relation to the antineoplastic activity of this commonly used drug.
Last edited by DatBtrue; 17th August 2010 at 01:31 PM.
 
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plang

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Bump for those still pounding away the nolvadex
 

P.Griffin

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Thanks for posting that. Very interesting topic, supports the use of peptides/gh in pct.
 

Jarconis

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Or just avoid nolvadex. I think everyone already knew that nolva kills igf lvls anyway.
 

viveutvivas

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Or just avoid nolvadex. I think everyone already knew that nolva kills igf lvls anyway.
Lots of stuff do at high dosages.

It is hard to tell what dosages in humans would correspond to the above. Most likely, it would be insane dosages.

Having said that, many BBs use insane dosages and stack different SERMS, which makes little sense, so that is an issue for them.

As for sane dosages, see this article , which shows that 5 mg per day is plenty, and higher doses make no difference.

Effect of lower versus higher doses of tamoxifen o... [Andrologia. 1985 Jul-Aug] - PubMed result

Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.

Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.
Abstract

Administration of the antiestrogen tamoxifen for one month to 12 patients with idiopathic oligozoospermia significantly increased the mean basal testosterone (T) level and the responses of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to constant luteinizing hormone releasing hormone (LHRH) infusion but did not significantly influence the mean oestradiol (E2) levels or the E2 over testosterone ratio. Mean sperm concentration and total sperm output increased by about 70% after a mean treatment period of 5.5 +/- 0.4 months. No statistically significant difference was found between the two subgroups of patients treated with either the lower (5 or 10 mg once daily) or higher dose of tamoxifen (10 mg twice daily) with respect to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio and the effect on sperm density and total sperm output. In both subgroups the sperm motility and morphology remained unchanged. In conclusion higher doses of tamoxifen in this study prove not to be superior to lower doses in improving mean sperm density and total sperm output. The relative small percentage of patients achieving normalisation of only these sperm parameters pleads for further search for more effective selection of patients and other more effective treatment modalities in patients with idiopathic oligozoospermia.
 
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