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This is the cycle I plan to run:
test e 300mg. two half cc's per week
Deca 250mg. two half cc's per week
inject both on tuesdays and fridays.
I know that Clomid and Nolvadex are both anit-e's and basically do the same thing, but what it the main difference. Should I take both or should I choose one over the other? And when do you start taking each one and how long?
This is the study taken from Pheendo's PCT. Tamox = Nolvadex. Read Pheendo's PCT sticky. Even if you do not follow his PCT plan, the post has lots of valueable information:
Tamox vs Clomid
Am J Physiol 1983 Feb;240(2):E125-30
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.
Adashi EY, Hsueh AJ, Bambino TH, Yen SS.
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.
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Br J Pharmacol 1978 Apr;62(4):487-93
Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.
Kurl RN, Morris ID.
1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.
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the following study was not available in my library, so i wasn't able to obtain the article or abstract. it may have to be purchased, so if someone is interested, here's the title and authors of the research.
Nippon Funin Gakkai Zasshi 1978 Oct;23(4):398-404
[The hormonal dynamics picture of tamoxifen treatment cases, in comparison of clomid treatment cases]
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Cochrane Database Syst Rev 2000;(2):CD000151
Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.
Vandekerckhove P, Lilford R, Vail A, Hughes E.
Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN.
I can't understand that ****! what the hell?
I am not trying to be a pain in the ass but can you explain it in english?
I don't think anyone but a doctor can understand that stuff.
can someone please explain it better.