seanlambo
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what is the difference and why do people say to use non-steroidal while on, and steroidals in pct?
Me too, like young David on AI, just wanted a real mother to love me. Unfortunately PhilABowl stole her from me...This guy at the gym told me he saw a movie called AI while on cycle, but he got gyno anyway.
I can't help it... she loved every inch! LOLMe too, like young David on AI, just wanted a real mother to love me. Unfortunately PhilABowl stole her from me...
I dont think SERMs eliminate estrogen. They will actually increase circulating estrogen in the body but just block it at certain receptors like breast tissue etc.Both AI's & SERM's work by eliminating estrogen, even though they do so by different methods. AI's are broken into 2 groups - steroidal & non-steroidal.
Right. From what I understand, this is actually preferrable to blocking estrogen entirely because estrogen has an anabolic effect as well, and your body needs estrogen for many processes.I dont think SERMs eliminate estrogen. They will actually increase circulating estrogen in the body but just block it at certain receptors like breast tissue etc.
please see:I dont think SERMs eliminate estrogen. They will actually increase circulating estrogen in the body but just block it at certain receptors like breast tissue etc.
wouldn't this indicateThe concentration of E2 decreased during the TOR therapy with 60 mg and 300 mg causing 82 and 71% decreases, respectively. PRL was significantly suppressed. Both these effects reflect the anti-oestrogenic action of TOR. SHBG increased significantly at both doses of TOR, probably due to a direct oestrogen-like effect of TOR in the liver. TE decreased as a consequence of the elevated SHBG.
later:Estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone and prolactin decreased proving the antiestrogenic activity of the drug. Sexual hormone binding globulin significantly increased by week 12 at both doses
earlier:The drug sensitized the pituitary to the action of the gonadotrophins; the LHRH-induced FSH and LH release showed a considerably increasing tendency during the toremifene therapy. Estradiol levels decreased statistically significantly and SHBG levels showed a statistically significant increase. A decreased level of prolactin is the sign of an antiestrogenic effect of toremifene on the hypophysis and, as a result, provides evidence for a direct influence of toremifene upon the pituitary.
The hormonal effects of toremifene were the most marked at the 2nd and at the 8th week. Estradiol decreased continuously, SHBG increased slightly and the high initial value of basal prolactin level decreased. The TRH-induced prolactin release was suppressed by tormifene after an 8-week period.
those recommendations on tamo use are pretty old, and possibly based on studies such as:Interestingly, studies have found that Nolva has NO effect on testosterone levels. Apparently, nolva's main effect is gyno prevention and allowing your body to return to a 'normal' state. It makes me question Nolva's importance and ability in 'getting the boys back' when used in post cycle therapy.
orTreatment of 9 patients with benign prostatic hyperplasia with 20 mg tamoxifen daily for 6 weeks resulted in a significant increase of LH (211%), FSH (215%), E2 (231%), total T (157%), free T (148%) and total DHT (148%) levels in blood. The increase of plasma free DHT (152%) levels was not significant and PRL concentrations in serum were unchanged during treatment.
andFSH levels showed a continuous increase in the patients during the three months of treatment, while the stimulation by LH-RH was not altered. In the case of LH the basal as well the stimulated levels increased. Mean levels of testosterone, 17-hydroxyprogesterone, androstenedione and estradiol increased significantly during treatment.
andAdministration 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.
but see also (very old):40 patients with oligoasthenozoospermia in infertile marriages were subjected to randomized treatment with 30 mg tamoxifen/day (n = 20), or with 30 mg tamoxifen/day and 150 mg testolactone/day (n = 20), to prevent elevation of estradiol levels during monotherapy with tamoxifen. In both groups there was a significant increase in FSH, LH and testosterone. The elevation of estradiol serum levels was significant in the tamoxifen group, and not significant in the group with combination therapy.
andTamoxifen treatment (20 mg/day) did not affect the gonadotropin levels, but it temporarily increased prolactin, induced sex hormone-binding globulin production, and suppressed peripheral serum progesterone, 17-hydroxyprogesterone, androstenedione, testosterone, and 5 alpha-dihydrotestosterone concentrations.
andwe have shown previously that tamoxifen inhibits LH and 8-bromo-cyclic AMP stimulated testosterone synthesis in a dose-dependent manner. The inhibitory effect of tamoxifen could not be reversed with 17 beta-estradiol. The present studies indicate that tamoxifen directly inhibits testosterone response to gonadotropin stimulation both in immature and mature hypophysectomized rats. When interstitial cells were incubated with pregnenolone, testosterone levels in the incubation medium were 27.0 +/- 1.9 ng/10(6) cells. Tamoxifen significantly inhibited pregnenolone-induced testosterone formation. Tamoxifen also significantly diminished adenylate cyclase activity whereas the binding of hCG to receptor was not affected. These results indicated that several steps of steroidogenesis are inhibited by tamoxifen.
orin both experiments, the administration of testosterone results in a significant decrease of serum FSH and in a total suppression of LH release. The administration of tamoxifen, in either dose, does not modify the elevated serum FSH and LH levels present in the orchidectomized animals, and does not antagonize the inhibitory effect on FSH and LH secretion exerted by the concomitant treatment with testosterone propionate. It is concluded that testosterone inhibits FSH secretion in orchidectomized rats acting as such, and not following aromatization to oestrogens.
on clomid:Tamoxifen was administered i.m. for 9 days to adult male rats in a daily dose of 100 micrograms or 1 mg. The treatment resulted in a significant reduction of the plasma levels of testosterone and LH, without modification of the plasma levels of FSH and of the testes weight. Upon incubation, the testes from the tamoxifen-treated rats produced less testosterone and 7 alpha-hydroxytestosterone, but metabolized [4-14C]testosterone in the same way as the control animals. Small doses of hCG (0.5 i.u. for 9 days) were unable to modify the tamoxifen effect on the testicular function, while tamoxifen significantly inhibited the increase of the plasma levels of testosterone induced by the administration of moderate doses of hCG (1.5 i.u. or 2.5 i.u. for 9 days) to hypophysectomized rats. Tamoxifen treatment, however, did not modify significantly the reactivity of the testes towards high doses of hCG (10 i.u.), administered either 2 h before sacrifice or for 9 days. It is concluded that a prolonged administration of tamoxifen in the rat has, besides an indirect effect resulting from a decrease of the LH levels, a direct inhibitory influence on the testicular testosterone formation, which can be reversed by high doses of hCG.
just wanted to show that all things are not as black and white as often proliferated. there is a wealth of information available, unfortunatley much of it contradictory.The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels.
THE INTERLOCUTORAll the subjects showed different response patterns. No general characteristic of the hormonal changes in the investigated group could be given. A consistent correlation between the within-individual levels of gonadotrophin and sex steroid changes could not be observed. It is concluded, within the limits of the used experimental design, that in healthy males a single administration of tamoxifen does not result in consistent changes in serum levels of either gonadotrophins or sex steroid hormones.
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