non steroidal/steroidal AI's
- 02-05-2008, 05:12 PM
- 02-06-2008, 03:44 AM
I think you got that backwards brother. Most people use non-steroidal AI's aka SERMS (Nolvadex, Arimidex, etc) after a cycle for post cycle therapy. Steroidal AI's (formestane, ATD, etc) are used a lot while ON for 2 main reasons - (1) to run along with gear that aromatizes so the gear DON'T aromatize and (2) to help boost gains. Some use steroidal AI's for PCT along with or sometimes in place of a SERM because some people can't get SERMS. Many people don't agree with this since the point of PCT is to get your body back to normal Test levels (back from being 'shutdown') and steroidal AI's alone can shut you down. This is like doing a cycle of Dianabol and using Superplex as the PCT - coming of of a steroid w/ a weaker steroid.
- 02-07-2008, 12:21 AM
I don't believe AIs and SERMs are the same thing, even though they are used at similar times. AIs disable or clog the aromatase enzyme to prevent testosterone from being converted to estrogen. SERMs block up the estrogen receptors so the body can ignore the estrogen in the system. The main reason for using either of them is to prevent your body from seeing a ton of estrogen.
02-07-2008, 01:07 AM
02-07-2008, 01:30 AM
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.
02-07-2008, 01:31 AM
02-07-2008, 01:45 AM
02-07-2008, 11:23 AM
Non steroidal AIs block estrogen production by competively blocking the aromatase enzyme from receptors. Steroidal AIs simply make every aromatase enzyme they come in contact with inert, therefore labeled as irreversible. They are more effective in reducing estrogen levels, usually less harsh on lipid profiles, but are not needed unless u are sensitive to gyno. They also have little to no rebound as they break down slowly in the body, naturally tapering down levels in the body, unlike non-steroidal which can cause flare up. That is the reason why steroidals r used in pct, the correct way to incorporate an AI in pct is to taper up on the AI as u taper down on the serm. They only reason u should use an AI on cycle is if u are using a substance that aromatizes into E, like test, however most designers/phs do not so there is no need.
Non-steroidal AIs - anastrozole, letrozole, atd
Steroidal AIs - formestane, exemastane(aromasin)
I am no authority here, this is just what I have found in researching the topic. If I am wrong please post, I would like to know.
02-07-2008, 11:26 AM
02-07-2008, 02:01 PM
In the case of Nolvadex, the 'invisibility' of the estrogen prevents gyno while your body slowly returns to its natural balance of testosterone and estrogen.
In the case of Clomid, it makes the estrogen invisible to the anterior pituitary also, which causes more FSH to be released, which in turn causes your testes to create more sperm and testosterone.
In the case of AIs, they block the creation of estrogen via the aromatase, which in turn causes the same cascade as Clomid.
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 PCT.
02-14-2008, 07:09 AM
Influence of toremifene on the endocrine regulation in breast cancer patients.
Eur J Cancer. 1994;30A(2):154-8
Számel I, Hindy I, Vincze B, Eckhardt S, Kangas L, Hajba A.
National Institute of Oncology, Budapest, Hungary.
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.
1. torm (a SERM) DOES in fact reduce serum level estrogen
2. use of an SHBG mod may be beneficial while using torm in PCT (even though the SHBG raising/test lowering effect apparently occured after about 12 weeks)
also, different translation:
The anti-estrogenic effect of 4-chloro-1,2-diphenyl-1-(4-[2-(N,N-dimethylamino)ethoxy]phenyl)1-butene (Toremifene) on the endocrine regulation in breast cancer patients
Eur J Cancer. 1994;30A(2):154-8
Számel I, Hindy I, Vincze B, Ady N, Eckhardt S.
Országos Onkológiai Intézet, Budapest.
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
Endocrine mechanism of action of toremifene at the level of the central nervous system in advanced breast cancer patients.
Cancer Chemother Pharmacol. 1998;42(3):241-6
Számel I, Hindy I, Budai B, Kangas L, Hajba A, Lammintausta R.
Clinical Research Department, National Institute of Oncology, Budapest, Hungary.
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.
Hormonal effects of toremifene in breast cancer patients.
J Steroid Biochem. 1990 Jun 22;36(3):243-7
Számel I, Vincze B, Hindy I, Kerpel-Fronius S, Eckhardt S, Mäenpää J, Grönroos M, Kangas L, Sundquist H, Hajba A.
National Institute of Oncology, Budapest, Hungary.
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.
Effects of tamoxifen on the levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), 17 beta-oestradiol (E2), total and free testosterone (T) and total and free dihydrotestosterone (DHT) in blood of patients with benign prostatic hyperplasia.
Exp Clin Endocrinol. 1983 Jul;82(1):21-8
Stahl F, Schnorr D, Rohde W, Poppe I, Geier T, Dörner G.
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.
Treatment of oligozoospermia by tamoxifen: no evidence for direct testicular action.
Andrologia. 1985 May-Jun;17(3):285-90
Krause W, Hübner HM, Wichmann U.
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.
Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.
Andrologia. 1985 Jul-Aug;17(4):369-78
Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.
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.
Tamoxifen and testolactone in therapy of oligozoospermia: results of a randomized study.
Eur Urol. 1988;14(6):447-9
Maier U, Hienert G.
Department of Urology, University of Vienna Medical School, Austria.
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.
Rapid endocrine effects of tamoxifen and testolactone in prostatic carcinoma patients.
Leinonen P, Bolton NJ, Kontturi M, Vihko R.
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.
Tamoxifen inhibits Leydig cell steroidogenesis: in vivo and in vitro studies.
Metabolism. 1982 Jun;31(6):543-7
Lin T, Murono EP.
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.
Tamoxifen does not block the inhibitory effect of testosterone on FSH release in rats.
Acta Endocrinol (Copenh). 1987 Jan;114(1):84-9
Negri-Cesi P, Celotti F, Melcangi RC, Zanisi M, Motta M.
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.
Influence of a prolonged tamoxifen administration on steroidogenesis by incubated rat testes.
J Steroid Biochem. 1987 Sep;28(3):301-5
Lacroix E, Eechaute W, Vanderstichele H, Leusen I.
Laboratory of Normal and Pathological Physiology, University of Gent, Belgium.
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.
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Fertil Steril. 1978 Mar;29(3):320-7
Vermeulen A, Comhaire F.
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.
however as with all studies care has to be taken to apply results to healthy adult males if the studies were made on eg. postmenopausal women or orchidectomized rats...
maybe those guys had it right:
Short- and long-term hormonal effects of a single dose of 50 mg tamoxifen administered to normal males.
Andrologia. 1984 Sep-Oct;16(5):465-70
Fauser BC, Dony JM, Doesburg WH, Thomas CM, Rolland R.
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.
02-14-2008, 01:50 PM
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