Torem is recommended often for PCT for PH/PS cycles. Nolva/Clomid is generally recommended for gear cycles but not Torem. Why is this if Torem helps to restore HPTA for methyl cycles. Preference? Old school vs new school?
most likely because of the higher doses needed in order to acheive the same from nolvaTorem has a higher incidence of side effects than Nolva.
Specifically liver, heart, and vision abnormalities.
Possibly, im not realy positive the reason why, i can just say what the results were.most likely because of the higher doses needed in order to acheive the same from nolva
I thought Nolva was more liver toxic than Torem, which has been cited as a reason for choosing Torem over Nolva in methyl PCT?
saying nolva is better? thats what im reading from that study, butFirst # is (torem) at 60 2nd (tamoxifen) at 20. the () are percentage. The # is incidence out of a 592 person study.
Cardiac Failure 2 (1) 1 (<1) -
Myocardial Infarction 2 (1) 3 (1.5)
Arrhythmia 3 (1.5) 1 (<1)
Angina Pectoris 1 (<1) 2 (1)
Ocular *
Cataracts 22 (10) 16 (7.5)
Dry Eyes 20 (9) 16 (7.5)
Abnorma Visual Fields 8 (4) 10 (5)
Corneal Keratopathy 4 (2) 2 (1)
Glaucoma 3 (1.5) 2 (1)
Abnormal Vision/Diplopia (only torem) 3 (1.5) -
Thromboembolic
Pulmonary Embolism 4 (2) 2 (1)
Thrombophlebitis - 2 (1) 1 (<1)
Thrombosis - 1 (<1) 1 (<1)
CVA/TIA 4 (2) 4 (2)
Elevated Liver Tests **
SGOT 11 (5) 4 (2)
Alkaline Phosphatase 41 (19) 24 (11)
Bilirubin 3 (1.5) 4 (2)
Hypercalcemia 6 (3) 6 (3)
* Most of the ocular abnormalities were observed in the North American Study in which on-study and biannual ophthalmic examinations were performed. No cases of retinopathy were observed in any arm.
** Elevated defined as follows: North American Study: SGOT >100 IU/L; alkaline phosphatase >200 IU/L; bilirubin >2 mg/dL. Eastern European and Nordic studies: SGOT, alkaline phosphatase, and bilirubin - WHO Grade 1 (1.25 times the upper limit of normal).
Which is why i would never recomend torem, Nolva seems safer too me, even though ALL serms have these risks associated with use.the doses used in PCT for torem are 2 times that amount, ive seen people use.
Which is why i would never recomend torem, Nolva seems safer too me, even though ALL serms have these risks associated with use.
and all increase prolactin,
Study1: The results of this study indicate that tamoxifen prevents not only the proliferative effect of estrogen but also inhibits the secretion mechanism of the cells.
Study2: tamoxifen was used together with bromocriptine resulting further reduction of tumor size and normalization of serum PRL level.
study3: The effects of oestrogen priming on the response of serum PRL, LH and TSH to dopamine (DA) infusion have been studied in hyperprolactinaemia. " TAM pretreatment showed a significant positive correlation with the greater decrement in PRL levels during E2 and TAM primed DA infusions."
study 2 bromo was used in it which is why it was lowered.study 1: proves Nolva reduces prolactin.
Study 2: the above excerpt shows Nolva reduces prolactin levels.
Study3: Is about dopamine infusion, with a pre-dopamine infusion does of either Nolva, or E2. Its a study about the effects of Dopamine on prolactin, not nolva.
So basically you just posted 2 more studies that help prove my point that Nolva reduces prolactin, and study 3 that proves that Dopamine reduces prolactin.
"tamoxifen was used together with bromocriptine resulting further reduction of tumor size and normalization of serum PRL level"study 2 bromo was used in it which is why it was lowered.
Actually it mimics the shape and chemical composition of estradiol. It binds to the same site as estrogen blocking the action of the receptor, hence it being a "SERM".either way, it doesnt decrease estroidal so it can still be a reason for delayed gyno,
Actually it mimics the shape and chemical composition of estradiol. It binds to the same site as estrogen blocking the action of the receptor, hence it being a "SERM".
The purpose of a SERM is not to have an aggregate effect on serum oestrogen or estradiol levels; but rather, to selectively bind to oestrogen receptors in certain tissues (mainly breast) to prevent glandular proliferation. As well, this study states that TAM did not prevent hyperprolactinemia, this is not directly corollary to increasing prolactin.Tamoxifen prevents sulpiride-induced weight gain in female rats.
Baptista T, de Baptista EA, Hernandez L, Altemus M, Weiss SR.
Department of Physiology, Medical School, Universidad de Los Andes, Mérida, Ven.
To evaluate its potential utility in counteracting neuroleptic-induced obesity, the effects of long-term administration of tamoxifen (TAM) on body weight (BW) and food intake (FI) of gonadally intact and sulpiride-treated (SUL) female rats were assessed. In addition, estradiol and prolactin serum levels were measured in rats treated with SUL. SUL plus TAM and SUL plus bromocriptine (BR). TAM, at doses of 10, 50 and 100 micrograms, significantly decreased BW gain: FI was significantly reduced at the doses of 50 and 100 micrograms. In addition, doses of TAM ranging from 5-100 micrograms completely prevented SUL-induced BW gain and hyperphagia. BR also prevented SUL effects on BW and FI. In contrast to BR, concomitant administration of TAM did not prevent SUL-induced hyperprolactinemia. Estradiol levels were not modified by SUL alone or SUL plus BR, but they were significantly increased in the animals treated with TAM plus SUL. Neuroleptic-induced obesity in female rats might be related to an alteration in gonadal steroid balance secondary to hyperprolactinemia. While BR might counteract neuroleptic-induced weight gain by preventing hyperprolactinemia, TAM might directly interact with estrogen receptors, or indirectly increase estradiol levels. The use of TAM in preventing neuroleptic-induced obesity in humans warrants further investigation.
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