Why isn't Torem recommended for gear PCT?

NasD

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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?
 
Rodja

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Tor is a new SERM and many have not even heard about it. IIRC, it is still in the trial stages.
 
NasD

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That would make sense. Test E/Cyp "bread and butter" cycle recommendations have been around forever so people are waiting until Torem is sorta tried and true before recommending?
 
Rodja

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BBers are creatures of habit as well. A lot of them do not like to deviate too far from their comfort zone, for better or worse.
 
crazyfool405

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torem is similar in action to nolva and the doses need to be much higher,

being that its similar to nolva it lowers igf1 output from the live which could inhibit gains.


juss my .02
 
Nightwanderer

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Let's not forget that Tamox is also dirt cheap aside from being time tested as effctive.
 

futurepilot

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Torem has a higher incidence of side effects than Nolva.

Specifically liver, heart, and vision abnormalities.
 
crazyfool405

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Torem has a higher incidence of side effects than Nolva.

Specifically liver, heart, and vision abnormalities.
most likely because of the higher doses needed in order to acheive the same from nolva
 
NasD

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I thought Nolva was more liver toxic than Torem, which has been cited as a reason for choosing Torem over Nolva in methyl PCT?
 

futurepilot

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most likely because of the higher doses needed in order to acheive the same from nolva
Possibly, im not realy positive the reason why, i can just say what the results were.


I thought Nolva was more liver toxic than Torem, which has been cited as a reason for choosing Torem over Nolva in methyl PCT?

I posted the study in another thread recently, lemme see if i can find it
 

futurepilot

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First # 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).
 
crazyfool405

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First # 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).
saying nolva is better? thats what im reading from that study, but
the doses used in PCT for torem are 2 times that amount, ive seen people use.

nolva is effective at 1/4 that dose mentioned,

nolva supperior? stronger?

i think so, just going by what worked for me, i never used torem
 

futurepilot

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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.
 
crazyfool405

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Effects of estrogen and tamoxifen on the ultrastructural characteristics of female rat prolactin cells as evaluated by immunogold technique.
Erensoy N, Cagatay P, Yilmazer S.

Department of Medical Biology, Cerrahpasa Faculty of Medicine, University of Istanbul, Turkey. [email protected]

Estrogens and antiestrogens are known to have effects on prolactin (PRL)-producing cells in the anterior pituitary. This study was planned to investigate the effects of estrogen and tamoxifen at immunohistochemical and immunoelectron microscopic levels on PRL cells of female rat pituitary. Animals were divided into three groups of eight adult female rats each. The first group was the control group. 200-microg/day of estrogen was administered subcutaneously for 11 weeks to 16 rats. Tamoxifen was administered to eight of them for the last 15 days. In diethylstilbestrol (DES)-induced group, serum PRL levels and pituitary weights were found to be elevated when compared with the control group. In the DES plus tamoxifen group the readings were close to that of the control group. PRL-positive cells were enlarged and strongly immunostained in DES-induced group when assessed by light microscopy. Tamoxifen prevented this effect. At the ultrastructural level, in the tamoxifen treated group, PRL-producing cells contained both immunopositive and immunonegative secretory granules. Numerous PRL-producing cells exhibited progressive morphological changes in the nuclei compatible with the apoptotic process. 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.


Effect of tamoxifen on the treatment of pituitary adenomas with bromocriptine]
[Article in Japanese]

Yamashita M, Hirakawa T, Tashiro Y, Matsuda T, Kibe M, Fukushima T, Tomonaga M.

Administration of 2-Br- alpha-ergocryptine (bromocriptine = CB-154) in combination with an estrogen-receptor blocking agent tamoxifen were performed in two patients with prolactinoma and non-functioning adenoma, respectively. Case 1 was a 50-year-old male with hyperprolactinemia, impaired pituitary function and visual disorders, in whom a large invasive sellar mass lesion was disclosed by CT scans, which extended supra- and parasellarly and extracranially into paranasal sinuses and pterygopalatine fossa on the left side. As the effect of bromocriptine therapy was partial in tumor size reduction and decrease of serum PRL level and it could not be gained further improvement except for the well recovered visual acuity, tamoxifen was used together with bromocriptine resulting further reduction of tumor size and normalization of serum PRL level. Unexpectedly the medication was ceased during and after a couple of bypass surgery for angina pectoris, and it was followed by elevation of serum PRL level and regrowth of the sellar tumor as well as impairment of vision. By tamoxifen therapy the visual acuity showed some improvement, but the serum PRL level and the tumor size remained as before. Then the combination therapy with bromocriptine and tamoxifen was started again. Case 2 was a 38-year-old female with three children, who had secondary amenorrhea, galactorrhea, borderline level of serum PRL with impaired pituitary function and visual disorders. Under the diagnosis of a non-functioning pituitary adenoma with supra-sellar extension, a craniotomy was done and intracapsular partial removal of the tumor was made, revealing a chromophobe adenoma in light microscopy and undifferentiated cell adenoma in electron-micrographs.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of oestrogens on the sensitivity of PRL, TSH and LH to the inhibitory actions of dopamine in hyperprolactinaemic patients.
Valcavi R, Harris PE, Foord SM, Dieguez C, Evans PJ, Peters JR, Hall R, Scanlon MF.

The effects of oestrogen priming on the response of serum PRL, LH and TSH to dopamine (DA) infusion have been studied in hyperprolactinaemia. Seven hyperprolactinaemic females (aged 22-57 years; basal PRL 911-5130 mU/l, normal less than 420 mU/l), had submaximal DA infusions (0.06 micrograms/kg/min) over 3 h. The DA was repeated at the same dose after pretreatment with ethinyl oestradiol (E2) 100 micrograms daily by mouth for 3 d, and after a further 2 week interval, following pretreatment with tamoxifen (TAM) 20 mg twice a day by mouth for 3 d. Ethinyl oestradiol pretreatment stimulated a rise in basal PRL levels in all subjects (mean +/- SE, mU/l; 2903 +/- 761 vs 2293 +/- 684, P less than 0.05) while TAM produced a higher but more variable increase in basal PRL levels (mean +/- SE, mU/l; 3402 +/- 757, P = n.s.). The individual increments in basal PRL levels after both E2 and TAM pretreatment showed a significant positive correlation with the greater decrement in PRL levels during E2 and TAM primed DA infusions (E2, r = 0.93, P less than 0.01, TAM, r = 0.83, P less than 0.05). E2 pretreatment produced a rise in basal LH levels in 5/7 patients, and there was a significant positive correlation between the rise in basal LH levels after E2 and the decremental change in LH levels in E2 primed DA infusions (r = 0.94, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
 
crazyfool405

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while it may reduce prolactin think of this....


estrodail and oestrogen plays a part in hyper prolactemia,

nolvadex doesnt reduce ESTROIDAL, which is why after using it, you may get prolactin induced gyno.
 

futurepilot

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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 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.
 
crazyfool405

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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.
study 2 bromo was used in it which is why it was lowered.

nolva will decrease the size due tpo inhibition of igf1 from the liver and bromo will decrease prolactin
 

futurepilot

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study 2 bromo was used in it which is why it was lowered.
"tamoxifen was used together with bromocriptine resulting further reduction of tumor size and normalization of serum PRL level"

they added tamox after bromo didnt reduce tumor/PRL to desired levels.
 
crazyfool405

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By tamoxifen therapy the visual acuity showed some improvement, but the serum PRL level and the tumor size remained as before.


either way, it doesnt decrease estroidal so it can still be a reason for delayed gyno,
 

futurepilot

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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".
 
crazyfool405

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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".

oestrogen not estroidal, ill dig up the study i found

i kno what a serm is.
 
crazyfool405

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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.
 
Mulletsoldier

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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.
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.

As well, it seems you may have missed the fact that Sulpride is an antipsychotic Dopamine antagonist; at higher dosages, it is postsynaptic at the D2 receptors, and at lower dosages it operates off presynaptic inhibition of Dopamine receptors - in short hand, it lowers serum Dopamine and therefore increases Serum Prolactin levels. Providing a study stating Tamoxifen did not counter this effect is hardly conclusive evidence of Tamoxifen increasing serum prolactin. Most compounds (aside from BR) fail at prolactin inhibition in the face of lowered Dopamine.
 

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