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  1. #1
    rambo's Avatar
    rambo is offline The Lord God
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    To those of you who like to parrot the phrase "TEST IS BEST"

    Well, you can't do it in this thread. If you've seen my other thread, you'll have seen that I have basically proven that no amount of Anti-E's will prevent me from getting gyno symptoms, even on a cycle of 350mg of prop a week, shot ED @50mg. So now I'm at a crossroads. I'll continue taking my anti-e's, and I'm going to attempt to jump into a non-test cycle, to salvage some of the hardness that the prop brought me. I'm thinking of jumping into 60mg of Var for 6 weeks, or maybe even Winny for 6. One or the other for now. I'm leaning towards var, but winny is exponentially cheaper, and I'm wondering if anyone out there has any advice that doesn't consist of "SHOOT UP TEST YOU PUSSY," because chances are I still look better than you. Carry on.

    Thanks.

  2. #2
    UnNaturalBuff is offline Member
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    who knows, maybe just keep some hgc, calis and viagra on hand and you might be good to go? :lol"

  3. #3
    rambo's Avatar
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    IGF had crossed my mind, but the effects of IGF-1 on tissue growth might induce the growth of any gyno tissue that might have occured either through puberty, or via this last short cycle. With estrogen levels that will rise and test levels that will drop, it might not be a good idea.
    Last edited by rambo; 08-27-2004 at 04:35 AM.

  4. #4
    Warrior's Avatar
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    TestisBest.com <- my views exactly

  5. #5
    J*U*icEd's Avatar
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    great!!!

  6. #6
    inheritmylife's Avatar
    inheritmylife is offline Anabolic Member
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    60mg of Var with some Proviron sounds like a good bet.

  7. #7
    w_rballs's Avatar
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    i personally would reccomend a dbol /deca /EQ/fina/winny stack. nothing like it in the world!! and who says u need test?? test is over rated


    j/k

    have u ever tried femara? and does all test affect u like that bro? i notice more from prop than i did with enanthate . also var only is decent, just make sure to throw some proviron in like inheritmylife said

  8. #8
    detroit's Avatar
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    Between Winny and Var. I'll take Winny any day...
    Actually, look into Masteron , same dosage as Prop, and same frequency of shots. Has very strong anti-e effect too. If your lean already, you cant go wrong with Masteron.

  9. #9
    Blown_SC is offline Retired Vet
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    I read about your problems with gyno last week I think... it's too bad bro..
    I agree with the bro above... Masteron looks to be a really cool compound... but that's only based on reading...
    If you decide to do Var, will you make it yourself?

  10. #10
    Da Bull's Avatar
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    Quote Originally Posted by detroit
    Between Winny and Var. I'll take Winny any day...
    Actually, look into Masteron, same dosage as Prop, and same frequency of shots. Has very strong anti-e effect too. If your lean already, you cant go wrong with Masteron.
    Masteron will harden you up.But it will do very little in the growth or strength department.

  11. #11
    monstercojones's Avatar
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    50 mgs winstrol ed with 50 mgs proviron ed should give you the benefits of var without actually paying out the ass for anavar . mabye that'll work bro.

  12. #12
    Alexander the Graet's Avatar
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    what about halostetin? better for strenght and androgenicity

  13. #13
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    Quote Originally Posted by rambo
    Well, you can't do it in this thread. If you've seen my other thread, you'll have seen that I have basically proven that no amount of Anti-E's will prevent me from getting gyno symptoms, even on a cycle of 350mg of prop a week, shot ED @50mg. So now I'm at a crossroads. I'll continue taking my anti-e's, and I'm going to attempt to jump into a non-test cycle, to salvage some of the hardness that the prop brought me. I'm thinking of jumping into 60mg of Var for 6 weeks, or maybe even Winny for 6. One or the other for now. I'm leaning towards var, but winny is exponentially cheaper, and I'm wondering if anyone out there has any advice that doesn't consist of "SHOOT UP TEST YOU PUSSY," because chances are I still look better than you. Carry on.

    Thanks.
    Cocky basterd

  14. #14
    Bryan2's Avatar
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    what exactly have you taken for anti es?
    i hear a femara nolva stack is supposed to be the best and if doesnt work try stacking with proviron i bet that will work!!!

  15. #15
    custom fit is offline Member
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    Quote Originally Posted by Bryan2
    what exactly have you taken for anti es?
    i hear a femara nolva stack is supposed to be the best and if doesnt work try stacking with proviron i bet that will work!!!
    Exaxtly!


    Some people are more prone to gyno than others, but I'm interesting in knowing how you "proven" no amount of anti-e's will help with gyno. There are numerous studies that show the reduction of gyno with anti-e's.

    What is your experience with Supps? I bet your new at this!

  16. #16
    Justincase is offline Associate Member
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    I say good luck to you.....you don't have to take test......it may be best but there
    is nothing in the world that would get me to use it if I were growing boobs.
    I too would look for another way!!!

  17. #17
    UrbanDawg's Avatar
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    1) TEST IS BEST is not a parrot phrase if the one saying it is speaking from experience and qualifying it as personal experience - not something they have merely read

    2) Having said that...... T E S T i s B E S T

    3) I feel ya for the gyno symptoms bro. When I was 13 or 14 I developed a bad gyno for a couple months. Looking back I would like to kill the doctor who laughed and said I guess you havent decided whether you want to tbe a boy or a girl.

    Dumb fukk shold have told me that my nuts are cranking out test so fast my body cant deal with the estrogen. He should said something positive like your twice the man those other boys are. Jerk gave me a fuking complex that took a few years to get over. And he never even figured out that I was experiencing puberty. Sometimes doctors are your worst enemies.


    So - im not pickin on you for reacting to the TEST IS BEST mantra if it gives you gyno. I have felt the stigma and humiliation of gyno.

    Wish you the best in your efforts to fiqure out a workoaround.

    Good luck Bro!


    Quote Originally Posted by rambo
    Well, you can't do it in this thread. If you've seen my other thread, you'll have seen that I have basically proven that no amount of Anti-E's will prevent me from getting gyno symptoms, even on a cycle of 350mg of prop a week, shot ED @50mg. So now I'm at a crossroads. I'll continue taking my anti-e's, and I'm going to attempt to jump into a non-test cycle, to salvage some of the hardness that the prop brought me. I'm thinking of jumping into 60mg of Var for 6 weeks, or maybe even Winny for 6. One or the other for now. I'm leaning towards var, but winny is exponentially cheaper, and I'm wondering if anyone out there has any advice that doesn't consist of "SHOOT UP TEST YOU PUSSY," because chances are I still look better than you. Carry on.

    Thanks.

  18. #18
    w_rballs's Avatar
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    Quote Originally Posted by custom fit
    Exaxtly!


    Some people are more prone to gyno than others, but I'm interesting in knowing how you "proven" no amount of anti-e's will help with gyno. There are numerous studies that show the reduction of gyno with anti-e's.

    What is your experience with Supps? I bet your new at this!




    rambo he is calling u out bro!
    hey custom rambo is definately not new. jsut a little FYI. he has been around a long time.

  19. #19
    Blown_SC is offline Retired Vet
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    Quote Originally Posted by w_rballs


    rambo he is calling u out bro!
    hey custom rambo is definately not new. jsut a little FYI. he has been around a long time.
    I believe Custom was referring to the gent he quoted.. Bryan2.. could be wrong though,... correct me if I am Custom...

  20. #20
    magicstick2003's Avatar
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    Quote Originally Posted by w_rballs
    have u ever tried femara? and does all test affect u like that bro? i notice more from prop than i did with enanthate. also var only is decent, just make sure to throw some proviron in like inheritmylife said
    I noticed the same thing as of now im on prop and test e (all done with the prop as of last night) i noticed the past few days beofre i decided to stop it (2 days short) that i had some sore nips and the nolva just didn;t seem to help, however today i havent; felt nething. Thats' weird how the different esters affect you.

  21. #21
    Da Bull's Avatar
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    Quote Originally Posted by Blown_SC
    I believe Custom was referring to the gent he quoted.. Bryan2.. could be wrong though,... correct me if I am Custom...
    Nope..he's talking to rambo.

  22. #22
    Blown_SC is offline Retired Vet
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    Quote Originally Posted by Da Bull
    Nope..he's talking to rambo.
    Sorry .. you're right.. I read it over a couple times.. my bad!

    EDIT: Hey Rambo.. what has your experience been with Winny/Var so far?
    Last edited by Blown_SC; 08-27-2004 at 04:16 PM. Reason: spelling

  23. #23
    SV-1's Avatar
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    Hey Rambo, if you haven't already you might want to give Aromasin /Exemestane a try. It's an aromatase inactivator unlike l-dex and femara which are aromatase inhibitors.





    AROMASIN Tablets for oral administration contain 25 mg of exemestane, an irreversible, steroidal aromatase inactivator. Exemestane is chemically described as 6-methylenandrosta-1,4-diene-3, 17-dione. Its molecular formula is C20H24O2.

    The active ingredient is a white to slightly yellow crystalline powder with a molecular weight of 296.41. Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in water.

    Each AROMASIN Tablet contains the following inactive ingredients: mannitol, crospovidone, polysorbate 80, hydroxypropyl methylcellulose, colloidal silicon dioxide, microcrystalline cellulose, sodium starch glycolate, magnesium stearate, simethicone, polyethylene glycol 6000, sucrose, magnesium carbonate, titanium dioxide, methylparaben, and polyvinyl alcohol.


    CLINICAL PHARMACOLOGY

    Mechanism of Action

    Breast cancer cell growth may be estrogen-dependent. Aromatase (exemestane) is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone ) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer.

    Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation, an effect also known as “suicide inhibition.” Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme.

    Pharmacokinetics

    Following oral administration to healthy postmenopausal women, exemestane is rapidly absorbed. After maximum plasma concentration is reached, levels decline polyexponentially with a mean terminal half-life of about 24 hours. Exemestane is extensively distributed and is cleared from the systemic circulation primarily by metabolism. The pharmacokinetics of exemestane are dose proportional after single (10 to 200 mg) or repeated oral doses (0.5 to 50 mg). Following repeated daily doses of exemestane 25 mg, plasma concentrations of unchanged drug are similar to levels measured after a single dose.

    Pharmacokinetic parameters in postmenopausal women with advanced breast cancer following single or repeated doses have been compared with those in healthy, postmenopausal women. Exemestane appeared to be more rapidly absorbed in the women with breast cancer than in the healthy women, with a mean tmax of 1.2 hours in the women with breast cancer and 2.9 hours in the healthy women. After repeated dosing, the average oral clearance in women with advanced breast cancer was 45% lower than the oral clearance in healthy postmenopausal women, with corresponding higher systemic exposure. Mean AUC values following repeated doses in women with breast cancer (75.4 ng•h/mL) were about twice those in healthy women (41.4 ng•h/mL).

    Absorption: Following oral administration of radiolabeled exemestane, at least 42% of radioactivity was absorbed from the gastrointestinal tract. Exemestane plasma levels increased by approximately 40% after a high-fat breakfast.

    Distribution: Exemestane is distributed extensively into tissues. Exemestane is 90% bound to plasma proteins and the fraction bound is independent of the total concentration. Albumin and a1-acid glycoprotein both contribute to the binding. The distribution of exemestane and its metabolites into blood cells is negligible.

    Metabolism and Excretion: Following administration of radiolabeled exemestane to healthy postmenopausal women, the cumulative amounts of radioactivity excreted in urine and feces were similar (42 ± 3% in urine and 42 ± 6% in feces over a 1-week collection period). The amount of drug excreted unchanged in urine was less than 1% of the dose.

    Exemestane is extensively metabolized, with levels of the unchanged drug in plasma accounting for less than 10% of the total radioactivity. The initial steps in the metabolism of exemestane are oxidation of the methylene group in position 6 and reduction of the 17-keto group with subsequent formation of many secondary metabolites. Each metabolite accounts only for a limited amount of drug-related material. The metabolites are inactive or inhibit aromatase with decreased potency compared with the parent drug. One metabolite may have androgenic activity (see Pharmacodynamics: Other Endocrine Effects, below). Studies using human liver preparations indicate that cytochrome P450 3A4 (CYP 3A4) is the principal isoenzyme involved in the oxidation of exemestane.

    Special Populations

    Geriatric: Healthy postmenopausal women aged 43 to 68 years were studied in the pharmacokinetic trials. Age-related alterations in exemestane pharmacokinetics were not seen over this age range.

    Gender: The pharmacokinetics of exemestane following administration of a single, 25-mg tablet to fasted healthy males (mean age 32 years) were similar to the pharmacokinetics of exemestane in fasted healthy postmenopausal women (mean age 55 years).

    Race: The influence of race on exemestane pharmacokinetics has not been evaluated.

    Hepatic Insufficiency: The pharmacokinetics of exemestane have been investigated in subjects with moderate or severe hepatic insufficiency (Childs-Pugh B or C). Following a single 25-mg oral dose, the AUC of exemestane was approximately 3 times higher than that observed in healthy volunteers. (See PRECAUTIONS.)

    Renal Insufficiency: The AUC of exemestane after a single 25-mg dose was approximately 3 times higher in subjects with moderate or severe renal insufficiency (creatinine clearance <35 mL/min/1.73 m2 ) compared with the AUC in healthy volunteers (see PRECAUTIONS).

    Pediatric: The pharmacokinetics of exemestane have not been studied in pediatric patients.

    Drug-Drug Interactions

    Exemestane is metabolized by cytochrome P450 3A4 (CYP 3A4) and aldoketoreductases. It does not inhibit any of the major CYP isoenzymes, including CYP 1A2, 2C9, 2D6, 2E1, and 3A4. In a clinical pharmacokinetic study, ketoconazole showed no significant influence on the pharmacokinetics of exemestane. Although no other formal drug-drug interaction studies have been conducted, significant effects on exemestane clearance by CYP isoenzymes inhibitors appear unlikely. However, a possible decrease of exemestane plasma levels by known inducers of CYP 3A4 cannot be excluded.

    Pharmacodynamics

    Effect on Estrogens: Multiple doses of exemestane ranging from 0.5 to 600 mg/day were administered to postmenopausal women with advanced breast cancer. Plasma estrogen (estradiol, estrone, and estrone sulfate) suppression was seen starting at a 5-mg daily dose of exemestane, with a maximum suppression of at least 85% to 95% achieved at a 25-mg dose. Exemestane 25 mg daily reduced whole body aromatization (as measured by injecting radiolabeled androstenedione) by 98% in postmenopausal women with breast cancer. After a single dose of exemestane 25 mg, the maximal suppression of circulating estrogens occurred 2 to 3 days after dosing and persisted for 4 to 5 days.

    Effect on Corticosteroids: In multiple-dose trials of doses up to 200 mg daily, exemestane selectivity was assessed by examining its effect on adrenal steroids . Exemestane did not affect cortisol or aldosterone secretion at baseline or in response to ACTH at any dose. Thus, no glucocorticoid or mineralocorticoid replacement therapy is necessary with exemestane treatment.

    Other Endocrine Effects: Exemestane does not bind significantly to steroidal receptors, except for a slight affinity for the androgen receptor (0.28% relative to dihydrotestosterone). The binding affinity of its 17-dihydrometabolite for the androgen receptor, however, is 100-times that of the parent compound. Daily doses of exemestane up to 25 mg had no significant effect on circulating levels of testosterone , androstenedione, dehydroepiandrosterone sulfate, or 17-hydroxy-progesterone. Increases in testosterone and androstenedione levels have been observed at daily doses of 200 mg or more. A dose- dependent decrease in sex hormone binding globulin (SHBG) has been observed with daily exemestane doses of 2.5 mg or higher. Slight, nondose-dependent increases in serum lutenizing hormone (LH) and follicle-stimulating hormone (FSH) levels have been observed even at low doses as a consequence of feedback at the pituitary level.

  24. #24
    Rickson's Avatar
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    Femara has worked better for me then other anti-e's so if you haven't tried it you might want to but personally I don't see anything wrong with a winny/proviron cycle.

  25. #25
    rambo's Avatar
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    Thanks, SV1. The cat above who called me "new", just doesn't know the whole story. I've run nolva, leading two weeks up to my first inject at 20mg a day, and ldex at .25 mg preloaded before the cycle. At first symptom I ran 80, 100, 120 and held at 120mg of nolva and the symptoms are barely susbiding. I've started femara at 3mg ED with the nolva, and will taper it off in place of the ldex. I guess the bottom line is that I don't want to F around with my body anymore if I know I'm not reacting well. How many more times can I do this before I develop even worse sides? It's like taking a chance with each time I try and cycle test that this time I won't catch it in time. That being said, if I were going to run Winny, I'd probably run it alone @ 60mg ED with proviron at 25mg ED, and milk thistle.

  26. #26
    Steroids101 is offline Member
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    Were you running anything other than the test? That sucks about being really sensitive to the gyno sides bro... You could probably get away with running EQ alone without too many sexual sides.... Good luck bro!

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