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Thread: confused, Nolva or Arimidex

  1. #1

    confused, Nolva or Arimidex

    been looking at a beginners cycle on this site

    I will be doing similar,

    Test e 500mgs/weel 1-12 weeks
    Dbol 30-40mgs/day weeks 1-6

    PCT weeks 14-16 clomid/nolva


    Just wondering to keep Estrogen levels at bay during cycle weather to take Arimidex 0.5mg EOD or nolva 10mg a day?

    reading the information on this site suggests they are similar but different


    can someone help please explain?

    Will Arimidex completely block estrogen conversion while Nolva will just keep the level of Estrogen down enough to hopefully avoid gyno etc?

    thanks

  2. #2
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    Nolva is SERM not AI! Its for PCT

    AI should be run during the cycle untill start of PCT, start with adex 0.25mg eod or aromasin 12,5mg eod and upper dose if needed.

  3. #3
    ok thanks,

    this is from this website

    "It must be noted possible side-effects such as Gynecomastia, water retention, high blood pressure and high cholesterol are all a possibility with this cycle as both Testosterone and Dianabol aromatize and cause a buildup in estrogen. If you’re nipples begin to get sore while on cycle you might try supplementing with 10mg of Nolvadex per day. If this does not work you are going to need an Aromatase Inhibitor such as Arimidex or Letrozole; 0.5mg every other day of either should suffice"

    I not to sure why it does not suggest taking an AI like arimidex 0.25 eod
    cheers

  4. #4
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    Use AI on cycle 2 control e2 nolva only binds to receptor sites it does not eliminate e2.

  5. #5
    so guys is Arimidex and Proviron the same thing?

    what dose of proviron would be the same as 0.25mg eod of arimadex?

    thanks

  6. #6
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    Quote Originally Posted by bobbyinhk
    so guys is Arimidex and Proviron the same thing?

    what dose of proviron would be the same as 0.25mg eod of arimadex?

    thanks
    No they are not the same thing!

    Get adex or aromasin!

  7. #7
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    Correct nolvadex will compete with the receptor in the mammary glands to stop estro from binding to it. Aromasin will reduce the actual amount of e in the body by stopping the testosterone from being converted to estro

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    Quote Originally Posted by bobbyinhk View Post
    so guys is Arimidex and Proviron the same thing?

    what dose of proviron would be the same as 0.25mg eod of arimadex?

    thanks
    Proviron is not an AI to begin with.

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  10. #10
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    Quote Originally Posted by jim230027 View Post
    Correct nolvadex will compete with the receptor in the mammary glands to stop estro from binding to it. Aromasin will reduce the actual amount of e in the body by stopping the testosterone from being converted to estro
    You'll want to run adex as an AI while on cycle. The nolva is as a post cycle. Super old school guys ran nolva on cycle but noone really does that anymore. Adex will suffice completely

  11. #11
    Thanks guys.

    And i see guys running clomid or nolva for PCT, some prefer to run one of them

    Any disadvantage of running both? besides cost?

    cheers

  12. #12
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    Quote Originally Posted by bobbyinhk View Post
    Thanks guys.

    And i see guys running clomid or nolva for PCT, some prefer to run one of them

    Any disadvantage of running both? besides cost?

    cheers
    If you're gonna just go with one nolva is the answer. I know some people turn into whiny teens on thier periods with too high of a dose of clomid lol. I've never used it though. Just straight nolva seems to do the trick

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    Quote Originally Posted by bobbyinhk View Post
    Thanks guys.

    And i see guys running clomid or nolva for PCT, some prefer to run one of them

    Any disadvantage of running both? besides cost?

    cheers

    “The following explains why it is prudent to use BOTH Nolvadex and Clomid together in your PCT. It is by Dr Scally - probably the foremost expert in the United States on this topic.” JimmyInk’dUp.

    Med Hypotheses. 2009 Jun;72(6):723-8. Epub 2009 Feb 23.
    Anabolic steroid -induced hypogonadism--towards a unified hypothesis of anabolic steroid action.
    Tan RS, Scally MC.

    Source
    HPT/Axis Inc., 1660 Beaconshire Road, Houston, TX 77077, USA.

    Abstract

    Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids . Anabolic-androgenic steroid (AAS), both prescription and nonprescription, use is a cause of ASIH. Current AAS use includes prescribing for wasting associated conditions. Nonprescription AAS use is also believed to lead to AAS dependency or addiction. Together these two uses account for more than four million males taking AAS in one form or another for a limited duration. While both of these uses deal with the effects of AAS administration they do not account for the period after AAS cessation. The signs and symptoms of ASIH directly impact the observation of an increase in muscle mass and muscle strength from AAS administration and also reflect what is believed to demonstrate AAS dependency. More significantly, AAS prescribing after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness. ASIH is critical towards any future planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent ASIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use. This paper proposes a unified hypothesis that the net effects for anabolic steroid administration must necessarily include the period after their cessation or ASIH.

    PMID: 19231088 [PubMed - indexed for MEDLINE]

    Future treatments:

    A treatment goal of HPTA restoration will have its basis in the regulation and control of testosterone production. The HPTA has two components, both spermatogenesis and testosterone production.

    In males, luteinizing hormone (LH) secretion by the pituitary positively stimulates testicular testosterone (T) production; follicle-stimulating hormone (FSH) stimulates testicular spermatozoa production. The pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates LH and FSH secretion. In general, absent FSH, there is no spermatozoa production; absent LH, there is no testosterone production. Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LHsecretion.

    In the case of ASIH, where the individual suffers from functional hypogonadism and the belief for eventual return of function, treatment is directed at HPTA restoration. A medical quandary for physicians presented with hypogonadal patients secondary to AAS administration is there is currently no FDA approved drug to restore
    HPTA function. Standard treatment to this point has been testosterone replacement therapy (TRT), human chorionic gonadotropin (hCG ), conservative therapy (‘‘watchful waiting” or ‘‘do nothing”), or off-label prescribing of aromatase inhibitors or selective estrogen receptor modulators (SERM).

    The primary drawback of testosterone replacement and hCG administration is that this therapy is infinite in nature. These treatments will remedy the signs and symptoms associated with hypogonadism, but do not alleviate the need for a life-long commitment to therapy. Further, administration serves to further HPTA suppression.

    Conservative therapy (‘‘watchful waiting” or ‘‘do nothing”) is the probably worst case option as this does nothing to treat the patient with ASIH. Also, conservative therapy will have the undesirable result of the nonprescription AAS user to return to AAS use as a means to avoid ASIH signs and symptoms.

    The aromatase inhibitors demonstrate the ability to cause an elevation of the gonadotropins and secondarily serum testosterone [62]. The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production
    [63–67].

    Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism. Patients received clomiphene citrate 50 mg per day for 4 months in an attempt to raise their testosterone level [68]. Clomiphene has been reported in a case study to reverse andropause secondary to anabolic–androgenic steroid use [69]. The patient received clomiphene citrate 50 mg twice per day in an attempt to raise his testosterone level. The patient when followed up after two months had a relapse, tiredness and loss of libido, after discontinuing clomiphene citrate. There are case study reports demonstrating the effectiveness of the combination of clomiphene and tamoxifen in HPTA restoration after stopping AAS administration [70–73]. Clomiphene is a mixture of the trans (enclomiphene) and is (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor [74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor.


    "Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen; it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondary gonadal sex hormones. " Dr Michael Scally

  14. #14
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    get aromasin

  15. #15
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    Quote Originally Posted by slumchop View Post
    get aromasin
    For PCT?

  16. #16
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    I don't take anything. I have adex and exestamine (aromasin) on hand just in case at all times some people are prone to gyno, more than others nolva for pct adex or aromasin during to fight estrogen

  17. #17
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    Quote Originally Posted by bstacked View Post
    I don't take anything. I have adex and exestamine (aromasin) on hand just in case at all times some people are prone to gyno, more than others nolva for pct adex or aromasin during to fight estrogen
    Do you have bloodwork to support this? If not, that's not a very wise decision. There are so many issues with unusually high E2 that you are unaware of. Most of which cannot be detected visually or felt until its too late.

    I hope you dont give this advice to others.

  18. #18
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    Like any drug, it can depend on the individual. Some fare best with aromas in or arimidex while some swear by Letro. Others can only function maximally using nolvadex or proviron/Masterone. On paper the obvious answer is aromas in but in real life situations everyone reacts differently and it will be up to you to find your way through the estrogen blocking drug maze. I personally do not do well on anything stronger than proviron or Masterone which do lower estrogen levels a little. One of my buddies does well on Letro while another has to combine nolvadex and Masterone to prevent brain fog and back acne. I have been able to avoid taking Anti-es for 17 years with no symptoms of Gyno. I have also kept all my hair regardless of which dht derivative I used. There are no set rules!
    Last edited by Ronnie Rowland; 02-18-2013 at 05:32 AM.

  19. #19
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    Quote Originally Posted by Ronnie Rowland;6397547[B
    ]I have been able to avoid taking Anti-es for 17 years with no symptoms of Gyno. I have also kept all my hair regardless of which dht derivative I used. [/B]There are no set rules!
    You are one lucky guy, Ron.

    Yes, there are no set of rules in this game.

  20. #20
    Mickey, this was an awesome post. I have always wondered if using a pct or ai or serm is only going to create either dependence, rebound effect or the need for another drug to counter the other one to counter the other one until after 2-3 yrs you have more pills lined up on the kitchen table at breakfast than an 85 year old grandma. Not for me! I have never experienced sides in the 3 or 4 cycles I did. I never used anything to go with my gear and all is well when I go off cold or the old school way of just taking 30 days to slowly lower my dosage of test.

    So do you and anyone else here agree that "if it aint broke, dont fix it?" Id prefer that way if its worked for me in the past. My only problem now is that at age 54 Im retaining water as I never did in my 20's. Same type of gear,also. Just slightly higher dosage now of dbol and test.

  21. #21
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    I honestly think Ronnie is an alien.

    But seriously, the "if it ain't broke don't fix it" rule dose not apply here. But rather than type a pile of garble this explains why, better than i can. Read it and tell me if this is something you want to gamble with..


    Cardiovascular Dangers of Excess Estrogen

    Conventional medical dogma states that estrogen is cardio-protective while androgens are pro-atherogenic. This fallacy is based on the mere fact that men have higher levels of heart disease than women.

    Excess estrogen in males has many harmful effects, and is definitely not cardio-protective. The following are just a few of the many research studies demonstrating the harmful cardiovascular effects of excess estrogen in males:

    1) Increases Risk of Stroke.
    After adjustment for age, hypertension, diabetes, adiposity, cholesterol, atrial fibrillation, and other characteristics were made in a group of 2,197 men aged 71 to 93 years of age, men with the highest blood levels of estradiol had a 2.2-fold greater risk of stroke, compared with those whose estradiol levels were lower. www .ncbi.nlm.nih.gov/pubmed/17310026

    2) Increases carotid artery thickness.
    In a study of 313 men whose average age was 58, carotid artery intima-media thickness was measured at baseline and then three years later. After adjusting for other confounding risk factors, higher levels of estradiol were associated with thickening of the carotid artery wall. Researchers concluded, “Circulating estradiol is a predictor of progression of carotid artery intima-media thickness in middle-aged men.” jcem.endojournals.org/content/91/11/4433.full

    3) Negatively affects lipids and other risk factors for CAD.
    In an angiographic trial of coronary atherosclerosis in a group of men with stable coronary artery disease, significant positive correlations between estradiol levels and other known atherosclerotic risk factors was observed. Researchers concluded, “Our results indicate a possible role of estradiol in promoting the development of atherogenic lipid milieu in men with coronary artery disease.” ncbi.nlm.nih.gov/pubmed/15860391

    4) Promotes coronary atherosclerosis.
    In another angiographic trial of coronary atherosclerosis in men aged 40-60 years, compared with healthy age-matched controls, men with coronary atherosclerosis had higher levels of estrone and a low level of testosterone in the presence of a high level of estradiol. Researchers concluded, “Low levels of total testosterone, testosterone/estradiol ratio and free androgen index and higher levels of estrone in men with coronary artery disease appear together with many features of metabolic syndrome and may be involved in the pathogenesis of coronary atherosclerosis.”
    ncbi.nlm.nih.gov/pubmed/15669538

    5) Associated with heart attacks.
    In a study of men having suffered an acute myocardial infarction (heart attack), a prior heart attack, and patients with normal coronary arteries, the results showed significantly higher levels of estradiol in both groups of heart attack patients compared with those without coronary disease. ncbi.nlm.nih.gov/pubmed/17435665

    6) Increases Blood Pressure
    Excessively high levels of estrogen cause production of superoxide, a potent free radical which damages cell structures and increases blood pressure.
    ncbi.nlm.nih.gov/pubmed/21411770

  22. #22
    Ronnie, you seem like just the guy to give me your 2 cents worth if you dont mind. I just started proviron 2 days ago and I started TREN A 4 days agi. I found that Proviron was only made by Bayer and they stopped making it 20 yrs ago. Ok so if Im getting knock offs, so be it. But... am getting provirons same ingredients that comes with each pill individually sealed in strips and it says Bayer on it. I started itching like crazy while napping 2 hrs or so ago and I woke up scratching like a dog with fleas. Never happened from any drug reaction before.

    questions:

    why would an UGL bother to counterfeit the packaging of individual pills with ther bayer name on it if its totally non existant? And how do we know then if no one has the real stuff, how can they counterfeit it if there is no template to go by? Is it just going to a medical library and looking up the formula? Wouldnt that be propriatary, and therefore illegal to do and almost impossible to get the real formula from Bayer?

    Also, could the extreme itching im getting be from the TREN A, a I started 4 days ago? I doubt it because I dId it 3 weeks ago for one day and got a loose stomach and stopped. Im pissed off because the tren A is the only thing in my stack thats letting me gain any muscle at all. Jeez!!!! In 4-5 days I gained more with tren A than with 10 weeks of sust and dbol. Im sure the last 2 set up a good base,though. And yeah, i got a bit of the sweats from the tren, but it was anxiety. Dont see what massive itching would have to do with it. Yet, itching from 2 days of proviron? It all makes no sense to me.


    Any thoughts on this, Ronnie. I hope no one has a more severe reaction than me and winds up in the emergency room. Maybe bringing this out now will help some poor guy who might be a bit too "aggresive" with his proviron. I only took one 25mg pill per day.

    Steroidsrx website had the proviron article that clued me in on this. They wont let me post it here as Im too new,they say.

  23. #23
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    ^^ Start your own thread bud. Thanks for understanding.

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