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Thread: Chosing anti-E's

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    Deacon's Avatar
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    Default Chosing anti-E's

    By Bask8kase;


    INFO: How to choose a good anti-e or anti-e combination

    --------------------------------------------------------------------------------

    Here's some information I put together to discuss the BASIC anti-e's. This is not an exhaustive list, but it touches on some of the more commonly discussed anti-e's

    Which anti-estrogen (anti-e) combination should I use?

    Direct Answer to the Question:

    My choices would change based on what I was using in my cycle:

    1. If I were not using deca in a cycle, then my first choice would be Arimidex alone since it is one of the strongest, most effective anti-e's.
    2. If I were running deca in a cycle, then I would use Proviron due to its secondary effect on erections to counteract deca dick.
    3. If I found via blood tests that my lipids (specifically HDL) where heavily and badly affected by my cycle, I would use Nolvadex with Arimidex, or Nolvadex with Proviron (based on whether deca was in the cycle, as noted in sections 1 and 2 above) or, I would choose Nolvadex alone, with a solid good PCT plan to prevent estrogen rebound (see below).

    Background Information:

    Clenbuterol is neither an anti-estorgen (anti-e) nor a steroid hormone; it is a beta-2-symphatomimetic. Clenbuterol is a strong anti-catabolic, which means it decreases the rate at which protein is reduced in the muscle cell, consequently causing an enlargement of muscle cells. For this reason, people use Clenbuterol after a cycle to minimize catabolisim and thus maintain maximum strength and muscle mass.

    Proviron, arimidex, and L-dex (liquid version of Arimidex) inhibit the aromitization of testosterone to estrogen while Nolvadex blocks the estrogen from doing any harm by blocking the estrogen receptors (estrogen antagonist).

    The good and the bad:

    Nolvadex is good to have on hand if you begin to have gyno symptoms, because it blocks the estrogen. By the time you see any bad symptoms due to estrogen, it's too late to use an aromitization inhibitor such as Proviron, arimidex, or l-dex.

    Again, Nolvadex does not control the amount of estrogen, it just blocks it from getting to receptors, so after you stop using Nolvadex, there might be a lot of estrogen still in your system that can do harm. Some have experienced a reboud effect when using Nolvadex: After they stop using it the estrogen that has built up in the system reaches estrogen receptors and causes problems that were delayed by using Novladex.

    Think of it like this:

    Proviron, arimidex, and l-dex prevent the fire from starting. Nolvadex suppresses/temporarily extinguishes the fire after it has already begun.

    Furthermore:

    Inhibitors such as a-dex and femara effect lipids(primarily HDL) because estrogen greatly contributes in the stabilization of cholesterol. If you inhibit the production of estrogen, the lipid environment can become "unstable." **

    Nolva being a SERM, helps eliminate blood estrogen by binding to the receptor, but doesn't prevent conversion (as noted above); in addition it mimics liver and bone estrogen which help in creating a healthy heart environment.**

    **--NOTE: The two paragraphs (immediately above) marked with asterisks are paraphrased paragraphs from a post by PHEEDNO at ANABOLICREVIEW.COM

    Extra info:

    SERM
    SELECTIVE ESTROGEN RECEPTOR MODULATORS

    The group of drugs classified as SERM selectively acts on estrogen receptors present in different tissues and organs: breast, uterus, bones. Their agonistic action on bone and lipid metabolism has been documented in clinical trials. Positive influence on bones appears as the inhibition of bone resorption (confirmed with bone markers) and estrogen-like increase in bone mineral density, and in consequence decrease in the risk of osteoporotic bone fractures. Their agonistic action on lipids is shown as the decrease in serum total cholesterol, LDL-cholesterol, without significant influence on HDL-cholesterol and TG.

    SERM do not stimulate the uterus and breast, contrary to estrogens which increase the risk of neoplasms. Their unfavorable influence on the activation markers of hemostasis and fibrinolysis was not found.
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    A NOTE FROM BASK8KACE TO ALL READERS: I AM NOT A HEALTH PROFESSIONAL. I do not advocate the use of steroids. Do not assume that I know how to use steroids. I AM NOT QUALIFIED TO GIVE MEDICAL ADVICE. I am under the impression that this board (SculptedByIron) exists as a forum for pretending. The information that I share throughout this board (SculptedByIron) is for entertainment purposes only and is not meant to evoke any action by those who read it. Do not act on any advice or suggestions that I provide.

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    Got this info somewhere, but can't remember where exactly. Fits into this thread so I thought I'd post it. BTW good thread Deac ALOT of confusion and different opinions when it comes to this subject.

    The Best Anti-E

    theres been a lot of talk on other boards about this lately, and a lot of bad information thrown out as well. i wanted to share the good info.

    somone keeps posting how letrozole is the strongest and doesnt negatively affect cholesterol. this is not true. letrozole is NOT the strongest and it DOES negative affect cholesterol/lipid profile in a bad way.

    aromasin(exemestane) is the best. this is why

    both arimidex/ldex/anastrozole and femara/letrozole hurt your cholesterol. the way these 2 anti e's work is they inhibit the aromatase enzyme. by inhibiting the enzyme which converts testosterone to estrogen, you reduce or even come close to eliminating estrogen production. we need some estrogen to be healthy. the major drawback to this is without estrogen, your lipid profile gets fucked.

    exemestane works differently. it does not stop the body from producing estrogen. rather, it makes it so the estrogen is unable to bind to receptors by deactivating the binding enzyme. if the estrogen cannot bind, you simply will not get bloated or get gyno. the estrogen is crippled due to exemestane. however, since the estrogen is still floating around, it will not negatively affect your lipid/cholesterol profile.

    anastrozole doesnt cause a rebound effect, and neither does exemestane, but letrozole does. this means after you stop the letrozole, your estrogen rebounds and goes pretty high for a while, eventually it normalizes. you can avoid this by tapering your letro dose down before stopping it, but that is a pain in the ass. higher than normal can mess many things up post cycle when you stop. since the hpta has a feedback loop is primarily controlled by estrogen, high estrogen will tell your hpta to produce less testosterone, because it thinks the high estrogen is caused by too much testosterone. this is fact. now post cycle, dont we want to raise our test levels, not lower them? of course! so rebounds are bad. if you use letro taper the dose off to zero over a couple weeks.

    fyi- nolvadex(tamoxifen) is a SERM(Selective Estrogen Receptor Modulator). this means on certain tissue it can act antagonisticaly or agonistically. in the case of lipid profiles, it acts agonistically. so, running tamoxifen with your anti e's will IMPROVE your cholesterol profile even if not on cycle or using any gear or other anti e's. its just plain good for cholesterol.

    one thing to keep in mind though when runing tamoxifen with letro. letro reduces blood levels of tamoxifen by over 50%. a study showed 2.5mg letro ed made nolva levels drop to 40% of what they were before adding letro. this does not mean you cant use tamoxifen with letro, it just means you need to use more, about double. 20mg of nolva will act like 8mg if running letro. so make sure you are aware of this because you will need to buy more nolva to compensate. this does not happen when mixing tamoxifen with anastrozole or exemestane, it only hppens with letro.

    also, many people and myself experince a reduction of libido on letro. this doesnt happen w/ ldex or exmestane as far as i know, and in my own experience, and ive run all 3 quite a bit.

    the best combo IS exemestane and tamoxifen together. your cholesterol will be as good as can be considering your on a cycle of steroids. the dose of aromasin will vary depending on the users needs and how much aromatizing gear is being taken. usually 10-25mg ed works well. run 10mg ed nolva to improve your cholesterol.

    second best combo i feel is anastrozole(ldex) and tamoxifen. ldex dose ranges from usually 15mg ed to 1mg ed. run 10mg nolva ed to improve cholesterol.

    thierd best is letro and nolvadex. letro doses usually range from 1-2.5mg ed. run 20mg ed nolva to improve cholesterol w/ letro.

    you do not need to run nolva with any of these 3, i do recomend it though as it will improve cholesterol compared to using the anti e's alone without nolva.

    so in order of strength, on a dose per dose basis(not mg per mg) aromasin is def the strognest, next is letro, and then ldex.

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    good info here.
    Didn't know about the femera E rebound

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    all your Anti-Es here:
    http://www.ag-guys.com/home.html

    mms sponsor

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    I didn't know about the Femara either...I'm currently on HRT and my Doc recently put me on 1 tab of Femara 1x a week...I'm about to start a cycle and was just planning on upping my dose of Femara...
    I can do all things through Him who strengthens me. Phil 4:13

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    So , now I'm confused, should we just use aromasin/nolva and drop all else?

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    Quote Originally Posted by bigtred
    So , now I'm confused, should we just use aromasin/nolva and drop all else?
    I don't think you need to "drop all else". I do think, it seems anyway, aromasin and nolva are the best choice. That being said the other 2 are also effective just be aware of some of the issues they might bring about and deal with them accordingly. For instance tapering your letro, running nolva with adex to improve your cholesterol ect. I know this topic is confusing and there are lots of different opinions, but most seem to agree on the aromasin/nolva stack as a good one.

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    Great thread, good info and input.

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