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Posted by Bask8Kace on AR
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.
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.
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.
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.