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What is a SERM? Nolvadex and Chlomid Explained
SERM is an acronym that stands for Selective Estrogen Receptor Modulator. SERMs bind with estrogen receptors, blocking some estrogen actions while at the same time permitting others. This means their action is different in various tissues, hence the "selective' descriptor. They selectively inhibit some while stimulating other estrogen-like actions. Compare this to aromatase inhibitors (AI), which block the conversion of androgens into estrogen. In other words, AIs prevent estrogen from being produced while SERMs prevent certain receptors from receiving and responding to estrogen.
Your body is always seeking to maintain balance. When you take a prohormone or steroid, your testosterone levels rise. In response to this, your body signals for the release of more estrogen to balance the increase in testosterone. When you end you cycle, testosterone quickly reduces (since it was artificially raised), but it can take some weeks for your body to react and begin reducing estrogen. For a period of time, your body could be pretty far out of whack, with too much estrogen and not enough testosterone. One of the primary effects of this is gynecomastia (the abnormal development of large mammary glands in males resulting in breast enlargement).
AIs fight this imbalance by preventing the body from producing aromatase, which signals the conversion of testosterone to estrogen. SERMs fight this imbalance by blocking the the androgenic effects of estrogen. Even many bodybuilders are paranoid about the effects of estrogen, it's important to remember that estrogen is necessary and must be balanced, not completely inhibited.
The advantage of a SERM over an AI is that SERMs don't affect estrogen levels, just how the body uses it. As far as the body knows, there's plenty of estrogen there, so it doesn't keep trying to make more. We take the SERM over a period of 3-5 weeks while out body naturally lowers the production of estrogen to match the lowered testosterone levels.
One of the problems with AIs is that by blocking estrogen production, levels remain out of balance and the body keeps trying to make more. Sometimes this can cause a rebound effect, so when the AIs is stopped, estrogen levels spike suddenly. This can result in manifestation of some of the adverse androgenic results. Because of this potential rebound effect, many experienced steroid users prefer to use limited (or no) AIs and instead rely on SERMs to block estrogen effects during post cycle therapy.
Two of the more common SERMs are Nolvadex (tamoxifen) and Chlomid (clomiphene citrate). In men, both these drugs oppose the negative feedback of estrogens on the hypothalamus and stimulate the release of Gonadotropin Releasing Hormone. The Luteinizing Hormone (LH) output by the pituitary will be increased as a result, which in turn can increase the production of testosterone. Although the effect is much the same, the methodology is very different. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, while Clomid, although a strong anti-estrogen at the hypothalamus, seems to exhibit weak activity at the pituitary.
Clomid stimulates the release more gonadotropin so that a faster and higher release of follicle stimulating hormone (FSH) and luteinizing hormone (LH) occurs. This results in an increase in testosterone production. Clomid is a weak synthetic estrogen that binds to estrogen receptors, blocking 'real' estrogen.
Nolvadex is a mixed estrogen agonist/antagonist of the same type as Clomid. Nolvadex also blocks 'real' estrogen from attaching to estrogen receptors and, in those tissues where it is an antagonist, causes the receptor to do nothing.
Sp that begs the question, should you use Chlomid or Nolvadex (or something else) for your PCT? In terms of clinical application, Nolvadex is commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. Both Clomid and Nolvadex will reduce post-cycle estrogen, so that the hypothalamus is stimulated to regenerate natural testosterone production.
Both compounds are classified as triphenylethylenes. Triphenylethylenes are very mild estrogens that don't little to no activity at the estrogen receptor, but are still highly attracted to it, thus blocking the receptor and preventing it from binding to 'real' estrogen. This essentially makes estrogen inert in that it has no receptor to bind to. Nolvadex is the stronger of the two as it can achieve results with 20-40 mg a day. Clomid requires doses of 100-150mg a day.
When it comes to which one to use, most experienced steroid users give the nod to Nolvadex. It's stronger and deactivates rebound estrogen faster and more effectively. Nolvadex also directly influences testosterone restoral, where Clomid may actually have a slight negative influence.
One of the effects of Nolvadex in an increase the responsiveness of luteinizing hormone (LH) to gonadtropin releasing hormone (GnRH), which means a stronger signal for producing testosterone. Nolvadex acts more potently as an estrogen in the liver, offering the positive estrogen benefits in this organ, while avoiding negative effects elsewhere. This translates to a potential positive impact on cholesterol levels.
One of the main reason experienced bodybuilders use Nolvadex is that it's safer in that it doesn't have the side-effects exhibited by Clomid. Clomid has been know to cause acne and even irreversible changes in eyesight.
Both drugs can reduce gains. Estrogen is responsible for a number of anabolic factors. When reducing the estrogen, we also reduce the potential gains being made. To prevent this, Nolvadex and Cholmid are not typically run on-cycle unless on encounters a problem with gynecomastia. [I got this article from prohormonedb.com]
SERM is an acronym that stands for Selective Estrogen Receptor Modulator. SERMs bind with estrogen receptors, blocking some estrogen actions while at the same time permitting others. This means their action is different in various tissues, hence the "selective' descriptor. They selectively inhibit some while stimulating other estrogen-like actions. Compare this to aromatase inhibitors (AI), which block the conversion of androgens into estrogen. In other words, AIs prevent estrogen from being produced while SERMs prevent certain receptors from receiving and responding to estrogen.
Your body is always seeking to maintain balance. When you take a prohormone or steroid, your testosterone levels rise. In response to this, your body signals for the release of more estrogen to balance the increase in testosterone. When you end you cycle, testosterone quickly reduces (since it was artificially raised), but it can take some weeks for your body to react and begin reducing estrogen. For a period of time, your body could be pretty far out of whack, with too much estrogen and not enough testosterone. One of the primary effects of this is gynecomastia (the abnormal development of large mammary glands in males resulting in breast enlargement).
AIs fight this imbalance by preventing the body from producing aromatase, which signals the conversion of testosterone to estrogen. SERMs fight this imbalance by blocking the the androgenic effects of estrogen. Even many bodybuilders are paranoid about the effects of estrogen, it's important to remember that estrogen is necessary and must be balanced, not completely inhibited.
The advantage of a SERM over an AI is that SERMs don't affect estrogen levels, just how the body uses it. As far as the body knows, there's plenty of estrogen there, so it doesn't keep trying to make more. We take the SERM over a period of 3-5 weeks while out body naturally lowers the production of estrogen to match the lowered testosterone levels.
One of the problems with AIs is that by blocking estrogen production, levels remain out of balance and the body keeps trying to make more. Sometimes this can cause a rebound effect, so when the AIs is stopped, estrogen levels spike suddenly. This can result in manifestation of some of the adverse androgenic results. Because of this potential rebound effect, many experienced steroid users prefer to use limited (or no) AIs and instead rely on SERMs to block estrogen effects during post cycle therapy.
Two of the more common SERMs are Nolvadex (tamoxifen) and Chlomid (clomiphene citrate). In men, both these drugs oppose the negative feedback of estrogens on the hypothalamus and stimulate the release of Gonadotropin Releasing Hormone. The Luteinizing Hormone (LH) output by the pituitary will be increased as a result, which in turn can increase the production of testosterone. Although the effect is much the same, the methodology is very different. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, while Clomid, although a strong anti-estrogen at the hypothalamus, seems to exhibit weak activity at the pituitary.
Clomid stimulates the release more gonadotropin so that a faster and higher release of follicle stimulating hormone (FSH) and luteinizing hormone (LH) occurs. This results in an increase in testosterone production. Clomid is a weak synthetic estrogen that binds to estrogen receptors, blocking 'real' estrogen.
Nolvadex is a mixed estrogen agonist/antagonist of the same type as Clomid. Nolvadex also blocks 'real' estrogen from attaching to estrogen receptors and, in those tissues where it is an antagonist, causes the receptor to do nothing.
Sp that begs the question, should you use Chlomid or Nolvadex (or something else) for your PCT? In terms of clinical application, Nolvadex is commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. Both Clomid and Nolvadex will reduce post-cycle estrogen, so that the hypothalamus is stimulated to regenerate natural testosterone production.
Both compounds are classified as triphenylethylenes. Triphenylethylenes are very mild estrogens that don't little to no activity at the estrogen receptor, but are still highly attracted to it, thus blocking the receptor and preventing it from binding to 'real' estrogen. This essentially makes estrogen inert in that it has no receptor to bind to. Nolvadex is the stronger of the two as it can achieve results with 20-40 mg a day. Clomid requires doses of 100-150mg a day.
When it comes to which one to use, most experienced steroid users give the nod to Nolvadex. It's stronger and deactivates rebound estrogen faster and more effectively. Nolvadex also directly influences testosterone restoral, where Clomid may actually have a slight negative influence.
One of the effects of Nolvadex in an increase the responsiveness of luteinizing hormone (LH) to gonadtropin releasing hormone (GnRH), which means a stronger signal for producing testosterone. Nolvadex acts more potently as an estrogen in the liver, offering the positive estrogen benefits in this organ, while avoiding negative effects elsewhere. This translates to a potential positive impact on cholesterol levels.
One of the main reason experienced bodybuilders use Nolvadex is that it's safer in that it doesn't have the side-effects exhibited by Clomid. Clomid has been know to cause acne and even irreversible changes in eyesight.
Both drugs can reduce gains. Estrogen is responsible for a number of anabolic factors. When reducing the estrogen, we also reduce the potential gains being made. To prevent this, Nolvadex and Cholmid are not typically run on-cycle unless on encounters a problem with gynecomastia. [I got this article from prohormonedb.com]
