Anti-E's & Aromatase Inhibitors

[vegas]

Arimidex
Anastrozole (Arimidex) is the aromatase inhibitor of choice. The drug is appropriately used when using substantial amounts of aromatizing steroids, or when one is prone to gynecomastia and using moderate amounts of such steroids. Arimidex does not have the side effects of aminoglutethimide (Cytadren) and can achieve a high degree of estrogen blockade, much moreso than Cytadren. It is possible to reduce estrogen too much with Arimidex, and for this reason blood tests, or less preferably salivary tests, should be taken after the first week of use to determine if the dosing is correct.

As an aromatase inhibitor, Arimidex's mechanism of action -- blocking conversion of aromatizable steroids to estrogen -- is in contrast to the mechanism of action of anti-estrogens such as clomiphene (Clomid) or tamoxifen (Nolvadex), which block estrogen receptors in some tissues, and activate estrogen receptors in others. During a cycle, if using Arimidex, there is generally no need to use Clomid as well, but (as mentioned in the section on Clomid) there may still be benefits to doing so.



Clomid
Clomid is not an anabolic/androgenic steroid. Since it is a synthetic estrogen it belongs, however, to the group of sex hormones. In school medicine Clomid is normally used to trigger ovulation. Clomid also has a strong influence on the hypothalamohypophysial testicular axis. It stimulates the hypo-physis to release more gonadotropin so that a faster and higher re-lease of FSH (follicle stimulating hormone) and LH (luteinizing hor-mone) occurs. This results in an elevated endogenous (body's own) testosterone level. Clomid is especially effective when the body's own testosterone production, due to the intake of anabolic/androgenic steroids, is suppressed. In most cases Clomid can normalize the tes-tosterone level and the spermatogenesis (sperm development) within 10- 14 days. For this reason Clomid is primarily taken after steroids are discontinued. At this time it is extremely important to bring the testosterone production to a normal level as quickly as possible so that the loss of strength and muscle mass is minimized. Even better results can be achieved if Clomid is combined with HCG or when Clomid is used after the intake of HCG.

Paradoxically, although Clomid is a synthetic estrogen it also works as an antiestrogen. The reason is that Clomid has only a very low estrogenic effect and thus the stronger estrogens which, for example, form during the aromatization of steroids, are blocked at the recep-tors. These would include those that develop during the aromatiz-ing of steroids. This does not prevent the steroids from aromatizing but the increased estrogen is mostly deactivated since it cannot at-tach to the receptors. The increased water retention and the possible signs of feminization can thus be reduced or even completely avoided. Since the antiestrogenic effect of Clomid is lower than those found in Proviron, Nolvadex, and Teslac it is mainly taken as a testosterone stimulant. Clomid is a medica-tion that promotes the production of the body's own stimulating hormone, gonadotropin, which in turn increases the testosterone level. It is, for example, administered to women as a so-called antiestrogen to trigger ovulation ("ovulation stimulator").


Nolvadex

This remedy is somewhat different from others since it is not an anabolic/androgenic steroid. For male and female bodybuilders, how-ever, it is a very useful and recommended compound which is con-firmed by its widespread use and mostly positive results. Nolvadex belongs to the group of sex hormones and is a so-called antiestrogen. The normal application of Nolvadex is in the treatment of certain forms of breast cancer in female patients. With Nolvadex it is pos-sible to reverse an existing growth process of deceased tissue and prevent further growth. The growth of certain tissues is stimulated by the body's own estrogen hormone. This is especially true for the breast glands in men and women since the body has a large number of estrogen receptors at these glands which can bond with the estro-gens present in the blood. If the body's own estrogen level is unusu-ally high an undesired growth of breast glands occurs. However, in healthy women and particularly in men this is not the case. Despite this, it is mostly male bodybuilders who use Nolvadex, and fewer women. At first sight this seems somewhat inconceivable but when taking a closer look, the reasons are clear. Bodybuilders who take Nolvadex also use anabolic steroids at the same time. Since most steroids aromatize more or less strongly, i.e. part of the substance is converted into estrogens, male bodybuilders can experience a sig-nificant elevation in the normally very low estrogen level. This can lead to feminization symptoms such as gynecomastia (growth of breast glands), increased fat deposits and higher water retention.

The antiestrogen Nolvadex works against this by blocking the es-trogen receptors of the effected body tissue, thereby inhibiting a bonding of estrogens and receptor. It is, however, important to un-derstand that Nolvadex does not prevent the aromatization but only acts as an estrogen antagonist. This means that it does not prevent testosterone and its synthetic derivatives (steroids) from converting into estrogens but only fights with them in a sort of "competition" for the estrogen receptors.


Here is some good info for those wanting to know.....Vegas

 

[Homer_J]

I'm not trying to hijack your thread Vegas - I just wanted to add this since it includes Femara & Aromasin. This is from BigKris23 over at Anabolex...

Start Quote:

Triplev you asked for it, so here it is...some info for the new guys on a few compounds that will help you win your war against prolactin, estrogen and progesterone...

Arimidex (anastrozole) (aromatase inhibitor)is a compound that can inhibit around 75% of estrogen conversion if taken properly. Someone on the board (I'm not sure who it was) said as a rule of thumb, use at least .25mg per 250mg of test per week...arimidex is also found in liquid forms like liquidex...Liquidex is anastrozole powder mixed with glycerin. There are a few different kinds of liquidex coming from different suppliers some are higher concentrations of arimidex per ml...others have added ingredients to enhance the absorbtion. Liquidex is much cheaper then arimidex in the tablet form....Studies have shown that arimidex decreases IGF-1 levels by around 18%

Femara (letrozole) is another compound that may be useful ...Femara is another aromatase inhibitor...that actually icreases IGF-1 levels by 24%...If used correctly, Femara can effectively inhibit about 80% of estrogen conversion. Femara also stimulates serum LH...I've yet to try femara, but I've heard that 1/2 a 2.5mg pill ed is an effective dose for moderate doses of test (I'm not sure about this...I'm just reporting what I heard.

Aromasin (exemestane) is in a class of it's own, it is a aromatase inactivator...It actually renders estrogen receptors useless. Instead of just inhibiting production, it cuts off production. Aromasin can effective prevent about 90-95% of estrogen conversion. A negative aspect of Aromasin is that it decreases IGF-1 levels by about 23-24%

Nolvadex is actually an anti-estrogen that can be useful if symtoms of gyno appear...A problem with nolvadex it supresses estrogen, but then when nolvadex use is discontinued, there is a rebound effect....if you need to use nolvadex, it's a good idea to run it until you start clomid therapy or add proviron after discontinuing use to off set the rebound. Nolvadex also decreases IGF-1 levels by about 25% so it will effect your gains to some extent.

Clomid is a weak anti-estrogen....it is better for the purposes of restoring natural test levels post cycle.

Proviron is a weak anti-estrogen and also a weak androgen...it can be helpful in preventing gyno. It doesn't compete with androgen receptors or lower IGF-1 levels...so it will not effect your gains. Proviron can also be helpful post cycle to boost libedo and improve the ability to get errections. Additionally, I've noticed that proviron puts me in a better mood post cycle...and it hardens muscles a bit. Not to mention, if take in low to moderate does in the am up waking, it does not effect htpa recovery. I'm a big supporter of proviron use both during and post cycle.

Also I must add Winstrol as an effective agent in combating progesterone related sides...Winstrol is very effective in preventing the conversion of progesterone while on deca durabolin....it is also somewhat effective in preventing the conversion or progesterone while using Fina...but not to the extent it does with deca because of the way fina binds to PR receptors.

RU-486 the controversial abortion pill may also be effective in blocking progesterone and as an anti-cortisol...because of the short half-life of the drug (20-30 hours) ed dosing is need. I've heard that 50-75mg ed is an effective dose...Aside from it being difficult to get, Ru-486 has a number of side effects that IMO outweigh the benefits. The first being that it hinders white blood cells and suppresses the immune system...another negative is that low cortisol can inhibit protein degradation and if taken at high doses and not tapered can shut down adrenals and ulimately kill you.

Lastly, there are a number of products that can help you prevent prolactin induced gyno. OTC drugs like Vitex (chasteberry) can help lower prolactin levels, but may cause an increase in progesterone. Bromocriptine can also lower prolactin but also reduces the bodys GH levels. There are a couple of other drugs that inhibit prolactin by raising dopamine levels....Deprenyl inhibits prolactin and improves depression...it also has been said to protect brain cells from free radical oxidation. L-Dopa and velvet bean (which actually contains L-Dopa) may also be helpful by similar means, they raise dopamine and inhibit prolactin. They also have been shown to raise GH levels and assist in burning fat.

Hopefully, this will be helpful to some people....it is by no means a complete list...feel free to comment and add to the list.

End Quote

I don't know about the 'estrogen rebound' from Nolvadex - I've never felt that. (Maybe some people have - I don't read the boards as much as I used to.)

Take care,
Homer_J

 

[FearMy6Pak]

nice info

 

[einstein1905]

That's all very good info....the studies showing so and so reduces or increases IGF-1 levels by X% are misleading though. There are several studies that show both increases and decreases in IGF-1 levels with all three AIs and nolva. I wouldn't conclude anything regarding their abilities to affect IGF-1 levels at this point.
A similar issue with HDL levels, as there have been studies that have shown each of the AIs can lower HDL levels, but there have also been studies showing that HDL levels are unaffected by the AIs. Nolvadex (tamoxifen) is pretty consistently shown to increase both HDL and IGF-1 levels, from what I've seen.

As for winstrol preventing the conversion of deca or fina to progestins, I'm not sure I buy that. If someone can explain how that works, I'd appreciate it. I also don't understand chasteberry, as it increases progesterone levels....progesterone can be a prolactin receptor agonist, hence prog/prolactin gyno.

I also don't get how exemestane would be the most beneficial AI (being type I, steroidal) on lipid levels. It reduces plasma estrogen more than other AIs, so how would it not affect HDL the most?

If anybody can answer these questions, you'll have my eternal gratitude.

Demeur??

 

[demeurj]

That's all very good info....the studies showing so and so reduces or increases IGF-1 levels by X% are misleading though. There are several studies that show both increases and decreases in IGF-1 levels with all three AIs and nolva. I wouldn't conclude anything regarding their abilities to affect IGF-1 levels at this point.
A similar issue with HDL levels, as there have been studies that have shown each of the AIs can lower HDL levels, but there have also been studies showing that HDL levels are unaffected by the AIs. Nolvadex (tamoxifen) is pretty consistently shown to increase both HDL and IGF-1 levels, from what I've seen.

As for winstrol preventing the conversion of deca or fina to progestins, I'm not sure I buy that. If someone can explain how that works, I'd appreciate it. I also don't understand chasteberry, as it increases progesterone levels....progesterone can be a prolactin receptor agonist, hence prog/prolactin gyno.

I also don't get how exemestane would be the most beneficial AI (being type I, steroidal) on lipid levels. It reduces plasma estrogen more than other AIs, so how would it not affect HDL the most?

If anybody can answer these questions, you'll have my eternal gratitude.

Demeur??

I wouldn't be surprised in Winny prevents the some progestin-like activity of deca/fina. My guess would be competitive inhibition of 5-alpha reductase; with the androgenic potential of Winny being much less than deca/fina. Furthermore, the aromatization of deca/fina is also enzyme mediated but likely one of the liver cytochromes not typical aromatase activity. That means that something as simple as grapefruit juice might increase or decrease the anabolic (and side effects). Another option is that Winny acts like Clomid. The androgenic effects of Winny are so weak in comparison to Deca/Fina that it essentially blocks the activity.

I had no idea people were using chasteberry for gyno. Last I heard it was almost useful for PMS. I saw one reference that said it binds to the estrogen receptor and stimulates the PRODUCTION of progesterone receptors but it doesn't activity the progesterone receptor. So it's conceivable that chasteberry may block the estrogen and progesterone receptors.

Exemestane can have a negative influence on estrogen and boost HDL at the same time by acting through different pathways. Although estrogen is important for HDL it clearly isn't the sole determinant of HDL. In fact, Pfizer has a drug in development that has doubled HDL levels in early trials.

 

[einstein1905]

I wouldn't be surprised in Winny prevents the some progestin-like activity of deca/fina. My guess would be competitive inhibition of 5-alpha reductase; with the androgenic potential of Winny being much less than deca/fina. Furthermore, the aromatization of deca/fina is also enzyme mediated but likely one of the liver cytochromes not typical aromatase activity. That means that something as simple as grapefruit juice might increase or decrease the anabolic (and side effects). Another option is that Winny acts like Clomid. The androgenic effects of Winny are so weak in comparison to Deca/Fina that it essentially blocks the activity.

I had no idea people were using chasteberry for gyno. Last I heard it was almost useful for PMS. I saw one reference that said it binds to the estrogen receptor and stimulates the PRODUCTION of progesterone receptors but it doesn't activity the progesterone receptor. So it's conceivable that chasteberry may block the estrogen and progesterone receptors.

Exemestane can have a negative influence on estrogen and boost HDL at the same time by acting through different pathways. Although estrogen is important for HDL it clearly isn't the sole determinant of HDL. In fact, Pfizer has a drug in development that has doubled HDL levels in early trials.

Thanks again......you know that if you keep answering my questions....I'm just going to keep coming back to you with more.

 

[finafreak]

Arimidex
Anastrozole (Arimidex) is the aromatase inhibitor of choice. The drug is appropriately used when using substantial amounts of aromatizing steroids, or when one is prone to gynecomastia and using moderate amounts of such steroids. Arimidex does not have the side effects of aminoglutethimide (Cytadren) and can achieve a high degree of estrogen blockade, much moreso than Cytadren. It is possible to reduce estrogen too much with Arimidex, and for this reason blood tests, or less preferably salivary tests, should be taken after the first week of use to determine if the dosing is correct.

As an aromatase inhibitor, Arimidex's mechanism of action -- blocking conversion of aromatizable steroids to estrogen -- is in contrast to the mechanism of action of anti-estrogens such as clomiphene (Clomid) or tamoxifen (Nolvadex), which block estrogen receptors in some tissues, and activate estrogen receptors in others. During a cycle, if using Arimidex, there is generally no need to use Clomid as well, but (as mentioned in the section on Clomid) there may still be benefits to doing so.



Clomid
Clomid is not an anabolic/androgenic steroid. Since it is a synthetic estrogen it belongs, however, to the group of sex hormones. In school medicine Clomid is normally used to trigger ovulation. Clomid also has a strong influence on the hypothalamohypophysial testicular axis. It stimulates the hypo-physis to release more gonadotropin so that a faster and higher re-lease of FSH (follicle stimulating hormone) and LH (luteinizing hor-mone) occurs. This results in an elevated endogenous (body's own) testosterone level. Clomid is especially effective when the body's own testosterone production, due to the intake of anabolic/androgenic steroids, is suppressed. In most cases Clomid can normalize the tes-tosterone level and the spermatogenesis (sperm development) within 10- 14 days. For this reason Clomid is primarily taken after steroids are discontinued. At this time it is extremely important to bring the testosterone production to a normal level as quickly as possible so that the loss of strength and muscle mass is minimized. Even better results can be achieved if Clomid is combined with HCG or when Clomid is used after the intake of HCG.

Paradoxically, although Clomid is a synthetic estrogen it also works as an antiestrogen. The reason is that Clomid has only a very low estrogenic effect and thus the stronger estrogens which, for example, form during the aromatization of steroids, are blocked at the recep-tors. These would include those that develop during the aromatiz-ing of steroids. This does not prevent the steroids from aromatizing but the increased estrogen is mostly deactivated since it cannot at-tach to the receptors. The increased water retention and the possible signs of feminization can thus be reduced or even completely avoided. Since the antiestrogenic effect of Clomid is lower than those found in Proviron, Nolvadex, and Teslac it is mainly taken as a testosterone stimulant. Clomid is a medica-tion that promotes the production of the body's own stimulating hormone, gonadotropin, which in turn increases the testosterone level. It is, for example, administered to women as a so-called antiestrogen to trigger ovulation ("ovulation stimulator").


Nolvadex

This remedy is somewhat different from others since it is not an anabolic/androgenic steroid. For male and female bodybuilders, how-ever, it is a very useful and recommended compound which is con-firmed by its widespread use and mostly positive results. Nolvadex belongs to the group of sex hormones and is a so-called antiestrogen. The normal application of Nolvadex is in the treatment of certain forms of breast cancer in female patients. With Nolvadex it is pos-sible to reverse an existing growth process of deceased tissue and prevent further growth. The growth of certain tissues is stimulated by the body's own estrogen hormone. This is especially true for the breast glands in men and women since the body has a large number of estrogen receptors at these glands which can bond with the estro-gens present in the blood. If the body's own estrogen level is unusu-ally high an undesired growth of breast glands occurs. However, in healthy women and particularly in men this is not the case. Despite this, it is mostly male bodybuilders who use Nolvadex, and fewer women. At first sight this seems somewhat inconceivable but when taking a closer look, the reasons are clear. Bodybuilders who take Nolvadex also use anabolic steroids at the same time. Since most steroids aromatize more or less strongly, i.e. part of the substance is converted into estrogens, male bodybuilders can experience a sig-nificant elevation in the normally very low estrogen level. This can lead to feminization symptoms such as gynecomastia (growth of breast glands), increased fat deposits and higher water retention.

The antiestrogen Nolvadex works against this by blocking the es-trogen receptors of the effected body tissue, thereby inhibiting a bonding of estrogens and receptor. It is, however, important to un-derstand that Nolvadex does not prevent the aromatization but only acts as an estrogen antagonist. This means that it does not prevent testosterone and its synthetic derivatives (steroids) from converting into estrogens but only fights with them in a sort of "competition" for the estrogen receptors.


Here is some good info for those wanting to know.....Vegas

Way to go Vegas good thread buddy

fina