Spiderman
New member
This is an article that I found on another board - I have read through it and thought it would be a good read for some people who had questions about gyno. I have added some of my own comments to the article but it is clear where this is done.
Oh brother... I could write a text book here, but I don't have the time. So I will give some quick short answers.
Basics on Prolactin, and most importantly that Dopamine regulation has a major effect on prolactin secretion:
http://arbl.cvmbs.colostate.edu/hboo...prolactin.html
Prolactin and progesterone are not the same thing, and are not simply connected via steroidogenesis pathways (scroll down til you get to the graphic with all the sterans "Major pathways in steroid biogenesis").
http://arbl.cvmbs.colostate.edu/hboo...dogenesis.html
Take a look (for those that are biochemically inclined) as to the interrelationship of the various steroids in the body. Note the reactions/enzymatic processes that connect them - these are what we typically seek to modulate with "anti-side effect" drugs (i.e. control aromatase CYP19, control Aldosterone CYP11B2, etc.)
Quickie on the drugs:
arimidex, letrozole - are aromatase inhibitors. For example, Anastrozole is a potent and selective non-steroidal aromatase inhibitor. It significantly lowers serum estradiol concentrations and has no detectable effect on formation of adrenal corticosteroids or aldosterone. These drugs do not directly effect estrogen/estradiol already in circulation. They just help reduce the production of estrogen/estradiol going forward.
[They do this by inhibiting the enzyme aromatase through reversable competition. Aromatse is the enzyme that converts androgens to estrogen. So this drug works by decreasing the amount of estrogen you are forming which is why they are best used throughout the cycle if you plan on using them, IMHO.] - Spiderman
aromasin/exemstane - these drugs work by selectively targeting and irreversibly binding to the aromatase enzyme, which is required to produce estradiol/estrogen. Basically they are steroidal aromatase inactivators. Again, similar to the aromatase inhibitors, these drugs do not directly impact estrogen that is already in circulation.
[With this being an irreversible binder to the aromatase enzyme it will not come off until the enzyme is metabolized.] - Spiderman
nolvadex - is a selective estrogen receptor modulator (SERM). Basically it blocks the actions of estrogen in breast tissues and certain other tissues by "occupying" the estrogen receptors on cells. With a SERM sitting in the estrogen receptor, there is no place for the real estrogen to "sit down" - like a game of musical chairs. The SERM fits in the estrogen receptor, but it does NOT send messages to the cell nucleus to grow and divide. This is why nolvadex can help in situations where circulating estrogen levels are already elevated. For example early signs of gyno indicate high circulating estrogen levels - nolvadex is the best initial treatment to block the circulating estrogen from binding, followed-up by either an aromatase inhibitor or an inactivator to stop additional estrogen in its tracks.
bromocriptine & dostinex (cabergoline) - these 2 drugs do not directly modify estrogen or progesterone regulation. These drugs are dopamine agonists that mimic the effects of dopamine in the brain by stimulating dopamine receptors. This increased stimulation of dopamine receptors, as I wrote above, will have a direct impact on prolactin levels - it will cause a marked decrease in prolactin secretion from the pituitary.
[Thus the reason why it will they are useless unless the gyno you are experiencing is from prolactin stimulation instead of estrogen stimulation. The common steroids that cause prolactin induced gyno are Tren and Nandrolone] - Spiderman
proviron - has 2 main effects. (1) it stongly binds with sex hormone binding globulin, SHBG. SHBG normally binds with testosterone and as a result only 1-3% of total testosterone is ever free to bind with receptors. By binding with SHBG, proviron basically helps elevate free test levels. (2) Proviron is 5-alpha reduced (since it is DHT like) and therefore it can't convert to estrogen, yet it nonetheless has a much higher affinity for the aromatase enzyme (which converts testosterone to estrogen). So it can act like an aromatase inactivator to some degree.
[While it is true that it will help elevate free testerone levels, it only does this temporarily, because when our bodies realize that the levels are too high we will increase our production of SHBG to bring them back down. IMO this is not a great estrogen blocker] - Spiderman
RU486/mifepristone - now this drug effects progesterone related side effects. The drug anti-progestational activity results from competitive interaction with progesterone at progesterone-receptor sites, and as a result the compound inhibits the activity of endogenous or exogenous progesterone.
[This is commonly referred to as "the morning after pill"] - addition by Spiderman
Oh brother... I could write a text book here, but I don't have the time. So I will give some quick short answers.
Basics on Prolactin, and most importantly that Dopamine regulation has a major effect on prolactin secretion:
http://arbl.cvmbs.colostate.edu/hboo...prolactin.html
Prolactin and progesterone are not the same thing, and are not simply connected via steroidogenesis pathways (scroll down til you get to the graphic with all the sterans "Major pathways in steroid biogenesis").
http://arbl.cvmbs.colostate.edu/hboo...dogenesis.html
Take a look (for those that are biochemically inclined) as to the interrelationship of the various steroids in the body. Note the reactions/enzymatic processes that connect them - these are what we typically seek to modulate with "anti-side effect" drugs (i.e. control aromatase CYP19, control Aldosterone CYP11B2, etc.)
Quickie on the drugs:
arimidex, letrozole - are aromatase inhibitors. For example, Anastrozole is a potent and selective non-steroidal aromatase inhibitor. It significantly lowers serum estradiol concentrations and has no detectable effect on formation of adrenal corticosteroids or aldosterone. These drugs do not directly effect estrogen/estradiol already in circulation. They just help reduce the production of estrogen/estradiol going forward.
[They do this by inhibiting the enzyme aromatase through reversable competition. Aromatse is the enzyme that converts androgens to estrogen. So this drug works by decreasing the amount of estrogen you are forming which is why they are best used throughout the cycle if you plan on using them, IMHO.] - Spiderman
aromasin/exemstane - these drugs work by selectively targeting and irreversibly binding to the aromatase enzyme, which is required to produce estradiol/estrogen. Basically they are steroidal aromatase inactivators. Again, similar to the aromatase inhibitors, these drugs do not directly impact estrogen that is already in circulation.
[With this being an irreversible binder to the aromatase enzyme it will not come off until the enzyme is metabolized.] - Spiderman
nolvadex - is a selective estrogen receptor modulator (SERM). Basically it blocks the actions of estrogen in breast tissues and certain other tissues by "occupying" the estrogen receptors on cells. With a SERM sitting in the estrogen receptor, there is no place for the real estrogen to "sit down" - like a game of musical chairs. The SERM fits in the estrogen receptor, but it does NOT send messages to the cell nucleus to grow and divide. This is why nolvadex can help in situations where circulating estrogen levels are already elevated. For example early signs of gyno indicate high circulating estrogen levels - nolvadex is the best initial treatment to block the circulating estrogen from binding, followed-up by either an aromatase inhibitor or an inactivator to stop additional estrogen in its tracks.
bromocriptine & dostinex (cabergoline) - these 2 drugs do not directly modify estrogen or progesterone regulation. These drugs are dopamine agonists that mimic the effects of dopamine in the brain by stimulating dopamine receptors. This increased stimulation of dopamine receptors, as I wrote above, will have a direct impact on prolactin levels - it will cause a marked decrease in prolactin secretion from the pituitary.
[Thus the reason why it will they are useless unless the gyno you are experiencing is from prolactin stimulation instead of estrogen stimulation. The common steroids that cause prolactin induced gyno are Tren and Nandrolone] - Spiderman
proviron - has 2 main effects. (1) it stongly binds with sex hormone binding globulin, SHBG. SHBG normally binds with testosterone and as a result only 1-3% of total testosterone is ever free to bind with receptors. By binding with SHBG, proviron basically helps elevate free test levels. (2) Proviron is 5-alpha reduced (since it is DHT like) and therefore it can't convert to estrogen, yet it nonetheless has a much higher affinity for the aromatase enzyme (which converts testosterone to estrogen). So it can act like an aromatase inactivator to some degree.
[While it is true that it will help elevate free testerone levels, it only does this temporarily, because when our bodies realize that the levels are too high we will increase our production of SHBG to bring them back down. IMO this is not a great estrogen blocker] - Spiderman
RU486/mifepristone - now this drug effects progesterone related side effects. The drug anti-progestational activity results from competitive interaction with progesterone at progesterone-receptor sites, and as a result the compound inhibits the activity of endogenous or exogenous progesterone.
[This is commonly referred to as "the morning after pill"] - addition by Spiderman
