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How Different Drugs Control Estrogen
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How Different Drugs Control Estrogen - 01-11-2013, 11:20 AM

– By drgoodbody

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.

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.

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.

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.

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.

Alright ya lazy fucks, that’s all the good doctor has time to write on the subject. Now go read something.

DrG


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