Vreemd hoor (ervan uitgaande dat je arimidex real was).
En aromasin heeft een lagere oestrogeen reductie dan arimidex he. Maar goed, valt te proberen, omdat het via een andere manier gaat.
arimidex was real (dokter)
niet helemaal mee eens met je statement over aromasin, dit is trouwens een interessante read:
When it comes to this comparison its more about type of estrogen suppression as opposed to "strength". Arimidex is a VERY potent sulfatase inhibitor, which inhibits estrone. It is a moderately strong aromatase inhibitor (weak as compared to aromasin, AIFM or letrozole). This is fine for women with breast cancer who produce percentage wise very high levels of estrone (the weak estrogen), which can be converted to estradiol (the strong estrogen) via aromatase.
For men this is generally not very good, especially for men on TRT since sulfatase inhibitors have very little effect on exogenous testosterone. Actually its generally not a good thing since it nearly completely eliminates estrone, while still allowing estradiol. If you have a choice as a man, you want estrone (weak estrogen) with near total elimination of estradiol (strong). AIFM and aromasin do inhibit sulfatase, though to a lesser extent than the competitive inhibitors (dex and letro). They are both potent aromatase inhibitors and highly suppress estradiol. Since exogenous test converts to estradiol via aromatase, AIFM and aromasin are much better suited.
Lowest doses of letrozole completely suppresses glandular production of estrone(E1). while it generally takes higher end doses of exemestane(aromasin) to come close to doing this. Exemestane dose dependantly decreases estradiol and to a lesser extent estrone. Basically aromasin at low doses is mostly peripheral, which means blocking conversion of estrone, testosterone and other aromatic precursors to estradiol. Whereas because they are competitive inhibitors that have high permeability through tissue types, arimidex and letrozole have high affinity and saturation of tissues like testes and adrenals, where estrone is produced. They highly block synthesis of aromatase in those tissues at even lowest doses.
Though aromasin/exemestane can produce high level suppression, particularly in low estrogen producers as well as those that generally produce less aromatase. (genetics, followed by factors like age and bodyfat). Keeping in mind that there are many endogenous and exogenous regulators of aromatase...ie, dopaminergics tend to down regulate aromatase mRNA, thus synthesis (not block, down regulate) but their use may require a lesser dose of AI (of either kind) that you are used to.
