If mag10 doesn’t convert into estrogen, then why would you need to take m, which helps with estrogen convertion? Can anyone explains this to me. Or am I just mis-informed.
Bump for Bill Roberts. I have had a question about this for a long time. I have some of my own theories but I would like to hear Bill’s reasoning first.
Estrogen suppression will encourage more T. T aromitizes to E, so the higher E, the less T produced so that no more E will be aromatized. Suppress E, and the body is tricked into making more T in attempt to raise E.
Wanted to add, this is how clomid works post cycle and clomid is used even after non-aromitizing cycles to help restart T.
Vitex is a more economical choice when using androgens that do not aromatize. Vitex is the T supporting herb in M.
Heb, I understand how clomid works to increase testosterone and that is by blocking estrogen receptors in the hypothalamus and pituitary. Consequently, the body thinks that there is less estrogen and it raises testosterone. Estrogen levels are not suppressed with clomid but generally rise. The only clomid like component of M is trihydroxystilbene (resveratrol). It is a SERM (selective estrogen receptor modulator) like clomid in that it blocks estrogens receptors in breast and uterine tissue, however, the effects of trihydroxystilbene on the hypothalamus and pituitary have not been evaluated thoroughly so we do not know how it affects testosterone levels yet. D-Glucarate has been reported to decrease circulating estrogen levels and is probably one of the more important ingredients in M. Tocotrienols help prevent and treat breast cancer but it is through estrogen dependant and independent mechanisms therefore I don’t understand what it has to do with estrogen blocking, suppression, or elimination. I wish that Brock or the other fellow who invented M would write an article to explain the scientific basis of this and the other ingredients. Joel, Vitex has only been shown to decrease prolactin in males and it has no effects on FSH, LH, or testosterone (Exp Clin Endocrinol Diabetes (1996)104:447-453). The decrease in prolactin may increase testosterone levels over a longer term study but this has yet to be demonstrated. Most normal males do not have a problem with excessive prolactin levels. I wish there were more information on this topic but it is really quite limited.
I would also like to add my theory as to why M (if it proves effective) or another anti-estrogen would be useful after an androgen cycle (estrogenic or non-estrogenic). If you are taking androgens this will stimulate an increase in aromatase levels in order to lower androgen levels whether or not the androgen can be aromatized or not. This increase in aromatase levels will most likely last post-cycle and will convert one’s natural testosterone, which will probably be suppressed anyway, to estrogens. These estrogens will further decrease testosterone levels making recovery even more difficult. Therefore if estrogen could be effectively blocked or cleared form the system by M or another anti-estrogen it would improve recovery time of natural testosterone levels.
Kenny thnak you very much for your imput. You seem very knowledgable and what you have explained I was able to understand. Thanks again.