Is “M” more similiar to clomid or arimidex in terms of estrogen suppression and LH production?

I would say that it is more like clomid than arimidex. Resveratrol (Trihydroxystilbene)in “M” is a naturally occuring stilbene and Clomid is actually a stilbene derivative. They are both selective estrogen receptor modulators (SERMS)as they act as estrogen in some tissues and block estrogen in other tissues. Resveratrol blocks estrogen in breast tissue but the jury is still out on if it blocks estrogen in the central nervous system like clomid does. There are no aromatase inhibitors like arimidex in “M” to my knowledge. Calcium D-glucarate increases estrogen excretion in the bile through the intestines and vitex reduces prolactin levels which can be inhibitory on LH/testosterone levels. By blocking prolactin production you may increase testosterone levels indirectly. Tocotrienols are used to treat estrogen dependant and do not act via an estrogen receptor-mediated pathway and must therefore act differently from estrogen antagonists. It works to reduce the effects of estrogen post-receptor and I don’t understand the mechanism well. I hope there will be detailed description of this process in the upcoming article on “M” Chris promised. If Bill, Brock, or Cy could give a sneak preview on this I would appreciate it.