letro nor adex gets rid of all estrogen in the body. Maybe if you really over did it, it could. 2.5mg letro will lower estrogens 46-62% depending on age. Letro is good for PCT, but aromasin is even better.
sorry 4thad, that is not true. it get's rid of 100% in this study:
Aromatase inhibition, testosterone, and seizures.Harden C, MacLusky NJ.
Department of Neurology and Neuroscience, Comprehensive Epilepsy Center, Weill Medical College of Cornell University, New York, NY, USA. clharden@med.cornell.edu
The effect of testosterone on brain excitability is unclear. The excitatory aspect of testosterone's action in the brain may be due to its conversion to estrogen via aromatase. We report herein a 61-year-old man with temporal lobe epilepsy and sexual dysfunction due to low testosterone levels. Use of an aromatase inhibitor, letrozole, normalized his testosterone level and improved his sexual functioning. Letrozole, in addition to standard antiseizure medication, was also associated with improved seizure control. This was sustained and, further, was associated with seizure exacerbation after withdrawing letrozole, and subsequent seizure improvement after restarting it. During the course of treatment, his serum testosterone level increased, sex hormone-binding globulin decreased (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels increased,
while serum estradiol levels remained undetectable . Letrozole may, therefore, have produced a central alteration in the testosterone/estrogen ratio, thereby impairing estrogen-mediated feedback control of the pituitary, resulting in the observed increase in circulating LH and FSH levels. This experience suggests that aromatase inhibitors should be further investigated as a beneficial treatment modality for male patients with epilepsy.
and 98% in this one:
Aromatase inhibition: translation into a successful therapeutic approach.Geisler J, Lønning PE.
Department of Medicine, Section of Oncology, Haukeland University Hospital, Bergen, Norway.
The development of the novel third-generation aromatase inhibitors and inactivators for breast cancer treatment is one of the most successful contemporary achievements in cancer therapy. Parallel to studies evaluating toxicity and clinical efficacy in metastatic disease, the endocrine effects of multiple compounds were evaluated, leading to the identification of the highly potent third-generation aromatase inhibitors based on estrogen deprivation and aromatase inhibition in vivo. Thus, translational studies have been of vital importance identifying the unique characteristics of these compounds. Whereas first- and second-generation aromatase inhibitors inhibit estrogen synthesis in vivo by up to 90%, the third-generation compounds anastrozole, exemestane, and
letrozole were found to cause > or =98% aromatase inhibition. This article summarizes and discusses the "translational research" that provided the background for the implementation of the third-generation aromatase inhibitors and inactivators into large clinical trials. The need for future translational research exploiting the mechanisms of resistance to these compounds for future improvement of endocrine therapy is emphasized.
