Spurfy
Active member
My hypothesis is that SERMs act partially by inhibiting the binding of xenoestrogens, and thus produce a much more robust effect on testosterone than would be predicted strictly based on a structure-function analysis.
Xenoestrogens significantly disrupt estrogen signalling by acting at the ER-alpha receptor (1) in ways that differ even from endogenous estrogens,SERMs act -- among other ways -- by blocking ER-alpha, thus preventing the binding of toxic xenoestrogens.
SERMs, and specifically toremifene, have been shown to prevent the occurrence of prostate cancer. (2) Prostate cancer can be specifically driven by xenoestrogens, and BPA has been shown to do this (3). Currently, there is no real hypothesis on why toremifene is effective in preventing prostate cancer -- I propose it works by inhibiting the binding of BPA and other xenoestrogens to receptors in the prostate.
1. Steroids. 2014 Mar; 81: 36–42.
2. J Urol. 2006 Sep;176(3):965-70; discussion 970-1.
3. Cancer Res. 2005 Jan 1;65(1):54-65.
Xenoestrogens significantly disrupt estrogen signalling by acting at the ER-alpha receptor (1) in ways that differ even from endogenous estrogens,SERMs act -- among other ways -- by blocking ER-alpha, thus preventing the binding of toxic xenoestrogens.
SERMs, and specifically toremifene, have been shown to prevent the occurrence of prostate cancer. (2) Prostate cancer can be specifically driven by xenoestrogens, and BPA has been shown to do this (3). Currently, there is no real hypothesis on why toremifene is effective in preventing prostate cancer -- I propose it works by inhibiting the binding of BPA and other xenoestrogens to receptors in the prostate.
1. Steroids. 2014 Mar; 81: 36–42.
2. J Urol. 2006 Sep;176(3):965-70; discussion 970-1.
3. Cancer Res. 2005 Jan 1;65(1):54-65.