OverMachoGrande
Senior Member
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I'm sitting here at home drinking a nice cup of green tea, when I came across an article saying that women who drink green tea have 13% lower estrogen levels, which is important to know considering estrogen (and IGF-1) cause breast cancer in women and prostate cancer in men. So I decided to google the terms "green tea IGF-1" and "green tea estradiol". Not surprisingly I found that the green tea polyphenols EGCG increased IGFBP-3 (which is shown to be low in men with male pattern baldness) and that these same polyphenols help to decrease circulating estrogen levels as well.
The study below shows that EGCG (a polyphenol found in green tea) can compete for binding to the estrogen receptors.
Also, if you look at the molecular structure of EGCG it looks similar to estradiol (and D.H.T.)!
Estrogen Receptor-Mediated Actions of Polyphenolic Catechins in Vivo and in Vitro
M. G. Goodin*, K. C. Fertuck, T. R. Zacharewski and R. J. Rosengren*,1
* Department of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand; and Department of Biochemistry and Molecular Biology, and National Food Safety and Toxicology Center, Michigan State University, East Lansing, Michigan 48824
Recent investigations have demonstrated that polyphenolic catechins inhibit breast cancer cell proliferation and tumor growth. However, the ER-mediated effects of the three predominant catechins (EGCG, ECG, and EGC) have not been extensively examined in vitro or in vivo. Therefore, EGCG, ECG, and EGC were examined for their ability to compete with [3H]-17ß-estradiol ([3H]-E2) for binding to ER and ERß and to elicit reporter gene activity in MCF-7 human breast cancer cells transiently transfected with either chimeric ER or ERß. EGCG and ECG displaced [3H]-E2 from GST-hERdef (D, E, and F domains of human ER fused to GST) or from full-length human ERß. Additionally, only EGCG elicited Gal4-hERdef and Gal4-mERßdef-mediated reporter gene expression (EC50 values: 28 and 19 µM, respectively) in MCF-7 cells cotransfected with a Gal4-regulated luciferase reporter gene. In cotreatment experiments, EGCG (1–50 µM) and ECG (1 µM) decreased E2-induced (1 nM) ERß-mediated gene expression 35–50%. In vivo, no catechin induced estrogenic responses (uterine weight or uterine peroxidase activity) in immature C57BL/6 mice. However, when mice were cotreated with E2 (10 µg/kg/day, 3 days) and either EGCG (30 and 50 mg/kg/day, 3 days) or ECG (50 mg/kg/day, 3 days), uterine peroxidase activity was increased 2.3-fold above that elicited by E2 alone. In conclusion, EGCG and ECG bind to ER and ERß, but only EGCG elicited ER-mediated gene expression in vitro. However, both of these compounds moderately increased E2-inducible responses in vivo.
http://toxsci.oxfordjournals.org/cgi/co ... t/69/2/354
The study below shows that EGCG (a polyphenol found in green tea) can compete for binding to the estrogen receptors.
Also, if you look at the molecular structure of EGCG it looks similar to estradiol (and D.H.T.)!
Estrogen Receptor-Mediated Actions of Polyphenolic Catechins in Vivo and in Vitro
M. G. Goodin*, K. C. Fertuck, T. R. Zacharewski and R. J. Rosengren*,1
* Department of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand; and Department of Biochemistry and Molecular Biology, and National Food Safety and Toxicology Center, Michigan State University, East Lansing, Michigan 48824
Recent investigations have demonstrated that polyphenolic catechins inhibit breast cancer cell proliferation and tumor growth. However, the ER-mediated effects of the three predominant catechins (EGCG, ECG, and EGC) have not been extensively examined in vitro or in vivo. Therefore, EGCG, ECG, and EGC were examined for their ability to compete with [3H]-17ß-estradiol ([3H]-E2) for binding to ER and ERß and to elicit reporter gene activity in MCF-7 human breast cancer cells transiently transfected with either chimeric ER or ERß. EGCG and ECG displaced [3H]-E2 from GST-hERdef (D, E, and F domains of human ER fused to GST) or from full-length human ERß. Additionally, only EGCG elicited Gal4-hERdef and Gal4-mERßdef-mediated reporter gene expression (EC50 values: 28 and 19 µM, respectively) in MCF-7 cells cotransfected with a Gal4-regulated luciferase reporter gene. In cotreatment experiments, EGCG (1–50 µM) and ECG (1 µM) decreased E2-induced (1 nM) ERß-mediated gene expression 35–50%. In vivo, no catechin induced estrogenic responses (uterine weight or uterine peroxidase activity) in immature C57BL/6 mice. However, when mice were cotreated with E2 (10 µg/kg/day, 3 days) and either EGCG (30 and 50 mg/kg/day, 3 days) or ECG (50 mg/kg/day, 3 days), uterine peroxidase activity was increased 2.3-fold above that elicited by E2 alone. In conclusion, EGCG and ECG bind to ER and ERß, but only EGCG elicited ER-mediated gene expression in vitro. However, both of these compounds moderately increased E2-inducible responses in vivo.
http://toxsci.oxfordjournals.org/cgi/co ... t/69/2/354
