Green Tea and Estrogen

“Japanese women’s relative freedom from breast cancer is independent of soy products: traditional soy foods aren’t the same as those so widely used in the US, for example, soy sauce doesn’t contain the so-called soy estrogens, and tea is used much more commonly in Japan than in the US, and contains health protective ingredients. The “estrogenic” and “antioxidant” polyphenolic compounds of tea are not the protective agents (they raise the level of estrogen), but tea’s caffeine is a very powerful and general anti-cancer protectant. The influential article in Lancet (D. Ingram, Lancet 1997;350:990-994. “Phytoestrogens and their role in breast cancer,” Breast NEWS: Newsletter of the NHMRC National Breast Cancer Centre, Vol. 3, No. 2, Winter 1997) used a method known to produce false results, namely, comparing the phytoestrogens (found in large amounts in soybeans) in the urine of women with or without breast cancer. For over fifty years, it has been known that the liver excretes estrogens and other toxins from the body, and that when (because of liver inertia) estrogen isn’t excreted by the liver and kidneys, it is retained in the body. This process was observed in both animals and humans decades ago, and it is also well established that estrogen itself suppresses the detoxifying systems, causing fewer carcinogens to be excreted in the urine. Ingram’s evidence logically would suggest that the women who have cancer are failing to eliminate estrogens, including phytoestrogens, at a normal rate, and so are retaining a higher percentage of the chemicals consumed in their diets. Flavonoids and polyphenols, like our own estrogens, suppress the detoxifying systems of the body.“ -Ray Peat, PhD

J Steroid Biochem Mol Biol 1998 Feb;64(3-4):207-15,
Effects of tea polyphenols and flavonoids on liver microsomal glucuronidation of estradiol and estrone.
Zhu BT, Taneja N, Loder DP, Balentine DA, Conney AH
Administration of 0.5 or 1% lyophilized green tea (5 or 10 mg tea solids per ml, respectively) as the sole source of drinking fluid to female Long-Evans rats for 18 days stimulated liver microsomal glucuronidation of estrone, estradiol and 4-nitrophenol by 30-37%, 15-27% and 26-60%, respectively. Oral administration of 0.5% lyophilized green tea to female CD-1 mice for 18 days stimulated liver microsomal glucuronidation of estrone, estradiol and 4-nitrophenol by 33-37%, 12-22% and 172-191%, respectively. The in vitro addition of a green tea polyphenol mixture, a black tea polyphenol mixture or (-)-epigallocatechin gallate inhibited rat liver microsomal glucuronidation of estrone and estradiol in a concentration-dependent manner and their IC50 values for inhibition of estrogen metabolism were approximately 12.5, 50 and 10 microg/ml, respectively. Enzyme kinetic analysis indicates that the inhibition of estrone glucuronidation by 10 microM (-)-epigallocatechin gallate was competitive while inhibition by 50 microM (-)-epigallocatechin gallate was noncompetitive. Similarly, several flavonoids (naringenin, hesperetin, kaempferol, quercetin, rutin, flavone, alpha-naphthoflavone and beta-naphthoflavone) also inhibited rat liver microsomal glucuronidation of estrone and estradiol to varying degrees. Naringenin and hesperetin displayed the strongest inhibitory effects (IC50 value of approximately 25 microM). These two hydroxylated flavonoids had a competitive mechanism of enzyme inhibition for estrone glucuronidation at a 10 microM inhibitor concentration and a predominantly noncompetitive mechanism of inhibition at a 50 microM inhibitor concentration.