Breast Cancer, Part 5 – Natural Approaches and Protection Against Dangerous Estrogens
Protecting Against Dangerous Estrogens:
- Green Tea
- Conjugated Linoleic Acid
- EPA and DHA
- Vitamins A, D, and E
Protecting Breast Cells Against Dangerous Estrogens
How to Use I3C
The stronger form of estrogen, estradiol, can be converted into the weakerform, estriol, in the body without using drugs. Estriol is considered to be amore desirable form of estrogen. It is less active than estradiol, so when itoccupies the estrogen receptor, it blocks estradiol’s strong “growth” signals. Using a natural substance the conversion of estradiol to estriolincreased by 50% in 12 healthy people (Michnovicz et al. 1991).
Furthermore, in female mice prone to developing breast cancer the natural substance reduced the incidence of cancer and the number of tumors significantly. The natural substance was indole-3-carbinol (I3C).Indole-3-carbinol (I3C) is a phytochemical isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage, mustard seed, etc.).
I3C given to 17 men and women for 2 months reduced the levels of strong estrogen, and increased the levels of weak estrogen. But more importantly, the level of an estrogen metabolite associated with breast and endometrial cancer, 16–a-hydroxyestrone, was reduced by I3C (Bradlow et al. 1991). When I3C changes “strong” estrogen to “weak” estrogen, the growth of human cancer cells is inhibited by54-61% (Telang et al. 1997).
Moreover, I3C provoked cancer cells to self-destruct (kill themselves via apoptosis). Induction of cell death is anapproach to suppress carcinogenesis and is the prime goal of cytotoxic chemotherapy. The increase in apoptosis induced by I3C before initiation of new tumor development may contribute to suppression of tumor progression. Nontoxic I3C can reliably facilitate apoptosis (12 week treatment in rats); thus, this phytonutrient may become a standard adjunct in the treatment of breast cancer (Zhang et al. 2003)
13C inhibits human breast cancer cells (MCF7) from growing by as much as 90% in culture; growth arrest does not depend on estrogen receptors (Cover et al. 1998).
Furthermore, I3C induces apoptosis in tumorigenic(cancerous) but not in non-tumorigenic (non-cancerous) breast epithelial cells (Rahman et al. 2003). I3C does more than just turn strong estrogen to weak estrogen. 16-a-Hydroxyestrone (16-OHE) and 2-hydroxyestrone (2-OHE) are metabolites of estrogen in addition to estriol and estradiol. 2-OHE is biologically inactive, while 16-OHE is biologically active; that is, like estradiol, it can send “growth” signals. In breast cancer, the dangerous16-OHE is often elevated, while the protective 2-OHE is decreased.
Cancer-causing chemicals change the metabolism of estrogen so that 16-OHE is elevated. Studies show that people who take I3C have beneficial increases in the “weak” estriol form of estrogen and also increases in protective 2-OHE.African-American women who consumed I3C, 400 mg for 5 days, experienced an increase in the “good” 2-OHE and a decrease of the “bad” 16-OHE. However, it was found that the minority of women who did not demonstrate an increase in 2-OHE, had a mutation in a gene that helps metabolize estrogen to the 2-OHE version. Those women had an eight times higher risk of breast cancer (Telang etal. 1997).
I3C Stops Cancer Cells from Growing
Tamoxifen is a drug prescribed to reduce breast cancer metastases and improve survival. I3C has modes of action similar to tamoxifen. I3C inhibited the growth of estrogen-receptor-positive breast cancer cells by 90% compared to 60% for tamoxifen. The mode of action attributed to I3C’s impressive effect was interfering with the cancer cell growth cycle. Adding tamoxifen to I3C gave a 5% boost (95% total inhibition) (Cover et al. 1999).
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