The Truth About Estrogen Dominance & Breast Cancer
Solid medical science and clinical studies have established that an underlying and untreated condition of “estrogen dominance” significantly increases your breast cancer risk: women who develop breast cancer have higher estrogen levels than women without breast cancer. Some studies have also shown that women who had been treated for breast cancer, and who continued to have high estrogen levels, had a return of the disease sooner than breast cancer survivors with lower estrogen levels. The reason is that one of estrogen’s functions in the body is to foster cell growth, or “cell proliferation.” At a cellular level, unchecked cell growth can be a precursor for cancer.
Estrogen dominance can lead to cancer in one of two ways: The first has to do with the concentration of each of the three different forms of estrogen–estrone, estradiol, and estriol–circulating within the body. Estrone and estradiol both work within the body to increase expression of the BCL2 gene that causes cell development and growth, particularly in hormone-sensitive tissue such a breast or uterine lining. If unopposed, this cell proliferation can lead to cancer. In fact, nearly every risk factor for breast and uterine cancer can be either directly or indirectly linked to an increase in estrone, estradiol, or their receptor activity. One such study in 2008 determined that high levels of estradiol were associated with significantly higher incidence of breast cancer recurrence(1). In many cases of breast cancer, a gene known as the P53 tumor suppressor pathway is disrupted. The P53 gene is the opposing force for the BCL2 gene; it causes natural cell death (know as apoptosis), and is responsible for balancing the effects of cell proliferation. In a nutshell: estrone and estradiol stimulate the production of the BCL2 gene, while progesterone stimulates the production of the P53 gene. When the body is experiencing estrogen dominance, what it desperately needs is progesterone to counter the effects of cell proliferation. Some studies have demonstrated that, by stimulating the P53 gene, progesterone can effect apoptosis (cell death) in cancer tumors(2)(3).
Note that Premarin, one of the most popular “synthetic” hormone replacement drugs, is composed of 49.3% estrone, almost ten times the amount that occurs naturally in the body–is it any wonder that this drug was found to increase risk of invasive breast cancer in post-menopausal women by 41 percent?
The second factor influencing your cancer risk has to do with how your body metabolizes its estrogen. Estrogen can be “metabolized” (converted) down a “bad” pathway–one that is more cancer inducing–or a “good” pathway–one that is more cancer protective. The chemical name for the “bad” pathway is 16-hydroxyestrone. The “good” pathways are 2-hydroxyestrone and 2-hydroxyestradiol. Each woman’s estrogen metabolism is different, so the balance between your “good” and “bad” pathways is unique. The balance of anti-carcinogenic and pro-carcinogenic estrogen can be investigated with a urine test (trademarked Estronex). Studies have demonstrated that post-menopausal women with more hydroxylation along the 2-pathways have a lower risk of breast cancer(4). Some studies suggest that this is also the case for pre-menopausal women, but due to the varying levels of menstruating women’s hormones, it is more challenging to conduct research. (Imagine trying to coordinate hundreds of volunteers to schedule blood draws on a certain representative day of their menstrual cycles!)
Our practice treats about 7,000 patients (of varying ages) each year with BHRT, and only a handful have developed breast cancer during more than two decades of prescribing bioidentical progesterone to balance the effects of estrogen dominance. When your body’s overabundance of estrogen is neutralized with bioidentical progesterone, your breast cells are no longer continuously exposed to high estrogen, and a causative factor for breast cancer is, for the most part, held in check.
(1) Cheryl L. Rock, Shirley W. Flatt, Gail A. Laughlin, et al., “Reproductive Steroid Hormones and Recurrence-Free Survival in Women with a History of Breast Cancer,” Cancer Epidemiology Biomarkers and Prevention 17 (2008): 614-20. https://www.ncbi.nlm.nih.gov/pubmed/18323413
(2) Formby, B., Wiley, T.S., “Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53,” Annals of Clinical & Laboratory Science. Nov-Dec;28(6):360-9 (1998). https://www.ncbi.nlm.nih.gov/pubmed/9846203
(3) Horita K1, Inase N, Miyake S, Formby B, Toyoda H, Yoshizawa Y. “Progesterone induces apoptosis in malignant mesothelioma cells,” Anticancer Research, Nov-Dec;21(6A):3871-4 (2001). https://www.ncbi.nlm.nih.gov/pubmed/11911261
(4) Roni T. Falk, Louise A. Brinton, Joanne F. Dorgan, et al., “Relationship of serum estrogens and estrogen metabolites to postmenopausal breast cancer risk: a nested case-control Study,” Breast Cancer Research 15 (2013): online 2013 Apr 22. https://www.ncbi.nlm.nih.gov/pubmed/23607871