Estrogen replacement therapy offers many potential health benefits for women when used correctly and in the right situations. The benefits and risks of estrogen replacement must be considered on an individual basis.
Some doctors are hesitant to recommend estrogen therapy replacement. This fear is based on a 2002 study known as the Women’s Health Initiative (WHI) estrogen-progestin trial. This study involving synthetic and not bioidentical hormone replacement was stopped early due to concerns of increased breast cancer incidence and heart attacks. The study focused on women over the age of 60 but then generalized to younger women on short-term therapy for menopause. Years later, with more thorough reviews of this research, researchers had a new consensus is that there is no increased risk of breast cancer for women under age 60 who take hormone replacement (HRT) for less than 5.6 years. As well, researchers found a benefit for women who take hormone replacement closer to menopause have reduced heart risk. The ultra-conservative North American Menopause Society summarizes breast cancer risk and estrogen replacement by stating:
Compared with women who received placebo, women who received CEE [synthetic estrogen] alone in the WHI showed a nonsignificant reduction in breast cancer risk after an average of 7.2 years of randomization, with 7 fewer cases of invasive breast cancer per 10,000 person-years of CEE [synthetic estrogen]. The nonsignificant pattern of reduction in breast cancer remained evident for up to a median 13-year cumulative follow-up…. Limited observational evidence suggests that HT [hormone therapy] does not further increase risk of breast cancer in women with a family history of breast cancer or in women after oophorectomy for BRCA1 or 2 gene mutation.
The conclusion is that current data does not support a high breast cancer risk with estrogen replacement, even with the less healthy synthetic estrogen.
The term bioidentical can be defined as “…chemical substances that are identical in molecular structure to human hormones.” It is intuitive that if one is to supplement a hormone, then it should be the same as your body makes. The concept of bioidentical hormones is opposite the still available synthetic hormones that are altered for patentable purposes by drug companies. Historically, the most prescribed synthetic hormones prescribed include conjugated equine estrogens (Premarin) and medroxyprogesterone acetate (Provera), and contraceptives that contain synthetic hormones.
Women that are given estrogen replacement by conventional doctors are sometimes given progestin. Synthetic hormone replacement is the use of synthetic progesterone, whose proper term is progestin. Typically, menopausal hormone replacement includes estrogen and progesterone to prevent the excessive build-up of the uterine lining and risk of endometrial cancer. There is research demonstrating that progestins increase the risk of breast cancer by causing abnormal cell proliferation. In addition, published research demonstrates that estrogen plus progestin increases breast cancer incidence and mortality in postmenopausal women. Oppositely, progesterone (bioidentical form) decreases the risk of breast cancer. This is because progestins exert different actions on cells than do the naturally occurring progesterone. Progestins such as medroxyprogesterone acetate (Provera) have significantly increased cell proliferation through interaction with cell growth factors, whereas progesterone had no effect. Progesterone blocks estrogen caused proliferation and healthier gene expression and is associated with decreased metastasis in estrogen-positive breast cancer.
A review of studies that looked at the evidence of comparing bioidentical hormones including estradiol, estriol, and progesterone was compared to non-bioidentical (synthetic) HRT. The author of this paper concluded “that bioidentical hormones are associated with lower risks, including the risk of breast cancer and cardiovascular disease, and are more efficacious than their synthetic and animal-derived counterparts.”
The optimal way to supplement estrogen is through topical administration on the skin, known as the transdermal route. This method bypasses the digestive tract and goes directly into the bloodstream and to your cells. Transdermal administration is a safer method than taking estrogen by pill (oral form). When the transdermal route is used, it reduces the formation of clotting factors associated with the oral form. The transdermal form also leads to better blood pressure control compared to the oral form. Also, the oral form is converted into estrone more readily, which does not have the symptom-relieving effect of estradiol.
Published research has shown many other advantages of the transdermal form as follows. The use of transdermal estrogen maintains a better blood estradiol level and fewer fluctuations in estrogen blood levels with the transdermal form. Both oral and transdermal estrogen has increased good HDL cholesterol and decreased LDL and total cholesterol. However, oral estrogens can raise triglyceride levels, whereas the transdermal form does not. Also, oral estrogen may increase inflammation markers such as C-Reactive Protein (CRP), while the transdermal form does not contribute to elevated CRP but may decrease it. And in terms of digestion, the transdermal form avoids the gut there is fewer problems with digestive upset compared to the oral form. And finally, the transdermal form is less likely to cause side effects such as vaginal bleeding and breast tenderness compared to the oral form.
The type of bioidentical estrogen used by holistic doctors is known as Biest. It contains a blend of estradiol and estriol. As mentioned, it is best administered transdermally. Biest should be given with its “balancer,” which is the hormone progesterone. Progesterone is given in the transdermal or oral form. Unlike estrogen, progesterone is safe and effective orally and is most effective in preventing endometrial build-up or endometrial cancer. Women take the combination of biest and progesterone replacement daily, with a drug holiday one day a week or three to five days in a row each month. If a premenopausal woman still has a menstrual cycle, then the hormones are discontinued during menses.
There is no consensus as to how long a woman should stay on estrogen replacement therapy. The North American Menopause Society takes the position that hormone therapy has been shown to prevent bone loss and fracture. They support the individualized use of hormone therapy for women younger than the age of 60 who are within 10 years of the start of menopause and have no medical reasons to not use it, and for the indications of vasomotor symptoms (hot flashes) and those at risk for bone loss and fracture. If a woman is aged 60 years or older and initiates hormone therapy 10 or 20 years from menopause, then they are less supportive except for ongoing vasomotor symptoms (hot flashes and night sweats) and bone loss. I have some female patients who take Biest and other bioidentical hormones well into their 70’s and even 90’s to maintain quality of life. These patients are monitored with the proper testing and evaluation of their symptoms.
Dr. Mark Stengler NMD, MS, is a bestselling author in private practice in Encinitas, California, at the Stengler Center for Integrative Medicine. His newsletter, Dr. Stengler’s Health Breakthroughs, is available at www.markstengler.com and his product line at www.drstengler.com
Chlebowski, R. T., Anderson, G. L., Gass, M., Lane, D. S., Aragaki, A. K., Kuller, L. H., Manson, J. E., Stefanick, M. L., Ockene, J., Sarto, G. E., Johnson, K. C., Wactawski-Wende, J., Ravdin, P. M., Schenken, R., Hendrix, S. L., Rajkovic, A., Rohan, T. E., Yasmeen, S., Prentice, R. L., WHI Investigators (2010). Estrogen plus progestin and breast cancer incidence and mortality in postmenopausal women. JAMA, 304(15), 1684-92.
Fournier A, Berrino F, Riboli E, Avenel V, Clavel-Chapelon F. 2005. Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort. International Journal of Cancer 114:448-454. https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.20710
Fournier A, Berrino F, Clavel-Chapelon F. 2007. Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study. Breast Cancer Research and Treatment 107:103-111. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211383/
Holtorf K. 2009. The Bioidentical Hormone Debate: Are Bioidentical Hormones (Estradiol, Estriol, and Progesterone) Safer or More Efficacious than Commonly Used Synthetic Versions in Hormone Replacement Therapy? Postgraduate Medicine 121:73-85. https://www.tandfonline.com/doi/abs/10.3810/pgm.2009.01.1949
Mohammed H, Russell I, Stark R, Rueda O, Hickey T, Tarulli G, Serandour A, Birrell S, Bruna A, Saadi A et al. 2015. Progesterone receptor modulates ERα action in breast cancer. Nature 523:313-317. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650274/
Murkes D, Lalitkumar P, Leifland K, Lundström E, Söderqvist G. 2012. Percutaneous estradiol/oral micronized progesterone has less-adverse effects and different gene regulations than oral conjugated equine estrogens/medroxyprogesterone acetate in the breasts of healthy women in vivo. Gynecological Endocrinology 28:12-15.
The 2017 hormone therapy position statement of The North American Menopause Society. 2017. Menopause 24:728-753. https://www.menopause.org/docs/default-source/2017/nams-2017-hormone-therapy-position-statement.pdf
Vogel L. 2017. Landmark trial overstated HRT risk for younger women | CMAJ News. Cmajnews.com. https://cmajnews.com/2017/04/12/landmark-trial-overstated-hrt-risk-for-younger-women-109-5421/
Whelan A. 2011. Defining bioidentical hormones for menopause-related symptoms. Pharmacy Practice 9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4132968/
Wood C, Branstetter D, Jacob A, Cline J, Register T, Rohrbach K, Huang L, Borgerink H, Dougall W. 2013. Progestin effects on cell proliferation pathways in the postmenopausal mammary gland. Breast Cancer Research 15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978455/
Zhou J, Yu Q, Chen R, Seeger H, Fehm T, Cahill M, Mueck A, Neubauer H. 2013. Medroxyprogesterone acetate-driven increase in breast cancer risk might be mediated via cross-talk with growth factors in the presence of progesterone receptor membrane component-1. Maturitas 76:129-133. [accessed 2019 Jan 29]. https://www.maturitas.org/article/S0378-5122(13)00197-7/fulltext