16 Oct Breast Cancer & BHRT
Breast cancer and bio-identical hormone replacement therapy is definitely a contested debate in today’s society. Then again, almost every day we are finding more and more items that we consume or are exposed to on a regular basis that is claimed to be carcinogenic. I don’t mean to be cynical but we need to look at the literature and dive deeper than just making claims without substance. All medical professionals should be following the golden medical rule, “Do no harm”. Now, what I am referring to is simply a motto with hormone replacement therapy, “Go low and start slow”. This meaning generally to use conservative dosing, sees how the patient and body respond and titrate accordingly. With hormone replacement therapy there are limitations to every rule, but as long as we abide by them and dose responsibly patients are at no more risk than many other daily exposures.
Breast cancer and hormone replacement therapy there is always a focus on estrogen levels and how they affect risk for cancers, etc. The concern is just since estrogen is the primary driving force surrounding breast cancer. Responsible dosing is important to ensure dosing is appropriate for individual patients since excess. If you have a headache and want to take a Tylenol, the headache could be subsided by 1 or 10 tablets. But why would you take 10 if you can relief the problem with 1? The same is true with hormones since excess just sits in body. The balancing act regarding estrogen and progesterone and the importance of progesterone is also very important to prevent estrogen dominance and opposed estrogen. Over a 12 year period and over 1,000 women evaluated, it was found that premenopausal women with progesterone deficiency had more than 5.4 times the risk of breast cancer than those with non-hormonal causes (Cowan, 1981). Almost all risk factors associated with breast cancer are directly or indirectly related to excess estrogen levels. It was found that progesterone can actually inhibit breast cancer cell growth and induce apoptosis or cell death (Formby, 1998).
We have addressed progesterone and its benefits relative to estrogen and lowering risk of breast cancer but it is important to discern progesterone vs. progestins. The World Health Initiative (WHI) trial was investigating risk with hormone replacement therapy but was using estrogen and progestins. During this trial they found a higher incidence of breast cancer than the group receiving estrogen alone. As shown above, bioidentical progesterone has been found to not only not increase breast cancer risk but actually reduce in contrast to synthetic progestins that increased risk (Fournier, 2005).
The role of hormone balance in the development and prevention of breast cancer is still and will continue to be a subject of controversy for some. As for me, the proof is in the literature. There are many benefits to its utilization from symptom control to quality of life that cannot be quantified by patients using bioidentical hormone replacement therapy. There is a contraindication of estradiol with patients with a history of breast cancer so other options need to be discussed. This concern does not address all hormone replacement therapy or all patients, so it is important to discuss these options with your provider.
Citations
Anderson GL, Judd HL, Kaunitz AM, et al. Effects of Estrogen Plus Progestin on Gynecologic Cancers and Associated Diagnostic Procedures: The Women’s Health Initiative Randomized Trial. JAMA. 2003;290(13):1739–1748. doi:10.1001/jama.290.13.1739
Cowan, L., et al. “Breast cancer incidence in women with a history of progesterone deficiency,” American Journal of Epidemiology, Volume 114, Issue 2, August 1981, Pages 209–217, https://doi.org/10.1093/oxfordjournals.aje.a113184
Fournier A, Berrino F, Clavel-Chapelon F. “Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study.” Breast Cancer Research and Treatment 2007.
Formby, B. & Wiley, T.S. (1998) Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53. Ann Clin Lab Sci, 28 (6): 360-369.
Micheli, A. , Muti, P. , Secreto, G. , Krogh, V. , Meneghini, E. , Venturelli, E. , Sieri, S. , Pala, V. and Berrino, F. (2004), Endogenous sex hormones and subsequent breast cancer in premenopausal women. Int. J. Cancer, 112: 312-318. doi:10.1002/ijc.20403