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Estriol & Breast Cancer

Is Estriol a Risk Factor for Breast Cancer?

We get asked this a lot, understandably, so we've broken down the science, the statistics, and the research to give you a look at how estriol affects cancer rates.

You probably know by now that there are different types of estrogen. These vital estrogens are used in different ways in the body. Estrogen hormones move around in the bloodstream - looking for receptors, like little doors, on the surface of cells.

There are two types of estrogen receptors in the breast – Alpha and Beta. The Alpha receptors promote breast cell growth, whereas the Beta receptors inhibit or reduce breast cell growth. Estrone and Estradiol bind to the Alpha Receptors whereas Estriol binds to the Beta receptors. Estradiol supplementation is associated with breast cancer promotion for those at risk, whereas Estriol is associated with breast cancer protection.

General practitioners often are unaware of the existence of, and difference between, the two types of estrogen receptors and so can end up lumping estrone, estradiol, and estriol together. This is a shame because many women who have had breast cancer, or who have some risk of breast cancer often don’t get the opportunity to try estriol as a supplementation tool.

Estrogen Receptors in the Breast



Promote Breast Cell Growth

Inhibit or Slow Breast Cell Growth

Estrone and Estradiol attach to the Alpha Receptors

Estriol attaches to the Beta Receptors

More likely to promote breast cancer cell development in those at risk

Very likely to protect the breast from breast cancer cell development

Is That The Whole Story?

Understanding breast cancer risk is not just an estrogen story. Estradiol is a very small part of a woman’s risk factor for developing cancer. Cancer cells grow all the time and we have special cells in the immune system that scurry around looking for those cancer cells and knocking them out.

What Affects Cancer Cell Growth?

To understand the wide range of factors that can affect cancer cell growth we have to look at the environment those cells attempt to grow in. Cancer cells need damaged DNA, and sugar, and an acidic environment, and lots of toxins which will damage the DNA. A combination of all these things will create a “dirty” or inflammatory environment where cancer cells can grow faster than the immune system can knock them out.

How Our Bodies Fight Cancer

When we are younger our internal cleaning processes are pretty good at destroying cancer cells before they start to build a mass and add blood vessels. Kids do get cancer, but these cancers are most often related to a genetic risk. We’re not talking about these types of cancers, we're talking about the increased risk for normal DNA being damaged and spinning out of control into cancer cell development.

As we get older, our lifestyle choices, and food choices, and the natural process of aging makes it harder for the immune cells to keep up. Here is a list of all the factors that can increase the risk of creating an inflammatory environment where DNA can be damaged and where cancer cells can grow and flourish:


The more risk factors apply to you, the greater your risk of developing cancer cells.

The Difference Between Estradiol and Estriol

Unopposed estradiol is definitely a risk factor for someone who has a LOT of other risk factors. Estradiol does make cells grow, that’s a big part of its biochemical MO. The key word however is “Unopposed”. Unopposed estradiol means using estrogen without balancing it with progesterone. We are talking bioidentical progesterone here - not the pharmaceutically made progestins that don’t behave in the body like progesterone does. Millions of women have been denied or are afraid of estrogen supplementation because of the faulty belief that estrogen “will cause cancer”. Estrogen balanced by progesterone is important for so many functions in the body: bone strength, memory formation, memory recall, skin function, vaginal and urinary health just to mention a few.

An Inventory of Risk

Rather than worry excessively about whether estrogen causes cancer, instead, to an honest inventory of all the risk factors associated with allowing cancer cells to grow and start changing those. Inflammation will destroy DNA and allow genetic mutations that can result in cancer cell growth. The key to cancer prevention is keeping the body free from inflammation.

Progestin .v. Progesterone

We said earlier in this post that general practitioners often are unaware of the existence of and difference between the two types of estrogen receptors and so can end up lumping estrone, estradiol and estriol together. These same doctors don’t understand the difference between bioidentical progesterone and the often harmful progestins made by pharmaceutical companies. They understand that that progestins are harmful and, when combining that a lack of understanding of the role of inflammation in the body decide to advise patients against using ANY hormones post menopause.

It is very possible to keep your body safe from overgrowth of cancer cells, just as it is possible to safely use estrogen and progesterone to help you be vibrant and strong for all the years you will live post menopause.

What About Topical Estriol?

One of the possible solutions to this is estriol. Estriol is the weakest of the estrogens, produced through non reversible metabolism of the other two estrogens - estradiol and estrone. It has 1/7 to 1/8th the potency of estradiol and is metabolized to non harmful metabolites that are not associated with breast cancer cell growth. Vaginal estriol is a local treatment; some estrogen does get into the bloodstream and move around the body, but most stays locally in the pelvic area. For the small amount of estriol that does reach breast tissue, it is active for about a quarter of the time that estradiol is. Therefore, if a woman is not getting relief from other strategies, low dose vaginal estriol may be a reasonable option.

Some Scientific Background

A frequently feared effect of the use of estrogen is in the pro-estrogenic effects on breasts and endometrium. The fact that there are two distinct types of estrogen receptors, estrogen receptor alpha (ER-A) and estrogen receptor beta (ER-B) is a crucial concept. 1, 2, 3 In the breast for example, the binding of estrogen hormones to estrogen receptor alpha promotes breast cell proliferation, whereas the binding of estrogen hormones to estrogen receptor beta inhibits breast cell proliferation and prevents breast cancer development. 4, 1 It is important to note that estrone and estradiol bind mostly to estrogen receptor alpha, thereby explaining the known breast cancer-promoting effects of these two hormones.5,6 On the other hand, estriol binds to estrogen receptor beta5,6, a characteristic that corresponds to a unique breast cancer protection effect amongst the estrogens.

1. Helguero LA, Faulds MH, Gustafsson JA and Haldosen LA. Estrogen receptors alfa (ERalpha) and beta (ERbeta) differentially regulate proliferation and apoptosis of the normal murine mammary epithelial cell line HC11. Oncogene 24: 44: 6605-6616, 2005.

2. Nilsson S, Makela S, Treuter E, Tujague M, Thomsen J, Andersson G, Enmark E, Pettersson K, Warner M and Gustafsson JA. Mechanisms of estrogen action. Physiol.Rev. 81: 4: 1535-1565, 2001.

3. Paruthiyil S, Parmar H, Kerekatte V, Cunha GR, Firestone GL and Leitman DC. Estrogen receptor beta inhibits human breast cancer cell proliferation and tumor formation by causing a G2 cell cycle arrest. Cancer Res. 64: 1: 423-428, 2004.

4. Bakken K, Alsaker E, Eggen AE and Lund E. Hormone replacement therapy and incidence of hormone-dependent cancers in the Norwegian Women and Cancer study. Int.J.Cancer 112: 1: 130-134, 2004.

5. Rich RL, Hoth LR, Geoghegan KF, Brown TA, LeMotte PK, Simons SP, Hensley P and Myszka DG. Kinetic analysis of estrogen receptor/ligand interactions. Proc.Natl.Acad.Sci.U.S.A. 99: 13: 8562-8567, 2002.

6. Zhu BT, Han GZ, Shim JY, Wen Y and Jiang XR. Quantitative structure-activity relationship of various endogenous estrogen metabolites for human estrogen receptor alpha and beta subtypes: Insights into the structural determinants favoring a differential subtype binding. Endocrinology 147: 9: 4132-4150, 2006.

**Disclaimer: We always recommend that women with a history or genetic risk of breast cancer talk to their doctors about the use of hormones and other medications in their healthcare regime.**