The story of estrogen
Approximately 75% of all breast cancers are “ER positive” (estrogen receptor positive), which means that they grow in response to estrogen. About 65% of these are also “PR positive” (progesterone receptor positive), meaning they grow in response to progesterone. In this article we will focus on estrogen.
Three types of estrogens are produced naturally in women.
- Estradiol (E2) is the major estrogen produced in a woman before menopause.
- Estrone (E1) is the dominant circulating estrogen during menopause
- Estriol (E3) occurs mostly in pregnant women where it increases to 300 to 500-fold in relation to non-pregnant women. E3 is also the type of estrogen prescribed as part of “bio-identical hormone replacement therapy”. Despite the fact that E3 is a relatively weak type of estrogen, it should not be considered exclusively harmless with regards breast cancer risk.
It is important to emphasise that all three types of naturally occurring estrogens have been shown in research studies to stimulate breast cancer.
Xenoestrogens are part of a group of synthetic and naturally occurring chemicals referred to as endocrine disruptors because of their capacity to mimic natural hormone function in the human body.
We all encounter and / or ingest several types of xenoestrogens during our lifetime.
Research indicates that xenoestrogens can contribute to the development of hormone dependent cancers, such as breast cancer. We will list and discuss how to minimise our exposure to, and the impact of, various common environmental and dietary xenoestrogens such has pesticides and petrochemicals in part two of This article.
The estrogen receptor
In order for estrogen or any chemical mimicking estrogen to have an effect on the cells and tissues of your body (whether for benefit or disease) it needs to interact with something called a receptor. Think of it as a lock and key scenario. In order to open a door you have to use the right key in the right lock. Estrogen is the key in this metaphor (whether a natural estrogen or a xenoestrogen). The lock or receptor that estrogen interacts with can be either estrogen receptor alpha or estrogen receptor beta.
It is estrogen receptor alpha that is implicated in the disease process of breast cancer, whereas estrogen receptor beta is actually protective against breast cancer. In fact chemicals (whether natural, dietary or synthetic) that target or activate estrogen receptor beta actually prevent and fight breast cancer.
The metabolism (i.e. breakdown) of estrogen in the body can result in a combination of several different metabolites (products). Some of these metabolites offer protection against breast cancer, while others increase the risk and severity of breast cancer even more so than estrogen itself. Testing the ratio of these estrogen metabolites can indicate whether a person is at a greater risk of developing breast cancer. These ratios also influence the disease process of breast cancer. In part two, we will examine the factors that impact on estrogen metabolism, including genetic and epigenetic influences. We will also explore diet and lifestyle choices you can make to influence the ratio of estrogen metabolites.
If estrogen influences the majority of breast cancers to some degree, why then don’t all women develop breast cancer? Furthermore, genetic breast cancer accounts for only around 15% of breast cancer. So it is apparent that our genes and estrogen don’t act alone to cause breast cancer. It always depends on environmental factors (referred to as epigenetic factors) that allow estrogen to become problematic and / or genes to be triggered. We will discuss specific environmental (e.g. dietary and lifestyle) changes that can make a difference in part two, which will be published in the next issue of the magazine.
Written by Dr Cornelia Botha