Dear Dr. Shani,
I’ve been told to avoid soy at all costs since breast cancer treatment, because it could encourage the return of my cancer. What’s the problem with soy? Is it really a cause of cancer?
To answer your question, let’s first look at how estrogen works in your body. Then we’ll look at whether eating soy after cancer is a problem.
Estrogen is produced by your ovaries, adrenal glands and fat tissue. It can also be produced by converting testosterone to estrogen, especially in men and in post-menopausal women.
Estrogen, a steroid hormone, is naturally produced in 3 forms: estrone, estradiol and estriol.
- Estradiol is by far the most potent of these three forms.
- Estrone is a less abundant and less potent “reserve” form of estradiol: it can be converted to estradiol if needed.
- Estriol is a breakdown product of estrone that also has the ability to bind to estrogen receptors. Estriol is typically far more abundant in the body than the other two types of estrogen. It is only about a quarter as potent as estradiol.
(At this point ask yourself: why would your body naturally produce three forms of estrogen, rather than just one?)
Once produced, estrogen is released to circulate in your blood, most often bound to a carrier protein called sex-hormone binding globulin (SHBG). It’s released by SHBG at various tissues, where it floats easily through cell membranes and binds to receptors specially shaped to accommodate estrogen molecules. Bound to its receptor, estrogen can enter the nucleus of the cell, where it affects the behavior of genes in hundreds of ways.
In your body’s native state, estrogen’s influences on cell behavior are constructive. (Your body wouldn’t produce estrogen if it wasn’t beneficial to your wellbeing.) Estrogen triggers maturation of female reproductive organs and regulates their functioning throughout life. It also strengthens your bones, keeps your skin and membranes moist and pliable and exerts a healthful influence on your cardiovascular system.
So when does estrogen become the “bad guy”?
Excess binding of estradiol – the most potent form of estrogen – is a key mechanism behind the formation of estrogen-positive breast cancers, uterine and ovarian cancers (and even some prostate and lung cancers). That’s why current drug therapies aimed at preventing recurrence of these cancers aim to interrupt this activity in one of two ways:
- by reducing the amount of estradiol your body produces (Arimidex, Aromasin or Femara)
- by blocking the binding of estrogen to estrogen receptors (selective estrogen receptor modifiers or SERMs, such as Tamoxifen and Faslodex).
But what causes excessive estrogen activity in the first place? Key reasons uncovered in recent years include:
- Obesity: since adipose (fat) cells produce estradiol, one consequence of today’s obesity epidemic is dangerously high production of estradiol.
- Drugs that affect hormonal activity: especially synthetic forms of estrogen used in hormone replacement therapy.
- Widespread exposure to xenoestrogens: xenoestrogens are chemical compounds with the ability to bind to estrogen receptors and potentially mimic estrogen’s effects on gene behavior. Examples are PCBs and phthalates found in soft plastics, whose amplification of estrogen activity has been linked to the rising incidence of unnaturally early puberty. There are also some naturally-occurring plant-derived xenoestrogens: some components of soy have the ability to bind to estrogen receptors.
Does that mean soy is dangerous for cancer survivors? Come back for part 2 to find out.