To Soy Or Not To Soy, Part 2
Many survivors of hormone-driven cancers are being told to avoid soy at all costs. We’re taking a closer look at the widespread idea that soy is a no-no after cancer. In part 1, we discovered that
Many survivors of hormone-driven cancers are being told to avoid soy at all costs. We’re taking a closer look at the widespread idea that soy is a no-no after cancer.
In part 1, we discovered that there are a number of substances, synthetic and natural, whose structure is similar to estrogen. This similarity of structure allows them to bind to estrogen receptors and potentially initiate estrogen-like activity within cells. Some of these substances, such as PCBS, phthalates or synthetic estradiol used in hormone replacement therapy, have been linked to undesirable health consequences, such as unnaturally early puberty and increases in female cancers.
Based on these results, it would be easy to assume that any substance known to bind to estrogen receptors, like the isoflavones in soy, should be avoided after diagnosis of a hormone-based cancer.
But is it that a valid conclusion?
To decide, let’s go where even the most conservative doctors go to inform their decisions. What does recent research say about the effect of soy consumption in survivors of hormone-based cancers?
Here are highlights from some large recent studies which specifically examined the effects of soy on breast cancer recurrence and survival:
- A 2009 study that followed over 5,000 breast cancer survivors for an average of 4 years found that regular soy intake was associated with up to 32% lower risk of breast cancer recurrence and up to 29% lower breast cancer mortality (depending on quantity of soy consumed) as compared to women who didn’t eat soy. This association held for ER+ or ER negative cancer, and for both users and nonusers of Tamoxifen. (Journal of the American Medical Association (JAMA), 2009) 1
- A 2010 study of 524 breast cancer survivors, followed for an average of 5 years, found risk of recurrence for postmenopausal women in the highest quartile of soy consumption was 33% lower than those who ate the least soy. This protective effect of soy was observed in women with estrogen and progesterone positive disease and those taking anastrozole (Arimidex) This study found no significant effect either positive or negative in premenopausal women: no benefit, but no harm either. (Canadian Medical Association Journal 2010) 2
- A 2012 analysis combined the data from three major studies of Chinese and American invasive breast cancer survivors (total of 9514 women, followed for an average of 7.4 years). Post-diagnosis soy consumption of >10 mg isoflavones/day was associated with a 25% reduced risk of cancer recurrence as well as a slightly reduced risk of all-cause and breast cancer mortality. (American Journal of Clinical Nutrition 2012) 3
The best available evidence to date demonstrates that dietary soy is at best significantly protective, and at worst not harmful to breast cancer survivors.
The mechanism of soy’s protective effect is not yet fully understood, and is the subject of much current study. But consider this: in part 1 I asked why your body produces both strong (estradiol) and weak (estriol) variants of estrogen. We know that estradiol, while a critical initiator of essential bodily processes, has the potential to drive cancer development if not sufficiently checked. Your body has the ability to increase and decrease estradiol production as needed, but there are many factors that can dysregulate this production “schedule”. As such, your body has developed another way to protect you. It maintains a large amount of circulating estriol, the weaker form of estrogen, that can plug into estrogen receptors and prevent excess estradiol from negatively affecting cell behavior.
And soy? It may look like a duck, but it doesn’t quack like a duck. Soy’s effect on estrogen receptors is weak, like that of estriol. When soy occupies estrogen receptors it doesn’t amplify harmful estrogenic activity, but instead protects you by blocking the activity of the real culprit: estradiol.