Whole-Food Guide for Breast Cancer Survivors (20 page)

10.
Hormone Harmony

We are indebted to Dr. Jonathan Wright for his groundbreaking work on women’s hormones and for allowing us to use his writings (wrightnewsletter.com) to express key concepts in this chapter.

Chapter Goal: Balance your hormones

It seems as if every day, we hear more bad news about estrogen. Both medical journals and the popular press warn us about its dangers. In fact, after derogatory news about pharmaceutical hormone replacement emerged from the Women’s Health Initiative in 2002, both the study and millions of women’s prescriptions were abruptly halted (NIH 2002). Moving farther into the second decade of the century, the subject of hormone replacement remains a source of intense controversy.

As we dig deeper, we find a more nuanced story: it is not estrogen itself that is the problem; it’s the type of estrogen to which we’re exposed, how it is metabolized by the body, and how it dances with progesterone and other hormones that matters (Kabat et al. 2006). In this chapter we’ll look closely at the facts, not the hyperbole, to help you sort through the evolving story surrounding this contentious hormone.

Meet Your Estrogens

While many of us have traditionally thought of estrogen as a single hormone, it is actually a family of hormones comprising several distinct molecules that the body secretes naturally, the most well known of which are estrone (E1), estradiol (E2), and estriol (E3). Along with progesterone, testosterone, 5-dehydroepiandrosterone (or 5-DHEA, commonly known as DHEA), and corticosteroids, estrogens are in the steroid group of hormones that are all made from the same basic building block: cholesterol.

Of the three plentiful forms of estrogen just mentioned, estradiol is the most potent. Primarily a growth hormone, estradiol shapes tissue growth in the vagina, breasts, endometrium, fallopian tubes, ovaries, bones, and, of course, the developing fetus. Before menopause, most of your estradiol is produced by the ovaries, with lesser amounts produced by the adrenal glands, the liver, and the breasts. Fat cells also secrete estradiol; hence heavier women tend to carry it in greater concentrations.

Estrone, a weaker estrogen derived from estradiol in the liver, serves as a backup form of estrogen. Although we stop manufacturing most estradiol after menopause, the adrenal glands continue to produce estrone after menopause and for the rest of our lives.

The third key estrogen compound, estriol, plays
its
pivotal role during pregnancy, when levels of this “weak” estrogen start to soar. Although scientists have considered estriol to be too weak to be relevant except during pregnancy, it now appears that this “weakness” might actually be its strength.

One study (Siiteri et al. 2002) that suggested this was conducted in Berkeley, California, where researchers examined frozen blood samples of fifteen thousand women who had been pregnant forty years earlier. They found that of all the study subjects, those with the highest levels of estriol relative to other estrogens during pregnancy had the lowest occurrence of breast cancer. Specifically, women with the
highest
level of estriol during pregnancy had a 58 percent
lower
risk of developing breast cancer than the women with the
lowest
estriol levels. It’s noteworthy that during pregnancy, estriol levels climb enormously, by one thousand times or more. Even after childbirth, estriol levels usually remain higher than they were before pregnancy.

To summarize, it’s clear from the data that all estrogens are not the same. And it gets even more interesting than that.

The “Daughter” Metabolites: E2, E4, E16

Over the last three decades, with evolving interest and tools, researchers have been paying fresh attention to an additional family of estrogen complexes. We might call them “daughter” metabolites because they are the estrogen by-products that emerge after estradiol, estrone, and estriol are processed, or detoxified, by the liver. The technical terms for these by-products are 2-hydroxyestrone (2-OHE), 4-hydroxyestrone (4-OHE), and 16α-hydroxyestrone (16α-OHE), and together they give us a very clear picture of whether the amounts and types of estrogen in your body are apt to cause trouble.

Once the body uses estrogen, like everything else, the estrogen heads to the liver for detoxification. Properly metabolizing and excreting estrogens, the essence of detoxification, is a critical but tricky task. If the estrogens are metabolized into 2-hydroxyestrone, they lose most of their aggressive activity; thus they are known as “good” estrogen metabolites. Research indicates that when levels of 2-hydroxyestrone are higher, the body resists cancer, and when these levels are low, cancer risk increases (Gaikwad et al. 2008). On the other hand, women who metabolize a larger proportion of their estrogens into 16α-hydroxyestrone and 4-hydroxyestrone show an elevated risk of breast cancer (ibid.).

Why would the liver use a pathway that could lead to adversity? Recall from chapter 9 that gut and liver health are intimately tied to estrogen metabolism. A liver that is compromised by toxicity, alcohol, or estrogen overload from environmental sources (see chapter 4), for example, will not do as good of a job at clearing out excess estrogen as a liver that’s at the peak of health. Likewise, a healthy population of gut bacteria actually helps to detoxify excess estrogen (via the containment of an enzyme called
beta-glucuronidase
). In effect, these desirable microbes provide the “bugpower” to help carry excess estrogen out of the body.

Where’s the proof? Examining this premise in context, among 10,786 premenopausal women studied in the 1990s, researchers observed that women who developed breast cancer had notably less 2-hydroxyestrone—a full 40 percent less—and more 16α-hydroxyestrone metabolites than women who did not develop breast cancer (Muti et al. 2000). Another study, this one on postmenopausal women, found that those with the highest ratio of estradiol to 16α-hydroxyestrone had a 30 percent lower risk of developing breast cancer than women with lower ratios (Meilahn et al. 1998). If we could only find a way to make sure the liver is turning out healthy estrogen metabolites, as opposed to unhealthy ones, we could lower our breast cancer risk. It turns out that we can, and we’ll get back to that part of the estrogen story shortly.

What Else Affects Our Estrogen Load?

To reiterate, it’s not estrogen per se that is the problem for women. Estrogen has played a vital role in reproduction and female well-being since the beginning of humanity. But the amounts of estrogen that our bodies need to metabolize, as well as the types of estrogen that proliferate in excess, have steadily expanded in the chemically laden, hyper-estrogenic world of the twenty-first century.

As we discussed extensively in earlier chapters, animal estrogens from factory-farmed meat and dairy products, plus xenoestrogens from chemicals, plastics, pesticides, and other contaminants, can wreak havoc with our balance of
natural
estrogens. Estrogen also dances with other hormones, and the nature of the dance can influence breast-cancer risk in an equally dramatic way.

ESTROGEN AND PROGESTERONE

Progesterone is a steroid hormone produced in the ovaries that is essential for normal breast development during puberty, for regulating the menstrual cycle, for maintaining a pregnancy, and for preparing for lactation and breastfeeding. While estrogen is the hormone that stimulates cell growth, progesterone is the hormone that inhibits growth, induces cell maturation, and initiates programmed cell death (apoptosis).

In his first book on natural progesterone, the late Dr. John Lee (2001) explains how “estrogen dominance” can affect women who have any amount of estrogen but have little or no progesterone to balance the effects of estrogen in the body. Please note that while synthetic progesterone (progestin), such as that used in the illustrious Women’s Health Initiative study mentioned earlier, is considered to be carcinogenic, natural progesterone is thought to be protective; in fact, many researchers agree that healthy levels of progesterone in the body may actually help protect you against breast cancer (Jerry 2007).

But as we grow closer to menopause, our progesterone levels begin to wane, a decade or even more before estrogen wanes. Here is where the state of estrogen dominance becomes apparent: our bodies make too little progesterone in relationship to estrogen. Not surprisingly, this is when we become most susceptible to breast cancer. Also not surprisingly, this is when many women begin talking to their doctors about supplementing with natural progesterone.

ESTROGEN AND THYROID HORMONE

The thyroid gland and estrogen share a close and somewhat complicated relationship. As on a seesaw, when one part is out of balance, it can readily throw the other one off as well. For instance, while an increase in estrogen does not lower production of thyroid hormones, it does cause a chain reaction that renders thyroid hormones less active. Fortunately, millions of women have been helped by research completed back in 1964, which established that adequate thyroid hormone helps estradiol metabolize more completely into the “good” estrogen metabolite, 2-hydroxyestrone (Fishman et al. 1965). Indeed, many, but not all, studies indicate that having an underactive thyroid slows the process of clearing estrogen from the body, thus creating a state of estrogen dominance, a known risk factor for breast cancer (Vasudevan, Ogawa, and Pfaff 2002). Clearly, this is an area that requires significantly more research and analysis. As always, we believe that balance is key: a thyroid gland that works properly—that is neither hyperactive nor hypoactive—will help keep the rest of your metabolism in balance. That is our goal!

ESTROGEN AND MELATONIN

Sleep habits also influence estrogen levels. Melatonin, the “sleep hormone” that we produce when we sleep in complete darkness, helps reduce excessive estrogen production. By simply sleeping in a completely dark room (and avoiding working night shifts, if possible), you take another powerful step in keeping your estrogen levels under control.

ESTROGEN, OBESITY, AND INSULIN

The current obesity epidemic has taken a toll on our hormonal balance, as reported in numerous journals over the past decade, including the
New England Journal of Medicine
(Yager and Davidson 2006) and the premier medical journal of the United Kingdom, the
Lancet
(Bianchini, Kaaks, and Vainio 2002). As we discussed in chapter 6, obese women have a higher risk of developing breast cancer for a variety of reasons. One key factor underlying this higher risk is an elevated level of circulating estrogens that is linked to greater amounts of adipose (fat) tissue. Adipose tissue serves as an additional site for estrogen production.

But there’s another hormone at play here as well. The liver produces a hormone called
sex hormone–binding globulin
(SHBG), which carries sex hormones around the body and regulates their access to tissues. In women, SHBG has a special affinity for estradiol; that is, the more SHBG we have, the more estradiol is “bound up.” This is, by and large, a good thing.

Obese women have lower levels of SHBG, making more estrogen available to breast tissue. Perhaps most ominously, research published in the
Journal of Clinical Investigation
showed that a high-fructose diet (containing high-fructose corn syrup, for example, present in virtually all processed foods and beverages) decreased levels of SHBG in the liver by a whopping 80 percent, resulting in higher levels of circulating estrogen (Selva et al. 2007). Fortunately, a foundational Eating for Health plan, plus the specific suggestions in chapter 6, will go a long way toward helping manage excess weight and insulin, and, in the process, controlling levels of estrogen and SBGH. We’ll provide several suggestions for lowering estrogen load later in this chapter.

Assessing Your Status

Dr. Jonathan Wright, medical practitioner since 1973 and author or coauthor of twelve health books, including
Stay Young and Sexy with Bio-Identical Hormone Replacement
(Wright and Lenard 2010), was the first to introduce an integrated, balanced pattern of bioidentical hormones for women, in the early 1980s. He has been prescribing, researching, and writing about them ever since. In fact, much of what we know about the various forms of estrogen and their actions in the body is due to his exhaustive investigation on the issue. Here’s what he has to say about assessing estrogen-related cancer risk.

First, Dr. Wright recommends a look at the “EQ” or
estrogen quotient
, a ratio first described by Dr. Henry Lemon of the University of Nebraska medical school. The EQ is the relationship of estriol to estradiol and estrone. The higher your EQ, mathematically derived as E3/(E1+E2), the better. Dr. Lemon, the originator of the EQ test, and colleagues (1966) tested estriol along with estrone and estradiol by having women collect their urine for twenty-four hours and then measuring the hormone levels in the specimens.

With the authorization of a doctor, nutritionist, or other health professional, the testing kits can be mailed to you at home, where you collect your specimen and send it back to the lab. Remember, it’s not the absolute amount of estriol that appears to be the most important number, but the relative amount of estriol compared with the sum of estradiol and estrone. According to Dr. Wright (2005), “In today’s environment, with the amount of estrogen-mimicking carcinogens increasing dramatically, it’s more important than ever to keep your level of estriol as high as possible. So I don’t see any reason why we shouldn’t…shoot for an EQ of 1.0 or above.” Interestingly, Dr. Wright also discovered that iodine raises the EQ for nearly all women.

The second test Dr. Wright recommends is commonly called the "
2:16
," referring to the relationship of the estrogen metabolites we discussed earlier (2-hydroxyestrone and 16α-hydroxyestrone). Testing the 2:16 ratio can be done separately or along with the EQ. You definitely want more “good” (2-hydroxyestrone) estrogen than “bad” (16α-hydroxyestrone) estrogen—substantially more if possible; any ratio below 1.0 is unfavorable. Although there’s no consensus concerning the ideal ratio, Dr. Wright recommends 2.0 or greater, if possible. This lab test will also report on your level of 4-hydroxyestrone, which also appears to have carcinogenic tendencies, as well as your level of another metabolite known as 2-methoxyestradiol, an extremely potent, natural anticarcinogenic form of estrogen made by all women’s bodies. For information on where to obtain these lab tests, refer to appendix B.