The human body manufactures estrogen as a necessary component in many processes; estrogen is always in the body, even in postmenopausal women. Copper, too, is always in the body and is another example of something that can distort the way genistein behaves in a test tube.39 Researchers at the University of California, Davis, recently did the same test tube study on genistein and produced the same negative results. They then put genistein in a test tube with the cancer cells and environmental estrogens. The result showed that genistein suppressed cancer cell growth.40 These studies on pure genistein, however, do not accurately reflect what occurs in a complex environment such as the human body.
Fortunately, the safety of soy isoflavones (including genistein) for human consumption has been confirmed by experiments with monkeys, the experimental model closest to humans.41 Monkeys treated for three years with soy or soy minus its isoflavones exhibited no abnormal cell growth; in fact, the result was just the opposite. The researchers concluded, “These findings suggest that high dietary levels of soy isoflavones do not stimulate breast or uterine proliferation in postmenopausal monkeys and may contribute to an estrogen profile associated with reduced breast cancer risk.” In addition, a new study clarifying the estrogenic effects of genistein on the uterus found that genistein may enhance cell growth for a few days, but then the effect stops. This is a new finding, and the results are different from those for estrogen drugs that perpetuate growth indefinitely.42 With any luck, issues surrounding how genistein behaves will be soon resolved.
It is important to remember that genistein also blocks the growth of estrogen-receptor-negative breast cancer cells. By incorporating soy and isoflavones in her diet, a woman can potentially stop breast cancer before it develops.43 The one caveat is that genistein may interfere with tamoxifen, and thus should not be taken by itself with that drug.44
One of the most exciting new findings is that genistein keeps amyloid from killing brain cells (without any negative effects on uterine cells), and has been suggested as an alternative to synthetic estrogens for the prevention ofAlzheimer’s disease.45 Studies of the popular estrogen drugs Premarin® and Prempro™ show that they may actually increase the risk of dementia.46
Everybody knows that vegetables are good for you, and they are especially good for women who want to avoid breast cancer. Vegetables enable the body to rid itself of excess estrogens. Meat eaters have about 50% more estradiol and estrone in their blood than do vegetarians.47 Women who eat the most vegetables, beans such as lentils, and fiber reduce their risk of breast cancer risk by 50%.48 As you will read next, compounds found in vegetables favorably affect the way estrogen behaves in the body.
The way estrogen is metabolized is critical to how it behaves. Fortunately, we can do more than cross our fingers and hope for the best. Certain compounds found in plants turn harmful estrogen into a more beneficial version. Chief among them is indole-3-carbinol (I3C), a phytochemical found in cruciferous vegetables such as broccoli. In China, where the risk of breast and prostate cancers is minuscule, consumption of cruciferous vegetables is more than three times that of the US.49
I3C helps convert “strong” estrogens into benign or even helpful estrogens such as 2-hydroxyestrone.50,51 It also acts very much like tamoxifen in blocking undesirable estrogenic effects in breast cancer cells, and its antiestrogen effects are enhanced with genistein.52
When digested, I3C is converted to other substances, including diindolylmethane (DIM). Some earlier research suggested that I3C’s beneficial effects were due to DIM. New research shows this is not the case, and that there are important differences in the effects of I3C and DIM on the metabolism of estrogen. Researchers recently stated, “This finding [of I3C’s effects] is inconsistent with the claim that DIM is the biologically active metabolite of I3C with regard to its antiestrogenicity.” DIM does not increase beneficial 2-hydroxylation of estrogen (at least in rats), but it does lower harmful 4- and 6-hydroxylations.53 By contrast, I3C, which partially converts to DIM during digestion, affects all three in a positive way. Moreover, DIM does not have the anti-estrogen effects of I3C.54
Another potential supplement for breast cancer prevention that has drawn a lot of interest is melatonin. Melatonin is associated with sleep because it builds up during the night, but it may ultimately end up being more associated with estrogen than with sleep. Studies show that melatonin plays a major role in how estrogen behaves. In estrogen-receptor-positive breast cancer cells, melatonin can bring cell growth to a halt.55 Research indicates that melatonin controls estrogen, and vice versa.55-57 In studies of rodents, melatonin shows great promise with regard to its ability to prevent breast cancer when given continuously, before and after exposure to a carcinogen, and when given to mice with the HER2/neu genetic alteration.58,59 Researchers have been unsuccessful in correlating blood levels of melatonin with breast cancer.60 This reflects melatonin’s complexity as a hormone that, like estrogen, comes in various forms and has several receptors. Without a doubt, melatonin plays a major role in breast cancer through its effects on estrogen and other cancer-related phenomena.
As an antioxidant, melatonin is not only powerful but also unique. Unlike vitamin E, which essentially has no further effects after it scavenges a radical, when melatonin gets a radical, it creates a new melatonin antioxidant; that is, it self-perpetuates. It also cooperates with other antioxidants like vitamins C and E.61 Antioxidants are very important in preventing cancer, and it has been reported that free radicals can activate or deactivate genes that are involved in breast cancer.62
In addition, melatonin may suppress cortisol, which is a stress-related hormone.63,64 It is interesting to note that the overwhelming majority of breast cancer patients say stress caused their disease.65 In a study of older women, 2 mg of melatonin per day reduced estradiol levels, enhanced sleep, and improved levels of DHEA.66 Melatonin is very potent, and as little as 0.3 mg per day may be enough to produce beneficial effects.
Breast cancer is a serious concern for most women. Understanding that there are different types of estrogen, that different estrogens have different effects, and that women can, to a certain degree, control their own estrogen (through dietary modification and supplement use) will help women make informed choices about estrogen exposure and reduce their risk of breast cancer. Recent discoveries about estrogen receptors and how they interact may finally unlock the mysteries of how estrogens work, and provide the basis for nontoxic treatment and effective prevention.
According to the Breast Cancer Fund, a woman’s risk of contracting breast cancer was 1 in 22 in the 1940s. Today, it is 1 in 7. There is no end to the theories as to why this risk has increased. “Endocrine disrupters” (chemicals that mimic hormones) are a likely suspect. They are wreaking havoc on wildlife and clearly affect brain cells in the developing embryo.67 So far, however, studies have failed to show a link between breast cancer and blood levels of these chemicals. Still, they remain suspect—especially in combination with other factors.
Mainstream dogma is that exposure to estrogen causes breast cancer. By “estrogen,” the mainstream means the body’s own estrogens. This line of thinking always links variables (such as having/not having children or the age at which menopause occurs) to estrogen exposure and, hence, breast cancer risk. While this viewpoint appears to have some validity, a few things are wrong with it, including the thorny question of why, all of a sudden, exposure to something that has been a part of the human body for eons would cause cancer. It also skirts the question of why long-term use of birth control pills containing estrogens does not increase the risk of breast cancer.68
Genes are another possible explanation for breast cancer. This depressing theory implies that whether or not people get breast cancer is beyond their control and that nothing can be done about it, except having the breasts removed as a preventive measure.69 New research may put an end to the notion that there is nothing a person can do about “bad genes.”
“Bad genes” do not necessarily come from parents. Sometimes they come from the environment. Eighty-five percent of the “family risk” for breast cancer may come from something besides an inherited gene.70 Moreover, it has now been discovered that there are genes that can modify “bad genes.”71,72 In other words, you may not have to live with “bad genes.”
In addition, a new study shows that even if a person has a genetic predisposition toward breast cancer, the cancer does not necessarily activate unless the person encounters something in the environment that activates it.73 For some women, that “something” could be meat. For the first time, eating meat has been linked to genes and breast cancer.73 Families tend to share not only genes but recipes as well, and it is becoming clear that what you eat may be more important than what you were born with.
In studies that search for the cause of breast cancer, certain things consistently emerge. One is that diets rich in vegetables, soy, and green tea reduce cancer risk, and diets rich in animal fats (especially from red meat) increase risk.73-79 In a study from the Barbara Ann Karmanos Cancer Institute at Wayne State University in Detroit, beef, pork and vegetables accounted for 85% of the alterations to DNA in women, with meat causing damage and vegetables preventing it.80 Damaged DNA lays the groundwork for cancer.
The case of red meat is interesting not only because cooking it creates carcinogens, but also because the use of hormone implants in cows (which dates back about 50 years) coincides with the beginning of a major increase in breast cancer in North America.81 Countries with the highest rates of breast (and prostate) cancer also are the countries that allow such implants. North America’s breast cancer rate is the world’s highest—higher than all of South America and northern and southern Europe combined.82 Australia and New Zealand, which allow hormones to be implanted in cattle, have similarly high rates of breast cancer. In Europe, such implants are banned.
It is not hard to figure out why. Cattle implants contain 17 beta-estradiol and other strong steroids, including synthetic estrogens. Cows are repeatedly implanted, and the implants are in the cows when they are slaughtered. Guidelines published by the US Department of Agriculture and the University of Nebraska advise implanting the strongest drug last, 70 days before slaughter.83 The strongest implants last 90-120 days. Besides being in the cows at the time of slaughter, over time the hormones build up in fat.84 Fifty percent of the hormones contained in a steak may be in the fat.84 Neither the FDA nor the USDA monitors the use of hormone implants, or tests for residues in beef. Testing for the metabolites of estradiol alone would be a major undertaking, as there are more than a dozen such metabolites, and this is just one estrogen. Cows are given other hormones as well, including “male” hormones. Heifers are fed melengesterol acetate, a synthetic progesterone used for birth control and promoting rapid weight gain.
It has been demonstrated that a diet high in beef fat activates hormone-related genes.85 Zeranol, a synthetic estrogen cow implant, causes breast cancer cells to grow in the test tube. The amount of Zeranol needed to cause this growth is 30 times less than the amount that the FDA deems to be safe.86 A follow-up study being conducted at Ohio State University hopes to ascertain how much Zeranol ends up on the dinner plate and in the tissue of women with breast cancer.87 The study, which began in 2002, is still in progress. Data from approximately 200 women have been collected and are being analyzed. This important study may shed some light on at least one hormone implant. Studies on the total amount of all hormones added to American beef have yet to be conducted.