Are soy products bad for breast cancer?

I have read the book "Anti Cancer - a new way of life" by David Schreiber, MD, PhD. I found this book very interesting and I can recommend it to anyone.

This is what he writes about soy;

"Some breast cancer patients have been advised NOT to consume soy-based products. In reality, the consensus in the scientific literature on this subject suggests that there is no dangerous effect from soy in breast cancer, aside from in certain experiments with dietary supplements in high doses, which is not advisable. It seems that soy consumed regularly (every day) may reduce the dangerous effects of xenoestrogens, especially when the soy is part of a diet rich in anticancer ingredients (green tea, cruciferous vegetables, etc) and is in normal quantities for food (avoid isoflavones suppliments). While awaiting more specific scientific data, the French Agency for Food Safety recommends that women who have had breast cancer restrict their consumption of soy to moderate amounts. (No more than one soy youghurt or one glass of soy milk a day.)

On the other hand, concentrated extracts of isoflavones sold as dietary supplement for use during menopause have been suspected of promoting tumor growth and should be avoided."

I took Estroven for about 4 years and I just learned it has isoflavones!  Little did I know.....

Two Places,  I was just watching a PBS show with Dr Schreiber.  I was surprised by your quote from his book because he definitely said that soy is full of omega 6.  Omega 6 stimulates inflammation and cell growth, including cancer cells.  He advised his audience to stay away from it for those reasons.  Confused....again.

My Onc. told me I should stay away from all soy products. His opinion is no one knows at this time in our culture if is good or not. I have decided I would rather side on the of no soy side.

2006 studies on soy are outdated.  A new study was released at the San Antonio breast conference

 Bee - done, if you stop "stalking".  All you do is disagree with everything I have every said.  Including quotations from my doctors.  I know what my personal circumstances are and you do not.  It is also strange how no matter where I post,,,,,you are there to disagree

As for acting so innocent - it was extremely uncalled for when you posted PM's that I sent to you.  There was no need to sink to that level, and the moderators seemed to agree since it was removed

PEACE

"Why can't someone figure out WHICH estrogens are actually making the attachments to the receptors? The pro-soy people say the phytoestrogens are protective of health because they are weaker than our own bodies estrogens, thus they lack the capacity to feed a tumor and they prevent a stronger estrogen from attaching to the receptor. How does anyone know which estrogens make the connection to the receptors? Has anyone looked? I'm totally not a science geek, but I don't think anyone has to be to see that there's a gaping hole here."

Althea, great questions!  I don't know the answer but here's what I think.  The soy studies seem to fall into two categories. There are those that are based on the consumption of soy within the diet of women and there are those that have been done on mice. Because heavy soy consumption over an extended period of years has so far tended to be an Asian phenomenon, the human soy studies so far have mostly come out of China. Most of the results have been favorable but the problem with those studies is that there are many other differences in the Asian diet & lifestyle vs. the west. Because of all the variables involved, it's impossible to directly correlate soy to the estrogen levels or breast cancer rates of the participants of the studies. So there is no way to know if the results are actually because of soy.  And there is no way to know if the results are applicable to those on a Western diet.  

With mice studies it's much easier to focus in on only the effect of soy and to see what the soy is actually doing within the body and to the estrogen levels.  In fact it's the mice studies that have shown that soy leads to an increase in breast cancer risk. The problem however is that nobody wants to make a definitive statement based on only mice studies and these mice studies are difficult it not impossible to replicate in humans. I think that's why doctors and dietitians in North America tend to be cautionary about soy (because of the mice studies) without being willing to take a clear stand. Of course, this is all just my speculation and frankly while I'm good at interpreting research, once we get into the details of what can be scientifically proven, I'm at a loss. So other theories are definitely welcome!

Sidebar: My apologies to all for taking this discussion off track; hopefully the discussion continues based on the main part of my post and not on this sidebar.  (Erica31/Daisy6, if I happen to post in the same thread as you it's not because I'm stalking you; it's because we have some of the same interests. I actually wanted to post in this thread when it first started up but I saw that you'd posted so, wanting to avoid a confrontation, I decided to not post here, despite my interest in the topic. But finally the discussion got to a point where I felt that I had some meaningful input so I decided to join in. Believe me, my posting here has nothing to do with your presence.  As for your saying that all I do is disagree with whatever you say, in fact on this topic you and I have been saying almost the exact same thing. Lastly, in the other thread the only reason I posted our PM exchange is because you wrote publicly that I'd sent you a nasty PM. I never did such a thing and in fact our single PM exchange about 2 years ago was actually very pleasant, so I posted that. The Mods did not delete that post; the Community deleted it after the Mods had come in and cleaned up the thread. I actually planned to delete that post myself since it was no longer relevant once your reference to my nasty PM had been deleted by the Mods however the Community beat me to it.  I would really appreciate it if you would please do everyone a favor and move on from this, not just here but across the whole discussion board. As I said the other thread, I have no interest in having a fight with you, but I will not let false accusations and lies about me stand unanswered. So now can we both just participate in a civil and interesting discussion about soy?) 

We are such complicated animals.

althea, here are the abstracts (or parts of the abstracts) from some of the mice studies. If you click on the links you will get the abstract and in most cases you'll also be able to access the full study.  I'd love to draw some conclusions about the type of soy etc. but honestly, this is way above my head!

• We have demonstrated that the isoflavone, genistein, stimulates growth of estrogen-dependent human breast cancer (MCF-7) cells in vivo (C. Y. Hsieh et al., Cancer Res., 58: 3833-3838, 1998). The isoflavones are a group of phytoestrogens that are present in high concentrations in soy. Whether consumption of genistein from soy protein will have similar effects on estrogen-dependent tumor growth as pure genistein has not been investigated in the athymic mouse tumor implant model. Depending on processing, soy protein isolates vary widely in concentrations of genistein. We hypothesize that soy isolates containing different concentrations of genistein will stimulate the growth of estrogen-dependent cells in vivo in a dose-dependent manner. To test this hypothesis we conducted experiments in which these soy protein isolates were fed to athymic mice implanted s.c. with estrogen-dependent tumors. Genistein content (aglycone equivalent) of the soy isolate diets were 15, 150, or 300 ppm. Positive (with 17β-estradiol pellet implant) and negative (no 17β-estradiol) control groups received casein-based (isoflavone-free) diets. Tumor size was measured weekly. At completion of the study animals were killed and tumors collected for evaluation of cellular proliferation and estrogen-dependent gene expression. Incorporation of bromodeoxyuridine into cellular DNA was used as an indicator of cell proliferation, and pS2 mRNA was used as an estrogen-responsive gene. Soy protein diets containing varying amounts of genistein increased estrogen-dependent tumor growth in a dose-dependent manner. Cell proliferation was greatest in tumors of animals given estrogen or dietary genistein (150 and 300 ppm). Expression of pS2 was increased in tumors from animals consuming dietary genistein (150 and 300 ppm). Here we present new information that soy protein isolates containing increasing concentrations of genistein stimulate the growth of estrogen-dependent breast cancer cells in vivo in a dose-dependent manner. Soy Diets Containing Varying Amounts of Genistein Stimulate Growth of Estrogen-dependent (MCF-7) Tumors in a Dose-dependent Manner
• Genistein, found in soy products, is a phytochemical with several biological activities. In the current study, our research focused on the estrogenic and proliferation-inducing activity of genistein. We have demonstrated that genistein enhanced the proliferation of estrogen-dependent human breast cancer (MCF-7) cells in vitro at concentrations as low as 10 nM, with a concentration of 100 nM achieving proliferative effects similar to those of 1 nM estradiol. Expression of the estrogen-responsive gene pS2 was also induced in MCF-7 cells in response to treatment with a concentration of genistein as low as 1 µM. At higher concentrations (above 20 µM), genistein inhibits MCF-7 cell growth. In vivo, we have shown that dietary treatment with genistein (750 ppm) for 5 days enhanced mammary gland growth in 28-day-old ovariectomized athymic mice, indicating that genistein acts as an estrogen in normal mammary tissue. To evaluate whether the estrogenic effects observed in vitro with MCF-7 cells could be reproduced in vivo, MCF-7 cells were implanted s.c. in ovariectomized athymic mice, and the growth of the estrogen-dependent tumors was measured weekly. Negative control animals received the American Institute of Nutrition (AIN)-93G diet, the positive control group received a new s.c. estradiol (2 mg) pellet plus the AIN-93G diet, and the third group received genistein at 750 ppm in the AIN-93G diet. Tumors were larger in the genistein (750 ppm)-treated group than they were in the negative control group, demonstrating that dietary genistein was able to enhance the growth of MCF-7 cell tumors in vivo. Increased uterine weights were also observed in the genistein-treated groups. In summary, genistein can act as an estrogen agonist in vivo and in vitro, resulting in the proliferation of cultured human breast cancer cells (MCF-7) and the induction of pS2 gene expression. Here we present new information that dietary genistein stimulates mammary gland growth and enhances the growth of MCF-7 cell tumors in ovariectomized athymic mice.  Estrogenic Effects of Genistein on the Growth of Estrogen Receptor-positive Human Breast Cancer (MCF-7) Cells in Vitro and in Vivo
• The estrogenic soy isoflavone, genistein, stimulates growth of estrogen-dependent human breast cancer (MCF-7) cells in vivo. Genistin is the glycoside form of genistein and the predominant form found in plants. It is generally believed that genistin is metabolized to the aglycone genistein in the lower gut. However, it is unclear if the rate of metabolism of genistin to genistein is sufficient to produce a level of genistein capable of stimulating estrogen-dependent breast cancer cell growth. Our hypothesis was that dietary genistin would stimulate tumor growth similar to that observed with genistein in athymic mice. To test this hypothesis, genistin or genistein was fed to athymic mice containing xenografted estrogen-dependent breast tumors (MCF-7). Mice were fed either genistein at 750 p.p.m. (parts per milllion) or genistin at 1200 p.p.m., which provides equal molar concentrations of aglycone equivalents in both diets. Tumor size was measured weekly for 11 weeks. At completion of the study, half of the animals per treatment group were killed and tumors collected for evaluation of cellular proliferation and estrogen-responsive pS2 gene expression. Incorporation of bromo-deoxyuridine into cellular DNA was utilized as an indicator of cellular proliferation. Dietary genistin resulted in increased tumor growth, pS2 expression and cellular proliferation similar to that observed with genistein. The remaining mice were switched to diets free of genistin and genistein. When mice were placed on isoflavone free diets, tumors regressed over a span of 9 weeks. Next, we examined how effectively and where metabolism of genistin to genistein occurred in the digestive tract. We present evidence that demonstrates conversion of genistin to its aglycone form genistein begins in the mouth and then continues in the small intestine. Both human saliva and the intestinal cell-free extract from mice converted genistin to genistein. In summary, the glycoside genistin, like the aglycone genistein, can stimulate estrogen-dependent breast cancer cell growth in vivo. Removal of genistin or genistein from the diet caused tumors to regress. Dietary genistin stimulates growth of estrogen-dependent breast cancer tumors similar to that observed with genistein
• Soy-based products consumed in Asian countries are minimally processed whereas in the USA many of the soy foods and soy ingredients are highly processed. Soy foods contain complex mixtures of bioactive compounds, which may interact with one another. The objective of this study was to evaluate the ability of various soy products containing genistin, the glycoside form of genistein, to affect growth of MCF-7 cells transplanted into ovariectomized athymic mice. Products investigated included soy flour, two crude extracts of soy (soy molasses and Novasoy®), a mixture of isoflavones and genistin in pure form. Each of the soy flour-processed products was added to the diet to provide equivalent amounts of genistein aglycone equivalents (750 p.p.m.). Tumors in the negative control animals regressed throughout the study while the tumors in the soy flour-fed animals remained basically the same size (neither grew nor regressed). In animals consuming soy molasses, Novasoy®, mixed isoflavones or genistin alone, tumor growth was stimulated when compared with animals consuming a control diet devoid of soy. These same dietary treatments resulted in increased cellular proliferation. Changes in mRNA expression of gene targets (estrogen responsiveness, cell cycle progression, apoptosis and aromatase activity) in tumors induced by the different diets were evaluated. The relative expression of pS2, progesterone receptor and cyclin D1 was increased in animals consuming the Novasoy®, mixed isoflavones and genistin. Bcl2 mRNA expression was low in most of the dietary treatment groups compared with positive (estradiol implant) controls. Aromatase expression was not affected in any of the treatment groups. The degree of soy flour processing affects the estrogenicity of products containing a constant amount of genistein. Collectively, these findings suggest that for postmenopausal women with estrogen-dependent breast cancer, the consumption of foods containing soy flour is more advisable than consuming isoflavones in more purified forms. Soy processing influences growth of estrogen-dependent breast cancer tumors
• We have demonstrated that genistein (GEN) stimulates growth of estrogen-dependent breast tumors in vivo. In this study, we evaluated whether dietary GEN can act in an additive manner with low circulating levels of 17β-estradiol (E2). We developed an E2 delivery system using silastic implants that yield low circulating plasma E2 levels similar to those observed in postmenopausal women....Further, we observed that these concentrations regulate the growth rate of MCF-7 breast tumors. Using this model, we demonstrated that dietary GEN in the presence of low levels of circulating E2 act in an additive manner to stimulate estrogen-dependent tumor growth in vivo. Results from this study suggest that consumption of products containing GEN may not be safe for postmenopausal women with estrogen-dependent breast cancer.  Genistein stimulates growth of human breast cancer cells in a novel, postmenopausal animal model, with low plasma estradiol concentrations
• In several epidemiological studies, a phytoestrogen-rich diet containing lignans and isoflavones is associated with reduced breast cancer risk, but experimental findings are controversial. In postmenopausal mammary cancer xenograft model, flaxseed (FS), a rich source of plant lignans, reduced breast cancer growth, while soy protein (SP), a rich source of isoflavones, enhanced it. The intake of phytoestrogens is increasing particularly among postmenopausal women, emphasizing the importance of elucidating their interactive effects on breast cancer. Our study determined the effect of FS and SP diets, alone and in combination, on the established human breast cancer MCF-7 tumor growth in ovariectomized athymic nude mice. Tumor bearing mice were divided into 4 groups and fed for 25 weeks either the basal diet (BD), or BD supplemented with 10% FS, 20% SP or 10% FS and 20% SP. After estrogen deprivation, FS regressed the tumor size similar to that of control. SP initially regressed the tumors but starting at week 13, the tumors regressed significantly less than in control and 43% of the tumors were regrowing until the end of the experiment and were significantly larger in size than in control. The combination of SP with FS reduced the tumor growth similar to that of control, as suggested also by the reduced tumor cell proliferation index. In conclusion, dietary FS did not stimulate the growth of estrogen responsive MCF-7 cancers in ovariectomized mice, while long-term consumption of SP did. Furthermore, FS reduced the tumor growth stimulating effect of SP to the same level as control, suggesting tumor growth attenuating effect of FS.  Flaxseed attenuates the tumor growth stimulating effect of soy protein in ovariectomized athymic mice with MCF-7 human breast cancer xenografts.
• This study determined the effect of the mammalian lignans enterolactone (ENL) and enterodiol (END) alone and in combination with the isoflavone genistein (GEN) on the growth of MCF-7 tumors in ovariectomized nude mice. Ovariectomized athymic nude mice with established MCF-7 tumors were fed a basal diet (AIN-93G) and divided into 5 groups that received daily subcutaneous injections (10 mg/kg body weight (BW)) of ENL, END, GEN, a mixture of these compounds (MIX), or vehicle as a negative control for 22 weeks. A positive control group was implanted with an estradiol pellet in order to establish an estrogenic tumor growth response. In the ENL- and END-treated mice, palpable tumors regressed significantly by 91 and 83%, respectively, resulting in final tumors that were similar to the negative control tumors. However, tumor cell apoptosis was significantly enhanced by the lignans. In the GEN-treated mice, tumors initially regressed significantly by 64% but regression ceased following prolonged treatment, resulting in final tumors that were significantly larger compared to negative control, ENL-, and END-treated mice, in part by increasing tumor cell proliferation. The MIX treatment significantly regressed palpable tumors by 87% similar to negative control group, with no effects on tumor cell apoptosis or proliferation. The isoflavone GEN alone promoted the growth of established MCF-7 human breast cancer xenografts after prolonged treatment while the mammalian lignans ENL and END did not. When these phytoestrogens were given in combination, no tumor growth-promoting effects were observed.  Mammalian lignans enterolactone and enterodiol, alone and in combination with the isoflavone genistein, do not promote the growth of MCF-7 xenografts in ovariectomized athymic nude mice
• Soy foods and nutritional supplements are widely consumed for potential health benefits. It was previously shown that isoflavone-supplemented diets, which contained equal genistein equivalents, differentially stimulated mammary tumor growth in athymic mice based on the degree of processing. This paper reports plasma pharmacokinetic analysis and metabolite identification using the parental mouse strain fed the same diets, which contained genistin, mixed isoflavones, Novasoy, soy molasses, or soy flour plus mixed isoflavones. Whereas the degree of soy processing did affect several parameters reflecting isoflavone bioavailability and gut microflora metabolism of daidzein to equol, stimulation of tumor growth correlated significantly with only the plasma concentration of aglycon genistein produced by the diets. This conclusion is consistent with the known estrogen agonist activity of genistein aglycon on mammary tumor growth. Conversely, plasma equol concentration was inversely correlated with the degree of soy processing. Although antagonism of genistein-stimulated tumor growth by equol could explain this result, the very low concentration of aglycon equol in plasma (12-fold lower relative to genistein) is inconsistent with any effect. These findings underscore the importance of food processing, which can remove non-nutritive components from soy, on the pharmacokinetics and pharmacodynamics of isoflavones. Such changes in diet composition affect circulating, and presumably target tissue, concentrations of genistein aglycon, which initiates estrogen receptor-mediated processes required for the stimulation of tumor growth in a mouse model for postmenopausal breast cancer. Soy processing affects metabolism and disposition of dietary isoflavones in ovariectomized BALB/c mice

Well, I just made the switch to almond milk. Not that bad, rather tasty! Now I'll wait and see if 5 years from now studies come out saying it causes cancer...

"So, the moral of the story - do the best you can with the best info you've got to work with to get the best outcome for yourself and your very individual body and most certainly mutated disease that is tuned to your very individual metabolism in order to obtain a quality of life that is worth living while existing in tandem with breast cancer."  

Lowrider, Well put!  I agree completely!!  I'm analytical by nature so I like to dig through the research but the one thing I know for sure after spending 5 years digging through BC research is that everything we know or believe today is subject to change tomorrow!  So do what you feel is right for you and move on from there.

althea, yeah the research was a bit much for me too.  I did skim a couple of the full reports - there was more there than I ever wanted to know about the effects of soy on prepubescent mice. The full reports go into a level of detail that I'm sure is meaningful and important to the scientists but it makes my eyes glaze over.  I will say that my conclusion on the type of soy used would be different than yours.  I think for the purity of the experiment, they would use the most pure soy compounds that they could.  And if they wanted to test the impact of genetically modified soy, that would be specifically noted. So my guess is that these experiments were done using organic soy.

Reading the detail on the studies I can certainly see how these would be impossible to replicate with humans. And that's part of what makes this such a complicated issue.

My naturopath oncologist said the same thing about the "good soy" being okay.  I also read Schreiber's "Anti Cancer" book and feel comfortable eating soy in moderation (edamame, tofu, etc maybe a couple times a week.. but not daily).

Personally, I also totally agree with Lowrider's "moral to the story". 

Maybe they kept the baby male hamsters in a cold cage? .

(edited to change to hamsters from my assumed mice)

The fact that soy is already in so much of our food is kind of the point! We are already getting it in so many places, why add more?

Beesie,

First, I referenced my sources for the soy story (The large scale study, the links below, and some of it I also found on this website, www.breastcancer.org). Also, no, I'm not here to promote my site. I'm here to make friends, get and give information.  I do share whatever information  I have on the topics at hand, most of what is links to other organizations' websites.But definitely if I have written on  something of relevence to the folks I talk to, I include it too. I also don't accept revenue of any kind for my site. It's  something I do to try and help the people who are helping me with whatever I found that I can use it to be constructive. I'm a writer of 25 years, mainly health.  Doing this has enabeld me to bring  something good from my breast cancer diagnosis.

BTW Bessie,

 I didnt answer all your questions on the Soy Debate article I posted.Were you pointed out the "May" and Possibly" terminology on the study. Yes, you are so right, it's all inconclusive. We see that by all the data the women on this site are pulling up. That's the whole point; nonconclusive though most of the data is leaning toward natural soy from whole foods. And yes, you can still have a "bottom line." The bottom line i,s based on the data it looks like natural soy from whole foods in moderation is safe. A messatge in there for premenopausal women too.

 I'd love to be able to  wait for definite proof before making my decisions about how to keep fighting cancer. But if we waited for proof and made no  decisions until we had it, we'd be hanging in the rafters all our lives on most of the issues.