Soy will not interfere with Tamifoxen

[Guest guest]

The issue with soy, is not that it "may" be a GM food, it most certainly "often is" a GM food. Suspicion is aroused because so many people oppose, and so many peope support soy. What is needed is for a large number of highly qualified nutritional experts to make their opinions concerning soy, known to readers.

 

-

June Black

Wednesday, July 26, 2006 7:19 AM

Re: Soy will not interfere with Tamifoxen

 

 

 

Please Read book written by Jane Plant "Your Life In Your Hands" It is a good book but I am allergic to soy. She won the battle against breast cancer but I still think soy is dangerous mainly for the fact that it may be a GM food.

June

 

 

 

-

Parhatsathid Napatalung

Tuesday, July 25, 2006 9:47 PM

Soy will not interfere with Tamifoxen

 

 

Should Women with Breast Cancer Eat Soy? by Mark Messina, Ph D Introduction There is probably no more controversial area relatedto the health effects of soy than the relationshipbetween soy intake and breast cancer risk. Concernover the possibility that soy consumption couldactually stimulate breast tumor growth has led to muchconfusion among oncologists and other healthprofessionals, and to frustration and eventrepidation, among breast cancer patients. This isparticularly ironic, because unarguably, it wasexcitement over the hypothesized anticancer effects ofsoy, an area first funded by the National CancerInstitute in 1991, which initially drew attention tothe health effects of soyfoods (1). This articleattempts to briefly highlight those studies mostpertinent to this controversy so that dietitians arebetter able to advise their clients about this issue. Background The low breast cancer mortality rates insoyfood-consuming countries, particularly Japan,combined with the knowledge that weak estrogens, suchas the soybean isoflavones, can exert antiestrogeniceffects in some situations, logically led tospeculation that soy might reduce breast cancer risk.Isoflavones, which are found in nutritionally relevantamounts only in soybeans, have a similar chemicalstructure to estrogen but have traditionallybeenconsidered to be weak estrogens. Early support forthe protective effects of soy against breast cancercame in the form of an animal study published in 1990,which reported that rats fed diets containing soydeveloped approximately 50% fewer chemically-inducedmammary tumors than control rats (2). One year later,a case-control study conducted in Singapore reportedthat soy intake was associated with an approximate 50%reduction in premenopausal breast cancer risk (3). The Case Against Soy There is a clear consensus that greater lifelongexposure to estrogen increases breast cancer risk. Theestrogen- like properties of soybean isoflavonestherefore provide a basis for concern about soyconsumption by breast cancer patients. In fact,although often overlooked, early on it was establishedthat at low concentrations, genistein, the mainisoflavone in soybeans, actually stimulates the growthof estrogen-receptor positive (ER+) breast cancercells in vitro (4). The growth of ER+ breast cancercells is stimulated by estrogen. Breast cancerpatients can have a mix of estrogen receptor negative(ER-) and ER+ cells, but typically, one type of cellpredominates and this determines treatment (5). ER+breast cancer patients respond well to tamoxifen, anantiestrogen, which is the most widely prescribedbreast cancer drug (6). Survival rates of ER+ breastcancer patients generally exceed those of ER- patients(7,8). Genistein does not stimulate the growth of ER-cells, and at high concentrations, the growth of bothER+ and ER- cells is inhibited by genistein (9). Theproposed explanation for this biphasic effect is thatat low concentrations the estrogenlike properties ofgenistein stimulate growth, whereas at higherconcentrations, the ability of genistein to influencemolecules that control cell growth, differentiation,and survival, results in growth inhibition. However,it is the lower concentrations that more closelyreflect the serum genistein concentrations in peoplewho eat soyfoods. The one animal study that markedlyraised awareness of the potential detrimental effectsof soy was published in 1998 by Helferich andcolleagues, and found that in ovariectomizedimmune-compromised rats implanted with ER+ breastcancer cells, mammary tumor growth is stimulated whenanimals are fed diets to which genistein has beenadded (10). Although a pharmacological dose ofgenistein (750 ppm) was used in this study, serumgenistein levels in these mice were comparable tothose found in people eating soyfoods. However, forseveral reasons, the applicability of this particularexperimental model to humans has been questioned. Oneelement of the study design that brought criticismfrom nutrition scientists was that isolated genistein,rather than soy, or even a combination of isoflavonesas found in soy, was added to the diet. However, thiscriticism has been directly addressed in a follow-upstudy. In recently published research, Helferich andcolleagues found that soy protein isolate containingvarying amounts of genistein stimulated tumor growthto the same extent as comparable amounts of isolatedgenistein (11). Two human studies, one published in 1996, and theother in 1998, made it difficult to ignore concernsabout soy, because both studies suggested soy exertsweak estrogenic effects on breast tissue. In the firststudy by Petrakis et al., breast nipple aspirate fluidsecretion increased over a 5 month period during whichtime women had consumed 38 g of soy protein isolateper day (12). Furthermore, soy intake was associatedwith a higher percentage of hyperplastic cells inthese women. Both results suggested a possibleincreased breast cancer risk based on previousepidemiologic observations. In the second study, aftertwo weeks of consuming 60 g textured vegetable proteinper day, McMicheal-Phillips found that breast cellproliferation (based on biopsies) increased markedlyin premenopausal women (13). However, this initialreport was a preliminary analysis and involved only 48subjects. In the final analysis by Hargreaves et al.,involving all 84 subjects, no effects on cellproliferation were noted nor were there changes inseveral other markers of estrogenicity (14). Butlevels of pS2, a protein upregulated by estrogen, didsignificantly increase. Consequently, theinvestigators concluded that soy exerted weakestrogenic effects on breast tissue but that thelong-term implications of this effect were unclear. The Case For Soy Epidemiologic studies conducted in Asia generally donot show that the adult consumption of soy reducespostmenopausal breast cancer risk but the low rate ofbreast cancer mortality in Japan and the superiorprognosis of Japanese breast cancer patients incomparison to patients of other ethnic groups areobservations often cited as support for soy intakebeing beneficial, or at the very least, not beingharmful, for breast cancer patients. However, thesekinds of data do not specifically address the effectof soy. Arguably, breast cancer rates might be evenlower, and prognosis even better, if soy was not partof the Japanese diet. Furthermore, women in Japanconsume soy throughout their lives, which may have avery different effect than first consuming soy onlyafter having been diagnosed with breast cancer. Animal studies generally show that the addition of soyprotein or isoflavones to a typical laboratory dietreduces chemically-induced mammary tumorigenesis,although the effects are somewhat inconsistent andoften not particularly robust (15,16). No studies showincreased mammary tumorigenesis when soy is fed toadult animals. However, with few exceptions, theanimal studies address tumor development, not effectson existing tumors. Thus, their relevance to breastcancer patients is unclear. An important exception isa study by Shao et al. They found that when intact(with a uterus) immunecompromised mice were implantedwith ER+ breast cancer cells, genistein injectionsactually decreased mammary tumor development (17).These findings are in contrast to those by Helferichand colleagues cited previously (10,11). Shao et al.did inject genistein, which raises questionsaboutextrapolating the results to humans, but recent databy Zhou et al. show that in intact mice, dietarygenistein also inhibits mammary tumor growth (18). The primary difference between the two studies inwhich genistein was protective, and the studies byHelferich and colleagues in which genistein and soyprotein isolate were tumorigenic (10,11), is that inthe latter studies, mice were ovariectomized. Thissuggests that in a low-estrogen (ovariectomized mice)environment such as may exist in postmenopausal women,genistein has proliferative and possibly estrogeniceffects, whereas in a high-estrogen environment, suchas may exist in premenopausal women, it isantiproliferative and possibly antiestrogenic. Overallhowever, the antiestrogenic effects of soy have notbeen easy to demonstrate. Furthermore, Shao et al.found that genistein inhibited the growth of ER- cellsin vivo, which suggests that the antiproliferativeeffects of genistein may not be due to antiestrogeniceffects even in the case of ER+ cells (17). In anyevent, it is unlikely that the results of animalstudies can resolve the complex issue of soyconsumption by breast cancer survivors. Recently, two studies looked at the effects ofisoflavone supplements on breast tissue density.Breast tissue density is an excellent marker of breastcancer risk. Density is increased in response tostimuli that increase risk, such as hormonereplacement therapy HRT), and is decreased in responseto compounds that decrease breast cancer risk, such astamoxifen and raloxifene (19). In one yearlong study,isoflavone (100 mg/day) supplements had no effect onbreast tissue density in premenopausal women (20), andin the other yearlong study, isoflavone 40 mg/day)supplements actually decreased breast tissue densityin women 56-65 years of age (21). Thus, these studiessuggest soy does not increase, and may decrease,breast cancer risk. Of course, both studies wereconducted in healthy women, not breast cancerpatients. Lessons from HRT The relationship between HRT and breast cancer risk isunclear. Fortunately, the results from severalrecently conducted prospective studies have done muchto clarify this relationship. These studies indicatethat the combination hormones (some form of estrogenin combination with a progestin) markedly increaserisk, as much as 2-3fold over the course of a women’slifetime, whereas estrogen by itself, raises risk onlyslightly (22). This suggests that soy, which at mostonly possesses estrogen-like activity (23), and mayeven lower serum progesterone levels (24), is notlikely to increase breast cancer risk in healthywomen. But again, the question arises as to whetherthis conclusion is relevant to breast cancer patients.However, the HRT data may provide some answers to thisquestion as well. Although many oncologists recommendagainst their patients using HRT, this position is notwithout controversy and recent studies have beenunable to demonstrate that HRT decreases survival inbreast cancer patients (25). Thus, since there are noconvincing data that HRT has a detrimental effect onthe survival of breast cancer patients, it seemshighly unlikely that soy would. Conclusion Only intervention studies in which the effect of soyconsumption on the survival of Western breast cancerpatients is examined can definitely determine whethersoyfoods are contraindicated for such women. Becausethis type of research is difficult and expensive toconduct, and may not be approved for ethical reasons,it is unlikely that such trials will be forthcoming.Furthermore, even if this research was undertaken, theresults would not be known for many years.Alternatively, some insight may be gained by studyingthe effects of soy on markers of breast cancer risk inboth healthy women and breast cancer survivors.Unfortunately, Asian epidemiologic studies focused ondiet and the survival of breast cancer patients maynot help to resolve this issue because these studieswould involve subjects who have consumed soythroughout their life, not beginning as an adult afterhaving been diagnosed with breast cancer. Untilfurther data are available, in the opinion of thisauthor, the evidence does not justify recommendingthat breast cancer patients who enjoy partaking ofsoyfoods stop doing so, nor do they justifyrecommending that breast cancer patients specificallybegin soy consumption solely for the purpose ofpreventing recurrence and enhancing survival.Therefore soy intake recommendations for breast cancerpatients are similar to those for healthy women.Overall the evidence suggests that the intake ofapproximately 15 g (range, 10 to 25 g) of soy proteinand 50 mg (range, 30 to 100 mg) of isoflavones per dayis safe and has the potential to exert healthbenefits. This amount of soy protein and isoflavonesis provided by approximately two servings oftraditional soy foods. Is it a matter of dose and form of soy? Often statements about breast cancer patients and soyemphasize that only large amounts of soy or pills arelikely to be harmful. However, the evidence does notappear to be consistent with this perspective. In thestudy by Petrakis et al. cited previously in the caseagainst soy, subjects consumed 38 g of soy proteinisolate per day, which provided about 80 mg ofisoflavones. This is certainly a significant amount ofsoy protein, far more than the approximately 8-10 gJapanese women typically consume (26). However, themore relevant issue is the 80 mg of isoflavones. Thisamount is found in only about 2-3 servings of soy, andis only a little more than twice the average dailyintake in Japan. Thus, this would not be consideredexcessive isoflavone exposure. Furthermore, in theother human study that raised concerns by Hargreaveset al., subjects consumed 60 g of textured vegetableprotein that contained only 45 mg (the amount found inabout 5 ounces of tofu) of isoflavones per day, arather modest amount (14). Also, as already mentioned,in vitro, higher genistein concentrations inhibit thegrowth of ER+ breast cells, whereas lowerconcentrations are stimulatory. Therefore, if soy isproblematic, the problem is not specifically a resultof excessive consumption. In regard to pills versussoyfoods, as noted above, the two human studiesraising most concern used soy protein, not isolatedisoflavones. Furthermore, in ovariectomized mice, soyprotein was shown to stimulate tumor growth to asimilar extent as isolated genistein (11). Conversely,isolated genistein (not soy protein or foods)inhibited tumor growth in intact mice (17,18), andisoflavone supplements (not soy protein or foods) hada favorable effect on breast tissue density inpostmenopausal women (21). Although the use of pillscan be debated on several grounds, the evidencesuggests that in regard to breast cancer risk,equivalent amounts of isoflavones from pills and foodswill produce similar effects. Soy and Tamoxifen? There is ample reason to speculate that soy might becontraindicated for women on tamoxifen. However, Gotohet al. found that tamoxifen and a diet containing 10%miso synergistically inhibited the development ofchemically induced mammary tumors in rats (15). Misois a fermented soybean paste. Furthermore, in a followup experiment, when treatment was delayed until tumorshad been allowed to grow for several weeks, thecombination treatment inhibited growth byapproximately 50% whereas tamoxifen alone wasineffective (15). Recently, Constantinou found that adiet containing approximately 16% soy protein andtamoxifen additively inhibited the development ofchemically induced mammary tumors (27). Clinicaldecisions shouldn’t be based on animal data, but thesetwo studies suggest research examining the effect ofsoy on the efficacy of tamoxifen should be rigorouslypursued. Isoflavones: More than Phytoestrogens Isoflavones are often referred to as phytoestrogensbecause they bind to estrogen receptors. It is clearhowever that not all ligands that bind to estrogenreceptors have similar physiological effects. Receptorbinding is only one small part of the story. The shapeof the ligand-receptor complex and how this complexinteracts with activation factors in the cell, andDNA, determines the overall effect on cells (28,29).Thus, it may be more appropriate to refer to theestrogen-like, rather than estrogenic effects, ofisoflavones. Furthermore, two very importantobservations are that isoflavones bind with muchgreater affinity to estrogen receptor beta (ERb) thanestrogen receptor alpha (ERa), and stimulatetranscriptional activity with much greater potencywhen bound to ERb than ERa (29,30). Until recently, the scientific community understoodthere to be only one type of estrogen receptor. But in1996, Swedish researchers identified a second estrogenreceptor, which they named ERb, to distinguish it fromthe original estrogen receptor, ERa (31). Thesereceptors have different tissue distributions, so forexample, ERb predominates in injured coronary vesselswhereas ERa predominates in the uterus. This suggeststhat isoflavones are natural selective estrogenreceptor modulators (SERMs). In contrast to estrogen,which exerts estrogenic effects on all tissues and asa result dramatically raises endometrial cancer risk,SERMs, such as the drugs tamoxifen and raloxifene,have estrogenic effects in some tissues, but either noeffects or antiestrogenic effects in other tissues. The ideal SERM would have antiestrogenic effects onthe breast, estrogenic effects on the bone, and eitherno effects or antiestrogenic effects on the uterus.Isoflavones have estrogenic effects on coronaryvessels (32) but not on the endometrium(33).Therefore, isoflavones do qualify as SERMs. Buttheir effect on breast tissue is still unclear. Bear in mind though that as noted previously,isoflavones also possess nonhormonal properties; forexample, they exert antioxidant effects under someexperimental conditions and influence the activity ofenzymes involved in the metabolism of estrogen, andthat regulate cell growth and differentiation (34,35).Thus, isoflavones are more than phytoestrogens and mayexert biological effects that have little to do withbinding to the estrogen receptor. Consequently, evenreferring to isoflavones as SERMs doesn’t fullydescribe their potential biological actions. Mark Messina has a PhD in nutrition and was a formerprogram director with National Cancer Institute (USA).He has organized and chaired four internationalsymposia on the role of soy in preventing and treatingchronic disease, owns his own consulting business,Nutrition Matters, Inc., and is an adjunct associateprofessor in the Department of Nutrition at Loma LindaUniversity (Loma Linda, CA). Close this window

 

 

 

Version: 7.1.394 / Virus Database: 268.10.4/396 - Release 7/24/2006

[Guest guest]

Thank you John for backing me up. I sometimes feel that I am Alice in Wonderland with all that is going on out there. I totally agree with you about people that are highly qualified to help us through this quagmire...........

June

 

 

 

-

John Polifronio

Wednesday, July 26, 2006 9:16 AM

Re: Soy will not interfere with Tamifoxen

 

 

 

The issue with soy, is not that it "may" be a GM food, it most certainly "often is" a GM food. Suspicion is aroused because so many people oppose, and so many peope support soy. What is needed is for a large number of highly qualified nutritional experts to make their opinions concerning soy, known to readers.

 

-

June Black

Wednesday, July 26, 2006 7:19 AM

Re: Soy will not interfere with Tamifoxen

 

 

 

Please Read book written by Jane Plant "Your Life In Your Hands" It is a good book but I am allergic to soy. She won the battle against breast cancer but I still think soy is dangerous mainly for the fact that it may be a GM food.

June

 

 

 

-

Parhatsathid Napatalung

Tuesday, July 25, 2006 9:47 PM

Soy will not interfere with Tamifoxen

 

 

Should Women with Breast Cancer Eat Soy? by Mark Messina, Ph D Introduction There is probably no more controversial area relatedto the health effects of soy than the relationshipbetween soy intake and breast cancer risk. Concernover the possibility that soy consumption couldactually stimulate breast tumor growth has led to muchconfusion among oncologists and other healthprofessionals, and to frustration and eventrepidation, among breast cancer patients. This isparticularly ironic, because unarguably, it wasexcitement over the hypothesized anticancer effects ofsoy, an area first funded by the National CancerInstitute in 1991, which initially drew attention tothe health effects of soyfoods (1). This articleattempts to briefly highlight those studies mostpertinent to this controversy so that dietitians arebetter able to advise their clients about this issue. Background The low breast cancer mortality rates insoyfood-consuming countries, particularly Japan,combined with the knowledge that weak estrogens, suchas the soybean isoflavones, can exert antiestrogeniceffects in some situations, logically led tospeculation that soy might reduce breast cancer risk.Isoflavones, which are found in nutritionally relevantamounts only in soybeans, have a similar chemicalstructure to estrogen but have traditionallybeenconsidered to be weak estrogens. Early support forthe protective effects of soy against breast cancercame in the form of an animal study published in 1990,which reported that rats fed diets containing soydeveloped approximately 50% fewer chemically-inducedmammary tumors than control rats (2). One year later,a case-control study conducted in Singapore reportedthat soy intake was associated with an approximate 50%reduction in premenopausal breast cancer risk (3). The Case Against Soy There is a clear consensus that greater lifelongexposure to estrogen increases breast cancer risk. Theestrogen- like properties of soybean isoflavonestherefore provide a basis for concern about soyconsumption by breast cancer patients. In fact,although often overlooked, early on it was establishedthat at low concentrations, genistein, the mainisoflavone in soybeans, actually stimulates the growthof estrogen-receptor positive (ER+) breast cancercells in vitro (4). The growth of ER+ breast cancercells is stimulated by estrogen. Breast cancerpatients can have a mix of estrogen receptor negative(ER-) and ER+ cells, but typically, one type of cellpredominates and this determines treatment (5). ER+breast cancer patients respond well to tamoxifen, anantiestrogen, which is the most widely prescribedbreast cancer drug (6). Survival rates of ER+ breastcancer patients generally exceed those of ER- patients(7,8). Genistein does not stimulate the growth of ER-cells, and at high concentrations, the growth of bothER+ and ER- cells is inhibited by genistein (9). Theproposed explanation for this biphasic effect is thatat low concentrations the estrogenlike properties ofgenistein stimulate growth, whereas at higherconcentrations, the ability of genistein to influencemolecules that control cell growth, differentiation,and survival, results in growth inhibition. However,it is the lower concentrations that more closelyreflect the serum genistein concentrations in peoplewho eat soyfoods. The one animal study that markedlyraised awareness of the potential detrimental effectsof soy was published in 1998 by Helferich andcolleagues, and found that in ovariectomizedimmune-compromised rats implanted with ER+ breastcancer cells, mammary tumor growth is stimulated whenanimals are fed diets to which genistein has beenadded (10). Although a pharmacological dose ofgenistein (750 ppm) was used in this study, serumgenistein levels in these mice were comparable tothose found in people eating soyfoods. However, forseveral reasons, the applicability of this particularexperimental model to humans has been questioned. Oneelement of the study design that brought criticismfrom nutrition scientists was that isolated genistein,rather than soy, or even a combination of isoflavonesas found in soy, was added to the diet. However, thiscriticism has been directly addressed in a follow-upstudy. In recently published research, Helferich andcolleagues found that soy protein isolate containingvarying amounts of genistein stimulated tumor growthto the same extent as comparable amounts of isolatedgenistein (11). Two human studies, one published in 1996, and theother in 1998, made it difficult to ignore concernsabout soy, because both studies suggested soy exertsweak estrogenic effects on breast tissue. In the firststudy by Petrakis et al., breast nipple aspirate fluidsecretion increased over a 5 month period during whichtime women had consumed 38 g of soy protein isolateper day (12). Furthermore, soy intake was associatedwith a higher percentage of hyperplastic cells inthese women. Both results suggested a possibleincreased breast cancer risk based on previousepidemiologic observations. In the second study, aftertwo weeks of consuming 60 g textured vegetable proteinper day, McMicheal-Phillips found that breast cellproliferation (based on biopsies) increased markedlyin premenopausal women (13). However, this initialreport was a preliminary analysis and involved only 48subjects. In the final analysis by Hargreaves et al.,involving all 84 subjects, no effects on cellproliferation were noted nor were there changes inseveral other markers of estrogenicity (14). Butlevels of pS2, a protein upregulated by estrogen, didsignificantly increase. Consequently, theinvestigators concluded that soy exerted weakestrogenic effects on breast tissue but that thelong-term implications of this effect were unclear. The Case For Soy Epidemiologic studies conducted in Asia generally donot show that the adult consumption of soy reducespostmenopausal breast cancer risk but the low rate ofbreast cancer mortality in Japan and the superiorprognosis of Japanese breast cancer patients incomparison to patients of other ethnic groups areobservations often cited as support for soy intakebeing beneficial, or at the very least, not beingharmful, for breast cancer patients. However, thesekinds of data do not specifically address the effectof soy. Arguably, breast cancer rates might be evenlower, and prognosis even better, if soy was not partof the Japanese diet. Furthermore, women in Japanconsume soy throughout their lives, which may have avery different effect than first consuming soy onlyafter having been diagnosed with breast cancer. Animal studies generally show that the addition of soyprotein or isoflavones to a typical laboratory dietreduces chemically-induced mammary tumorigenesis,although the effects are somewhat inconsistent andoften not particularly robust (15,16). No studies showincreased mammary tumorigenesis when soy is fed toadult animals. However, with few exceptions, theanimal studies address tumor development, not effectson existing tumors. Thus, their relevance to breastcancer patients is unclear. An important exception isa study by Shao et al. They found that when intact(with a uterus) immunecompromised mice were implantedwith ER+ breast cancer cells, genistein injectionsactually decreased mammary tumor development (17).These findings are in contrast to those by Helferichand colleagues cited previously (10,11). Shao et al.did inject genistein, which raises questionsaboutextrapolating the results to humans, but recent databy Zhou et al. show that in intact mice, dietarygenistein also inhibits mammary tumor growth (18). The primary difference between the two studies inwhich genistein was protective, and the studies byHelferich and colleagues in which genistein and soyprotein isolate were tumorigenic (10,11), is that inthe latter studies, mice were ovariectomized. Thissuggests that in a low-estrogen (ovariectomized mice)environment such as may exist in postmenopausal women,genistein has proliferative and possibly estrogeniceffects, whereas in a high-estrogen environment, suchas may exist in premenopausal women, it isantiproliferative and possibly antiestrogenic. Overallhowever, the antiestrogenic effects of soy have notbeen easy to demonstrate. Furthermore, Shao et al.found that genistein inhibited the growth of ER- cellsin vivo, which suggests that the antiproliferativeeffects of genistein may not be due to antiestrogeniceffects even in the case of ER+ cells (17). In anyevent, it is unlikely that the results of animalstudies can resolve the complex issue of soyconsumption by breast cancer survivors. Recently, two studies looked at the effects ofisoflavone supplements on breast tissue density.Breast tissue density is an excellent marker of breastcancer risk. Density is increased in response tostimuli that increase risk, such as hormonereplacement therapy HRT), and is decreased in responseto compounds that decrease breast cancer risk, such astamoxifen and raloxifene (19). In one yearlong study,isoflavone (100 mg/day) supplements had no effect onbreast tissue density in premenopausal women (20), andin the other yearlong study, isoflavone 40 mg/day)supplements actually decreased breast tissue densityin women 56-65 years of age (21). Thus, these studiessuggest soy does not increase, and may decrease,breast cancer risk. Of course, both studies wereconducted in healthy women, not breast cancerpatients. Lessons from HRT The relationship between HRT and breast cancer risk isunclear. Fortunately, the results from severalrecently conducted prospective studies have done muchto clarify this relationship. These studies indicatethat the combination hormones (some form of estrogenin combination with a progestin) markedly increaserisk, as much as 2-3fold over the course of a women’slifetime, whereas estrogen by itself, raises risk onlyslightly (22). This suggests that soy, which at mostonly possesses estrogen-like activity (23), and mayeven lower serum progesterone levels (24), is notlikely to increase breast cancer risk in healthywomen. But again, the question arises as to whetherthis conclusion is relevant to breast cancer patients.However, the HRT data may provide some answers to thisquestion as well. Although many oncologists recommendagainst their patients using HRT, this position is notwithout controversy and recent studies have beenunable to demonstrate that HRT decreases survival inbreast cancer patients (25). Thus, since there are noconvincing data that HRT has a detrimental effect onthe survival of breast cancer patients, it seemshighly unlikely that soy would. Conclusion Only intervention studies in which the effect of soyconsumption on the survival of Western breast cancerpatients is examined can definitely determine whethersoyfoods are contraindicated for such women. Becausethis type of research is difficult and expensive toconduct, and may not be approved for ethical reasons,it is unlikely that such trials will be forthcoming.Furthermore, even if this research was undertaken, theresults would not be known for many years.Alternatively, some insight may be gained by studyingthe effects of soy on markers of breast cancer risk inboth healthy women and breast cancer survivors.Unfortunately, Asian epidemiologic studies focused ondiet and the survival of breast cancer patients maynot help to resolve this issue because these studieswould involve subjects who have consumed soythroughout their life, not beginning as an adult afterhaving been diagnosed with breast cancer. Untilfurther data are available, in the opinion of thisauthor, the evidence does not justify recommendingthat breast cancer patients who enjoy partaking ofsoyfoods stop doing so, nor do they justifyrecommending that breast cancer patients specificallybegin soy consumption solely for the purpose ofpreventing recurrence and enhancing survival.Therefore soy intake recommendations for breast cancerpatients are similar to those for healthy women.Overall the evidence suggests that the intake ofapproximately 15 g (range, 10 to 25 g) of soy proteinand 50 mg (range, 30 to 100 mg) of isoflavones per dayis safe and has the potential to exert healthbenefits. This amount of soy protein and isoflavonesis provided by approximately two servings oftraditional soy foods. Is it a matter of dose and form of soy? Often statements about breast cancer patients and soyemphasize that only large amounts of soy or pills arelikely to be harmful. However, the evidence does notappear to be consistent with this perspective. In thestudy by Petrakis et al. cited previously in the caseagainst soy, subjects consumed 38 g of soy proteinisolate per day, which provided about 80 mg ofisoflavones. This is certainly a significant amount ofsoy protein, far more than the approximately 8-10 gJapanese women typically consume (26). However, themore relevant issue is the 80 mg of isoflavones. Thisamount is found in only about 2-3 servings of soy, andis only a little more than twice the average dailyintake in Japan. Thus, this would not be consideredexcessive isoflavone exposure. Furthermore, in theother human study that raised concerns by Hargreaveset al., subjects consumed 60 g of textured vegetableprotein that contained only 45 mg (the amount found inabout 5 ounces of tofu) of isoflavones per day, arather modest amount (14). Also, as already mentioned,in vitro, higher genistein concentrations inhibit thegrowth of ER+ breast cells, whereas lowerconcentrations are stimulatory. Therefore, if soy isproblematic, the problem is not specifically a resultof excessive consumption. In regard to pills versussoyfoods, as noted above, the two human studiesraising most concern used soy protein, not isolatedisoflavones. Furthermore, in ovariectomized mice, soyprotein was shown to stimulate tumor growth to asimilar extent as isolated genistein (11). Conversely,isolated genistein (not soy protein or foods)inhibited tumor growth in intact mice (17,18), andisoflavone supplements (not soy protein or foods) hada favorable effect on breast tissue density inpostmenopausal women (21). Although the use of pillscan be debated on several grounds, the evidencesuggests that in regard to breast cancer risk,equivalent amounts of isoflavones from pills and foodswill produce similar effects. Soy and Tamoxifen? There is ample reason to speculate that soy might becontraindicated for women on tamoxifen. However, Gotohet al. found that tamoxifen and a diet containing 10%miso synergistically inhibited the development ofchemically induced mammary tumors in rats (15). Misois a fermented soybean paste. Furthermore, in a followup experiment, when treatment was delayed until tumorshad been allowed to grow for several weeks, thecombination treatment inhibited growth byapproximately 50% whereas tamoxifen alone wasineffective (15). Recently, Constantinou found that adiet containing approximately 16% soy protein andtamoxifen additively inhibited the development ofchemically induced mammary tumors (27). Clinicaldecisions shouldn’t be based on animal data, but thesetwo studies suggest research examining the effect ofsoy on the efficacy of tamoxifen should be rigorouslypursued. Isoflavones: More than Phytoestrogens Isoflavones are often referred to as phytoestrogensbecause they bind to estrogen receptors. It is clearhowever that not all ligands that bind to estrogenreceptors have similar physiological effects. Receptorbinding is only one small part of the story. The shapeof the ligand-receptor complex and how this complexinteracts with activation factors in the cell, andDNA, determines the overall effect on cells (28,29).Thus, it may be more appropriate to refer to theestrogen-like, rather than estrogenic effects, ofisoflavones. Furthermore, two very importantobservations are that isoflavones bind with muchgreater affinity to estrogen receptor beta (ERb) thanestrogen receptor alpha (ERa), and stimulatetranscriptional activity with much greater potencywhen bound to ERb than ERa (29,30). Until recently, the scientific community understoodthere to be only one type of estrogen receptor. But in1996, Swedish researchers identified a second estrogenreceptor, which they named ERb, to distinguish it fromthe original estrogen receptor, ERa (31). Thesereceptors have different tissue distributions, so forexample, ERb predominates in injured coronary vesselswhereas ERa predominates in the uterus. This suggeststhat isoflavones are natural selective estrogenreceptor modulators (SERMs). In contrast to estrogen,which exerts estrogenic effects on all tissues and asa result dramatically raises endometrial cancer risk,SERMs, such as the drugs tamoxifen and raloxifene,have estrogenic effects in some tissues, but either noeffects or antiestrogenic effects in other tissues. The ideal SERM would have antiestrogenic effects onthe breast, estrogenic effects on the bone, and eitherno effects or antiestrogenic effects on the uterus.Isoflavones have estrogenic effects on coronaryvessels (32) but not on the endometrium(33).Therefore, isoflavones do qualify as SERMs. Buttheir effect on breast tissue is still unclear. Bear in mind though that as noted previously,isoflavones also possess nonhormonal properties; forexample, they exert antioxidant effects under someexperimental conditions and influence the activity ofenzymes involved in the metabolism of estrogen, andthat regulate cell growth and differentiation (34,35).Thus, isoflavones are more than phytoestrogens and mayexert biological effects that have little to do withbinding to the estrogen receptor. Consequently, evenreferring to isoflavones as SERMs doesn’t fullydescribe their potential biological actions. Mark Messina has a PhD in nutrition and was a formerprogram director with National Cancer Institute (USA).He has organized and chaired four internationalsymposia on the role of soy in preventing and treatingchronic disease, owns his own consulting business,Nutrition Matters, Inc., and is an adjunct associateprofessor in the Department of Nutrition at Loma LindaUniversity (Loma Linda, CA). Close this window

 

 

 

Version: 7.1.394 / Virus Database: 268.10.4/396 - Release 7/24/2006

[Guest guest]

Soy impairs the enzyme that produces active thyroid hormone, it

causes goiter, thyroiditis, cancer, and impairs libido.

 

I agree with June that soy is dangerous but these dangers apply

to natural as well as frankensoy.

 

Duncan

 

> Posted by: " June Black " june1 junemesquite

> Wed Jul 26, 2006 7:20 am (PDT)

>

> Please Read book written by Jane Plant " Your Life In Your Hands "

> It is a good book but I am allergic to soy. She won the battle against

> breast cancer but I still think soy is dangerous mainly for the fact

> that it may be a GM food. June