<\/p>\n
Fontes:<\/strong><\/span><\/p>\n http:\/\/www.westonaprice.org\/soy-alert<\/a><\/p>\n 1998, FDA NCTR Reports: Our results may be interpreted that soy phytoestrogen genistein is a chromosomal mutagen.<\/span><\/p>\n www.ncbi.nih.gov\/pubmed\/9729267<\/a><\/p>\n 1999, FDA Scientists Against Soy: NIH NIEHS scientists Dr. Doerge and Dr. Sheehan have for decades consistently proven highly toxic soy-cause of multiple adverse body & brain effects, especially caused to most developmentally fragile fetus, infants, and children.<\/p>\n www.alkalizeforhealth.net\/Lsoy2.htm<\/a><\/p>\n 2001, NIEHS Report: Dietary (soy) genistein produced effects in multiple estrogen-sensitive tissues in male and female mice consistent with estrogenicactivity\u2026…within exposure ranges in humans.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11738518<\/a><\/p>\n 1999 & 2004, Phytoestrogens are compounds found in plant foods (largely soybeans) that exhibit estrogen-like activity, and display both estrogen-like activity and anti-estrogen effects. Interindividual diversity and complexity in dietary phytoestrogen absorption and metabolism make their bioactivity unpredictable.Their actions in specific cells are determined by many factors; levels of estrogen receptor-alpha and -beta, and the diverse cocktail of co-activators and co-repressors present in any given cell type. Overall, it is na\u00efve to assume that exposure to these compounds is always good. Inappropriate or excessive exposure to phytoestrogens may be detrimental to health.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/10548876<\/a><\/p>\n Soy, Cause of Multiple Cancers<\/strong> 2004, Findings suggest that oxidative DNA damage by (soy) isoflavone metabolites play a role in tumor initiation and that cell proliferation by isoflavones via Estrogen Receptors (ER) to Estrogen response elements (ERE) was largely consistent with cell proliferative activity of isoflavones.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/14992594<\/a><\/p>\n Leukemia: Soy-Cause of Infant Leukemia 2010, Genistein is a bioflavonoid enriched in soy products. High levels of maternal soy consumption linked to the development of infant leukemia. Genistein induced infant leukemia.<\/span><\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/20638367<\/a><\/p>\n Maternal Diet and infant Leukemia <\/strong><\/p>\n A Role for DNA topoisomerase II inhibitors caused to fetus in utero: 10 fold increase risk of infant acute myeloid leukemia with increased maternal consumption of DNA topo-2 inhibitor containing foods.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/9876473<\/a><\/p>\n Soy is in fact an established topoisomerase II inhibitor and in fact an inhibitor of several other essential enzymes<\/span><\/strong><\/p>\n Dietary topoisomerase II-poisons: Contribution of soy products to infant leukemia-DNA topoisomerase are nuclear enzymes inducing transient breaks in the DNA allowing DNA strands to pass through each other. Maternal exposure to low doses of dietary topoismerase II poisons, including genistein may contribute to development of infant leukemia. This study found at:<\/p>\n excli.de\/Vol1\/hengstleretal02-02.pdf<\/span><\/a><\/p>\n Timing of phytoestrogen use is important. Recent studies have indicated that soy phytoestrogens could be contributive factors in some forms of breast cancer, penile birth defects, and infantile leukemia. Genistein might increase the risk of leukemia because it inhibits the enzyme topoisomerase which result in double strand DNA breaks which are mutagenic. Genistein may not be safe for women with estrogen-dependent breast cancer. Soy phytoestrogens or isoflavones have been definitely shown to depress thyroid function and to cause infertility in every animal species studies so far. Soy isoflavone can act like estrogen, stimulating development and maintenance of female characteristic or block cells from using cousins of estrogen.<\/p>\n www.genistein.net\/cancer.html<\/a><\/p>\n 2007, Study demonstrates that biologically relevant concentrations of soy genistein flavonoids can induce abnormalities in mixed-linage leukemia.Particularly alarming knowing mother\u2019s metabolism can lead to higher flavonoid concentration on fetal side. Raise public awareness and set guidelines for marketing flavonoid supplements to reduce risk of infant leukemias.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/17468513<\/a><\/p>\n 2011, Isoflavone research revealed adverse effects on reproductive system. This is also the case with tumor-promoting effects on breast tissue. Questions about the effectiveness and safety of isoflavones have to be clarified. There are concerns about the maternal consumption of isoflavones due to the development of leukemia in infants.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/21438720<\/a><\/p>\n Soy-Cause of Bladder Cancer<\/strong><\/p>\n USC Study reports soy increases risk of bladder cancer<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/12496060<\/a><\/p>\n Colon Cancer, Gastric Cancer, & Intestinal Tumorigenesis<\/strong><\/p>\n 2005, Soy increases colon epithelial cell proliferation measures in the sigmoid colon a common location of colon cancer. In the cecum and sigmoid colon the proliferation count increased as the serum (soy) genistein concentration increased. Cells that multiply indiscriminately can encourage the cause of colon cancer.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/16155276<\/a><\/p>\n 2007, Maternal consumption to soy protein isolates increased the percentage of animals bearing multiple colon tumors. IGF-1 was elevated in soy protein isolate during pregnancy and casein-fed group thereafter. Elevated levels of insulin or IGF-1 are associated with increased colorectal cancer risk in humans and rodents.In summary, dietary exposure to a soy protein-based diet during pregnancy followed by the switch to casein at delivery increased colon tumor multiplicity (a measure of tumor promotion) in the male progeny as later adults. The present results raise the possibility that colon cancer, which conventionally is considered to be a cancer of the elderly, may be influenced by dietary\/metabolic perturbations or programming occurring during development.<\/p>\n joe.endocrinology-journals.org\/content\/195\/1\/79.full<\/a><\/p>\n 2007, Soy isoflavone genisten can affect cell metabolism by specifically inhibiting protein tyrosine kinase (PTK) and\/or interacting with the estrogen receptors (ERs). Synthesis of GAGs\/PGs (glycosaminoglycans\/proteoglycans by colon cancer cell line HT-29 cells in the presence of genistein was dependent on their type and localization which implies the active participation of the PTK interaction with ERs, which was further supported by the observed growth stimulation at low concentrations of genistein.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/18225578<\/a><\/p>\n 2012, Soy food which is rich in isoflavones are structurally similar to 17 B-estradiol. We found an increasing trend in risk of gastric cancer associated with higher isoflavone intake among female hormone drug users.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/22170362<\/a><\/p>\n 2008, \u2026.genistein in the diet enhanced intestinal tumorigenesis in male mice. This study demonstrates that although genistein can enhance EGCG (antioxidant found in teas and many supplements) bioavailabilty this combination enhances intestinal tumorigenesis in male mice.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/18684728<\/a><\/p>\n 2007, Several adverse effects of soy supplementation in female rats were observed. 5 of 21 rats fed soy supplement died before the end of the experiment while all animals on the control diet survived. Density of normal crypts lining the colonic mucosa was reduced, indicating gastrointestinal damage. Uterine weights, serum estradiol and serum isoflavone levels were increased in soy-supplemented diets. These adverse effects of soy isoflavones need further examination in target population of consumption of soy supplements.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/17157426<\/a><\/p>\n Intestinal Damage <\/strong><\/p>\n A high dose of soy genistein may potentially compromise intestinal growth. Study found at:<\/p>\n jn.nutrition.org\/content\/134\/6\/1303 <\/a> www.ncbi.nlm.nih.gov\/pubmed\/1897396<\/a><\/p>\n Pancreatic Cancer:<\/span> FDA Study: hypertrophy\/hyperplasia. Antinutritional components inhibit growth goitrogens, phytoestrogens, and saponins, lysinoalanine damage to kidneys allergenic response in humans.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/8142044<\/a><\/p>\n Pancreatic Cancer<\/span>: Neoplastic nodules including carcinomas. Any possible adverse effects may result from phytic acid and saponins in soybeans.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/7884560<\/a><\/p>\n Pancreatic Cancer:<\/span> USDA Study Confirms Soy-Cause of proliferative pancreatic lesions<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/2745924<\/a><\/p>\n 1986, Animal studies have indicated a link between pancreatic cancer and high fat and\/or high protein diets as well as raw soybean consumption. Nitrosamines may also be related to pancreatic cancer. (Soy contains nitrosamines).<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/3775080<\/a><\/p>\n Toxic Factors In Edible Legumes <\/strong><\/p>\n Best known of the anti-nutritional factors causing nutritional stress due to toxic components found in soybeans is trypsin inhibitors that inhibit growth. Recent evidence implicates pancreatic hypertrophyas one of the main physiologic responses to trypsin inhibitors. Many legumes such as soy contain hemagglutinins also inhibit growth. Other toxic components in soybeans include goiterogenic factors, cyanogenetic glucosides, saponins and alkaloids.<\/p>\n http:\/\/www.ajcn.org\/cgi\/content\/abstract\/11\/4\/281<\/a><\/p>\n Maternal Consumption of Soy Is Related to Breast Cancer in Offspring<\/strong><\/p>\n Maternal soy genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/9538161<\/a><\/p>\n Maternal exposure to genistein can increase mammary tumorigenesis in offspring, mimicking the effects of in utero estrogenic exposure\u2026increasing susceptibility.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/10425307<\/a><\/p>\n Maternal exposure increases carcinogenic induced mammary tumors in female rat offspring<\/strong><\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/10425307<\/a><\/p>\n Perinatal exposure on induced mammary carcinoma\u2026.5mg genistein in utero did increase number of mammary cancer lesions\u2026perinatal genistein is an endocrine disruptor and increases multiplicity of induced mammary carcinoma in rats<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/10737721<\/a><\/p>\n Soy-Cause Of Breast Cancer in Women and\/or Men<\/strong> 2009, Environmental estrogens affect breast development in male rats: NIEHS study; Clearest evidence to date: Abnormalities which could have the potential to become cancerous developed in the mammary gland tissue of male rats that were exposed to either the soy-based phytoestrogens genistein or ethinyl estradiol- an estrogen used in birth control pills. Findings support a growing concern that exposure to low levels of estrogen\u2026.might increase the risk of breast cancer. Genistein and ethinyl estradiol exposure in multigenerational and chronic studies induce similar proliferative lesions in mammary gland.<\/p>\n www.environmentalhealthnews.org\/ehs\/newscience\/environmental-estrogens-affect-breast-development-in-male-rats<\/a><\/p>\n Similar across all generations exposed to genistein\u2026..predominant tubuloalveolar growth in females and lobuloalveolar in males. Hyperplasia in male rats was similar induced by genistein or ethinyl estradiol\u2026substantiate previous reports that mammary gland hyperplasia in the male rat is most sensitive markers for estrogenic endocrine disruption.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/19383540<\/a><\/p>\n Journal National Cancer Institute: Chemical structure of isoflavones is similar to that of estrogens, and isoflavones bind to both estrogen receptors ERa and ERb and exert estrogen-like effects. The main soybean isoflavone genistin may stimulate the growth of estrogen sensitive tumors. Research recommendation is that the impact of isoflavones on breast tissue needs to be evaluated at the cellular level in women at high risk for breast cancer.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/16985246<\/a><\/span><\/p>\n 2008, Low concentrations of the soy phytoestrogen genistein induce Proteinase Inhibitor 9 and block killing of breast cancer cells by immune cells. A significant population consumes levels of genistein in soy products that may be high enough to induce PI-9, perhaps potentiating the survival of some preexisting breast cancer by enabling them to evade immunosurveillance.<\/p>\n www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2584580<\/a><\/p>\n 2004, DNA damage by isoflavone metabolites plays a role in tumor initiation and that cell proliferation by isoflavones via estrogen receptors induces tumor promotion and or progression, resulting in cancer of estrogen-sensitive organs.<\/p>\n www.ncib.nlm.nih.gov\/pubmed\/14992594<\/a><\/p>\n Soy-Causes Proliferation of Breast Cancer Cells<\/strong><\/p>\n Nurses should become more knowledgeable about soy foods for women at high risk, or with history of breast cancer should avoid high intake of soy supplements.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/19726393<\/a><\/p>\n 2004, An E-screen assay revealed that genistein and daidzein enhanced proliferation of estrogen-sensitive breast cancer MCF-7 cells.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/14992594<\/a><\/p>\n 2004, Genistein, at 1microM, stimulated the growth of MCF-7 cells and insulin-like growth Factor-I receptor pathway is involved in the proliferative effect of low-dose genistein in MCF-7 breast cancer cells.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15126563<\/a><\/p>\n Estrogenic properties of soy isoflavones, genistein can stimulate growth of breast cancer.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/14578162<\/a><\/p>\n 2010, Genistein is a major isoflavone with known hormonal and tyrosine kinase-modulating activities. Genistein has been shown to promote the growth of estrogen receptor positive breast cancer cells. Breast cancer cells are particularly susceptible to the growth-promoting effects of genistein across a wide range of doses.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/20067990<\/a><\/p>\n Soy Blocks Anti-Estrogen Breast Cancer Drugs<\/strong><\/p>\n 2001, Soy phytoestrogens, genistein and daidzein may stimulate existing breast tumor growth and antagonize the effects of tamoxifen. Women with current or past breast cancer should be aware of the risk of potential tumor growth when taking soy products.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11573864<\/a><\/p>\n Soy interrupts the actions of pharmaceutical drugs in treatment for breast cancer.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/17640169<\/a><\/p>\n 2008, Dietary genistein can negate the inhibitory effects of tamoxifen on estrogen-stimulated growth of MCF- 7 breast cancer cells.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/18815740<\/a><\/p>\n Soy-Cause of Uterine Cancer<\/span>– Seen in mice injected with Genistein as Soy Estrogen As Newborns<\/p>\n www.niehs.nih.gov\/news\/newsroom\/releases\/news-archive\/2001\/may31\/index.cfm<\/a><\/p>\n Uterine Cancer: <\/span>NIEHS: At 18 months, uterine adenocarcinoma was 35% for genistein and 31% for DES\u2026suggest genistein is carcinogenic if exposure occurs during critical periods of differentiation. Soy based infant formulas\u2026should be closely examined in children.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11389053<\/a><\/p>\n Soy causes cancer and progression in estrogen sensitive organs\u2026.uterus and vulva<\/p>\n www.ncbi.nlm.nih.gov\/pubmend\/14992594<\/a><\/p>\n Adverse effects on Uterus\u2026etc. Abnormal pathology in 3 women\u2026all 3 improved after withdrawal of soy. Additional information on phytoestrogen is necessary to ascertain safety.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/18396257<\/a><\/p>\n Soy exposure during pregnancy and lactation causes long-lasting adverse effects into adulthood. Soy Increases Risk of Diabetes: <\/strong><\/p>\n 2007, Serum insulin and leptin concentrations were decreased by soy protein isolates. (Low levels of insulin may cause of diabetes type 1. Leptin is a hormone involved in regulating appetite, body weight, fat and glucose activity. The absence of leptin leads to uncontrolled food intake and resulting obesity).<\/p>\n joe.endocrinology-journals.org\/content\/195\/1\/79.full<\/a><\/p>\n 2005, Findings demonstrate that genistein directly acts on pancreatic B-cells, leading to activation of the cAMP\/PKA signaling cascade to exert an insulinotropic effect, providing a novel role of soy isoflavones in the regulation of insulin secretion.2004, Logistic regression analyses showed soy milk formula consumption at 4-6 and 7-12 months of age was associated with a twofold higher risk of type 1 Diabetes.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15331209<\/a><\/p>\n 2011, Indeed, higher soy food intake was associated with a weakly elevated diabetes risk across ethnic groups among Caucasian, Japanese American, and Native Hawaiian men and women.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/20924394<\/a><\/p>\n 2006 Soy Genistein acutely stimulates insulin secretion in pancreatic beta-cells through cAMP-dependent protein kinase pathway. Evidence that genistein increases rapid glucose-stimulated insulin secretion in both insulin-secreting cell lines and mouse pancreatic islets. Genistein elicited a significant effect at concentration as low as 10 nmol\/l. Insulinotropinic effects of genistein is primarily mediated through protein kinase A.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/16567527<\/a><\/p>\n 2008, Soy isoflavones may influence insulin action by means of their well-known receptor-mediated estrogenic activity. Isoflavones also bind to peroxisome proliferator-activated receptors that are strongly associated with insulin action.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/1855850<\/a><\/p>\n 2007, Results support the hypothesis that diabetes may have a role in the development of breast cancer, influencing risk via both sex hormone and insulin pathways. Our results also show that the diabetes-breast cancer association we observed only in low\/intermediate soy consumers.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/17440036<\/a><\/p>\n 2004, Soyfood consumption and development of glycosuria, (glucose in the urine) an important indicator of diabetes.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15042129<\/a><\/p>\n Soy-Cause of Severe and Irreversible Adverse Brain Effects<\/strong><\/p>\n 2008, Endocrine disrupting chemicals (EDCs) exert hormone-like activity and exposure to these compounds may induce both short- and long-term deleterious effects. The EDCs examined included estradiol, androgen active compounds, soy phytoestrogens, and atrazine. Effects on behavior and hypothalamic neuroendocrine systems were examined. All EDCs impaired reproduction. Several hypothalamic neural systems proved to be EDC responsive, including arginine vasotocin, catecholamines, and gonadotropin releasing hormone system.Exposure to EDCs during embryonic development has consequences beyond impaired function of the reproductive axis. Behavioral alterations reveal both direct and indirect effects of exposure to EDC.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/18006066<\/a><\/p>\n Soy isoflavones provide a useful model to investigate the actions of endocrine disruptors. Isoflavonoids act in vivo through both ERalpha and ERbeta. Small physiologically relevant exposure levels can alter estrogen dependent gene expression in the brain and affect complex behavior in wide range of species.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15720476<\/a><\/p>\n FDA Study: \u201cFDA Scientists Against Soy\u201d NIH scientists Drs. Doerge and Sheehanreport, \u201cThus during pregnancy in humans, (soy) isoflavones per se could be a risk factor for abnormal brain and reproductive tract development. Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. \u2026.the public will be put at potential risk from soy isoflavones in soy protein, isolatewithout adequate warnings and information.\u201d<\/p>\n www.alkalizeforhealth.net\/Lsoy2.htm<\/a><\/p>\n 2001 Studies show that soybean-based formulas contain large quantities of phytoestrogens, particularly isoflavones. Because of experimental data suggesting possible deleterious effects of phytoestrogens on neuroendocrine maturation, thereduction of soy content in formulas must be considered.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11760676<\/a><\/p>\n Soy phytoestrogens influence estradiol estrogenic induced mechanism results inmodified brain functions:<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11602649<\/a><\/p>\n 2004, Major source of endocrine disrupting substances soy derived isoflavones are most abundant and most studied are known endocrine disruptors. Isoflavones exert estrogenic and antiestrogenic properties. Soy daidzein can be metabolized to the potent equol. Equol has important ability to bind testosterone and in turn inhibits the action of androgen. Specific influence of dietary soy phytoestrogens on consumptive, learning and memory and anxiety-related behaviors is identified.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15454683<\/a><\/p>\n Soya isoflavone content of rat diet can increase anxiety and stress hormone release in the male rat. Major changes in behavioral anxiety and stress hormones<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/12618915<\/a><\/p>\n 2005, Soy isoflavonoids provide a useful model to investigate the actions of endocrine disruptors. Isoflavonoids act in vivo through both ERalpha and ERbeta.Their neurobehavioural actions are largely anti-estrogenic. Small physiologically relevant exposure levels of soy isoflavonoids can alter estrogen-dependent gene expression in the brain and affect complex behavior in a wide range of species.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15720476<\/a><\/p>\n Evidence for soy genistein cytotoxicity in rat brain<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15147835<\/a><\/p>\n Small doses of soy genistein or daidzein can alter estrogen-dependent gene expression in brain and complex behavior.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11836071<\/a><\/p>\n 2004, Results indicate that long-term consumption of a diet rich in soy isoflavones can have marked influences on patterns of increased aggressive behavior and decreased social behavior.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/15053944<\/a><\/p>\n 2010- Endocrine disruptors, chemicals that disturb the actions of endogenous hormone, have been implicated in birth defects associated with hormone-dependent development. Phytoestrogens are a class of endocrine disruptors found in plants. \u2026.soy phytoestrogens. Effects of genistein on reproductive development and spatial learning required exposure throughout the pre-and postnatal periods.<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/20053350<\/a><\/p>\n Placental transfer of soy genistein to levels similar to those in maternal brain,crosses rat placenta and can reach fetal brain from maternal \u2026relevant to those observed in humans<\/p>\n www.ncbi.nlm.nih.gov\/pubmed\/11297868<\/a><\/p>\n Soy Damages Multiple Brain Neuro-Transmitter Systems<\/strong><\/p>\n 2008, Endocrine disrupting chemicals (EDCs) exert hormone-like activity and exposure to these compounds may induce both short- and long-term deleterious effects. The EDCs examined included estradiol, androgen active compounds, soy phytoestrogens, and atrazine. Effects on behavior and hypothalamic neuroendocrine systems were examined. All EDCs impaired reproduction. Several hypothalamic neural systems proved to be EDC responsive, including arginine vasotocin, catecholamines, and gonadotropin releasing hormone system.Exposure to EDCs during embryonic development has consequences beyond impaired function of the reproductive axis. Behavioral alterations reveal both direct and indirect effects of exposure to EDC.<\/p>\n
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\n<\/span>Soy-Cause of Pancreatic Cancer<\/strong><\/p>\n
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\n<\/span>Soy-Cause of Thymus Masses<\/strong><\/p>\n
\nwww.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2039948\/
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