Monday, August 27, 2012

Study Evidence Proving Soy-Causes CANCERS, and Cancer Proliferation:

Soy-Cause of Multiple Cancers:

2004, Soy isoflavones, genistein and daidzein induces cell proliferation and their metabolites cause oxidative DNA damage which plays a role in isoflavone-induced cancer. Oxidative DNA damage by isoflavone metabolites plays a role in tumor initiation and that cell proliferation by soy isoflavones via estrogen receptors or estrogen response element binding induces tumor promotion and/or progression, resulting in cancer of estrogen-sensitive organs.

Soy-Cause of Leukemia:

2010, High levels of maternal soy consumption during pregnancy have been linked to infant leukemia

2008, 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’s 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.

2002, National Cancer Institute: There remains a mechanistic concern associated with the ability of soy isoflavones (i.e., genistein) to inhibit topoisomerase, possibly leading to DNA strand breaks, Mouse lymphoma cell mutagenesis experiments conducted with and without metabolic activation revealed statistically significant increases in mutation frequency with investigational soy isoflavone drug product concentrations; such increases were dose related and increases in the frequency of both small and large colonies were observed. In similar experiments there were statistically significant increases in revertants (mutant change in DNA). Statistically significant increase in the frequency of micronucleated polychromatic erythrocytes was also seen 24 hours after treatment. The apparent risk of isoflavone ingestion may ultimately depend on the dose and developmental timing of exposure.

(Soy is in fact an established number one inhibitor of topoisomerase II).

1998, Maternal Diet and infant Leukemia: 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.

2002, 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 topoisomerase II poisons, including genistein may contributes to development of infant leukemia. (Vol 1)

2007. Study demonstrates that biologically relevant concentrations of soy genistein flavonoids can induce abnormalities in mixed-linage leukemia. Particularly alarming knowing mother’s metabolism can lead to higher flavonoid concentration on fetal side, raises public awareness of necessity to set guidelines for marketing flavonoid supplements to reduce risk of infant leukemia.

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.

1998, Phytoestrogen genistein is an isoflavone found in soy products. Genistein is a competitive inhibitor of tyrosine kinases and the DNA synthesis related enzyme, topoisomerase-II. Exposure of mammalian cells to genistein results in DNA damage that is similar to that induced by the topoisomerase-II inhibitor and chromosomal mutagen, m-amsa. Our results may be interpreted that genistein is a chromosomal mutagen.

2006, Concern has been raised about potential adverse effects due to estrogenic and other activities of the soy isoflavones. In the mouse lymphoma assay, genistein induced an increase of predominately small colonies indicating that genistein acts as a clastogen (material that can cause breaks in chromosomes, leading to sections of the chromosome being deleted, added, or rearranged. A mutagen that can lead to carcinogenesis). This observation is in agreement with published data on the inhibitory action of genistein on topoisomerase II, which is known to lead to chromosomal damage with a threshold dose response.

Soy is a topoisomerase inhibitor that interferes with the action of essential topoisomerase enzymes. Topoisomerase enzymes control the changes in DNA structure by catalyzing the breaking and rejoining of the phosphodiester backbone of DNA strands during the normal cell cycle. Topoisomerase inhibitors block the ligation step of the cell cycle, generating single and double stranded breaks that harm the integrity of the genome. Soy genistein possess strong topoisomerase inhibitory properties that cause DNA damaging properties, causing carcinogenicity.

Soy-Cause of Pancreatic Cancer:

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).

1991 FDA, CFSAN report: Chronic feeding of soy trypsin inhibitors can cause hypertrophy and hyperplasia of the pancreas and lead to adenomas and carcinomas of the exocrine pancreas.

1994, Soy cause of pancreatic hypertrophy/hyperplasia. Antinutritional components inhibit growth goitrogens, phytoestrogens, and saponins, lysinoalanine cause damage to kidneys, and allergenic response in humans.

1995, Pancreatic Cancer: Neoplastic nodules including carcinomas. Any possible adverse effects may result from phytic acid and saponins in soybeans.

1989, Pancreatic Cancer: USDA Study: proliferative pancreatice lesionw hypertrophy and hyperplasia of the rat pancreas produced by short-term dietary administration of soya-derived protein and soybean trypsin inhibitor.

1962, Toxic Factors In Edible Legumes and Their Elimination: 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 hypertrophy as 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.

Soy Cause Bladder Cancer:

2002, Dietary soy and increased risk of bladder cancer. USC Study. The soyfood-bladder cancer risk association did not differ significantly between men and women and was not explained by other dietary factors. The soy-cancer relationship became stronger when the analysis was restricted to subjects with longer (> or =3 years) duration of follow-up. To our knowledge, this is the first epidemiological report on the effect of dietary soy on bladder cancer risk.

Soy Cause Colon Cancer, Gastric Cancer, & Intestinal Tumorigenesis:

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.

2007, Soy isoflavone genistein 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.

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.

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.

2008, ….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) bioavailability this combination enhances intestinal tumorigenesis in male mice.

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.

Soy Increases Risk of Breast Cancer in Males and Females:

1998, High maternal estrogen exposure during pregnancy increases breast cancer risk among daughters.

2007, Increased incidence of hyperplasia of the mammary gland and calcification of renal tubules were observed in continuously exposed 100 and 500 ppm males, with a weaker induction of male mammary gland hyperplasia in 500 ppm males exposed only as adults or exposed only in utero and through lactation. Mammary lesions varied with sex and regimen. The relevance of the adverse effects observed here to human phytoestrogen exposures requires further study. (www not found. Article: “Reproductive and Developmental Toxicity of Phytoestrogens.” Source: Birth Defects Res A Clin Mol Teratol 2007 May;79(5):402. KB Delclos, CC Weis, RR Newbold).

1999, Maternal exposure to genistein can increase mammary tumorigenesis in offspring, mimicking the effects of in utero estrogenic exposure…increasing susceptibility.

2000, Perinatal exposure on induced mammary carcinoma….5mg genistein in utero did increase number of mammary cancer lesions…perinatal genistein is an endocrine disruptor and increases multiplicity of induced mammary carcinoma in rats

2008, NIH, National Toxicology Program report: (Soy) Genistein is a naturally occurring isoflavone that interacts with estrogen receptors and multiple other molecular targets. “Concerns” have been raised regarding potential adverse effects of genistein, particularly with regard to reproductive toxicity and the induction of potentiation of carcinogenesis due primarily to its weak estrogenic activity. There is also minimal transfer of genistein to rat pups via the dams’milk. In soy group there were significant effects on the onset of aberrant estrous cycles. Pituitary gland weights were significantly increased. There was a significant positive trend in the incidences of mammary gland adenoma or adenocarcinoma. There were positive trends in the incidences of adenoma or carcinoma in the pars distalis of the pituitary gland of females in males a significant positive trend occurred in incidences of combined adenoma or carcinoma of the pancreatic islets. There was some evidence of carcinogenic activity of genistein in female rats based on increased incidences of mammary gland adenoma or adenocarcinoma and pituitary gland neoplasms. The effects of genistein on common hormonally related spontaneous neoplasms of female rats are consistent with an estrogenic mechanism of toxicity.

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.

2009, NIEHS, Environmental estrogens affect breast development in male rats: 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….might increase the risk of breast cancer. Genistein and ethinyl estradiol exposure in multigenerational and chronic studies induce similar proliferative lesions in mammary gland.

2009. Similar across All generations exposed to genistein…..predominant tubuloalveolar growth in females and lobuloalveolar in males. Hyperplasia in male rats was similar induced by genistein or ethinyl estradiol…substantiate previous reports that mammary gland hyperplasia in the male rat is most sensitive markers for estrogenic endocrine disruption.

1998, Phytoestrogen genistein is an isoflavone found in soy products. Genistein is a competitive inhibitor of tyrosine kinases and the DNA synthesis related enzyme, topoisomerase-II. Exposure of mammalian cells to genistein results in DNA damage that is similar to that induced by the topoisomerase-II inhibitor and chromosomal mutagen, m-amsa. Our results may be interpreted that genistein is a chromosomal mutagen.

Soy Hormone Disruptors Proliferate Breast Cancer Cells:

2006, 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.

2001, 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 whey taking soy products.

2004, An E-screen assay revealed that genistein and daidzein enhanced proliferation of estrogen-sensitive breast cancer MCF-7 cells.

2009, 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.

2004, Estrogenic properties of soy isoflavones, genistein can stimulate growth of breast cancer.

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.

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.

2011, We show that genistein can induce estrogen-dependent MCB-7 tumor cell growth and increase breast cancer-associated aromatase expression and activity in vitro. Genistein could negate the growth inhibitory actions of aromatase inhibitor fadrozole (anti-estrogen breast cancer drugs). Increasing risk for adverse interactions with breast cancer treatment is of major concern and should be considered with care.

Soy Blocks Action of Anti-Estrogen Prescribed Breast Cancer Drugs;

2007, Soy drug-like effects interrupt the actions of pharmaceutical drugs.

2008, Dietary genistein can negate the inhibitory effects of tamoxifen on estrogen-stimulated growth of MCF- 7 breast cancer cells.

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.

2008, Genistein, a soy isoflavone, stimulates growth of estrogen-dependent human tumor cells. Anti-estrogens and aromatase inhibitors are frontline therapies for estrogen-dependent breast cancer. Genistein can reverse the inhibitory effects of anti-estrogen letrozole on tumor growth and adversely impact breast cancer therapy. Caution is warranted for consumption of dietary genistein by women with estrogen-dependent breast cancer taking tumor inhibitors such as letrozole.

2011, Soy genistein could negate the growth inhibitory actions of aromatase inhibitor fadrozole (anti-estrogen breast cancer drugs). Increasing risk for adverse interactions with breast cancer treatment is of major concern and should be considered with care.

Soy-Cause of Uterine Cancer

2001, FDA NIEHS, The developing fetus is uniquely sensitive to perturbations with estrogenic chemicals. DES is the classic example. Phytoestrogen use in nutritional and pharmaceutical applications for infants and children is increasing. We investigated the carcinogenic potential of genistein, a naturally occurring plant estrogen in soy. At 18 months (mice study) the incidence of uterine adenocarcinoma was 35% for genistein and 31% for DES. Data suggest that genistein is carcinogenic if exposure occurs during critical periods of differentiation. Use of soy –bead infant formulas in the absence of medical necessity and the marketing of soy products that appeal to children should be closely examined.

2001, Increased uterine cancer seen in mice injected with genistein, as soy estrogens. Newborn mice given genistein developed cancer of the uterus later in life, scientists at the National Institute of Environmental Health Sciences reported today. In the study, published in the June issue of Cancer Research, the scientists treated female mice for five days after birth with genistein, a substance in soy that is similar to the female hormone, estrogen.

2001, Uterine Cancer, NIEHS Report: At 18 months, uterine adenocarcinoma was 35% for genistein and 31% for DES…suggest genistein is carcinogenic if exposure occurs during critical periods of differentiation. Soy based infant formulas…should be closely examined in children.

2004, Soy causes cancer and progression in estrogen sensitive organs….uterus and vulva.

2008, Adverse effects on Uterus…etc. Abnormal pathology in 3 women…all 3 improved after withdrawal of soy. Additional information on phytoestrogen is necessary to ascertain safety.

2007, Long-term high-dose dietary (soy daidzein metabolite) equol exerts uterotropic effects at the cellular and molecular level which question the safety of uncontrolled and unlimited consumption of soy by women with intact uteri.

Soy Increases Risk of Diabetes:

2007, Serum insulin and leptin concentrations were decreased by lifetime 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).

2008, Soy isoflavones may influence insulin action by means of their well-known receptor-mediated estrogenic activity. Isoflavones also bind to peroxisome proliferators-activated receptors that are strongly associated with insulin action.

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.

2004, Soyfood consumption and development of glycosuria, (glucose in the urine) an important indicator of diabetes.

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.

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.

2000, Twice as many diabetic children had received soy formula in infancy as compared to non-diabetic children.

Soy is in truth loaded with multiple toxins that damage physiological, reproductive and neurological health. For additional soy phyto-toxic study evidence proving the cause of disease and disorders look at:,

Overwhelming study evidence repeatedly PROVES the FDA is protecting a highly powerful U.S. soy phyto-toxic multi-billion dollar industry, over and above their known soy-cause of pain and suffering from severe and fatal human disease. Is this NOT a crime?

An FDA investigation and accountability is long past due! What will you do about deliberate FDA massive destruction of health? What can be done to STOP the FDA from knowingly and willingly concealing soy-poisoning from a trusting American public?

Gail Elbek

Investigative researcher


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