Study Evidence That Soy-Causes Gene Mutations: Genotoxic (Causing DNA Damage):
1998, FDA NCTR report: Our results may be interpreted that soy phytoestrogen genistein is a chromosomal mutagen. www.ncbi.nlm.nih.gov/pubmed/9729267
2006, National Institute of Mind Health, NIMH Confirms: “Tiny, Spontaneous Gene Mutation May Boost Autism Risk. Our results show conclusively that these tiny glitches are frequent in autism, occurring in at least 10% of the cases, and primarily in the sporadic form of the disease, which accounts for 90% of affected individuals.” www.nimh.nih.gov/press/gene-mutations-autism.cfm
2004, Phytoestrogens are a matter of public concern, results point to genotoxicity of (soy) phytoestrogens. www.ncbi.nlm.nih.gov/pubmed/15177650
1991, Genotoxic effects of genistein: A variety of genotoxic effects of phytoestrogens have been reported. Genistein effects occur at relevant low dietary concentrations. No dose is without risk, the dose defines the poison. www.ncbi.nlm.nih.gov/pubmed/17688899
2004, Genotoxicity, DNA Damage: Recent studies indicated that genistein and/or daidzein induced cancer of reproductive organs in rodents…we examined the ability of genistein daidzein and their metabolites to cause DNA damage and cell proliferation. DNA damage by isoflavone metabolites plays a role in tumor initiation by isoflavones via estrogen receptors to estrogen response elements. www.ncbi.nlm.nih.gov/pubmed/14992594
2003, Genotoxic activity of soy daidzein, exhibit genotoxic potential in vitro www.ncbi.nlm.nih.gov/pubmed/14644352
2007, “Concerns” about potential detrimental or other genotoxic effects persist about soy-derived phytoestrogens. This review focuses on soy phytoestrogen, genistein, critically examining dose as a crucial determinant of cellular effects. In toxicology, the well accepted principle of “the dose defines the poison” applies to many toxicants and can be invoked to distinguish genotoxic effects of natural dietary products such as genistein. www.ncbi.nlm.nih.gov/pubmed/17688899
Soy Is A Highly Toxic Isoflavone ESTROGENIC HORMONE DISRUPTOR (Containing: Genistein, Daidzein (Equol), Glycitein):
Hormone disruptors adversely manipulate, interrupt, and aggravate natural hormone systems throughout the human body and brain. Hormone disruptors especially threaten the health of the reproductive system, multiple neuron systems, thyroid (immune system), pancreas, and in fact all hormone systems. Although dangerous for all people, hormone disruptors are of greatest risk during prenatal and early postnatal development when organ and neural systems are forming. The relationship between endocrine disruptors and central nervous system is comprised of multiple feedback loops. The consequences of hormone disruptors causing hormone system failure are critical to health... if not fatal.
2004, Soy causes agonistic and antagonistic properties on ER (Estrogen Receptor) alpha and ER Beta in human cells and functions as an endocrine disruptor. www.ncbi.nlm.nih.gov/pubmed/15084758
1999, NIH report, Phytoestrogens such as soy isoflavones, and organochlorine compounds (pesticides and polychlorinated biphenyls) are two broad classes of putative endocrine disruptors- chemicals that may have the capability to alter a woman’s hormonal milieu. The U.S. public is exposed to dietary sources of phytoestrogens… In addition, residues of organochlorine compounds can be detected in a large proportion of the population. Although phytoestrogens and organochlorine compounds are suspected of being important environmental determinants of hormone-related neoplasia, there are few epidemiological studies testing these hypotheses. http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~0jBvA2:1
2010, Soy As An Endocrine Disruptor: Cause For Caution: Endocrine disrupting compounds (EDCs) alter the function of the endocrine system and consequently cause adverse health effects. Phytoestrogens, natural plant compounds abundantly found in soy and soy products, behave as weak estrogen mimics or as anti-estrogen. They are considered to be EDCs. Supporting evidence that consumption of phytoestrogens is beneficial is indirect and inconsistent. Lifetime exposure to estrogenic substances, especially during critical periods of development, has been associated with formation of malignancies and several anomalies of the reproductive systems. Phytoestrogen consumption in infants, through soy-based formulas is of particular concern. Possible adverse effects should not be taken lightly. www.ncbi.nlm.nih.gov/upbmed/21175082
1998, We investigated the estrogenic activity of environmental chemicals and (soy) phytoestrogens in competition binding assays with ER alpha or ER beta protein. All environmental estrogenic chemicals compete with 17b-estradiol for binding to both ER subtypes. Phytoestrogens, including soy genistein stimulate the transcriptional activity of both ER subtypes at concentrations of 1-10nM. The estrogenic potency of phytoestrogens is significant, especially for ER-beta, and they may trigger many of the biological responses that are evoked by the physiological estrogens. www.ncbi.nlm.nih.gov/pubmed/975150
2005, Male reproductive abnormalities and falling sperm counts prompt interest into threats to global fertility. Little is known about the effects of dietary estrogens on male reproductive health. These non-steroidal estrogens are potent endocrine disruptors that modulate normal physiological functions. Phytoestrogens have become major component in food diet over the last few decades. Soy formula is another common source of phytoestrogen. This use is of particular concern since most vulnerable periods for estrogenic insult are pre-and neonatal periods when irreversible damage can be inflicted on the developing germinal epithelium. www.ncbi.nlm.nih.gov/pubmed/16234205
2008, NIH, National Toxicology Program reports: (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. www.ncbi.nlm.nih.gov/pubmed/18685716
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. All EDCs impaired reproduction. Male sexual behavior proved to be a sensitive index of EDC exposure and embryonic exposure to a variety of EDCs consistently resulted in impaired male sexual behavior. Exposure to EDCs during embryonic development has consequences beyond impaired function of the reproductive axis. www.ncbi.nlm.nih.gov/pubmed/18006066
2011, The increasing incidence of (male) hypospadias is partly attributed to increased gestational exposure to endocrine disruptors. Gestational exposure to (soy) genistein altered the urethral expression of 277 genes. Among the most affected were hormonally regulated genes. Genistein affected tyrosine kinase receptors. Gestational exposure to genistein contributes to hypospadias by altering pathways of tissue morphogenesis, cell proliferation and cell survival. www.ncbi.nlm.nih.gov/pubmed/21421236
2005, Soy isoflavonoids are plant phytoestrogens are increasingly advocated as a natural alternative to estrogen replacement therapy. As weak estrogen agonists/antagonists with a range of other enzymatic activities, the isoflavonoids provide a useful model to investigate the actions of endocrine disruptors. Activational and organizational effects of these compounds on the brain are reviewed. Isoflavonoids act in vivo through both ERalpha and ERbeta. Their neurobehavioural actions are largely anti-estrogenic, either antagonizing or producing an action in opposition to that of estradiol. Small, physiologically relevant exposure levels can alter estrogen-dependent gene expression in the brain and affect complex behavior in a wide range of species. Implications for these findings in humans, particularly in infants, remain uninvestigated and are a subject of increasing public interest. http://www.ncbi.nlm.nih.gov/pubmed?term=Phytoestrogenaction in the adult and developing brain
1997, Compounds within several major groups of chemicals, including organocholine pesticides, polychlorinated biphenyls, phenolic compounds and phthalate esters,have been identified as being weakly oestrogenic by in vitro and vivo screening methods. Many of these compounds are widespread and persistent in the evniromment. In addition to exposure to man-made chemicals, the consuption of plant-derived estrogens in foodstuffs poses a potential risk to human health as (soy) phytoestrogens are more potent estrogens and their intake by some infants is likely to be considerable. www.ncbi.nlm.nih.gov/pubmed/9414467
2000, FDA NCTR: Genistein principal soy isoflavone in diet to male and female rats. Endocrine responsive tissues including brain, liver, mammary, ovary, prostate, testis, thyroid and uterus showed significant dose-depended increases in total (soy) genistein concentration. Female liver contained the highest amount of blood concentrations and physiologic effects of genistein. www.ncbi.nlm.gov/pubmed/10917909
2004, Among the issues raising concerns about human exposure to soy phytoestrogens is how such exposure may affect responsiveness and sensitivity of the exposed subjects to additional xenobiotics, particularly drugs and environmental chemicals with estrogenic or other endocrine disruptor activities. www.ncbi.nlm.nih.gov/pubmed/15320740
2007, Endocrine disrupting chemicals (EDCs) cause defects in sexual behavior and reproductive ability due to their steroid-like or anti-steroid like properties. In addition, endocrine systems such as the hypothalamus-pituitary-thyroid (HTP) axis may be targets of endocrine disruption. There may be multiple targets for interference by various EDC substances suspected of having endocrine disruptor activity, such as (soy) genistein as well as glycitein and daidzein. A striking example is genistein, on one had inhibits thyroid peroxidase enzyme in the thyroid and on the other hand also displays estrogenic and anti-estrogenic effects by interacting with Estrogen Receptor-beta. EDC can act in a transgenerational manner by epigenetic and modification of genes. www.ncbi.nlm.nih.gov/pmc/articles/PMC2174406/
2003, Native soybean lectins (cause intestinal disorders, diarrhea, nausea, vomiting, nutritional deficiencies, immune allergic reactions, possible death) could potentially have deleterious effects on young animals. www.ncbi.nlm.nih.gov/pubmed 12710487
2002, In postmenopausal subjects, mean lutenizing hormone (LH)secretion decreased after discontinuing soy, suggesting a residual estrogenic effects. In a premenopausal woman enhanced LH secretion was observed after soy treatment, suggesting there may be subpopulations of women who are highly sensitive to soy isoflavones. www.ncbi.nlm.nih.gov/pubmed/11925465
2008, Developmental effects of exposure to endocrine disruptors can influence adult characteristics in mammals, but could also have evolutionary consequences. The effects of a continuous pre-and post-natal exposure to high levels of dietary soy isoflavones was evaluated on sexual maturity, morphometric parameters and DNA methylation status in mice. Individuals from a population subjected to a high consumption of soy isoflavones (plant-estrogens) can show alterations in characters that may be of importance from an evolutionary perspective, such as epigenetic and morphometric characters or sexual maturation. www.ncbi.nlm.nih.gov/pubmed/18793434
In truth, soy is loaded with multiple toxins capable of severely damaging physiological, reproductive, and neurological health for all people, and especially the most vulnerable developing fetus, infants, and children. For additional soy phyto-toxic study evidence proving the cause of disease and disorders look at:
http://causingcancers.blogspot.com
http://genderchaos.blogspot.com
http://reproductivedefects.blogspot.com
http://neurodefects.blogspot.com
http://soyhypothyroidism.blogspot.com
http://fetalchildtoxic.com
http://causingcancers.blogspot.com
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 acknowledgement of soy-causation of human pain and suffering from severe and fatal disease. Is this NOT a crime?
What can be done to STOP the FDA from knowingly and willingly concealing soy-poisoning from a trusting American public? An FDA investigation and accountability is long past due!
Gail Elbek
Investigative researcher
gaelbek@yahoo.com
