How Soy Irreversibly Maculinizes Female Brain, and Feminizes Male Brain:
2002, Neurobehavioral effects of dietary soy phytoestrogens; These studies used a commercially available diet rich in phytoestrogens (Phyto-rich) verses a diet relatively free of phytoestrogens (Phyto-free). The phyto-rich diet fed to adult male and female rats produced anxiolytic effects. When learning and memory parameters were examined the visual-spatial memory (VSM), the diet treatments significantly changed the typical sexually dimorphic pattern of VSM. Phyto-rich females executed the VSM task in a manner similar to that of phyto-free fed males. Phyto-rich males VSM was comparable to Phyto-free fed females. Results indicate that consumption of dietary phytoestrogens resulting in high plasma isoflavone levels (in many cases over a relative short interval of consumption) can significantly alter sexually dimorphic brain region, anxiety, learning, and memory. These findings identify biological actions of phytoestrogens on the brain and behavior. www.ncbi.nlm.nih.gov/pubmed/11836067
2001, NCTR/FDA report: Soy phytoestrogen genistein, the principal isoflavone in soybeans has adverse effects on animal reproduction. Since adult physiology and behavior are sensitive to perturbation by developmental estrogens, exposure to genistein during development may produce behavioral alterations. Results indicate that developmental genistein treatment, at levels that decrease maternal and offspring body weight, causes subtle alterations in some sexually dimorphic behaviors. www.ncbi.nlm.nih.gov/pubmed/10828262
2006, Neonatal (soy) genistein or BPA alters sexual differentiation de-masculinized males and de-feminized females. Endocrine active compounds…phytoestrogen genistein. Acute exposure to Endocrine Active Compounds alter AVPV Development www.ncbi.nlm.nih.gov/pubmed/16427766
2007, Soy de-masculinizes male, de-feminizes females…(Soy) Genistein exposure during critical developmental periods could disrupt brain differentiation. www.ncbi.nlm.nih.gov/pubmed/17109964
2003, Evidence Soy de-feminizes female brain: www.ncbi.nlm.nih.gov/pubmed/13129486
2010, Maternal exposure to daidzein alters behavioral and estrogen receptor alpha expression in adult female offspring. Females exposed to daidzein showed significantly less ERalpha expression in bed nucleus of the stria terminals and medial amygdale in the brains of female mice. Findings show that maternal exposure to daidzein has a masculinization effect on memory and social behavior, suggesting a potential role of ER alpha distribution in the brain. www.ncbi.nlm.nih.gov/pubmed/20505512
1996. Reversal of sex roles in genetic female mice by disruption of estrogen receptor gene. Deficiency of normal estrogen receptor gene function led to behavioral change in female mice, aggression was increased. Disruption of ER gene led to a pattern of hormonal and neural changes which caused female to lose their normal female-typical behavior and to behave more like males. www.ncbi.nlm.nih.gov/pubmed/8990081
2005, De-masculinize male mice: John Hopkins School of Medicine: Exposure to endocrine disrupting chemicals adversely affects reproductive development and behavior in males. Aggressive behaviors were decreased whereas defensive behaviors were increased in males that received the low-does genistein diet. Exposure to genistein during critical periods of sex differentiation results in concurrent and persistent de-masculinization in male mice. Given the popularity of soy infant formulas the influence isoflavone exposure on reproductive and behavioral health in boys and men should be considered. www.ncbi.nlm.nih.gov/pubmed/15708785
2003, Johns Hopkins, AB Wisniewski et al, Perinatal (soy) genistein exposure results in transient and lasting alterations in masculinization of the reproductive system. Exposure to genistein during gestation and lactation demasculinizes the reproductive system in rats. www.ncbi.nlm.nih.gov/pubmed/12629420
2011, Genistein impairs early testosterone production via estrogen receptor alpha. It is well known that genistein, an isoflavone found in soybeans and soy products, mimics the actions of estrogens and that fetal testis is responsive to estrogens. Genistein inhibits testosterone secretion by fetal Leydig cells in mice during early fetal development within the “masculinization programming window.” Results suggest that fetal exposure to phytoestrogens can affect the development and function of the male reproductive system. www.ncbi.nlm.nih.gov/pubmed/21624456
2001, FDA, National Center For Toxicological Research (NCTR) report: Effects of dietary exposure to the weak estrogen, (soy) genistein have been assessed using a number of techniques with validated gender related outcome measures. Findings indicate dose-related alterations of the volume of the sexually dimorphic nucleus of the medial preoptic area were observed in genistein-exposed male rats. Observations indicate that dose-related effects of developmental and chronic dietary exposure to genistein can be observed in the rodent. Additional studies are necessary to further predict the effect(s) of genistein on human gender-based development. www.ncbi.nlm.nih.gov/pubmed/11488560
1993- The results confirm that low doses of genistein have non-androgenizing, pituitary-sensitizing effects while higher doses of genistein mimc the more typical effects of estrogens….defining the reproductive consequences of environmental estrogen exposure during critical periods of central nervous system development. www.ncbi.nlm.nih.gov/pubmed/8448414
2007, Genistein is a phytoestrogen, abundant in soybeans that can bind estrogen receptors and sex hormone binding proteins, exerting both estrogenic and antiestrogenic activity. Results demonstrate that genistein acts similarly to estradiol. In this avian model embryonic exposure to phytoestrogens may have life-long effects on sexual differentiation of brain structures and behaviors. www.ncbi.nlm.nih.gov/pubmed/17274996
2007, Isoflavones, the most abundant phytoestrogens in soy food are structurally similar to 17beta-estradiol. It is known that 17beta-estradiol induces cell death in anteroventral periventricular nucleus (AVPV) in rat brain. There is evidence that consumption of soy isoflavones reduces the volume of AVPV, (controls sex typical physiology and behaviors). These findings proved direct evidence that consumption of soy isoflavones, influences the loss of ERbeta-containing neurons in male AVPV. www.ncbi.nlm.nih.gov/pubmed/17266774
2003, Sexually dimorphic brain volumes (sexually dimorphic nucleus of the hypothalamus preoptic area SDN-POA, and anteroventral periventricular AVPV nucleus: male characteristics/female characteristics and behaviors) are influenced by estrogens. In summary, consumption of dietary phytoestrogens (estrogen mimics) can alter hormone-sensitive hypothalamic brain regions in rodents. www.ncbi.nlm.nih.gov/pubmed/12943716
2001, Males fed the soy phytoestrogen diet had significantly higher phytoestrogen concentrations in a number of brain regions, (frontal cortex, amygdale & cerebellum) and in frontal cortex. Dietary phytoestrogens significantly sex-reversed the normal sexually dimorphic expression of the visual spatial memory (VSM). In females VSM was enhanced, in males VSM was inhibited by the same phytoestrogen diet. www.ncbi.nlm.nih.gov/pubmed/11801187
Study Evidence That Soy = Dangerous HORMONE DISRUPTOR:
Endocrine disruptors adversely manipulate, interrupt, and aggravate natural hormone systems throughout the human body and brain, with highest disruptor threat targets the reproductive, multiple neuron systems, and the immune system. 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 endocrine system is most important for the developmental process and the consequences when this hormone system malfunctions are critical to health if not fatal.
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
1998, We investigated the estrogenic activity of environmental chemicals and 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
2011, The increasing incidence of hypospadias is partly attributed to increased gestational exposure to endocrine disruptors. Gestational exposure to 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=Phytoestrogen action in the adult and developing brain
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
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
2002, Concerns have been raised about the potential adverse effects on reproductive health and immune status of farm animals following exposure to environmental compounds that disrupt normal hormonal actions. These compounds range from natural plant estrogens, (genistein), to growth promoting pharmaceuticals to chemicals spread in water, sewage, sludge or detergents, plastics, pesticides (DDT), and industrial chemicals. These compounds are commonly termed ‘endocrine disrupting compounds or endocrine disruptors’ due to their ability to disrupt hormone synthesis, storage or metabolism. Susceptibility of target tissues is related to the stage of development, cumulative exposure dose and the immune status of the individual. Effects that are observed in the adult may be due to exposure to endocrine disruptors during fetal life. www.ncbi.nlm.nih.gov/pubmed/12142238
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
1997, Man-made chemicals potential risk to human health include phytoestrogens comparing to plastics, pesticides etc. 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 genistein concentration. Female liver contained the highest amount and male whole brain contains the least 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
2004, Feeding with a soy formula should not be recommended for the prevention of allergy or food intolerance in infants at high risk of allergy or food intolerance: www.ncbi.nlm.nih.gov/pubmed/15266499
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 genistein as well as glycitein and daidzein (soybean isoflavones). 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
In truth, soy is loaded with multiple toxins that severely damage physiological, reproductive and neurological health. For additional soy phyto-toxic study evidence proving the cause of disease and disorders look at:
http://causingcancers.blogspot.com
http://causingautism.blogspot.com
http://reproductivedefects.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 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
gaelbek@yahoo.com
