Soy-Damage Caused To Reproductive Organs….Male
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
2011, Soy isoflavones induced changes in the morphology of seminiferous epithelium of rat testes. Estradiol levels of rats receiving phytoestrogen were significantly higher than control group. Testosterone levels were significantly lower. www.ncbi.nlm.nih.gov/pubmed/21167684
2011, The increasing incidence of 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
2010, Soy genistein and daidzein have the capacity to bind estrogen receptors and affect gene expression. Increasing use of soy–based products has raised concerns about the potential of these products to cause reproductive toxicity. Isoflavones have the capacity to act directly as mitogens in Leydig cells, inducing Leydig cell division. Perinatal exposures of male rats to soy isoflavones affected Leydig cell differentiation, and they imply that including soy products in the diets of neonates has potential implications for testis function. www.ncbi.nlm.nih.gov/pubmed/20554919
2007, In the high phytoestrogen fed group, sperm counts were significantly decreased. Exposure to adult male rat to a high phytoestrogen diet disrupts spermatogenesis…likely due to disruption of estrogen’s actions in the testis. www.ncbi.nlm.nih.gov/pubmed/17244728
2001, Little is know about the influence of phytoestrogens (estrogen-like) molecules on brain. We found that dietary phytoestrogens: significantly decrease body and prostate weights and significantly change sexually dimorphic brain region (AVPV) in male rats. Influence of significant concentrations of phytoestrogen on brain structure should be considered. www.ncib.nlm.nih.gov/pubmed/11733689
2005, Phytoestrogens, derived from plants, (especially soy products), are molecules structurally and functionally similar to estradiol. In summary consumption of dietary phytoestrogens (estrogen mimics) can alter hormone-sensitive hypothalamic brain sexually dimorphic brain volumes in (male and female) rodents during adulthood. www.ncbi.nlm.nih.gov/pubmed/12943716
2008, Endocrine disrupting chemicals (EDCs) exert hormone-like activity and exposure to these compounds may induce deleterious effects including functional alterations that contribute to decreased reproduction and fitness. 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. www.ncbi.nlm.nih.gov/pubmed/18006066
2012, Exposure to soy isoflavones (estrogenic agents) caused a decrease in testosterone production in Leydig cells and contributes to deficiencies in reproductive capacity. www.ncbi.nlm.nih.gov/pubmed/22155228
2000, National Center for Toxicological Research sferguson@nctr.fda.gov. Developmental neurotoxicity of endocrine disruptors: focus on estrogens. Need for assessing the neurotoxicity of these compounds following developmental exposure. Attention comes from literature on the effects of developmental exposure to exogenous estrogen on later behavioral and neuropathiological alterations. Ongoing studies at NCTR on four such estrogen mimics; Soy genistein, methoxychlor, nonylphenol and ethinyl estradiol. Volume of the sexually dimorphic nucleus of the medial preoptic area was reduced by genistein….” www.ncbi.nlm.nih.gov/pubmed/11233764
1998, Phytoestrogens have estrogenic and/or anti-estrogenic activity. Evidence from studies of various animal species has demonstrated that ingestion of high levels of phytoestrogens can produce adverse effects on reproductive endpoints including fertility. Studies in animals also show that exposure to high doses of phytoestrogens during development can adversely affect brain differentiation and reproductive development in rodents. In humans, high doses of phytoestrogens in infants should be addressed as a matter of priority so that any risks can be established. www.ncbi.nlm.nih.gov/pubmed/988630
2008, 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. In vitro studies have proven genistein to induce apoptosis of testicular cells at certain levels, thus raising concerns about effects it could have on male fertility. www.genistein.net/cancer.html
2004, Results demonstrate that rats fed a mixture of dietary soy isoflavones showed significantly altered testicular microsomal steroidogenic enzyme activity profiles during development at Post-Natal Day 28 as a result of early exposure to isoflavones at levels obtainable by humans. lib.bioinfo.pl/pmid:15698548
2004, Soy Isoflavones are known endocrine disruptors. Isoflavones genistein and daidzein have similar molecular weights and structural characteristics to that of 17-beta estradiol, exert estrogenic and antiestrogenic properties. Major source of endocrine disrupting substances soy derived isoflavones are most abundant and most studied are known endocrine disruptors. Daidzein can be further metabolized to the potent and abundant molecule equol that has the unique ability to specifically bind 5 alpha-dihydro-testosterone, and to act in turn to inhibit the action of this potent androgen. www.ncbi.nlm.nih.gov/Pubmed/15454683
2008, The isoflavone genistein is the most estrogenically active molecule present in soy. Results show that genistein through an estrogen receptor (ER)-mediated action, affects reproductive and nonreproductive organs, modulates gene expression in the whole body of male mice in a dose-and time-dependent manner, at all developmental ages. www.ncbi.nlm.nih.gov/pubmed/18281260
2008, Soy is associated with lower sperm concentration www.ncbi.nlm.nih.gov/pubmed/18650557
2010, Soy genistein inhibits 3beta-HSD activity convert cholesterol into testosterone. www.ncbi.nlm,.nih.gov/pubmed/20453869
2010, Soy and soy-based products are widely consumed by infants and adult individuals. These studies show that long-term exposure to dietary soy and phytoestrogens may affect male reproductive function resulting in a decrease in sperm count and fertility. www.ncbi.nlm.nih.gov/pubmed/20171261
2001, Soy Alters Testicular activity at levels obtainable by humans. www.ncbi.nlm.nih gov/pubmed/15698548
2010, Soy is reproductive endocrine disruptor: decreased male fertility. www.ncbi.nlm.nih.gov/pubmed/19919579
2005, Soy isoflavones are estrogen mimics that bind estrogen receptors and limited data exists regarding the influence of soy-derived dietary isoflavones in the brain. When animals were switched from phytoestrogen-rich diet volume of the sexually dimorphic nucleus of the preoptic area was decreased in males. www.ncbi.nlm.nih.gov/pubmed/15811581
2005, Dietary estrogens, soy, and male fertility causes “estrogenic insult” www.ncbi.nlm.nih.gov/pubmed/16234205
2008 Soy case of gynecomastia associated with soy product consumption www.ncbi.nlm.nih.gov/pubmed/18558591
2008 Soy-cause of Erectile Dysfunction in adulthood. www.ncbi.nlm.nih.gov/pubmed/17673432
2011. A number of reports demonstrate adverse effects of soy isoflavones due to their estrogen-like properties has increased. Loss of libido and erectile dysfunction is associated with soy product consumption. This case emphasized the impact of soy isoflavones in the regulation of sex hormone and associated physical alterations. www.ncbi.nlm.nih.gov/pubmed/21353476
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
Soy Damage to Female Reproductive System:
2009, Genistein, a natural isoflavone compound found in soy products affects diverse cell functions, including proliferation, differentiation and cell death. An earlier study by our group showed that genistein has cytotoxic effects on mouse blastocysts and is associated with defects in their subsequent development in vitro. In this study genistein induced a significant reduction in the rate of oocyte maturation, fertilization, and in vitro embryo development. Genistein decreased placental and fetal weights. With aid of in vivo mouse model we showed that consumption of drinking water containing genistein led to decreased oocyte maturation and in vitro fertilization, as well as early embryonic developmental injury. Our findings support inhibition of retinoic acid receptors in blastocysts treated with genistein during oocyte maturation. www.ncbi.nlm.nih.gov/pubmed/19490995
2005, FDA NIEHS study: In summary, neonatal treatment of mice with genistein caused abnormal estrous cycles, altered ovarian function, early reproductive senescence, and subfertility/infertility at environmentally relevant doses. www.ncbi.nlm.nih.gov/pubmed/15930323
1993, Estrogen exposure during critical periods of development promotes androgenization of the brain which is reflected in altered morphology, behavior, and cyclic hormone secretion in females. There is dose-response characteristics of neonatal exposure to the isoflavonoid phytoestrogen genistein on pituitary sensitivity to gonadotropin release in the sexually dimorphic nucleus of the preoptic area in female rats. Results confirm that low doses of genistein have nonandrogenizing, pituitary-sensitizing effects, while higher doses of genistein mimic the more typical effects of estrogens. Morphologic and physiologic endpoints more completely defines the reproductive consequences of environmental (soy isoflavone genistein) estrogen exposure during critical periods of central nervous system development. www.ncbi.nlm.nih.gov/pubmed/8448414
2011, Developmental exposure to estrogenic compounds can disrupt sexual differentiation and adult reproductive function in many animals including humans. Phytoestrogens in the diet comprise a significant source of estrogenic exposure to humans, particularly infants who are fed soy-based infant formula. Rodent models have used various dosing strategies to mimic the phytoestrogen levels in human populations. Studies clearly demonstrate that environmentally relevant doses of genistein have significant negative impact on ovarian differentiation, estrous cyclicity and fertility in the rodent model. Additional studies of reproductive function in humans exposed to high levels of soy phytoestrogens during development are warranted. www.ncbi.nlm.nih.gov/pubmed/20955782
2009, Genistein at 500ppm and ethinyl estradiol (prescribed estrogen drug) produced similar effects in continuously exposed rats, including decreased body weights, accelerated vaginal opening, and altered estrogen cycles in young animals. These compound-specific effects appeared to be enhanced in the offspring of prior exposed generations. www.ncbi.nlm.nih.gov/pmc/articles/PMC2706590/
2008, Disruption of female reproductive physiology following neo-natal exposure to soy phytoestrogens is associated with decreased GnRH activation and kisspeptin fiber density in the hypothalamus compared to control groups. The anteroventral periventricular (AVPV), Kisspeptin fiber density was significantly lower in the estradiol benzoate and Genistein groups, a known mechanism by which these endocrine disrupting compounds can impair female reproductive function. www.ncbi.nlm.nih.gov/pubmed/1865497
2009, FDA, NIEHS report: Oral exposure to genistin…form of soy genistein during neonatal life adversely affects the female reproductive system. Developmental exposure to estrogens is associate with adverse consequences later in life; ovarian, vaginal opening, abnormal estrous, decreased fertility, delayed parturition. www.ncbi.nlm.nih.gov/pubmed/20049207
2009, Adverse transfer through generations: Exposure to Genistein at 500ppm and ethinyl estradiol at 50ppb produced similar effects in continuously exposed rats, including decreased body weights, accelerated vaginal opening and altered estrous cycles in young animals. …a reduction in litter size was evidence in genistein-treated animals. These compound-specific effects appeared to be enhanced in the offspring of prior exposed generations. www.ncbi.nlm.nih.gov/pubmed/19159674
2005, NIEHS Soy adverse effects on female development on reproduction following neonatal soy exposure. Altered ovarian function early reproductive senescence, and infertility at relevant doses, pregnancy was not maintained. www.ncbi.nlm.nih.gov/pubmed/15930323
2006, FDA, NIEHS report, Soy genistein during development alters ovarian differentiation inhibiting oocyte next breakdown….. www.ncbi.nih.gov/pubmed/16192398
2002, FDA, NIEHS report: Neonatal exposure to genistein demonstrate alterations in ovary….warrant further soy-based food investigations.2002. www.ncbi.nlm.nih.gov/pubmed/12297547
2007, Disruption of female reproductive system by soy phytoestrogen genistein in adulthood. www.ncbi.nlm.nih.gov/pubmed/17250991
2008, Infant girls fed soy show reestrogenization at 6 months. Examination of infants for plausible effects of estrogens is valid and repeatable www.ncbi.nlm.nih.gov/pubmed /18335112
2009, Neonatal exposure to soy genistein disrupts ability of female mouse to support embryo implantation = reproductive failure. www.ncbi.nlm.nih.gov/pubmed/19005167
2007, FDA, NIEHS report; Soy genistein causes deleterious effects on the developing female reproductive system in adulthood. Altered ovarian differentiation, disrupted ovarian function and estrous cyclicity caused by neonatal exposure, reduced fertility altered mammary gland and behavioral endpoints. Further trangenerational effects were observed in neonatal treatment with genistein at environmentally relevant doses caused adverse consequences on female mice development which is manifested in adulthood. Feeding genistein found in soy formula are similar to those obtained from injecting genistein in mice. www.ncbi.nlm.nih.gov/pubmed/17604387
2009, Basal and gonadotropin-stimulated P(4) secretion were inhibited in granulose cells cultured in presence of daidzein (soy) phytoestrogen. Expression of ER alpha and ER beta mRNA, as well as ERbeta protein, was up-regulated by daidzein. Daidzein actions suggest disadvantageous effects of the phytoestrogen on reproductive processes in females. www.ncbi.nlm.nih.gov/pubmed/19617652
2010, Soy-based infant formula contain high levels of the estrogenic isoflavone genistein leading to “concern” that neonatal genistein exposure could cause acute and/or long-term adverse effects on reproductive and other organs. Neonatal genistein treatment caused increased relative uterine weight, down-regulation of progesterone receptor in uterine epithelia, genistein was also seen in the neonatal ovary, and thymus, which had an increase in the incidence of multioocyte follicles (MOF) and decrease in thymic weight. Increased MOF’s persisted into adulthood in neonatally treated genistein females. www.ncbi.nlm.nih.gov/pubmed/20357267
In truth, soy is 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:
http://causingcancers.blogspot.com
http://causingautism.blogspot.com
http://foodhealthroulette.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
