Study Truth About The Multiple Adverse Health Effects Caused By Early Exposure To Soy:
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 is of particular concern. Possible adverse effects should not be taken lightly. www.ncbi.nlm.nih.gov/upbmed/21175082
FDA Scientists Against Soy:
1999, 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. www.alkalizeforhealth.net/Lsoy2.htm
1998, FDA NCTR
Reports: Our results may be interpreted that soy phytoestrogen genistein is a
chromosomal mutagen. www.ncbi.nlm.nih.gov/pubmed/9729267
2001, NIEHS Report: Dietary (soy) genistein produced effects in multiple estrogen-sensitive tissues in male and female mice consistent with estrogenic activity…...within exposure ranges in humans. www.ncbi.nlm.nih.gov/pubmed/11738518
1999, 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 naïve to assume that exposure
to these compounds is always good. Inappropriate or excessive exposure to
phytoestrogens may be detrimental to health.
www.ncbi.nlm.nih.gov/pubmed/10548876
Evidence That Early Exposure to Soy Hormone Disruptors Can Masculinize Female Brain, and Feminize Male Brain:
Soy de-masculinized male, and de-feminized females…(Soy) Genistein during critical period could disrupt brain differentiation. www.ncbi.nlm.nih.gov/pubmed/17109964
Neonatal (soy) genistein or BPA alters sexual differentiation de-masculinizing males and de-feminizing females… Phytoestrogenic genistein is a endocrine active compounds (EAC). Acute exposure to EAC alter AVPV Development www.ncbi.nlm.nih.gov/pubmed/16427766
2011, Developmental exposure to estrogenic compounds can disrupt sexual differentiation in 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. Studies clearly demonstrate that environmentally relevant doses of genistein have significant negative impacts on ovarian differentiation, estrous cyclicity, and fertility in the rodent model. Additional studies of reproductive function in human populations exposed to phytoestrogens during development are warranted. www.ncbi.nlm.nih.gov/pubmed/20955782
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
Masculinize Female Brain:
Soy De-feminizes female brain. Reversal of sex roles in genetic female mice by disruption of estrogen receptor gene. www.ncbi.nlm.nih.gov/pubmed/13129486
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
De-feminize female mice: 2010, Females exposed to (soy)daidzein showed significantly less ERalpha expression in bed nucleus of the stria terminalis and medial amygdale. 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 brains….
www.ncbi.nlm.nih.gov/pubmed/20505512
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-dose (soy) 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
Feminize Male Brain:
2003 study, 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 de-masculinizes the reproductive system in rats. www.ncbi.nlm.nih.gov/pubmed/12629420
2011 study; A Lehraiki et al. It is well known that genistein, an isoflavone found in soybeans and soy products, mimics the actions of estrogens …. Genistein inhibits testosterone secretion by fetal Leydig cells during early fetal development within the “masculinization programming window." These 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/ppubmed/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, has an organizational effect on vasotocin system and copulatory behavior. In this avian (quail) 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
Maternal Diet Transfers Toxic Soy Estrogenic Endocrine Disruptors To Her Developing Fetus:
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. www.ncbi.nlm.nih.gov/pubmed/20638367
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. www.ncbi.nlm.nih.gov/pubmed/9876473
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. Raise public awareness and set
guidelines for marketing flavonoid supplements to reduce risk of infant
leukemias. www.ncbi.nlm.nih.gov/pubmed/17468513
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. ….soy phytoestrogens. Effects of genistein on reproductive development and spatial learning required exposure throughout the pre-and postnatal periods. www.ncbi.nlm.nih.gov/pubmed/20053350
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.
Placental transfer of genistein to levels similar to those in maternal brain. Crosses rat placenta and can reach fetal brain from maternal consumption …relevant to those observed in humans www.ncbi.nlm.nih.gov/pubmed/11297868
2002, Johns Hopkins study; Primary goal of this study
was to compare effects of perinatal rat exposure with life-long exposure to
genistein, an estrogenic compound in soy on the endocrine and immune system in adulthood. These data illustrate that
exposure to genistein during pregnancy and lactation exerts long-lasting effects
on the endocrine and immune systems in adulthood. www.ncbi.nlm.nih.gov/pubmed/12520091
2007, Concern has been raised of potential adverse effects due to the estrogenic and other activities of isoflavones. To assess the teratogenic and fetal toxic potential of genistein several rat studies were conducted. Treatment related anomalies were observed at concentrations of > or = 10microg and 100 microg/mL, all embryos were malformed. Adverse effects in the pups were observed. On basis of definitive Prenatal development study the NOAEL for maternal toxicity and adverse effects on embryonic development was considered to be 100mg/kg/day when administered orally by dietary admix. www.ncbi.nlm.nih.gov/pubmed/17433519
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. This study demonstrates in mammals that 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
Maternal soy genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring. www.ncbi.nlm.nih.gov/pubmed/9538161
Maternal exposure to genistein can increase mammary tumorigenesis in offspring, mimicking the effects of in utero estrogenic exposure…increasing susceptibility. www.ncbi.nlm.nih.gov/pubmed/10425307
Soy-Cause of Thymus Masses: Developmental soy exposure during pregnancy and lactation causes long-lasting adverse effects into adulthood.
www.ncbi.nlm.nih.gov/pmc/articles/PMC2039948/
2007, Fetal programing of colon cancer in adult rats. Maternal-only soy protein isolate increased the percentage of animals bearing multiple colon tumors. joe.endocrinology-journals.org/content/195/1/79.full
(Soy) Daidzein and genistein are found in higher concentrations than BPA in fetal amniotic fluid www.ncbi.nlm.nih.gov/pubmed/16112541
Maternal soy exposure to fetus; evidence of soy phytoestrogens found in amniotic fluid.
www.ncbi.nlm.nih.gov/pubmed/11888703
2005 Phytoestrogens transfer between mother and fetus…..placental transfer…the effects of fetal exposure to phytoestrogens should be studied further. www.ncbi.nlm.nih.gov/pubmed/16194669
2009 Soy genistein has cytotoxic effects on embryo development. Fetal and infant damage. www.ncbi.nlm.nih.gov/pubmed/19490995
Since dietary phytoestrogens account for a significant proportion of human exposure to potential endocrine modulators, and since the placenta does not represent a barrier to daidzein or related estrogenic isoflavones, the consequences of these exposures early in life should be examined and monitored carefully. www.ncbi.nlm.nih.gov/pubmed/11875621
2002, Soy Causation of inappropriate thyroid hormone levels can also have
a devastating effect on the developing human brain especially during the first
12 weeks of pregnancy when the fetus depends on the mother’s thyroid hormones
for brain development. www.rense.com/general3/soy.htm
Exposure To Soy Hormone Disruptors Prove Adverse Male Reproductive Effects:
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
(Soy) Genistein exposure predicts future adverse reproductive effects www.ncbi.nlm.nih.gov/pubmed/20955782
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
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
Soy Alters Testicular activity at levels obtainable by humans.
www.ncbi.nlm.nih gov/pubmed/15698548
Soy is reproductive endocrine disruptor: decreases male fertility.
www.ncbi.nlm.nih.gov/pubmed/19919579
Soy is associated with lower sperm count; www.ncbi.nlm.nih.gov/pubmed/18650557
Soy genistein inhibits 3beta-HSD activity convert cholesterol into testosterone. www.ncbi.nlm,.nih.gov/pubmed/20453869
2004, Soy Isoflavones are known endocrine disruptors. Isoflavones genistein and daidzein have similar molecular weights and structural characteristics to that of 17-beta estradiol, exerting estrogenic and antiestrogenic properties. Soy phytoestrogens 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
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
Dietary estrogens, soy, and male fertility results in “estrogenic insult” www.ncbi.nlm.nih.gov/pubmed/16234205
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
Soy cause of gynecomastia (breast growth) in males associated with soy product consumption. www.ncbi.nlm.nih.gov/pubmed/18558591
Soy-cause of Erectile Dysfunction in adulthood. www.ncbi.nlm.nih.gov/pubmed/17673432
Maternal vegetarian diet associated with hypospadias......soy phytoestrogens have a deleterious effect on the developing male reproductive system. www.ncbi.nlm.nih.gov/pubmed/10619956
Endocrine disruptors and soy genistein damage to male urethral development www.ncbi.nlm.nih.gov/pubmed/21421236
2001, Neonatal exposure to genistein reduces expression of estrogen receptor alpha and androgen receptor in testes of adult mice and affects male reproductive organs at molecular levels in adulthood. www.ncbi.nlm.nih.gov/pubmed/11873863
2011, Fetal exposure to phytoestrogens can affect the development and function of the male reproductive system www.ncbi.nlm.nih.gov/pubmed/21624456
Exposure to soy phytoestrogens in perinatal period affects androgen secretion by testicular leydig cells in adult rat. Phytoestrogens have ability to regulate Leydig cells. www.ncbi.nlm.nih.gov/pubmed/17569756
2008, Soy isoflavones can act like estrogen, stimulating development and maintenance of female characteristics, 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
Exposure To Soy Hormone Disruptors Prove Adverse Female Reproductive Effects:
2009, Adverse soy-transfer through generations: 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
NIEHS Report; Deleterious effects on female reproductive system in adulthood. www.ncbi.nlm.nih.gov/pubmed/17604387
Disruption of female reproductive system by soy phytoestrogen genistein in adulthood. www.ncbi.nlm.nih.gov/pubmed/17250991
Infant girls fed soy show reestrogenization at 6 months…..Examination of infants consuming soy for plausible effects of estrogens is valid and repeatable www.ncbi.nlm.nih.gov/pubmed /18335112
Reproductive failure; soy genistein causes failure to support egg www.ncbi.nlm.nih.gov.pubmed/19005167
2011, Developmental exposure to estrogenic compounds can disrupt sexual differentiation in 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. Studies clearly demonstrate that environmentally relevant doses of genistein have significant negative impacts on ovarian differentiation, estrous cyclicity, and fertility in the rodent model. Additional studies of reproductive function in human populations exposed to phytoestrogens during development are warranted. www.ncbi.nlm.nih.gov/pubmed/20955782
Soy adverse effects on female development on reproduction following neonatal soy exposure NIEHS report. Altered ovarian function early reproductive senescence, and infertility at relevant doses, pregnancy was not maintained. www.ncbi.nlm.nih.gov/pubmed/15930323
NIEHS: Soy genistein during development alters ovarian differentiation inhibiting oocyte next breakdown. www.ncbi.nlm.nih.gov/pubmed/16192398
NIEHS: Neonatal exposure to genistein demonstrate alterations in ovary….warrant further soy-based food investigations. www.ncbi.nlm.nih.gov/pubmed/12297547
Neonatal exposure to soy genistein disrupts ability of female mouse to support embryo implantation = reproductive failure. www.ncbi.nlm.nih.gov/pubmed/19005167
NIEHS Report: Oral exposure to genistin…a 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…i.e. ovarian, vaginal opening, abnormal estrous, decreased fertility delayed parturition. www.ncbi.nlm.nih.gov/pubmed/20049207
2004, In utero (fetal) exposure to genistein: There is pronounced ductal hyperplasia, lactational changes, and fibrosis were observed in mammary glands from genistein group. Postnatal exposure to pharmacological levels of genistein induces profound morphological changes in the mammary glands of adult female rats. There is also potential of genistein to modulate toxicological effects of other toxicant mixtures. Effects of in utero exposure to environmental toxicants and potential interaction with postnatal genistein there is enlargement of the thoracic mammary glands observed in female rat offspring at 200 days of age. www.ncbi.nlm.nih.gov/pubmed/14514955
2006, Dietary component, such as fat or phytochemicals in plant foods, can have an opposite effect on breast cancer risk if exposed in utero through a pregnant mother or at puberty. Dietary exposure during pregnancy often has similar effects on breast cancer risk among mothers and their female offspring. There is extensive programming of the mammary gland during fetal life and subsequent reprogramming at puberty and pregnancy. Thus, dietary exposure during pregnancy and puberty may play an important role in determining later risk by inducing epigenetic changed that modify vulnerability to breast cancer. www.ncbi.nlm.nih.gov/pubmed/17261753
2011, Isoflavones are non-nutritive components of soy responsible for estrogenic responses. There is evidence of potential adverse effects e.g., stimulation of estrogen-dependent mammary tumors and aberrant peri-natal development. Studies of the major soy isoflavone genistein were conducted in pregnant and lactating rats to quantify placental and lactational transfer to plasma and brain to better understand biological effects observed in multi-generational studies. The information derived from these studies also makes it possible to predict internal exposures of children to genistein from soy infant formula. www.ncbi.nlm.nih.gov/pubmed/21034763
BRAIN: Evidence That Soy Estrogenic Endocrine
Disruptors Causes Adverse Brain Functions:
Several
brain regions
that control mood, cognition, memory, bonding, and coordination are
sensitive
to soy's estrogenic hormone disruptors, enzyme inhibition, heavy metals,
and anti-nutrients. Soy is a proven neuro-endocrine disruptor
capable of acting as an agonist, antagonist, or modulator of the
synthesis
and/or metabolism of neuro-peptides, neuro-transmitters, or
neuro-hormones that
alter multiple behavioral processes throughout the brain. It is
repeatedly study proven that during most
fragile brain development, fetal, infant, and/or child exposure to soy
estrogenic
endocrine disruptors can cause irreversible adverse interruptions and
rearrangements
of multiple brain systems related to an assortment of developmental
brain
disorders.
1999, FDA Study: “FDA Scientists Against Soy”: NIH scientists Drs. Doerge and Sheehan report, “Thus 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. ….the public will be put at potential risk from soy isoflavones in soy protein, isolate without adequate warnings and information.” www.alkalizeforhealth.net/Lsoy2.htm
2011, NIH web site: Effects of genistein in maternal diet on reproductive development and spatial learning in male rats.. exposure to pregnant females is toxic to multiple organs and reproductive behavior in male offspring…. Also alters learning and memory. Sex based differences in behavior….. sensitive to endocrine disruption… www.ncbi.nlm.nih.gov/pmc/articles/PMC2834867/
2008, Genisein, a
phytoestrogen found abundantly in soy products stimulates brain protein synthesis
rates. In the cerebral cortex, the
cerebellum and the hypothalamus, results suggest that dietary genistein
elevates the rat of protein synthesis in the brain. Estrogen receptors of the brain are at least
partly related to the rate of brain protein synthesis caused by genistein.
2002, Small doses
of soy genistein or daidzein can alter estrogen-dependent gene expression in
brain and complex behavior www.ncbi.nlm.nih.gov/pubmed/11836071
Soy Significantly
Increases VASOPRESSIN:
2003, Soy Isoflavones form one of the main classes of phytoestrogens and
exert
estrogenic and anti-estrogenic effects on the central nervous system.
Effects
are not limited to reproductive behavior, but include effects on
learning and anxiety and actions on the hypothalmic-pituitary axis. The
group fed soy isoflavones 150 microg/g diet spent significantly less
time in active social interaction, displayed anxiogenic effects, and had
significantly elevated stress-induced corticosterone concentrations.
Stress-induced
plasma vasopressin concentrations were also significantly elevated.
Major changes in behavioral measures of anxiety and in stress hormones
can result from the soy isoflavone. These changes are as striking as
those seen following drug administration. (Elevated vasopressin is
reported cause of autism).www.ncbi.nlm.nih.gov/pubmed/12618915
GAMA:
2007, It is
surprising that contrary to estrogen, isoflavones, specifically soy isoflavones
genistein and daidzein are toxic to
primary neuronal culture at high concentrations. Toxic effect of genistein and daidzein could
be due to their inhibition of the GAMA(A) receptor resulting in further
enhancement of excitation by glutamate and leading to cellular damage. www.ncbi.nlm.nih.gov/pubmed/17245525
OXYTOCIN: Oxytocin, another neurotransmitter is related to pair bonding, enhances interpersonal trust, and the
ability to infer the emotions of others from facial cues.
2011, Phyotestrogens
have widespread effects in the adult human brain which have been previously
reviewed in detail elsewhere. Genistein
stimulates ER (estrogen receptor) -beta mRNA expression in the PVN,
(paraventricular nucleus), an effect opposite to that of 17b estradiol. PVN is primary site of oxytocin
production. ER-alpha is required for the
up-regulation of oxytocin. Consumption
of prepared phytoestrogen supplement attenuated estrogen-dependent upregulation
of oxytocin in the rat ventromedial nucleus.
www.ncbi.nlm.nih.gov/pmc/articles/PMC3074428/
CHOLINE:
1986, Results suggest
that soy lecithin preparation exposure has a major effects on cholinergic
synaptic development and reactivity, followed by secondary changes in other
neurotransmitter pathways. www.ncbi.nlm.nih.gov/pubmed/3455608
(Choline acetyltranserase
forms the Choline Neurotransmitter System).
Cholinergic systems are implicated in numerous neurologic functions, and
excess cholinergic neuron differentiation can lead to aberrant brain
development. www.nbi.nlm.nih.gov/pubmed/17211134
Catecholaminergic
Neurotransmitter System: Transporter
system for dopamine to norepinephrine networks related to higher cognitive
functions such as attention, focus, and motor functions. ADHD is believed to result from abnormalities
in the frontal regions of the brain particularly prefrontal cortex. Underpinning these abnormalities are
disturbances of catecholamine neurotransmission.
1986, Previous work
has shown that exposure of developing rats to soy lecithin preparations
influences macromolecular constituents of immature brain cells and causes
abnormal behavioral patterns.
Catecholamine transmitter levels were profoundly disturbed. Transmitter uptake capabilities were affected
by developmental exposure to soy lecithin as was tyrosine hydroxylase
activity. The patterns of effects
indicated that the altered transmitter utilization rate probably reflected a
change in impulse activity in the affected neuron populations with promotion of
activity in the midbrain + brainstem and reduced activity in the cerebral
cortex. These data indicate that dietary
supplementation with soy lecithin preparations throughout peri-natal
development alters synaptic characteristics in a manner consistent with
disturbances in neural function. www.ncbi.nlm.nih.gov/pubmed/2876756
Soy Inhibits DOPAMINE:
Correlation exists
between dopamine and expression of cognitive capacities. Inadequate dopamine levels
contribute to cognitive impairment.
2001, Genistein
inhibits protein tyrosine kinases that regulate dopamine function interfering
with cellular signaling cascades that regulate neurotransmitter transporters in
humans. These data provide several lines of evidence showing that PTK
inhibition rapidly reduces human
dopamine transporter activity that controls levels of dopamine. This PRK’s
represent cellular signaling cascades that acutely regulate
neurotransmitter transports. www.ncbi.nlm.nih.gov/pubmed/11181926
1995, Tyrosine
kinases are abundant in the adult CNS. Soy genistein inhibits tyrosine kinases
suggesting a changing role in neurotransmitter release caused by
kinase-regulation of dopamine. Genistein
increases endogenous dopamine release. www.ncbi.nlm.nih.gov/pubmed/7595495
Soy genistein
significantly potentiated dopamine release in males. Genistein exposure may act similarly to
estradiol (potent estrogen) in augmenting dopamine release. www.ncbi.nlm.nih.gov/pubmed/11836070
Soy Inhibits
Essential Enzyme Tyrosine Kinases Related To Brain Dysfunction:
1991, Long-term
potentiation (related to learning and long-term memory) in the hippocampus is
blocked by tyrosine kinase inhibitors such as genistein. Tyrosine kinases
participate in a kinase network with serine and threonine kinases.
2001, Tyrosine kinase
inhibitors, soy genistein, inhibits the glutamate-induced proliferation of astrocytes
(which are important for many brain functions).
SEROTONIN:
Brain cell changes
are involved in the interplay between estrogen and serotonin’s effects on mood
and cognition. Serotonin functions are
implicated in depression, anxiety disorders, and some aspects of
schizophrenia.
2003, Soy and social
stress affect serotonin neurotransmission in primates. Prescribed estrogens and soy phytoestrogen increased
serotonin reuptake transporter that was accompanied by increased serotonin
synthesis and neuronal firing. www.ncbi.nlm.nih.gov/pubmed/12746737
ZINC DEFICIENCY: Relatively high levels
of zinc are found in the brain, especially hippocampus. Zinc plays an important role in the
transmission of the nerve impulse between brain and cells. Deficiency of zinc during pregnancy and
lactation has been shown to be related to many congenital abnormalities of the
nervous system in the offspring.
2011, Levels
of estradiol of rats receiving phytoestrogens were significantly higher than
control group. In high levels, estradiol is a dangerously potent endogenous estrogen. Soy treated group showed
statistically significant decreased concentrations of zinc in blood serum. (Study evidence links low zinc levels to brain
disorders including autism). www.ncbi.nlm.nih.gov/pubmed/21167684
Iron & Zinc
Deficiency:
2002, Plant-based diets reduces dietary iron and zinc
absorption. Monitoring methods are
needed to detect and prevent possible iron and zinc deficiency with plant-based
diets.
2007, Zinc and iron
bioavailabilty was lower for GMO soybeans possibly due to its higher content of
antinutrient factors, especially soybean levels of phytate.
2000, Researchers testing soy formula found that it caused negative zinc balance in every infant to whom it was given, even when the diets were additionally supplemented with zinc. There is a strong correlation between soy phytate content in formula and poor growth. www.rense.com/general3/soy.htm
Soy Heavy Metals: 2000, Soy infant formulas contain other neurotoxins: aluminum, cadmium and fluoride. Studies found aluminum concentrations in soy-based formulas were 100-fold greater compared to human breast milk. Cadmium content was 8-15 times higher. Fluoride content of soy-based formulas ranged from 1.08 to 2.86 parts per million. www.rense.com/general3/soy.htm
2007, High Levels of Aluminum
in Soy: Aluminum content of soy formula is 10 times greater than milk based
formula and 100 times greater than unprocessed milk. Aluminum has a toxic effect on the kidneys of
infants, and implicated as causing Alzheimer’s in adults. Soy formulas lack cholesterol that is
absolutely essential for the development of the brain and nervous system; and
lack lactose and galactose, which play an equally important role in the
development of the nervous system. www.westonaprice.org/soy/infant.html
2000, Another way
that soybeans may affect brain function is because of the phytic acid
content. Also known as phytates, they
block the uptake of essential minerals in the intestinal tract: calcium,
magnesium, iron and especially zinc. Both
phytates ands soy protein reduce iron absorption. www.rense.com/general3/soy/htm
Breast Feeding Transfers Soy Toxins to Infants:
Lactational exposure to soy could result in estrogen-like actions on female reproductive system www.ncbi.nlm.nih.gov/pubmed/18047477
2008, Genistein passed from the lactating mother to the suckling offspring at levels sufficient to activate gene expression in the reproductive and nonreproductive tissues of mouse pups. In the liver, Estrogen Receptor-alpha and ER-beta messengers RNA and two target genes, CYP17 and the progesterone receptor were modulated by soy genistein. ER-alpha protein level followed an opposite regulation by genistein and estradiol.www.ncbi.nlm.nih.gov/pubmed/18281260
2002, Early exposure to genistein exerts long-lasting effects on the endocrine and immune systems. Data illustrate that exposure to soy genistein during pregnancy and lactation exerts long-lasting effects on the endocrine and immune systems in adulthood. www.ncbi.nlm.nih.gov/pubmed/12520091
Evidence Of Phyto-Toxic Soy INFANT FORMULAS: Soy Infant Formulas Are Repeatedly Proven As Developmentally Toxic:
2000, Twice as many diabetic children had received soy formula in infancy as compared to non-diabetic children. www.rense.com/general3/soy/htm
2011, Compared with
girls fed non-soy-based infant formula, soy-fed girls were at 25% higher risk
of early menarche throughout the course of follow-up. ….observable manifestation of endocrine-disrupting effects of soy isoflavone exposure. www.ncbi.nlm.nih.gov/pubmed/22324503
2009, Bulletin of Academy of National Medicine. Infant Nutrition Nutritional quality during the first weeks of life can influence health during both infancy and adulthood. Exclusive long-term breast feeding is strongly recommended. Soy-based formulas are not recommended for healthy infants. www.ncbi.nlm.nih.gov/pubmed/19718896
Soy phyto-estrogens and male reproductive function. Caution…soy formula should be avoided www.ncbi.nlm.nih.gov/pubmed/19919579
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, the reduction of soy content in formulas must be considered. www.ncbi.nlm.nih.gov/pubmed/11760676
2010 Soy isoflavones, genistein and daidzein are widely consumed with evidence for potential adverse effects. Study
results show that soy protein isolate (soy formula) is an efficient
isoflavone delivery vehicle capable of providing significant proportions
of the total dose into the circulation in the active aglycone form for
distribution to hormone receptor-bearing tissues and subsequent
pharmacological effects that determine possible health risks. www.ncbi.nlm.nih.gov/pubmed/20225898
2010 Uterine fibroids are the most common pelvic tumors in U.S.
women as well as the most common cause for hysterectomy. The results
showed an association between early fibroid diagnosis and having been
fed soy formula during infancy. www.ncbi.nlm.nih.gov.pmc/articles/PMC2854791
2011,
Compared with girls fed non-soy-based infant formula or milk formula,
early soy-fed girls were at 25% higher risk of menarche. Results
also suggest that girls fed soy products in early infancy may have an
increase risk of menarche specifically in early adolescence and may be
the manifestation of mild endocrine disrupting effects o f soy
isoflavone exposure. This soy formula association with menarche
warrants more in-depth evaluation.
www.ncbi.nlm.nih.gov/pubmed/22324503
2003,
Soy infant formula contains high levels of isoflavones, genistein and
daidzein which are commonly referred to as phytoestrogens. Infants
consuming soy formula have high levels of phytoestrogens, in a magnitude
greater than levels shown to produce physiological effects in adult
women consuming a high soy diet. Take a “Precautionary approach to these pharmacologically active compounds” www.ncbi.nlm.nih.gov/pubmed/12919490
2011, Developmental exposure to estrogenic compounds can disrupt sexual differentiation in 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. Studies clearly demonstrate that environmentally relevant doses of genistein have significant negative impacts on ovarian differentiation, estrous cyclicity, and fertility in the rodent model. Additional studies of reproductive function in human populations exposed to phytoestrogens during development are warranted. www.ncbi.nlm.nih.gov/pubmed/20955782
2001, NIEHS report: Dietary (soy) genistein produced effects in multiple estrogen sensitive tissues in males and female consistent with estrogenic activity within exposure ranges in humans.
Autoimmune Thyroid Disease: Infant feeding of soy formula may affect autoimmune diseases later in life. This retrospective analysis documents the association of soy formula feeding in infancy and autoimmune thyroid disease. Dr. Fort Study. www.ncbi.nlm.nih.gov/pubmed/2338464
Estrogen regulates thymic development and immune function. Genistein
administration to mice that produced serum genistein concentrations
similar to those reported in human infants consuming soy formula and had
demonstrable effects. Genistein had similar effects on many estradiol
target genes, affecting genes involved in transcription, apoptosis, cell
cycle and thymic development and function. www.ncbi.nlm.nih.gov/pubmed/16484547
Thymic and Immune Deficiency; Soy-fed human infants capable of significant thymic and immune changes abnormalities.” www.ncbi.nlm.nih.gov/pubmed/12032332
2004,
Logistic regression analyses showed soy formula consumption at 4-6 and
7-12 months of age was associated with a twofold higher risk of type 1
Diabetes. www.ncbi.nlm.nih.gov/pubmed/15331209
2002, Frequency of
feedings with soy-based milk formulas in early life was significantly higher in
children with autoimmune thyroid disease. Inappropriate thyroid hormone levels can also have devastating effects on the developing human brain. www.rense.com/general3/soy.htm
New Zealand speaks out against soy formula as a hazard to developmental health. U.S.
FDA, "Given the DES tragedy, it would be foolish to ignore the
possibility that some phytoestrogens constitute a developmental hazard."
www.kidalog.net/soyformula.html
Soy is a Food Allergen, Causes Asphyxiation Related To Infant Death, & May
Be Misdiagnosed as SIDS:
2006, FDA Section
201(qq) of the Act 21 defines “major food allergens” as one of eight foods or
food groups- milk, eggs, fish, shellfish, nuts, wheat and soybeans. As with most common food allergens, allergic
reactions to soy may result in life-threatening symptoms, such as
anaphylaxis. Furthermore, even low
levels of soy protein may cause adverse effects in some sensitive individuals. FDA considers an “adverse effect” to be any
objective sign of an allergic reaction.
Food fillers such as soy lecithin are another soy allergen:
Renal Damage; Soy diet exacerbated renal damage, significantly exacerbates the clinical course of this autoimmune disease. www.ncbi.nlm.nih.gov/pubmed/16039550
BPA and Soy Combination
= Toxic Cocktail:
2011, Bisphenol A
(BPA) and Genistein, the predominant component of soy products are both known
environmental estrogens. We investigated
the developmental toxicity of BPA and Genistein and their combined effects.
Genistein as a teratogen was solid… The combined effect of BPA and Genistein
was generally additive action…
2010, Teratogenic effects and fetal toxicity of environmental estrogenic endocrine disruptors have become a great concern in recent years. Combination bispenal A (BPA) and Genistein on rat embryos are investigated. Both BPA and Genistein produced concentration-dependent inhibition of embryonic development. Analyses reveal a significant synergistic interaction between BPA and Genistein for most end points, as indicated by enhanced developmental toxicity of BPA after co-exposure with Genistein. Serious malformations and higher abnormal frequency of the central nervous system were induced by the combination BPA and Genistein. Findings suggest that Genistein may be embryotoxic and teratogenic to humans. These two estrogenic chemicals have a synergistic effect on embryonic development. Pregnant women should not take soy supplements. www.ncbi.nlm.nih.gov/pubmed/20299547
1997, In addition to
exposure to man-made chemicals (pesticides, polychlorinated biphenyls, phenolic
compounds, phthalate esters, and organochlorine), the consumption of
plant-derived estrogens in foodstuffs poses a potential risk to human health as
phytoestrogens are more potent estrogens and their intake by some infants is
likely to be considerable. www.ncbi.nlm.nih.gov/pubmed/9414467
Genistein Genotoxicity: A variety of genotoxic effects of phytoestrogens have been reported. Genistein effects occur at relevant low dietary concentrations…the dose defines the poison. www.ncbi.nlm.nih.gov/pubmed/1768899
New Zealand
speaks out against soy formula as a hazard to developmental health. U.S.
FDA, "Given the DES tragedy, it would be foolish to ignore the possibility
that some phytoestrogens constitute a developmental hazard." www.kidalog.net/soyformula.html
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 naïve to assume that exposure to these compounds is
always good. Inappropriate or excessive exposure to phytoestrogens may be
detrimental to health. www.ncbi.nlm.nih.gov/pubmed/10548876
Ask "why" the FDA will NOT disclose their acknowledgment of several hundred published studies (many from their own scientists), of which for decades continuously PROVE the soy phyto-toxic cause of horrific severe and irreversible developmental brain and body adverse effects as critical public health information?
Please care to pass this urgently important adverse health information on to your family, friends, and neighbors.
Thank you very much,
Gail Elbek
@SoySorry gaelbek@yahoo.com
