Soy-Cause Of Brain Disorders

THE CAUSE OF AUTISM & NEUROLOGICAL DISORDERS

Hundreds of Published Studies Conclude: SOY PLANT-TOXINS DAMAGE THE BRAIN: Soy multiple phyto-toxins disrupt normal development of multiple neurotransmitter systems, sever synaptic connectors, and cause a number of adverse cascading brain cell effects. Soy is repeatedly study proven to dangerously interrupt normal neurotransmitter levels of; vasopressin, oxytocin, dopamine, glutamate, choline, serotonin, and GABA that regulates brain cell excitotoxicity.

Functioning Neurotransmitter systems are critical in the development and maintenance of: Complex social and emotional behavior, Stress, Anxiety, Bonding, Communications, Cognition, Aggression, Recognition, and Memory. Soy can dangerously manipulate several neurotransmitter systems resulting in deficits in social and behavioral processing that are also reported in the cause of autism, and in fact multiple brain disorders.

Soy causation of hypo-thyroidism is also scientifically proven as related to cause damage to brain neurons, due to the hypothalamic-pituitary-thyroid axis. Studies conclude that soy's adverse effects on the thymus and thyroid also encourage immune deficiency disease.

Soy contains phytic acid and heavy metals proven to adversely affect the brain by blocking absorption of necessary minerals directly involved in brain and body health.

Soy phytates are also proven to cause gastrointestinal distress that are common complaints in autistic children.

Evidence That Soy's Multiple Toxins Cause Adverse Brain Development & Functions:

2005, As weak estrogen agonists/antagonists with a range of other enzymatic activities, the (soy) isoflavonoids provide a useful model to investigate the actions of endocrine disruptors. Isoflavonoids act in vivo through both ER (Estrogen Receptor) –alpha and ER-beta. Their neurobehavioral 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 affects complex behavior in a wide range of species. 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, soy phytoestrogens, and atrazine. Effects on behavior and hypothalamic neuroendocrine systems were examined. All EDCs impaired reproduction. Several hypothalamic neural systems proved to be EDC responsive, including arginine vasotocin, catecholamines, and gonadotropin releasing hormone system. Exposure to EDCs during embryonic development has consequences beyond impaired function of the reproductive axis. Behavioral alterations reveal both direct and indirect effects of exposure to EDC. www.ncbi.nlm.nih.gov/pubmed/18006066

2008, Genistein, 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 rate 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. www.ncbi.nlm.nih.gov/pubmed/18681983

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

2001, Males fed the soy phytoestrogen diet had significantly higher phytoestrogen concentrations in a number of brain regions, (frontal cortex, amygdale & cerebellum); in frontal cortex, expression of calbindin (a neuroprotective calcium-binding protein) decreased, while COX-2 (an inducible inflammatory factor prevalent in Alzheimer’s disease) increased. 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. Findings suggest that dietary soy derived phytoestrogens can influence learning and memory and alter the expression of proteins involved in neuro-protection and inflammation in rats. www.ncbi.nlm.nih.gov/pubmed/11801187

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

2005, Genistein-induced neuronal differentiation is associate with activation of extracellular signal-regulated kinases and upregulation of p21 and N-cadherin. http://onlinelibrary.wiley.com/doi/10.1002/jcb.20626/abstract

2010, Serious malformation and a higher abnormal frequency of the central nervous system were induced by the combination of BPA and Genistein. Our findings suggest that genistein is embryotoxic and teratogenic to humans. BPA alone may not be a potential teratogen, but these two estrogenic chemicals have a synergistic effect on emybryonic development when present together during the critical period of major organ formation. Pregnant women should not take soy supplements. www.ncbi.nlm.nih.gov/pubmed/20505512

2003, Significant alterations in MBH-POA (medial basal hypothalamic preoptic area) and amygdale 5a-reductasee activities were detected in animals receiving the phytoestrogen-containing versus the phytoestrogen-free diets. www.ncbi.nlm.nih.gov/pubmed/10352124

2002, Neurobehavioral effects of dietary soy phytoestrogens. These studies used a commercially available diet rich in phytoestrogens via a diet free of phytoestrogens. Results indicate that consumption of dietary phytoestrogens resulting in very high plasma isoflavone levels (many cases over a short interval of consumption) can significantly alter sexually dimorphic brain regions, anxiety, learning and memory. www.ncbi.nlm.nih.gov/pubmed/11836067

2007, AVPV (essential part of neural pathways mediating hormonal feedback) neurons containing estrogen receptor-beta in adult male rats are influence by soy isoflavones. These findings provide direct evidence that consumption of soy isoflavones influence the loss of ERbeta-containing neurons in male anteroventral periventricular nucleus AVPV. www.biomedcentral.com/1471-2202/8/13

2009, Autism is probably attributable to a combination of a common genetic background and a possible prenatal exposure or alteration in fetal environment during pregnancy. www.ncbi.nlm.nih.gov/pubmed/19581261

Soy Damage to Multiple Brain Neurotransmitter Systems:
Neurotransmitters are chemicals that relay, amplify, and modulate signals between neurons and other cells. Release of neurotransmitters are most commonly driven by arrival of an action potential at the synapse, or driven by electrical potentials. Neurotransmitters are divided into amino acids, peptides, and monoamines. Neurotransmitters activate “excitatory” and/or “inhibitory” receptors. However, some receptors that activate complex metabolic pathways that produce effects are neither excitatory of inhibitory.

Soy Inhibits GABA A chief “Inhibitory” brain neurotransmitter, also plays an important role in the control of dopamine-mediated brain functions: Both are stated causes of autism, and both are caused by soy phyto-toxicity:

2007, Autism is a complex neurodevelopmental disorder . It is in agreement with the evidence of lower levels of GABA-A receptors in autistic brains, and joined by other variants could explain the autistic phenotype and its heterogeneity. www.ncbi.nlm.nih.gov/pubmed/17598645

2007, Neurotoxic Effects of soy genistein and daidzein could be due to their inhibition of the GABA (A) receptor resulting in further enhancement of excitation by glutamate and leading to cellular damage. (GABA, Gamma-aminobutyric Acid. Inhibition of GABA can cause: anxiety disorders, panic attacks, seizure disorders, headaches, Parkinson’s Cognitive impairment, depression, bipolar, infertility, lowers insulin levels). www.ncbi.nlm.nih.gov/pubmed?term=Genistein and daidzein induce neurotoxicity at high concentrations in primary rat neuronal cultures

2007, Genistein and daidzein induce neurotoxicity at high concentrations in primary rat neuronal cultures. Soy isoflavones possess estrogen-like activity. Specifically genistein and daidzein are toxic to primary neuronal culture at high concentrations, indicating a significant cellular damage. Both genistein and daidzein increases intracellular calcium level (CA2)i, significantly. The toxic effect of soy genistein and daidzein could be due to their inhibition of the GABA(A) receptor resulting in further enhancement of excitation by glutamate and leading to cellular damage. http://ncbi.nlm.nih.gov/pubmed/17245525

Soy Significantly Increases VASOPRESSIN- Causing adverse changes in social and emotional communication, bonding, aggression, and anxiety.

2003, Soya isoflavone content of rat diet can increase anxiety and stress hormone release in the male rat. Rats fed the soy isoflavone diet spent significantly less time in active social interaction. The soy isoflavone group had significantly elevated stress induced corticosteroid concentrations. Stress-induced plasma vasopressin concentrations were also significantly elevated in the soy group compared to soy-free rats. Major changes in behavioral measures of anxiety and in stress hormones can result from soy isoflavone content in rat diet. These changes are as striking as those seen following drug administration. www.ncbi.nlm.nih.gov/pubmed/12618915

2003, Dietary exposure to genistein increases vasopressin. Vasopressin was significantly elevated in the 1250ppm genistein group, consistent with known actions of estradiol. These data are consistent with known actions of estradiol and may explain our finding in a previous study that estrogenic endocrine disruptors such as genistein increased sodium preference in rats exposed to genistein in their diet. www.ncbi.nlm.nih.gov/pubmed/12660364

2005, Soy contains phytoestrogens, which are nonsteroidal polyphenolic compounds with the ability to bind and activate nuclear estrogen receptors. Soy isoflavones act as transcriptional activators of estrogen receptors (ERs) in vitro. These effects are generally greater in the presence of ER-b, but significant activation through ERa is also observed. In the brain, soy diets and isolated phytoestrogens can also mimic estrogen-transcriptional actions. Soy isoflavones increases brain-derived neurotropic factor, and choline acetyl transferase mRNA levels in the frontal cortex, and increase vasopressin levels in the hypothalamus. Phytoestrogens genistein, daidzein and equol are all found in the brains of rat on high soy diets. http://ajpregu.physiology.org/content/289/1/R103/full

1979, Results: Androgen inhibition and estrogen stimulation of vasopressin levels. www.ncbi.nlm.nih.gov/pubmed/511789 as related to: 2012, Estrogenic agents, soy isoflavones inhibit testosterone (androgen) production. www.ncbi.nlm.nih.gov/pubmed/22155228).

2004, Impaired vasopressin system is a strong candidates for involvement in autism susceptibility. www.ncbi.nlm.nih.gov/pubmed/15098001

2010, Syrian hamsters on the phytoestrogen-rich diet also had lower vasopressin receptor expression in the lateral septum but higher vasopressin expression in the lateral hypothalamus indicating that altered behavior might result from changes within vasopressin signaling pathways. Similarly, male rats on genistein and daidzein displayed increased anxiety and elevated stress-induced plasma vasopressin and corticosterone levels. Male monkeys fed soy protein isolate containing 1.88mg isoflavones/g protein over 18 months demonstrated higher frequencies of intense aggressive and submissive behaviors as well as decreased time spent in physical contact with other monkeys. Phytoestrogens 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. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074428/

Soy Manipulates OXYTOCIN: Oxytocin is critical for pair bonding, enhancing interpersonal trust, and the ability to infer the emotions of others from facial cues.

2011, Phytoestrogens 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/

2001, Soy isoflavones antagonize reproductive behavior and estrogen receptor alpha and beta dependent gene expression in the brain. Soy diminishes the up-regulation of oxytocin receptor in the hypothalamus. There is significant decrease in receptive behavior probably due to anti-estrogenic soy effects in the brain. www.ncbi.nlm.nih.gov/pubmed/11416015

2003, Genistein increased oxytocin, oxytocin receptor, and ERalpha mRNA. www.ncbi.nlm.nih.gov/pubmed/12504828

Soy Adverse Effects on CHOLINE Or Catecholamine Neurotransmitter System: Is a 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.

1985, Pregnant rat dams were fed a 5 or 2% soy lecithin preparation. Results indicate that dietary soy lecithin preparation enrichment during development leads to behavioral and neurochemical abnormalities in the exposed offspring. Onlinelibrary.wiley.com/doi/10.1002/dev.420180105/abstract

1986, Previous work has shown that exposure of developing rats to soy lecithin preparations (SLP) influences macromolecular constituents of immature brain cells and causes abnormal behavior patterns. Both catecholamines were profoundly disturbed in an age-dependent, regionally-selective manner. Transmitter uptake capabilities were also affected by developmental exposure to SLP, as was tyrosine hydroxylase activity. The altered transmitter utilization rate 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 SLP throughout perinatal development alters synaptic characteristics in a manner consistent with disturbances in neural function. www.ncbi.nlm.nih.gov/pubmed/2876756

1986, Results suggest that soy lecithin preparation exposure has a major effect on cholinergic synaptic development and reactivity, followed by secondary changes in other neurotransmitter pathways. www.ncbi.nlm.nih.gov/pubmed/3455608

1999, Soy phytoestrogens may function as estrogen agonists in regulating (increasing) choline acetyltransferase and nerve growth factor mRNA’s in the frontal cortex and hippocampus in the brain of female rats. www.ncbi.nlm.nih.gov/pubmed/10352122

(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

2008, Soy phytoestrogens stimulate catecholamine synthesis via estrogen receptors, but in high concentrations, phytoestrogens inhibit catecholamine secretion induced in adrenal cells, and brain neurons. www.ncbi.nlm.nih.gov/pubmed/18591472

Soy-Cause Of Dysfunctional DOPAMINE System: Derived from the amino acid tyrosine, examples include adrenaline, norepinephrine, and dopamine, having important physiological effects as neurotransmitters and hormones. Soy is established tyrosine inhibitor, thus inhibits essential neuron systems. 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 (Protein Tyrosine Kinases) inhibition rapidly reduces human dopamine transporter activity that controls levels of dopamine. This PTK’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

2003, Endogenous estrogen may play an important role in regulating the activity of dopamine neurons in mid-limbic systems, and that soy isoflavones exert an estrogen-like effect on the dopaminergic systems in the amygdale. www.ncbi.nlm.nih.gov/pubmed/14566409

Soy Inhibits Essential Enzyme, Tyrosine Kinase, Related To Brain Dysfunction:

2002, NIH confirms that genistein is the active form of the soy isoflavone, genistin. It has both phytoestrogens, and has protein tyrosine kinase inhibiting properties that are involved in central nervous system regulation of neurotransmission inhibition by genistein. (Neurotransmission inhibition is a cause of multiple brain disorders to include autism. In this study, the NIH is looking for benefits, not the adverse developmental brain effects caused by soy isoflavone and tyrosine inhibition of neurotransmitters systems). http://clinicaltrials.gov/ct2/show/NCT00042380

Kinase enzymes that specifically phosphorylate tyrosine amino acids are termed tyrosine kinases. Receptor tyrosine kinases (RTK)s are the high-affinity cell surface receptors for many polypeptide growth factors, cytokines, and hormones. Of the 90 unique tyrosine kinase genes identified in the human genome, 58 encode receptor tyrosine kinase proteins. Receptor tyrosine kinases have been shown to be key regulators of normal cellular processes. Soy is a well-known inhibitor of tyrosine kinases.

1997, The phosphorylation of proteins on tyrosine residues is now recognized as having a critical role in regulating the function of mature cells. The brain exhibits one of the highest levels of tyrosine kinase activity in the adult animal and the synaptic reason is particularly rich in tyrosine kinases and tyrosine phosphorylated proteins. Involved in the regulation of synaptic function. Tyrosine phosphorylation is involved in the modification of synaptic activity. Changes in the activities of tyrosine kinases and or protein tyrosine phosphatases which are associated with synaptic structures leads to both short-term and long-lasting changes in synaptic and neuronal function. www.ncbi.nlm.nih.gov/pubmed/9364450

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. www.ncbi.nlm.nih.gov/pubmed/1656271

1993, We report that genistein, a specific tyrosine kinase inhibitor, decreases tyrosine kinase activity and the content of phosphotyrosine proteins in cultured primary cortical neurons. Genistein inhibits protein synthesis by >80% in a dose-dependent manner and concurrently decreases ternary complex formation by 60%. Genistein depresses tyrosine kinase activity and concomitantly stimulates PKC activity. Protein tyrosine kinase participates in the initiation of protein synthesis in neurons. www.ncbi.nlm.nih.gov/pubmed/8228995

2001, Tyrosine kinase inhibitors, soy genistein, inhibits the glutamate-induced proliferation of astrocytes (which are important for many brain functions). http://ncbi.nlm.nih.gov/pubmed/11733703

2003, Genistein inhibits glutamate release and Ca(2+) influx from hippocampal synaptosomes. Genistein, a broad range inhibitor of tyrosine kinases did inhibit the intracellular CA(2+) and decrease glutamate release evoked by a drug stimulus in a dose-dependent manner. www.ncbi.nlm.nih.gov/pubmed/12421598

1998, Modulation of Ca2+ channel activity by protein kinases constitutes one of the major mechanisms regulating neuronal functions. PTK inhibitors on whole–cell Ba2+ currents (1Ba) were analyzed. Genistein and daidzein suppressed IBa. We estimated that specific PTK inhibition by genistein reduced 1Ba by 30%. Results suggest that the activity of neuronal Ca2+ channels can be modulated by protein tyrosine kinases in the nervous system that are mediated by Ca2+ channel modulation. www.ncbi.nlm.nih.gov/pubmed/9560456

1998, Genistein and daidzein inhibited L-type Ca2+ current in young rat ventricular cells. We investigated the developmental differences in the effects of genistein, an inhibitor of tyrosine kinases on Ca2+ in neonatal and adult rats. Genistein inhibits the basal L-type Ca2+ in rat ventricular cells and the inhibition of L-type Ca2+ by genistein is greater in immature cells than in adult cells. www.ncbi.nlm.nih.gov/pubmed/9592031

2005, Ca2+ and cAMP are important second messengers that regulate multiple cellular processes. Findings indicate highly coordinated interplay between Ca2+ and cAMP signaling in electrically excitable endocrine cells. www.jbc.org/cgi/content/abstract/280/35/31294 (Evidence of cascading brain-damaging effects).

2002, A role for tyrosine kinase in expression of (long-term potentiation) LTP. Tyrosine phosphorylation of proteins occurs in both the presynaptic and postsynaptic areas. We report that LTP was associated with increased calcium influx and glutamate release. LTP is also associated with an increase in phosphorylation of the alpha-subunit of calcium channels and ERK in synaptosomes prepared from dentate gyrus and these effects were inhibited when LTP was blocked by the tyrosine kinase inhibitor genistein. LTP was accompanied by increased protein synthesis and increased phosphorylation of CREB in entorhinal cortex, effects that were also blocked by genistein. www.ncbi.nlm.nih.gov/pubmed/12099488

(Long-term potentiation (LTP) is a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously. It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength. Memories are thought to be encoded by modification of synaptic strength. LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.

Soy inhibition of tyrosine kinase results in multiple cascading brain-modifying effects proven to disturb normal brain development and functions. Another example: Nerve growth factor triggers a sequence of tyrosine kinase-dependent phosphorylation steps that modulate glutamate (important excitatory neurotransmitter important for learning and memory release) and calcium influx having an impact on expression of long-term potentiation in dentate gyrus, of which failure is due to soy inhibition of tyrosine kinase. Because of the hippocampus' well established role in LTP, some have suggested that the cognitive decline seen in individuals with AD may result from impaired LTP).

Soy Manipulations Of 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

2003, Conjugated equine estrogen (estrogen drug), and soy phytoestrogen increased serotonin. Increase in serotonin was accompanied by increased 5-HT synthesis and neuronal firing. www.ncib.nlm.nih.gov/pubmed/12746737

Soy Modifies BDNF: A family of proteins that induce the development, survival, and function of neurons. High levels contribute to seizures, epilepsy, and hyperalgesia or increase sensitivity to pain.

1999, Both estradiol and soy phytoestrogens significantly increased the mRNA levels of BDNF (brain-derived neurotrophic factor) compared to controls in the frontal cortex of female rats. www.ncbi.nlm.nih.gov/pubmed/10081916

2005, Estrogenic effects of soy isoflavones on neurons have been observed in various studies. Soy contains numerous phytochemicals including isoflavones, phytic acid, trypsin inhibitors, saponins. Soy isoflavones are referred to as phytoestrogens because they bind to the estrogen receptors and affect estrogen-mediated processes. Soy isoflavones can exert both agonistic and antagonistic estrogenic effects, and have inhibitory effects on tyrosine kinase, topoisomerase and angiogenesis. Soy can affect synthesis of acetylcholine, and neurotrophic factors such as BDNF and nerve growth factor in the brain of the female rat. Frontal cortex choline acetyltransferase mRNA levels and BDNF were significantly higher in rats receiving soy isoflavones. DNA fragmentation was detected in homogenates of brain tissue from rats receiving either dose (2mg/day or 2mg/day) genistein. Genistein can modulate the dopaminergic system. Soy isoflavones affect ChAT (choline acetyltransferase) expression and activity. ChAT mRNA levels in soy isoflavones-treated rats were significantly higher in the frontal cortex. Genistein decreases the expression of GABAa receptors in the plasma membrane of rat cerebellar granule cell bodies and dendrites, and inhibits GAMA-activated currents in HEK293 cells. It has also been reported that glycine receptors are inhibited by genistein. Soy isoflavones can affect the viability of neurons and cognitive function by acting as an estrogenic agonist and they can also utilize differential distribution and regulation of ERa and ERb in the brain. ERa is involved in mediating sexual and aggressive behavior, whereas, ERb modulates emotional and cognitive behavior.

Protein tyrosine phosphorylation is involved in various responses in the brain including neuroregeneration, synaptic plasticity and neuronal injury. Genistein is known to inhibit tyrosine kinase which is generally considered to be detrimental to a neuron. It was also reported that high concentrations of genistein induced neuronal apoptosis in primary cortical neurons, blocked tyrosine kinase activity and contributed to H2O2-induced apoptosis in human neuroblastoma cells. Tyrosine-kinases are highly expressed ins several brain regions including the hippocampus, and are reported to be involved in the induction of long-term potentiation in the hippocampus, which is crucial to learning and memory. Long-term potentiation is also reportedly associated with increased calcium influx and glutamate release. Protein tyrosine physphorylation contributes to synaptic plasticity. Three families of tyrosine kinases are implicated in memory. Because genistein is a tyrosine kinase inhibitor it can inhibit long term potentiation, which will also suppress calcium channels and extracellular-signal-related kinase in synaptosomes prepared from dentate gyrus. Genistein inhibits protein synthesis and phosphorylation of cAMP response element binding protein in entorhinal cortex. Inhibitory activity of long-term potentiation by genistein is associated with the inhibition of high-threshold voltage-activated calcium currents (VGCC). Genistein inhibits the Ca2+ dependent glutamate release by partially inhibiting p-/Q-type VGCC and by inhibiting N-type and unidentified BGCCs, in rat hippocampal synaptosomes.

It is reasonable to assume that rats consuming soy isoflavones have impaired spatial memory. Large amounts of genistein are needed to inhibit tyrosione kinases in the brain and suppress cognitive function in vivo. Thus soy isoflavones, especially genistein as a tyrosine kinases inhibitor can induce impairment of memory processing and cognitive function when concentration of genistein in vivo is excessive. Soy isoflavones can affect brain function by ER-mediated processes and by inhibiting tyrosine kinase. Genistein (one of soy isoflavones) can have negative influences on cognitive function when it is present at a high level due to its action as a tyrosine kinase inhibitor which enables it to block long-term potentiation and cognitive function.

(Study title, “Soy isoflavones and cognitive function” by YB Lee et al. Journal of Nutritional Biochemistry, Vol 16, Issue 11, Page: 641-49).

Mitochondrial: Critical to cell function. Proper transport and distribution of mitochondrial in axons and at synapse are critical for the normal physiology of neurons. Efficient control of mitochondrial retention at particular stations, where energy production and calcium homeostasis capacity are demanded is essential for neuronal development and function. There are complex mobility patterns of axonal mitochondria: distribution in axons and at synapses, and the impact on synaptic function. Mitochondrial diseases include: Diabetes, visual loss, multiple sclerosis, Leigh syndrome, varying degrees of cognitive impairment, learning disabilities, dementia, hearing loss, myoclonic epilepsy, stokes, gastrointestinal disorders, poor growth, loss of muscle coordination, muscle weakness, liver, kidney disease, respiratory disorders, etc, etc.

Soy Inhibits Mitochondrial Functions:

2002, Genistein is an isoflavone soy derivative that binds to estrogen receptors with selective estrogen receptor modulated (SERM) properties. FDA recommendations of soy for cholesterol reduction prompted investigation into the potentially estrogen role of dietary soy phytochemicals in the brain. 50nM genistein significantly reduces neuronal apoptosis in an estrogen receptor-dependent manner, while the importance of apoptosis in the brain has been recognized with regard to the developing brain as well as degeneration in response to disease or stroke. We developed a model to test for apoptotic toxicity in primary cortical neurons caused by 17 beta estradiol and genistein and found; brain cell apoptosis confirmed loss of mitochondrial function, DNA laddering, nuclear condensation and fragmentation, and caspase activation were confirmed. Both 17beta estradiol and genistein reduced the number of apoptotic neurons and reduced the number of neurons containing active caspase-3. Results demonstrate that genistein and 17beta-estradiol have comparable anti-apoptotic properties in primary cortical neurons and these properties are mediated through estrogen receptors. www.ncbi.nlm.nih.gov/pubmed/12441188

(Caspases: Programmed cell death. Essential in cells for apoptosis in developmental and most other stages of adult life. Failure of apoptosis is one of the main contributions to tumor development and autoimmune diseases).

2000, Inhibition of mitochondrial proton FOF1-ATPase/ATP synthesis by (soy) phytochemicals. In conclusion the ATP synthase is a target for dietary phytochemicals, (genistein) with potential for cytotoxicity. www.ncbi.nlm.nih.gov/pmc/articles/PMC1572158/

(ATP, adenosine triphosphate, provides the energy for many cellular processes, including active transport of molecules across cell membranes, motility, and metabolism).

2005, Mitochondria are important targets of estrogen action. Another class of compounds, phytoestrogens which are found in our diet can also inhibit the activity of Complex 1 (NADH dehydrogenase). Phytoestrogens, genistein (found in soy beans) can inhibit the ATPase activity in rat brain mitochondria. www.ncbi.nlm.nih.gov/pmc/articles/PMC548143/

(NADH Dehydrogenase: Enzyme located in the mitochondrial transport chain involved in respiratory complexes. Mutations in subunits of Complex I can cause mitochondrial diseases, including Leigh syndrome (rare neurometabolic disorder that usually affects infants between 3 months and 2 years old, but sometimes teenagers and adults. Mutations in mitochondrial DNA cause degradation of motor skills and eventually death. The disease is characterized by movement disorders, loss of heal control and motor skills, continuous crying in infants, and seizures). Complex I defects may play a role in the etiology of Parkinson’s disease. Complex I was significantly decreased in patients with bipolar disorder. Complex I deficiency showed decreased oxygen consumption rates and slower growth rates. Exposure to pesticides (besides soy, is another endocrine disruptor) can also inhibit Complex I and cause disease symptoms to include liver dysfunction. Alteration in Complex I leads to decreased mitochondrial electron transfer activities and decreased ATP synthesis).

2005, Genistein produced mitochondrial depolarization as an early step in the induction of apoptosis. We identified the mitochondria permeability transition pore (PTP) as a potential target of genistein activity. There results indicate that the induction of apoptosis by pharmacological concentrations of genistein occurs via mitochondrial damage with the involvement of the PTP. www.ncbi.nlm.nih.gov/pubmed/15749635

2002, Further analyses showed that genistein induces mitochondrial permeability transition by the generation of reactive oxygen species due to its interaction with respiratory chain at the level of mitochondrial complex III. Addition of genistein to isolated rat liver mitochondria induces swelling, loss of membrane potential and release of accumulated Ca2+. www.ncbi.nlm.nih.gov/pubmed/12460676

Soy Suppresses MET:

MET: Important gene in brain development particularly in the neocortex and cerebellum. Mutations to the MET receptor tyrosine kinase gene have been associated with renal cell carcinoma,. A genetic variant which disrupts MET transcription is associated with autism. Soy is an established tyrosine kinase inhibitor, this inhibiting MET, as involved in the cause of autism.

2006, Low concentrations of genistein was associated with down-regulation of MET. Genistein suppresses MET expression. www.ncbi.nlm.nih.gov/pubmed/16619504

Soy Effects on Cortisol Production: Cortisol is important for fetal development, immune system function, development of fetal lungs, and for normal brain development; emotions and cognitive function. Soy suppresses cortisol levels. Low levels of cortisol in the body are associated with multiple cascading adverse health effects including Addison’s disease. Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, clinical depression, and physiological stressors such as hypoglycemia, illness, fever, trauma, fear, pain, physical exertion, or temperature extremes. Cortisol levels may also differ for individuals with autism or Asperger’s syndrome.

1999, Phytoestrogens alter adrenocortical function: Genistein and daidzein suppress glucocorticoid and stimulate androgen production. Phytoestrogens influence a variety of biological processes. In human fetal and postnatal adrenal cortical cells, genistein and daidzein decreased ACTH-stimulated cortisol production to basal levels. In the adult adrenocortical cell line, H295, genistein daidzein and 17B estradiol decreased cAMP-stimulated cortisol synthesis in a similar fashion. Genistein and daidzein in postnatal adrenocortical cells, DHEA and DHEA-S were markedly increased. In H295 cells, basal and cAMP-stimulated DHEA production were similarly increased by the phytoestrogens and 17B estradiol. Genistein and daidzein specifically inhibited the activity of 21-hydroxylase (P450c21 steroidal enzyme). Consumption of foods containing phytoestrogens alter adrenocortical function. www.ncbi.nlm.nih.gov/pubmed/10404819

2002, Inhibitory effects of soy phytochemicals on cortisol production was examined in human adrenal H295R cells. Daidzein induced reduction of cortisol. Daidzein and genistein strongly and significantly inhibited steroidogenic enzymes 2beta-HSD. Daidzein and genistein significantly inhibited P450c21 steroidogenic enzyme activity. Daidzein is a competitive inhibitor of 3beta-HSD II and P450c21 steroidal enzymes. www.ncbi.nlm.nih.gov/pubmed/1198020

Soy-Cause of Vitamin D Deficiency: 2004, Content analysis of soybean milk showed very low calcium, phosphate, magnesium and vitamin D levels compared to cow’s-based infant formulas. This case highlights the unsuitability of soybean milk as the sole provider of infant nutrition and demonstrates the false perception that soybean milk is a healthy food for infants. It is necessary to be cautious about health claims for soybean milk…. www.ncbi.nlm.nih.gov/pubmed/15009584

Soy Modulation of Calbindin D28k-modulates calcium channel activity and neuronal firing. Calbindin D28k is a neuroprotective calcium-binding protein that is found in a number of neuroendocrine cells, particularly in the cerebellum. (Soy is an established endocrine disruptor).

2001, Males fed the soy phytoestrogen diet had significantly higher phytoestrogen concentrations in a number of brain regions, (frontal cortex, amygdale & cerebellum); in frontal cortex, expression of calbindin decreased while COX-2 (an inducible inflammatory factor prevalent in Alzheimers’ disease) increased. 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. Findings suggest that dietary soy derived phytoestrogens can influence learning and memory and alter the expression of proteins involved in neuro-protection and inflammation in rats. www.ncbi.nlm.nih.gov/pubmed/11801187

1999, In animals fed a phytoestrogen containing diet, males displayed significantly higher calbindin-D28k levels compared to females. Females exhibited significantly lower calbinin-D28 levels. Phytoestrogen content in diets apparently influence MBH-POA (medial basal hypothalamic preoptic area) calbindin levels prenatally. Altered calbindin-D28 levels modify sexually dimorphic brain structure during neural development by buffering ca2+ that is associated with programmed cell death. www.ncbi.nlm.nih.gov/pubmed/10320769

2006, Soybean isoflavones changes calbindin D-28k (CB) immunoreactivity in the hippocampus in female rats as well as male rats, correlating between calcium levels and phytoestrogens. In the dentate gyrus, CB immunoreatvity in females and males was significantly lower than controls. www.ncbi.nlm.nih.gov/pubmed/1681163

2000, Phytoestrogens are plant estrogenic-like molecules. Calcium binding proteins are associated with protecting against neurodengenerative diseases. In male rats on a phytoestrogen containing diet, plasma phytoestrogen levels were 78-fold higher than the control group, and the medial basal hypothalamic and preoptic area (mbh-poa) phytoestrogen content was 8-fold higher, demonstrating the passage of phytoestrogens into the brain. Independent brain site, i.e., mbh-poa, or amygdale, the abundance of calbindin from male phytoestrogen fed rats was significantly lower than controls. In the amygdale a similar pattern of expression was seen to that of the calbindin results. Consumption of phytoestrogens via a soy diet for a relatively short interval can (1). Significantly elevate plasma and brain phytoestrogen levels, and (2). Decrease brain calcium-binding proteins. www.ncbi.nlm.nih.gov/pubmed10720621

2000, Brigham Young Neuroscience Center researcher found that consumption of phytoestrogens via a soy diet for a relatively short interval can significantly elevate phytoestrogens levels in the brain and decrease brain calcium binding proteins. www.rense.com/general3.soy.htm

Iron & Zinc Deficiency Caused by Soy’s Phytic Acid Content:
Zinc is an essential trace element for all forms of life. Numerous aspects of cellular metabolism are zinc-dependent. Relatively high levels of zinc are found in the brain, especially hippocampus. Zinc plays an important role in brain development due to transmission of nerve impulses 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.

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 and soy protein reduce iron absorption. 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

1988, Results suggest that the low bioavailability of zinc from soy formula is a function of its phytate concentration. www.ncbi.nlm.nih.gov/pubmed/3189220

2002, Phyto-containing legumes and movement toward 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. www.ncbi.nlm.nih.gov/pubmed/12030275

2011, In the isoflavone-treated group, statistically significant decreased concentrations of zinc. The exposure of rats to genistein and daidzein during intrauterine life until sexual maturity influenced the mineral metabolism of the organism by significant decreases of zinc concentration in serum. Estradiol levels of rats receiving phytoestrogen were significantly higher than control group. www.ncbi.nlm.nih.gov/pubmed/21167684

2007, Zinc and iron bioavailability was lower for GMO soybeans possibly due to its higher content of antinutrient factors, especially soybean levels of phytate. www.ncbi.n.m.nih.gov/pubmed/18034754

2011, Levels of estradiol of rats receiving phytoestrogens were significantly higher than control group. 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

1999, Soy infant formulas may also contain phytate, which may negatively affect trace element absorption. Zinc absorption was significantly higher in low-phytate soy formula than from regular soy formulas. Reducing phytate content in soy formula had beneficial effect on zinc and copper absorption. www.ncib.nlm.nih.gov/pubmed/10075335

2001, Dialysability of all the minerals (calcium, phosphorus, magnesium, iron and zinc) analyzed from soy-protein based formulas showed significant differences. www.nbci.nlm.nih.gov/pubmed/11702418

2004, Even in low doses, phytic acid is a potent inhibitor of iron absorption, and low absorption of iron is a major factor in the etiology of iron deficiency in infants. www.ncbi.nlm.nih.gov/pubmed/15743020

Copper: The body needs trace amounts of copper to stay healthy, soy causes dangerous overdose of copper.

2003, Survival (rat) time in the soy protein isolate (SPI as in soy infant formulas) group was shorter than in control group. Copper concentrations in the livers of rats in the SPI diet groups were approximately 80% higher than in rats fed the control diet. Results indicate that SPI enhances copper uptake into the liver cells and promotes liver cell damage in rats. Recommendations to individuals suffering from Wilson’s (too much copper builds up in the liver, brain and/or eyes causing serious illness, eventually causing death) disease to avoid consuming soy protein may be warranted. www.ncbi.nlm.nih.gov/ubmed?term=soy protein isoflavone enhances hepatic copper accumulation and cell damage in LEC rats

Manganese: Soy Causes Toxic Manganese Levels, Another Soy-Cause of Dysfunctional Dopamine System:

2004, Manganese is an essential mineral nutrient found at high levels in plants such as soy. Excessive Manganese exposure increases the risk of adverse neurological effects. Well meaning but inadequately informed parents may perceive plant-based beverages such as soy beverages as an alternative to infant formula. Soy beverages should not be fed to infants because they are nutritionally inadequate and contain manganese at levels which may present an increased risk of adverse neurological effects. www.jacn.org/content/23/2/124.full

2006, Manganese can cause a neurotoxic syndrome due to its interactions with monoamine systems, especially dopamine. Perturbations of the dopamine system are known to underlie a number of neurobehavioral problems, including ADHD. Manganese in soy-based infant formula can contain up to 80 times the Manganese concentrations of breast milk. Ingestion of soy formula in infancy could influence overabsorption of manganese and neurobehavioural consequences. We conclude that, during infancy the ingestion of high levels of manganese, as found in soy-based infant formula, is associated with a variety of behavioral deficits. http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~5nPFQZ:3:BODY

2002, Neonatal exposure to high levels of manganese has been indirectly implicated as a causal agent in ADHD, since Manganese toxicity and ADHD both involve dysfunction in brain dopamine systems. Results support neonatal manganese exposure is related to brain dopamine levels and neurocognitive deficit in the rodent. www.ncbi.nlm.nih.gov/[pubmed?/term=Effects of neonatal dietary manganese exposure on brain dopamine levels and neurocognitive functions

2008, Newborn babies are fed infant formula high in the toxic metal manganese. Two University of California campuses affirm that manganese in infant formula may damage the infant brain and trigger aberrant behavior. David Goodman affirms that the soy infant formula currently on shelves permits an estimated manganese dose about 120 times the amount found in mother-s milk. Excess manganese is stored in body organs, about 8% in the brain, in proximity to dopamine-bearing neurons responsible in part for neurological development. Infants given soy formula may be at risk for brain and behavioral disorders. www.soyonlineservice.com.nz/articles/goodman.htm

SELENIUM Although toxic in large doses, selenium is an essential micronutrient. Too much selenium can cause gastrointestinal disorders, fatigue, irritability and neurological damage. Selenium and iodine are 2 minerals which are critically important in the proper functioning of the thyroid. Hypothyroidism during pregnancy, can cause mentally damaged offspring.

2008, Soy products typically contain a significant amount of selenium and the soy phytoestrogens may also influence selenium status. Selenium in a soy supplement was determined to be bioavailable. Isoflavones in the soy supplement may have interfered with the bioefficacy of selenium. https://kb.osu.edu/dspace/handle/1811/580?mode=full

2002, Effect of the application of selenium fertilizer on selenium content of soybean and its products. Significant differences were found in that soybean cultivars exhibited different accumulation of selenium. Selenium enriched protein derived from selenium enriched soybean increases selenium intake. www.ncbi.nlm.nih.gov/pubmed/12835506

2009, Selenium and arsenic levels in soybeans from different production regions of the United States. Whole soybeans were analyzed for total arsenic and selenium content. Arsenic levels were .1ppm or less. Selenium levels in soybeans varied from .07 - .90 ppm in the major production areas across the USA. www.osti.gov/energycitations/product.biblio.jsp?osti_id-6511424

1998, Selenium absorption from the soy isolate source was very high indicating that the selenium present is well absorbed from this soybean plant source. www.ncbi.nlm.nih.gov/pubmed/3772518

Soy Contains Toxic Metals: Having a devastating influence on mental, emotional, and physical health and well-being.

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

2003, Our own concern is the high amounts of fluoride and aluminum in soy formula. Infants fed soy formula there was an increase of 200% in autoimmune thyroid disease compared to breast-fed infants. A study concluded aluminum content in soy formula for 1-3 month old infants could result in intake of 363 micrograms/kg/day. Soy based formulas contains about 6-15 times more cadmium than milk based formulas, as well as high amounts of fluoride. Fluoride and phytates in soy formula will induce zinc deficiency. www.westonaprice.org/soy/notmilk.html

2006, There was significant difference in the fluoride content of infant formulas from distinct batchers in most brands. Milk formula varied in fluoride concentrations; 0.014 to 0.045, and soy formula was 0.253 to 0.702 mg F/L. www.ncbi.nlm.nih.gov/pubmed/17119712

(Fluoride toxicity can cause a variety of symptoms: abdominal pain, vomiting, hypocalcemia, headache, muscle weakness, or spasm, seizures etc.).

1987, Soy-based or milk-free formula contained about 8-15 times more cadmium than milk-based formulas. Canadian and U.S. ready-to-use formulas contained 900 and 230 ng/g fluoride attributed to the level of fluoride in the processing water used by the manufacturers. www.ncbi.nlm.nih.gov/pubmed/3624190

1999, Soy formulas contained approximately 6 times more cadmium that cow’s milk formulas, and diets with a cereal content had 4-21 times higher mean levels. Compared to breast-fed infants the exposure of dietary cadmium from weaning diets can be up to 12 times higher in children fed infant formulas. www.ncbi.nlm.nih.gov/pubmed/10789373

(Toxic overexposure of cadmium occurs art very low levels. Toxic heavy metal cadmium is a known carcinogen. Cadmium is a bio-accumulating substance which means that the body absorbs and holds it and isn’t able to expel it at a rate fast enough to be safe).

Additional Study Evidence Proving Soy-Cause of Brain Disrupting Effects:

2001, Visual spatial memory is inhibited in males (rat) by dietary soy phytoestrogens. Furthermore, males fed the phytoestrogen diets had significantly higher phytoestrogen concentrations in a number of brain regions (frontal cortex, amygdale, and cerebellum): in frontal cortex the expression of CALB (neuroprotective calcium-binding protein) decreased, while COX-2, an inducible inflammatory factor prevalent in Alzheimer’s disease increased. Results suggest that dietary phytoestrogen significantly sex-reversed the normal sexually dimorphic expression of visual spatial memory. These findings suggest that dietary soy derived phytoestrogens can influence learning and memory and alter the expression of proteins involved in neural protection and inflammation in rats. www.ncbi.nlm.nih.gov/pubmed/11801187

2003, 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 volumes in rodents during adulthood. www.ncbi.nlm.nih.gov/pubmed12943716

2004, Results indicate that long-term consumption of a diet rich in soy isoflavones can have marked influences on patterns of aggressive and social behavior. Frequencies of intense aggressive and submissive behavior were elevated relative to monkeys fed the control diet. Time spent by these monkeys in physical contact with other monkeys was reduced by 68%. www.ncbi.nlm.nih.gov/pubmed/15053944

2004, Dietary soy isoflavones alter regulatory behaviors, metabolic hormones and neuroendocrine function in male rats. This study demonstrates that consumption of a soy-based diet, significantly alters several parameters involved in maintaining body homeostatic balance, energy expenditure, feeding behavior, hormonal, metabolic and neuroendocrine function in male rats. www.ncbi.nlm.nih.gov/pubmed/15617573

2009, Administration of soy phytoestrogen genistein and 17B-estradiol induced rapid cAMP response element-binding protein (CREB) phosphorylation in the rat hypothalamus. Genistein induced a dose-dependent increase in CREB phosphorylation in the medial preoptic area and anteroventral periventricular nucleus. These results demonstrate that genistein induces estrogen-like rapid action on CREB phosphorylation in the neonatal central nervous system in vivo. http://ncbi.nlm.nih.gov/pubmed/19840237

2002, Soy isoflavone supplements containing a mixture of soy phytoestrogens inhibited estrogen-dependent female sexual behavior and was estrogen for both ER alpha and ER beta dependent gene expression in the hypothalamus. However, at 55ppm genistein had differential activity through ER alpha and ER beta in the hypothalamus. Genistein increased ER beta mRNA expression in the paraventricular nucleus of the hypothalamus by 24%.... www.ncbi.nlm.nih.gov/pubmed/12021182

2001, We show that genistein, a potent plant-derived isoflavone displaying estrogenic activity at low nanomolar concentrations, is toxic to rat primary cortical neurons…. Findings provide evidence for a delayed and prolonged activation of p42/44 mitogen-activated protein kinase (MAPK) and raise caution about potential side effects in the nervous system with genistein use. www.ncbi.nlm.nih.gov/pubmed/11561064

2001, Ingestion of soy containing isoflavones was correlated with the suppression of tau. Tau is an important protein in early brain development and plays an important role in growth of axons. (Axons make contact with other cells, usually other neurons but sometimes muscle or gland cells at junctions called synapses). http://ncbi.nlm.nih.gov/pubmed/10352122

1999, “FDA Scientists Against Soy”: Docket # 98P-0683. NIEHS Scientists Drs. Doerge and Sheehan report, “We oppose this health claim because there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzein, demonstrate toxicity in estrogen sensitive tissues and in the thyroid. This is true for a number of species including humans. Thus during pregnancy in humans, (soy) isoflavones per se could be a risk factor for abnormal brain and reproductive tract development. Development is recognized as the most sensitive life stage for estrogen toxicity because of the indisputable evidence of a very wide variety of frank malformations and serious functional deficits in experimental animals and humans. Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. Taken together, the findings presented here are self-consistent and demonstrate that genistein and other isoflavones can have adverse effects in a variety of species, including humans. ….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

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

2005, Evidence from rodents shows that certain phytoestrogens act as estrogen receptors in the brain. We sought to determine the estrogenic profile of food-borne phytoestrogens in neuronal cell lines. At sub-micromolar concentrations genistein, daidzein stimulated ERalpha and ERbeta-dependent transcription in neuronal cells co-transfected with ERs and estrogen-response element containing promoters. In neuronblastoma cells expressing endogenous ERs, genistein mimicked estrogen regulation of progesterone receptor mRNA levels. Results demonstrate that food-borne phytoestrogens particularly those found in soy act as estrogen-response elements in neurons. www.nclb.nlm.nih.gov/pubmed/15713532

2000, Dr. Bernard A. Schwetz FDA Director of National Center for Toxicological Research: (former employee of Dow Company) Adverse effects on reproductive tissues have been primary focus of attention, but effects from endocrine disruptors on other organ systems and processes, such as carcinogenesis have also been reported. Chemicals with estrogenic activity can affect the development and function of neural tissues through several different mechanisms. Experimental approaches to detect neurotoxic effects of estrogenic chemicals include neurobehavioral, neuropathological, and neurochemical endpoints. Genistein, a naturally occurring estrogen mimic is found in soy beans and soy products on which multigenerational studies are in progress. These studies will compare toxicity in neural, immune and reproductive systems and evaluate potential carcinogenicity. At dose levels that decreased maternal and offspring body weight, there were subtle alterations in some sexually dimorphic behaviors… Moderate doses of genistein also decreased the volume of sexually dimorphic nucleus of the hypothalamus in male offspring. Overall toxicity profile of chemicals to which humans are exposed is very important in order that the FDA may conduct sound risk assessments. www.ncbi.nlm.nih.gov/pubmed/11233764

2002, Neurobehavioral effects of soy phytoestrogens; The soy phytoestrogen diet fed to adult male and female rats produced anxioloytic effects. Results indicate that consumption of dietary phytoestrogens resulting in very high plasma isoflavone levels can significantly alter sexually dimorphic brain regions, anxiety, learning, and memory. The findings of these studies identify the biological actions of phytoestrogens. www.ncbi.nlm.gov/pubmed/11836067

2001, Soy phytoestrogens influence estradiol estrogenic induced mechanism results in modified brain functions: www.ncbi.nlm.nih.gov/pubmed/11602649

2005, Soy isoflavonoids provide a useful model to investigate the actions of endocrine disruptor. Isoflavonoids act in vivo through both ERalpha and ERbeta. Their neurobehavioural actions are largely anti-estrogenic. Small physiologically relevant exposure levels of soy isoflavonoids can alter estrogen-dependent gene expression in the brain and affect complex behavior in a wide range of species. www.ncbi.nlm.nih.gov/pubmed/15720476

2004, Results indicate that long-term consumption of a diet rich in soy isoflavones can have marked influences on patterns of increased aggressive behavior and decreased social behavior. www.ncbi.nlm.nih.gov/pubmed/15053944

2004 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. Exert estrogenic and antiestrogenic properties….equol act in turn to inhibit the action of testosterone/androgen. Influence of soy on learning and memory and anxiety behaviors is identified, and insulin levels affected by dietary isoflavones are discussed. www.ncbi.nlm.nih.gov/pubmed/15454683

2003, Soya isoflavone content of rat diet can increase anxiety and stress hormone release in the male rat causing major changes in behavioral anxiety and stress hormones. www.ncbi.nlm.nih.gov/pubmed/12618915

2004, Phytoestrogens: implications in neurovascular research: Differences in dietary phytoestrogen consumption result in large variations in somatic phytoestrogen content. These molecules affect estrogen and estrogen receptor function in several ways, having both agonist and antagonist effects on estrogen receptors. Similar to estrogens, dietary phytoestrogens appear to affect certain aspects of vascular, neuroendocrine and cognitive function. This article reviews health effects of estrogen, isoflavones and their hormonal mechanism of action, brain penetration by isoflavones. www.ncbi.nlm.nih.gov/pubmed/16181093

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

2004, Evidence for genistein cytotoxicity in rat brain www.ncbi.nlm.nih.gov/pubmed/15147835

1999, Environmental chemicals, (soy is in fact classified as environmental chemical) which mimic the actions of estrogen have the potential to affect any estrogen responsive tissue. Inappropriate exposure to environmental estrogens at critically sensitive stages of development could potentially perturb the organizational activities of estrogen on selected neuronal populations in the CNS. http://joe.endocrinology-journals.org/content/160/3/R1.abstract

2007, Effects of soy milk and isoflavone supplements on cognitive performance in healthy women- In contrast to predictions, soy did not improve attention, visual long-term memory, short-term memory. Also soy milk group showed a decline in verbal working memory compared to soy supplement and control groups. www.ncbi.nlm.nih.gov/pubmed/17435957

2009, Genistein is a phytoestrogen found at high levels in soybeans. In vitro and in vivo studies showed that high concentrations of genistein caused toxic effects. Zebrafish embryos were exposed to genistein. Genistein–treated embryos showed decreased heart rates, retarded hatching times, decreased body length, and increased mortality in a dose-dependent manner. Genistein treatment increased malformation of survived embryos such as pericardial edema and spinal kyphosis were observed. Assay results showed apoptotic DNA fragments in brain. This study also confirmed the estrogenic potential of genistein in the brain…. This study demonstrated that high concentrations of genistein caused teratogenic effects on zebrafish embryos and confirmed the estrogenic potential of genistein. www.ncbi.nlm.nih.gov/pmc/articles/PMC2739649/

2003, Estrogens exhibit complex effect on brain structure function and behavior. Body weights are significantly decreased in Phytoestrogen fed animals, and had significantly higher plasma adrenocorticotrophin and hippocampal glucocorticoid receptor levels. Lifelong consumption of dietary phytoestrogens alters the hypothalamic-pituitary-adrenal axis in male rats. www.ncbi.nlm.nih.gov/pubmed/127273197

2012, Phytoestrogens are promoted as safe, natural alternatives to estrogen therapies, yet their safety is poorly understood. Once daily treatment of female rats with soy phytoestrogen genistein resulted in subtle deficits in performance on cognitive tasks. Genistein treatment in concentrations similar to those achieved in humans, impaired the delayed spatial alternation task very similar to that observed with 17B-estradiol. www.ncbi.nlm.nih.gov/pubmed/21945133

Dangers of Soy Tofu:

2003, Soy-induced neuro-degeneration. A positive correlation between tofu consumption and brain atrophy in men. Has been shown that the soy phytoestrogen genistein inhibits neuroprotetive functions in cell cultures, recent in-vivo findings strengthen the case for possible soy –induced neurodegeneration. Genistein has been shown to suppress both DNA synthesis and the effects of brain derived neurotrophic factor (BDNF) in the hippocampus and cerebral cortex. Seems reasonable that some individuals may chose to avoid soy until proven safe …avoidance of soy also seems reasonable and should not be discouraged as alarmist. www.ncbi.nlm.nih.gov/pubmed/15142435

1996, Tofu and other soybean foods contain isoflavones bearing structural resemblance to steroidal hormones and have significant estrogen agonistic or antagonistic activities related to estrogen receptors and/or with enzymes involved in estrogen metabolism. There is evidence that estrogens modulate neural and synaptic plasticity during aging. We found an association of consistently high levels of tofu consumption in mid-life with low cognitive test scores and with Alzheimer’s disease in late life. www.jacn.org/content/19/2/242.full

2000, Poor cognitive test performance, enlargement of ventricles and low brain weight were each significantly and independently associated with higher midlife tofu consumption, indicative of cognitive impairment and brain atrophy in late life. www.ncbi.nlm.nih.gov/pubmed/10763906

2008 High tofu intake is associated with worse memory in elderly Indonesian men and women. Honolulu study also reported increased risk for cognitive impairment and other dementia markers with high tofu (soybean curd) intake. www.ncbi.nlm.nih.gov/pubmed/18583909

2009, The natural selective estrogen receptor modulator DT56a or Femarelle, (derived from tofu + flaxseed) is derived from the soybean. DT56a exerts an estrogen-like effect on selective areas related to mood, cognition, and homeostasis control, presenting a specific pattern of interaction with brain function. www.ncbi.nlm.nih.pubmed/19295450

2000, The Trouble With Tofu- Soy and the Brain: Men who consumed soy tofu at least twice weekly had more cognitive impairment. Consumption of phytoestrogens via a soy diet for a relatively short interval can significantly elevate phytoestrogen levels in the brain and decrease brain calcium-binding proteins. Soy’s ability to interfere with enzymes and amino acids may have direct consequence for the brain. High amounts of protein tyrosine kinases are found in the hippocampus a brain region involved with learning and memory. Soy is a tyrosine kinases inhibitor. www.rense.com/general3.soy.htm

Alzheimer’s Disease:

2001, Males fed the soy phytoestrogen diet had significantly higher phytoestrogen concentrations in a number of brain regions, (frontal cortex, amygdale & cerebellum); in frontal cortex, expression of calibindin decreased, while COX-2 (an inducible inflammatory factor prevalent in Alzheimers’ disease) increased. Findings suggest that dietary soy derived phytoestrogens can influence learning and memory and alter the expression of proteins involved in neuro-protection and inflammation in rats. www.ncbi.nlm.nih.gov/pubmed/11801187

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://genderchaos.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

@SoySorry

Monday, August 27, 2012

THE CAUSE OF AUTISM & NEUROLOGICAL DISORDERS