I would like to start this off by saying, this is not anti-vaccine, rather a way to help educate on the glutamate connection to vaccines.  There are a number of ways in which vaccines can lead to elevated glutamate levels and induce neuroinflammation, excitotocitiy, and ‘immunoexcitotoxicity’, therefore, resulting in increased sensitivity to glutamate. Here are a few examples:

1. Ingredients- Glutamate is often used to stabilize a vaccine and can be added as an ingredient (MSG, hydrolyzed protein, etc.) and/or a by-product and contaminant of the various manufacturing processes in every vaccine currently available. An example of a manufacturing process resulting in free glutamate, is the fermentation of growth mediums containing amino acids. Glutamate and other amino acids are also added during the culturing of the virus to support the viral growth. Currently there is no requirement for end-product testing of glutamate in vaccines. Therefore, it is impossible to know how much glutamate might be present in any particular vaccine. https://www.cdc.gov/…/do…/appendices/B/excipient-table-2.pdf

2. Immune Activation- Vaccines are made to induce an immune response in the hopes to protect against certain antigens in the future. Microglia are activated as part of the immune response to vaccines. What are microglia? Microglia are a type of glial cell located in the brain and the spinal cord. They act as the first and main* form of immune defense in protection against foreign invaders in the central nervous system (CNS). When the microglial are chronically activated (either from a single stimuli or multiple stimuli exposure such as vaccines or chronic underlying infections) they result in disruption of brain function, neuronal loss and send a surge of damaging cytokines and exictiotoxic levels of glutamate (aka glutamate storm). This process also severally damages the mitochondria and suppress mitochondrial function (ie mito dysfunction/ often low tone). “Because glutamate can also activate microglia and enhance cytokine-induced neurodegeneration, a vicious cycle is created in which immune cytokines can stimulate release of glutamate, and glutamate in turn enhances cytokine production and release. Moreover, cytokines inhibit glutamate transporters, which play a critical role in removal of excess extracellular glutamate. Intimately linked to excitotoxicity is the generation of destructive free radicals” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486922/ Interestingly enough, boys have a higher concentration of microglia in early life compared to girls. Which may play into, why males are more prone to autism. There is also evidence that viruses can enhance the toxicity of glutamate. It is not the virus that causes the damage, it is actually the surge in glutamate in response to the virus that causes the damage and this should be considered when using live viruses. “Many events can activate the microglial immune cytokines, including introduction of heavy metals, aluminum, oxidized LDL, amyloid, viruses, mycoplasma, bacteria, and glutamate,” http://www.jpands.org/vol9no2/blaylock.pdf It has also been shown to be an early event in Alzheimers, Parkinsons, ALS, viral encephalopathy, stroke, etc…

3. Metals in certain vaccines- Glutamate in conjunction with metals (specifically aluminum and mercury) enhance the toxicity of each other and can lead to glutamate receptor and transporter (allows the removal of glutamate and conversion to GABA) dysfunction. Glutamate also has aluminum binding capacities that can act to hold aluminum in the system.

4. GAD enzyme impairment- “An enzyme called glutamic acid decarboxylase (GAD) is needed for glutamate to make the conversion to GABA, but there are several factors that may interfere with this enzyme and impede the conversion process, which means a build up of glutamate and inhibited the formation of GABA. Response time may be delayed or capacity to convert may be impaired. It is believed that problems with the GAD enzyme may be the primary underlying issue that results in too much glutamate. For example, the rubella virus, which is found in the MMR vaccination can decrease the activity of glutamic acid decarboxylase (GAD)by as much as fifty percent. Thus, one of the reasons children begin to exhibit some of the symptoms of autism immediately after vaccination, as we mentioned earlier GABA is critical in speech and brain function.” http://www.holistichelp.net/…/how-to-increase-gaba-and-bal…/

Mice who were treated with thimerosal, the vaccine mercury, after birth then showed glutamate receptor dysfunction: “”Hippocampal architecture and glutamate receptor and transporter immunoreactivity are disrupted in SJL mice by postnatal thimerosal¬”…….NR¬1 and NR2b glutamate receptor immunoreactivity patterns are abnormal in the hippocampi of thimerosal treated SJL mice…… Neuronal glutamate transporter immunoreactivity patterns are abnormal in the hippocampi of thimerosal¬-treated SJL mice……¬Seizure related increases in extracellular glutamate are noted in temporal lobe epilepsy.” “Further, immune response genes may be linked to other heritable factors mediating toxin-induced CNS damage, such as systems regulating antioxidant45 or DNA methylation46 status, apoptosis pathways,47 glutamatergic transmission or excitotoxicity,48 metallothionein isoforms,49 or proinflammatory cytokine responses.50 As a central role is implicated for the Th1-type cytokine, interferon-italic gamma (IFN-italic gamma), in mercury-induced autoimmunity51 and general autoimmune disease susceptibility,52 we included C57 mice in our strain comparison; similar to SJL mice, C57 mice show a Th1-type cytokine predominance, including increased levels of IFN-italic gamma gene expression at baseline,53 yet are less sensitive than SJL mice to autoimmune sequelae following mercury or other Th1-dependent, autoimmunity-provoking challenges.54, 55 BALB mice, in contrast, demonstrate predominance of Th2-type cytokines, with reduced basal levels of transcripts representing IFN-italic gamma relative to C57 and SJL mice,53 and resistance to Th1-initiated autoimmune diseases.56 The susceptibility to the neurotoxic effects of low-dose postnatal thimerosal closely paralleled these immune vulnerabilities.” react-text: 2005 http://www.nature.com/mp/journal/v9/n9/full/4001529a.html

“Intriguingly, the elevation of anterior pituitary secreting hormones occurred exclusively in male but not in female thimerosal-treated mice, demonstrating for the first time the gender bias of thimerosal-mercury toxicity with regard to endocrine system. Our results indicate that higher dose of neonatal thimerosal-mercury (20× higher than that used in human) is capable of inducing long-lasting substantial dysregulation of neurodevelopment, synaptic function, and endocrine system, which could be the causal involvements of autistic-like behavior in mice.” react-text: 2010 https://academic.oup.com/…/Transcriptomic-Analyses-of

“A current hypothesis about methylmercury (MeHg) neurotoxicity proposes that neuronal damage is due to excitotoxicity following glutamate uptake alterations in the astrocyte. , ……we measured the effects of acute exposure to either 10 or 100 microM MeHg through the microdialysis probe, on glutamate extracellular levels in 15 awake animals. …… immediate and significant elevations in extracellular glutamate at 10 microM (9.8-fold, P<.001) and at 100 microM (2.4-fold, P=.001). This in vivo demonstration of increments of extracellular glutamate supports the hypothesis that dysfunction of glutamate neurotransmission plays a key role in MeHg-induced neural damage.” – This then indicates that a lower dose of mercury can be significantly more excitotoxic. So when we hear that vaccine companies have LESSENED mercury to trace amounts, these researchers have shown that damage still can occur. It would appear that glutamates are highly sensitive to the effects of mercury and this again shows even more evidence to a mechanism of vaccine injury, especially as far as autism is concerned. Is mercury the only cause of glutamate receptor and transporter immunoreactivity? It’s hard to say as NIH and CDC don’t seem to fund those types of studies but here is one from Japan that would make one wonder about MMR:” react-text: 2015 https://www.ncbi.nlm.nih.gov/pubmed/12460659 /react-text .

“Mercury in extremely small concentrations (nanomolar concentrations) can activate microglia, trigger excitotoxicity and induce significant mitochondrial dysfunction. Blocking the glutamate receptors (that trigger excitotoxicity) also blocks most of the neurotoxic effect of mercury at these concentrations. That is, most of lower-dose effects of mercury in the brain are secondary to excitotoxicity. The mitochondria produce most of the energy used by neurons and a number of studies have shown that suppressing mitochondrial function by itself is not enough to alter brain function, but it is enough to magnify excitotoxic damage. That is, it is the excitotoxicity that is disrupting brain function and development.” http://www.ageofautism.com/2008/04/dr-blaylock-on.html

plenty of articles here: http://www.ageofautism.com/…/autism-and-glutamate…

Microglial Activation

“The vaccine is different from a natural infection in that the vaccine produces brain immune stimulation for very prolonged periods.
It has been proven, in both animal studies and human studies, that systemic infections or immune activation by vaccines, rapidly activate the brain’s microglial system and can, in the case of vaccines, do so for prolonged periods. Once the primed microglia are reactivated by the subsequent vaccination or infection, the microglia activate fully and pour out their destructive elements as discussed above.
With a natural infection, the immune system quickly clears the infection and then shuts off the immune activation, thus allowing repair of what damage was done. This shutting down of the microglia is very important. There is evidence that with repeated and excessive vaccine-triggered immune stimulation, the microglia do not shut down. So, we see that giving a live, immunosuppressant vaccine early in life can dramatically increase the risk of autoimmune disorders, increase microglial brain injury as well as increase the risk of infection by other immune-suppressing viruses and pathogenic organisms. Most of these will be spaced within one month of each other, which means the priming and activation cycle of the microglia will be continuous.”

“A newer study has shown conclusively, that mitochondrial activation using a vaccine adjuvant not only suppresses mitochondrial function but that the damage cause by this mitochondrial suppression is actually produced by excitotoxicity. Blocking excitotoxicity completely blocks the microglial-induced neurotoxicity and mitochondrial damage cause by the vaccine.
A great number of studies have shown that activating the systemic immune system repetitively worsens neurological disorders caused by other things and can initiate neurodegeneration itself, that is prolonged. The inflammatory cytokines interact with glutamate receptors to dramatically increase excitotoxic damage. We know that autistic children have elevated CSF and blood levels of glutamate, which confirms the presence of the excitotoxic process.” http://www.ageofautism.com/2008/04/dr-blaylock-on.html

“As increasing evidence indicates that astrocytes and microglial cells play a major role in synapse maturation and function, and there is evidence of deficits in glial cell functions in ASDs, one current hypothesis is that glial dysfunctions directly contribute to their pathophysiology.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751265/

“Evidence indicates that children with autism spectrum disorder (ASD) suffer from an ongoing neuroinflammatory process in different regions of the brain involving microglial activation.” “It is plausible that by reducing brain inflammation and microglial activation, the neurodestructive effects of chronic inflammation could be reduced and allow for improved developmental outcomes. Future studies that examine treatments that may reduce microglial activation and neuroinflammation, and ultimately help to mitigate symptoms in ASD, are warranted.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523548/

“Two basic processes seem to be responsible for the chronic stimulation of brain immunity: repeated, closely spaced inoculation without allowing brain recovery, and inoculation with live viruses or contaminant organisms that persist in the brain.” http://www.jpands.org/vol9no2/blaylock.pdf

“A compelling amount of research has shown that repeated stimulation of the systemic immune system results in first priming the brain’s immune cells (called microglia) in the developing brain, followed by an intense microglial reaction with each successive series of vaccinations. When activated, especially chronically, microglia secrete a number of inflammatory cytokines, free radicals, lipid per oxidation products, and two excitotoxins—glutamate and quinolinic acid. Because of the critical dependence of the developing brain on a timed sequence of cytokine and excitatory amino acid fluctuation, sequential vaccination can result in alterations in this critical process that cause brain damage and abnormal pathway development. The evidence suggests that this overstimulation and persistent activation of the microglia is the central mechanism causing autism.” (http://beyondhealth.com/…/ExcessiveHungerandAutism.pdf)

“Growing evidence indicates that there is a close correlation between brain inflammation (by microglial released inflammatory cytokines and glutamate) and seizures, just as we see with excessive brain immune stimulation with vaccines. Using lipopolysacchride as a vaccine-based immune stimulant, scientists have induced seizures in experimental animals of various species.57,58 A considerable amount of evidence links excitotoxicity and seizures. In addition, a number of the newer anti-seizure medications work by blocking glutamate receptors or preventing glutamate release. One of the central mechanisms linking excessive immune stimulation with seizures, as with vaccines, is the induced release of the excitotoxin glutamate and quinolinic acid from immune stimulated microglia and astrocytes.59-61 In many cases these seizures are clinically silent or manifest as behavioral problems, often not recognized by pediatricians as seizures. Yet, they can alter brain function and eventually result in abnormal brain development. Even the CDC and American Academy of Pediatrics recognize that infants and children with a history of seizure should not be vaccinated. It is also known that autistic children who regress, that is begin to show a sudden worsening of mental development, have a significantly higher incidence of seizures, both clinical and subclinical, than those who do not regress. Interestingly, studies have shown that during early brain development after birth the number of glutamate receptors (that trigger the seizures) increase steadily until the age of two when it peaks.62 Thereafter they decline in number. This means that the immature brain is significantly more susceptible to seizures than the more mature brain and this is when your child is being given 24 vaccine inoculations, many of which are associated with a high incidence of seizure.” Growing evidence indicates that there is a close correlation between brain inflammation (by microglial released inflammatory cytokines and glutamate) and seizures, just as we see with excessive brain immune stimulation with vaccines. Using lipopolysacchride as a vaccine-based immune stimulant, scientists have induced seizures in experimental animals of various species.57,58”http://articles.mercola.com/…/the-danger-of-excessive…

“Males have overall more microglia early in postnatal development (postnatal day (P) 4), whereas females have more microglia with an activated/amoeboid morphology later in development, as juveniles and adults (P30-60)”. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296888/

Additional Resources

“These results suggest that neonatal exposure to MSG interferes with early development of the auditory brainstem and impacts expression of calcium binding proteins, both of which may lead to diminished auditory function.” https://www.ncbi.nlm.nih.gov/pubmed/28087338