My son suffered vaccine injury from the MMR his senior year of high school. That was 18 years ago, 18 years lost to vaccine injury. During this time he was misdiagnosed with Schizophrenia and Autistic Catatonia. He developed early onset dementia, Systematic Inflammatory Response Syndrome, Generalized Epilepsy, Hashimoto's Thyroiditis and Encephalitis, autoimmune post-infectious encephalitis. Further testing recently revealed sky high GAD 65 autoantibodies in plasma, and he has been diagnosed with GAD65 autoimmune limbic encephalitis. I just came across a study linking the MMR with Type 1 Diabetes. It states that "chicken embryo cell culture proteins in the MMR vaccine can cause the development of antibodies against chicken GAD 65 which cross-react with human GAD65 protein to cause type 1 diabetes." High GAD65 autoantibodies is also associated with other autoimmune disorders including seropositive autoimmune limbic encephalitis.

Thanks for sharing your story! Wish everything can become better for you and your daughter.

my son's recent lab work identified a GAD 65 level of 65 (range is 0/5.0) . A year ago it was 1.0 He has been undergoing monthly LD IVIG infusions for CVID & PANS. We don't see his Immuno Dr for another week, but I am freaking out.

I don't have any experience with autism however I'm 41 and just found out I have gad 65 autoantibodies the past year have had anxiety,brain fog ,horrible allergic reactions to food at least once a day among other issues am learning about this and hopefully this helps from what I understand gluten/ grains play a big role in causing this abnormal immune reaction and causing inflammation there are products that help with gabba support that seem helpful catechola calm is one with no side effects and has diminished that jumpiness I've had in the past hope this helps someone good luck to all and God bless

This is amazing! Thank you for sharing this!
Jackie Murphy

Teresa, you are amazing! I am curious if MSG (whether in food, formula or especially vaxxes) fits in here. Here are some interesting studies re: MSG, GAD, hippocampus, seizures, learning:

"Excitotoxic neonatal damage induced by monosodium glutamate reduces several GABAergic markers in the cerebral cortex and hippocampus in adulthood"
International Journal of Developmental Neuroscience DOI:10.1016/j.ijdevneu.2009.07.011
Monosodium glutamate (MSG) administered to neonatal rats during the first week of life induces a neurodegenerative process, which is represented by several neurochemical alterations of surviving neurons in the brain, where signalling mediated by GABA is essential for excitation threshold maintenance. GABA-positive cells, [3H]-GABA uptake, expression of mRNA for GABA transporters GAT-1 and GAT-3, and expression of mRNA and protein for two main GABA synthesizing enzymes, GAD65 and GAD67, were measured at postnatal day 60, after MSG neonatal treatment in two critical cerebral regions, cerebral cortex and hippocampus. GABA-positive cells, [3H]-GABA uptake, and mRNA for GAT-1, were significantly diminished in both cerebral regions. In the cerebral cortex, MSG neonatal treatment also decreased the mRNA for GAD67 and protein for GAD65 without significant changes in its corresponding protein and mRNA, respectively. Moreover in the hippocampus, mRNA and protein for GAD65 were increased, whilst GAD67 protein was elevated without significant changes in its mRNA. Clearly these results confirm the GABA cells loss after MSG neonatal treatment in both cerebral regions. As most of the GABAergic markers measured were reduced in the cerebral cortex, this region seems to be more sensitive than hippocampus, where interesting compensatory changes over GAD65 and GAD67 proteins were observed. However, it is possible that others neurotransmission systems are also compensating the GABA-positive cells loss in the cerebral cortex, and that elevations in two main forms of GAD in the hippocampus are not sufficient to maintain the neural excitation threshold for this region.

"Monosodium glutamate neonatal treatment as a seizure and excitotoxic model."
Brain research. 1317:246-56.
Monosodium glutamate (MSG) subcutaneously administrated to neonatal rats induces several neurochemical alterations in the brain, which have been associated with an excitotoxic process triggered by an over activation of glutamate receptors; however there are few systematic studies about initial changes in intracerebroventricular (i.c.v.) Glu levels produced by MSG in the brain. Thus, to characterize these changes, rat pups were injected with a MSG solution at 1, 3, 5 and 7 postnatal days (PD), and i.c.v. Glu levels and hippocampal total content of related amino acids (Asp, Glu, Gln, Gly, Tau, Ala and GABA) were estimated before, immediately and after each injection. Behavioral and EEG responses were also monitored after MSG administrations. Significant rise in i.c.v. Glu levels were found, mainly in response to the first and second injection. Moreover, the total content of all amino acids evaluated also increased during the first hour after the first MSG administration but only Glu and GABA remained elevated after 24 h. These biochemical modifications were accompanied with behavioral alterations characterized by: screeching, tail stiffness, head nodding, emprosthotonic flexion episodes and generalized tonic-clonic convulsions, which were associated with electroencephalographic pattern alterations. Altered behavior found in animals treated with MSG suggests an initial seizure situation. Although four MSG administrations were used, the most relevant findings were observed after the first and second administrations at PD1 and PD3, suggesting that only two MSG injections could be sufficient to resemble a seizure and/or excitotoxic model.

"Effect of early glutamate exposure on EAAT-3 and GAT-1 protein expression in cells of the dentate gyrus and CA1 region of the adult rat hippocampus."
Archives of medical research. 42(6):433-8.
Glutamate and GABA transporters are cell surface proteins localized on neurons and glial cells that mediate the reuptake of glutamate and GABA from the extracellular space. In different models of the acquisition of epilepsy, important changes in the expression of these transporters have been demonstrated, although to date no such studies have been performed using the monosodium glutamate (MSG)-induced seizure model in neonatal rats.
Following repeated MSG administration, we used immunofluorescence techniques to quantify the number of cells expressing the EAAT-3 and GAT-1 transporters at postnatal days (PD) 14 and 60 in the dentate gyrus (DG) and CA1 region of the hippocampus.
EAAT-3 and GAT-1 were expressed around the soma of granular cells and in the soma and dendrites of pyramidal cells in both experimental (MSG) and control (NaCl) rats. In the DG, MSG administration significantly increased the number of granular cells double-labelled for EAAT-3/Neun at PD 60 but not PD 14. No significant changes were observed at either PD 14 or 60 in terms of the number of cells expressing GAT-1 in the DG or CA1.
The findings suggest that the selective long-term increase in EAAT-3 expression in granular cells following neonatal MSG treatment reflects an important compensatory or protective response to the excitotoxic and seizure-promoting effects of early glutamate exposure in adult animals.

"Neonatal exposure to monosodium glutamate disrupts place learning ability in adult rats."
Pharmacology, biochemistry, and behavior. 82(2):247-51.
The activation of glutamatergic NMDA receptors of the hippocampus is closely associated with expression of place learning. Neonatal exposure to monosodium glutamate leads to abnormal expression of NMDA receptor subunits in the hippocampus, but its effect on place learning is unknown. Place learning acquisition and retrieval were assessed in mature adult rats after subcutaneous injection of monosodium glutamate (4 mg/g body weight) in eight neonatal rat pups at postnatal days one, three, five, and seven. Eight untreated rats were used as controls. At four months of age, the rats were challenged over a period of nine days with a place learning task. The task used an acquisition-retrieval paradigm in a Morris maze. Place learning acquisition was impaired in the experimental rats, which were unable to reduce their escape latencies during the nine training days. Controls improved between the fifth and ninth days of training. Test trials showed that retrieval of spatial information was also impaired in the experimental animals. These results show that both place learning acquisition and retrieval abilities in mature rats are impaired by neonatal treatment with monosodium glutamate. These findings may be related to the abnormal expression of NMDA receptor subunits in the hippocampus.

Thank you for all of your supportive and interesting comments. Our kids are very sick and the injustice of how they got that way plus the complete disregard of getting them better seems more like a Grimm's Fairy Tale lately instead of America 2012. (go canary party!)

Thank you, dan. Her eyes tell it all.

I was given a German measles (Rubella) booster at age 15. A week later, I fell apart and have been very ill ever since. I went from straight-A's, full of energy to extreme fatigue, severe stomach cramps, very foggy thinking, etc. I could no longer attend school, and slept 14 hours a day for years. When I was awake, just the basic things were a struggle for me, for I felt like I was not getting enough oxygen to function. That was 21 years ago. Today, I take the exact same supplements as my kids who are in managed recovery from Asperger's, PDD, NOS, ADHD, Bipolar, etc. I still have some fatigue, but my focus has returned. As an adult, I got the Hep B vaccine and TB tests. I became more fatigued after each one, not even thinking to blame the vaccine because for me, the symptoms started about a week later, and kept getting worse, so it was too gradual to notice. And the docs told me that vaccines don't cause any such symptoms, only allergy problems the day of the vaccine. If I had a time machine, I would not do any vaccines next time around.

@Garbo - The BLAST tool will look for matches with any genetic sequence that is in the database. The problem is narrowing down the results as there are so many possible permutations that might align. If there is a particular contaminate you are interested in, you can filter results for it.

@kathy - Please email me (jeffc3497-at-gmail-dot-com) if you want to trade ideas.

My daughter has a menstural dysfunction called polymenorrhea. That is she has such a short cycle she never stops having a period.

The gynocologist years ago pointed to her brain and said inside her brain about behind her nose is the pitiutary gland that is suppose to regulate this, and there lies her problem.

They now know that the anterior part of that little bitty gland is were the problem is for polymenorrhea. But to make matters more confusing is there are part of the hypothalmus that regulate the anterior of the pituitary so the problem could just well be there as it could the pituitary. I do worry much about a tumor and the problem being Cushings or some type of almost CUshings but not - we have a lot of that almost in our family.

My daughter also had Kawaskas as a child.
The treatment now for it is to give doses of IVIG (immunogoblins) or IgGs that comes from 1000 blood donors They say they don't know how they work.
At the same time her spleen swells up making her stomach huge.
This study right here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1418627/

tells what happens when they damaged pituitary of rats.

The IgG part of the immune system becomes low. IgAs too (and they are for regulation of the intestines. It also lowers the IgMs.

Short quote from this study says:
"The influence of anterior pituitary hormones on the gastrointestinal tract of humans and animals has been reported. Hypophysectomy (HYPOX) in the rat causes atrophy of the intestinal mucosa, reduction of gastric secretion and intestinal absorption, and increased susceptibility to infections". -----"

I guess I shouldn't comment on this but somewhere I know I read that

IgG's also regulate the production of T-cells, and without the IgG's the T- cells are more active?? So during Kawasakis my daughter perhaps stopped producing IgGs and her T cells in her spleen ???

Pituitary is important but it is in turn regulated by the hypothalmus.
Which basically is the entire endocrine system.

The hypothalmus is the main thing that the EPA regulates and demands companies to save, look at - when making pesticides. And they are darn well suppose to give these rats time to develop problems - group one killed and looked at a age two months old, three months old, right on up to two years old. and so forth.

The authorites above us cannnot tell us that they don't have rat's brians, with hypothalmuses frozen or put in formaldhyde bottles some where for vaccines.
Rat brains and studies of the hypothalmus are as common and goes hand in hand as peanut butter and jelly.

And those I don't even want to think about it being human brains and not just fats - but that freezer accident -- of course it is going to show damage to the hypothalmus.

@Jeff C.
That is facinating info. Would those tools also work for known contaminants in the vaxxes?
Avian leukovirus, porcine circovirus, human endogenous retrovirus?

Jeff, would like to pick your brain on the comment you made on HLA types. HLA DR4's usually are more autoimmune types...Dr Torres's research at Utah State had some great studies on this. My son has stiff man syndrome symptoms/PANDAS/PITAND and multiple pathogenic infections.

Hi Teresa, thank you for sharing your findings with us. It will be parents that finally figure this mess out, your diligence is an inspiration for the rest of us.

If you want to dig into the cause of the antibody cross-reactivity, here are a couple of links:

The GAD65 amino acid (AA) sequence can be found at this link toward the bottom of the page. Edit out the numbers so you only have the 585 AA sequence shown by the letters.

http://www.uniprot.org/uniprot/Q05329

Using the BLAST tool, you can search for sequences that closely match portions of the GAD65 AA sequence. In particular, look for AA sequences matches from antigens within the vaccines your daughter received. Use the "protein blast" function.

http://blast.ncbi.nlm.nih.gov/

If you know your daughter's HLA haplotype (you may have this as it is often done in autoimmune testing), you can perform binding strength predictions at this next link below. This can give you an indication of how likely your daughter would be to generate autoantibodies to this particular AA sequence based on her genetics.

http://tools.immuneepitope.org/main/html/tcell_tools.html

Email me if you would like more info. I've been using these tools to try and unravel my son's autoimmune conditions. Good luck and thanks for sharing what you've found with us.

A waterfall of information. Thanks, Teresa. More important now with my grandson recently diagnosed with Lyme, mycoplasma and high titers in the MMR, varicella, HHV-6.
You're the best!
Maurine

Teresa,

Each person is different, but I suspect if your daughter is similar to my wife in some aspects of this condition then there may well be a progression of problems as she ages if the immune issues are not controlled. I wrote a bit about the anti-GAd issue last December here at AoA. You may or may not have read it, but for you and others who may not have I think you could find it helpful. If this is progressively related to subsequent problems, as in our case, diabtetes, arthritis, and numerous other potential health problems are very possible.

Here is some of what I said in that thread followed with the link. There is more in the thread related to this besides these quotes so you may want to go and read the rest. I think what I posted there may be helpful, and at least shows that our vaccine concerns have been merited.

Thread name - "No One Knows"

Reportedly, "glycine exerts a cytoprotective effect against heat, hypoxia, anoxia, ischemia, and nephrotoxic drugs-metals, antibiotics, radiocontrast agents,cyclosporine, and cis-platinum (4-8)" and if the child and/or mother is challenged by these effects it may cause biological changes in immunity/autoimmunity that distrurbs the cells that develop relevant to to the first esposures to non self in the child, namely the gut through bacteria, yeast, viruses, and food. The mother'sw milk may be innoculted against such responses as it is associated with her already and by extension the baby. The glycine receptors could therefore be seeing a out of normal response in such children, but not to the degree that it seen in regressive autism where the vaccine containing glycine and possibly aluminum exert a multiplied effect conveying a signal artifically that there is a high amount of toxcicity present as the infant of aven fetus is in a very malleable response state to reach a proper response level. If this becomes a statically high or abnormally high, but flucuating state it could cause cahnges in the continued compliment response and of HLA-DR and HLA-DQ and other parts of ths immune system. So, in this altered state the body may produce intentionally higher levels of Anti-glutamic acid decarboxylase (GAD) antibodies which reduces Gaba, but would likely increase glycine levels in the blood that would be cell protective. At first this would indicate a redcution in Advanced Gylcation Endproducts as glycylglycine has been shown to reduce AGE's, but it may be that after some time the system orients to the glycine setpoint and the production of AGE's rises to unhealthy levels. It could be that the static change in glycine response means other amino acid levels would need to be raised as well to reduce AGE's. This procees seems to possibly be able to effect Nerve Growth Factor. The aluminum may alter the adaptive immune system that can activate the innate immune system ending up increasing osteopontin and other pathogens that may not be dealt with properly by the effected immune system like strep illicit Opsonin {Osteopontin also functions as an Opsonin}and these may activate the complement system. It appears C1Q and other complement regulators are involved too.For the gluten/giladin skeptics{wheat) both wheat and milk have proline and glutamic acid and the combo along with the lack of proper enzyme function to break them down properly certain in infants may lead to the epitope cross reactivity that connects their specific glutamic acid content to immune reactivity. If their peptides enter the circulation they appear to have opiate effects as well, but the immune reaction is more detrimental I think.

in a preceeding post to that I posted in that thread...

Following up on the Glycine-Glutamate is partially a rehash of things many of you may know, but the elements that may trigger or bring about anti-GAD antibodies pre-or postnatally seem to be part of the picture and the glycine element in vaccines may be a huge trigger for the cell effects proposed to be caused by it mentioned in the last post in the article "Scientific Link to Autism Identified". It is not the single problem that follows as other immune disruptions appear to be occurring as well. Glyphosate may be elevationg this problem too.

A pathogenetic model of autism involving Purkinje cell loss through anti-GAD antibodies.

Abstract

"Autism is a medical enigma, lacking truly effective treatments. Both genetics and environmental factors are recognized as players in the development of autism spectrum disorders (ASDs). Nevertheless, the exact mechanism(s) for the development of ASDs is (are) not known primarily because current understanding about the etiology of the disease is limited. Selective loss of Purkinje cells and the cerebellar atrophies are the neurological abnormalities most consistently found in persons diagnosed with autism. Because Purkinje cells are involved in motor coordination, working memory and learning, loss of these cells are likely to cause symptoms defining behavioral parameters of ASD. Currently the mechanism(s) for the loss of Purkinje cells in the cerebella of autistic individual is (are) not understood. Here we postulate a hypothesis for the development of autistic symptoms, severity of which is based on the extent of Purkinje cell loss triggered by Glutamate acid decarboxylase antibody (GAD-Ab). This model accommodates any genetic basis of autism and immunogenic triggers resulting GAD-Ab in the blood of the mother while pregnant with the child diagnosed autistic after birth or of an individual diagnosed with autism some time in the life time. Identification and characterization of GAD-Abs from pregnant mothers with a family history of autism, from children with autistic siblings, and individuals diagnosed with autism may allow find preventive and new therapeutic avenues."

http://www.ncbi.nlm.nih.gov/pubmed/18514431

More info on Glycine, Gaba, and Glutamate acid decarboxylase antibodies{anti-GAD antibodies}

Wiki - Glutamate decarboxylase

http://en.wikipedia.org/wiki/Glutamate_decarboxylase

GABA and Glycine

From the info here it can be theorized that not only would anti-GAD antibodies disrupt Gaba production, but also possibly causes neuronal autoimmune responses via altered epitope signaling effects.

http://www.acnp.org/g4/gn401000008/default.htm

Anti-glutamic acid decarboxylase (GAD) antibodies

Anti-GAD antibodies target an enzyme called Glutamic Acid Decarboxylase. This enzyme is responsible for converting glutamic acid to GABA,a chemical found in high concentrations in the cerebellum. It is believed that the lack of GABA results in cerebellar ataxia. Patients with cerebellar ataxia of an unknown cause should have an anti-GAD test. The anti-GAD antibodies have also been associated with a disease characterized by stiffness of the muscles, called "stiff person syndrome". The stiff person syndrome and cerebellar ataxia do not necessarily occur together in patients with anti-GAD antibodies. Anti-GAD antibodies are particularly common in diabetes mellitus and autoimmune diseases such as thyroid disease and rheumatoid arthritis. The treatment for anti-GAD antibodies is corticosteroids or prednisone to reduce the abnormal immune response. If this is ineffective infusion of immunoglobulin intravenously (IVIG) or a procedure called plasma exchange can be used.

http://www.ataxiacenter.umn.edu/aboutataxia/sporadic/gad/home.html

Again, the synergy of other factors such as aluminum and mercury are not dismissed due to anti-GAD/Gaba/Glycine issues, but are likely a co-occurring event regarding aluminum in those who have a vaccine reaction.

Here is the link to that thread - "No One Knows"

http://www.ageofautism.com/2011/12/no-one-knows.html

Good Morning-

and thank you, Alison for your kind words and support.

I just wanted to post a few additional facts. This gives more description of GAD65 as I continue to research more:

http://staging.mml.cws.net/test-catalog/print.php?unit_code=81596
Clinical Information

Glutamic acid decarboxylase (GAD) is a neuronal enzyme involved in the synthesis of the neurotransmitter gamma-aminobutyric acid (GABA). Antibodies directed against the 65-kd isoform of GAD (GAD65) are seen in a variety of autoimmune neurologic disorders including stiff-man (Moersch-Woltman) syndrome, autoimmune cerebellitis, brain stem encephalitis, seizure disorders, neuromyelitis optica and other myelopathies, myasthenia gravis, Lambert-Eaton syndrome, and dysautonomia.

GAD65 antibody is also the major pancreatic islet antibody and an important serological marker of predisposition to type 1 diabetes. GAD65 autoantibody also serves as a marker of predisposition to other autoimmune disease that occur with type 1 diabetes, including thyroid disease (eg, thyrotoxicosis, Graves' disease, Hashimoto's thyroiditis, hypothyroidism), pernicious anemia, premature ovarian failure, Addison's disease, (idiopathic adrenocortical failure) and vitiligo.

Adding too that GAD65 can also be found in the testis:

http://www.millipore.com/catalogue/module/c100779#0

Glutamic acid decarboxylase (GAD) is responsible for the conversion of glutamic acid to gamma-aminobutyric acid (GABA), the major inhibitory transmitter in higher brain regions, and putative paracrine hormone in pancreatic islets. Two molecular forms of GAD (65 kDa and 67 kDa) are highly conserved and both are expressed in the CNS, pancreatic islet cells, testis, oviduct and ovary.

Also- Studies illustrating that vaccination can be related to pancreatitis -- more connecting dots.

Acute pancreatitis associated with MMR vaccination http://www.ncbi.nlm.nih.gov/pubmed/12830760

Pancreatitis Caused by Measles, Mumps, and Rubella Vaccine http://journals.lww.com/pancreasjournal/Abstract/1991/07000/Pancreatitis_Caused_by_Measles,_Mumps,_and_Rubella.18.aspx

Acute Pancreatitis Caused by Parotiditis Vaccine http://journals.lww.com/pancreasjournal/Citation/1994/05000/Acute_Pancreatitis_Caused_by_Parotiditis_Vaccine.18.aspx

Severe necrotizing pancreatitis following combined hepatitis A and B vaccination http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1780095/
Pancreatitis following human papillomavirus vaccination https://www.mja.com.au/journal/2008/189/3/pancreatitis-following-human-papillomavirus-vaccination