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GAD65, Diabetes, Autoimmunity And Autism

Meg sick age 5

By Teresa Conrick

Lab results recently have shown my daughter's autoimmune condition is connected to GAD65, an autoantibody, often related to TYPE 1 DIABETES. Here is a brief description on Wiki of GAD65 :

"-Glutamate decarboxylase or glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2." 

Those are two things we know a lot about with an Autism diagnosis - GLUTAMATE and GABA, in fact I wrote last year about some of the research on GLUTAMATE  and how it related to Autism ---  "Glutamate receptors are responsible for the glutamate-mediated post-synaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation. Furthermore, glutamate receptors are implicated in the pathologies of a number of neurodegenerative diseases due to their central role in excitotoxicity and their prevalence throughout the central nervous system."

This would then explain symptoms Meg can exhibit as her body is not converting GLUTAMATE [EXCITATORY] into GABA [INHIBITORY] and to my surprise, a very recent study showed that my daughter is NOT THE ONLY ONE with an Autism diagnosis and an autoimmune process related to GAD65:

Presence of GAD65 autoantibodies in the serum of children with autism or ADHD.  

"Antibodies against glutamic acid decarboxylase 65 (GAD65) have been detected in the serum of patients with several neurological disorders....GAD65 antibodies were detected in the serum of 15% of children with autism (N = 20), 27% of children with ADHD (N = 15) and of none of the controls (N = 14).....Serum anti-GAD65 antibodies may be a common marker of subgroups of patients with autism and ADHD. Reactions of serum antibodies with the cells in the cerebellum in these patients suggest direct effects on brain function. The subgroup of children with autism and ADHD that tests positive for GAD65 antibodies needs further characterization in a larger study."

It seems that I have come face to face with an enemy in my daughter's body -- but where did it come from and what does it mean?  Knowing does not make it any easier BUT is does provide a valid and viable medical road to explore.  Doctors who keep telling parents like me that ----your child has autism ---- autism is based on behavioral symptoms ----- there are no medical tests --- --well, that needs to stop.

Here is a current snapshot of what I am learning and dots that connect:

Multiplicity of the antibody response to GAD65 in Type I diabetes 
 

"Autoantibodies to GAD65 (GAD65Ab) are present in the majority of patients with Type I diabetes (TID) and serve as an important marker of the disease." 

Central nervous system destruction mediated by glutamic acid decarboxylase-specific CD4+ T cells. http://www.ncbi.nlm.nih.gov/pubmed/20348424

"High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed  in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus."

Epilepsy and cerebellar ataxia associated with anti-glutamic acid decarboxylase antibodies.

"Anti-glutamic acid decarboxylase (GAD) antibodies are described in stiff-person syndrome and also in other neurological syndromes, including cerebellar ataxia and epilepsy"

So it appears that GAD65 can neurologically damage and yet also damage the pancreas.  More dots connecting:

"GADs catalyze the formation of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain. Two forms, GAD1/GAD67 and GAD2/GAD65, have been identified in humans. They are expressed in the brain, pancreas, ovary, and oviduct. Abnormalities in GADs are related to several neurological disorders including epilepsy and schizophrenia. GAD2/GAD65 is an autoimmune target in insulin-dependent diabetes mellitus."

That is interesting as both GAD65 and GAD 67 have been shown to be impaired  in those with an Autism diagnosis.  Pertinent also as my daughter has developed seizures related to estrogen.  If you dig to the next level of how the body begins this autoimmune process, we end up back to what we all have seen in many of our children's descent into Autism  -- vaccinations -- infections  -- mitochondrial dysfunction - abnormal immune response:

VACCINATIONS

"The identification of clusters of cases of T1DM [ type 1 diabetes mellitus] occurring in consistent temporal time periods allowed a link between the hemophilus vaccine and T1DM to be established. The current findings indicate the there are also clusters of cases of T1DM occurring 2-4 years post-immunization with the pertussis, MMR, and BCG vaccine. The data are consistent with the occurrence of clusters following mumps infection and the progression to T1DM in patients with antipancreatic autoantibodies."


"Cohort data from Denmark in all children born from January 1, 1990 to December 31, 2000 was analyzed toassess the association between immunization and type 1 diabetes in all Danish children and in a subgroup where childrenhad a sibling with type 1 diabetes. Pediatric vaccines were associated with a statistically significant increased risk of type1 diabetes in 12 of 21 endpoints in the general population."


INFECTIONS

"Antigens of pathogenic microbes that mimic autoantigens are thought to be responsible for the activation of autoreactive T cells. Viral infections have been associated with the development of the neuroendocrine autoimmune diseases type 1 diabetes and stiff-man syndrome, but the mechanism is unknown. These diseases share glutamic acid decarboxylase (GAD65) as a major autoantigen.....a pathogenic association between these autoimmune diseases is conceivable. Molecular mimicry has been postulated to represent the environmental cause of autoimmune diseases. Both type 1 diabetes and SMS have been associated with microbial infections."

Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease with a predominantly non-hereditary etiology that results in a destruction of pancreatic beta cells by autoaggressive T lymphocytes. Our results demonstrate that mono- and polyclonal GAD65-specific T cells from IDDM patients can be stimulated by viral and bacterial peptides with little apparent sequence homology with autoantigenic epitopes.


MITOCHONDRIA


"Since the rate-limiting step in GABA biosynthesis is the decarboxylation of glutamate by GAD, it is important to understand how GAD is regulated. So far, we know that GAD is regulated at the transcriptional level by alternate splicing and at the post-translational level by protein phosphorylation, palmitoylation and activity-dependent cleavage. Here, we present new evidence of the presence of GAD65 associated with mitochondria in the axon terminal and project a model in which ATP generated by mitochondrial GAD65 may serve an important function in providing energy for GAD65 mediated GABA biosynthesis and packaging into synaptic vesicles by vesicular GABA transporter (VGAT)."

"Mitochondrial metabolism plays a pivotal role in the pancreatic beta cell by generating signals that couple glucose sensing to insulin secretion. We have demonstrated previously that mitochondrially derived glutamate participates directly in the stimulation of insulin exocytosis. The aim of the present study was to impose altered cellular glutamate levels by overexpression of glutamate decarboxylase (GAD) to repress elevation of cytosolic glutamate."


ABNORMAL IMMUNE RESPONSE

"Treatments that tolerize, deviate, or alter the anti-GAD65 response in NOD mice typically delay or prevent insulitis and diabetes..... Part of the charm of the molecular mimicry model is the provision of a single epitope as the initiator, which could likely manifest as a sequential pattern of autoimmunity as described in the evolution of autoimmunity in young NOD [nonobese diabetic] mice."


"That autoimmune mechanisms are involved in the pathogenesis of IDDM [Type 1 (insulin-dependent) diabetes mellitus] is supported by the findings of experimental studies which showed that monoclonal antibodies for rubella virus capsid protein recognise B-cell epitopes on human and rat islet cells),and that T-cell clones from patients with congenital rubella elicit cytotoxic responses to GAD65, a B-cell autoantigen."

So there seems to be quit a bit of evidence showing that it is possible for GAD65 to be an important avenue of research to both Autism, Diabetes and autoimmunity.  It was interesting that the American Academy of Pediatrics published a study in 1999:

Previous Exposure to Measles, Mumps, and Rubella—but Not Vaccination During Adolescence—Correlates to the Prevalence of Pancreatic and Thyroid Autoantibodies
 

"ABSTRACT. Objective. This study was designed to determine whether a relationship exists between previous exposure to measles, mumps, and rubella (MMR) by natural infection or vaccination or by new immunization with MMR vaccine, and either the presence or levels of autoantibodies against thyroid cell and pancreatic b-cell antigens. Methods. Antibodies against MMR and autoantibodies
against thyroglobulin, thyroid peroxidase, pancreas islet cells (ICA), islet cell surface, glutamic acid decarboxylase 65k autoantibodies, and insulin were studied before, and 3 months after, vaccination with combined MMR vaccine in 386 school children between 11 and 13 years of age....The vaccination changed neither the prevalence nor the level of autoantibodies."

It seems that vaccination of MMR ---during adolescence---- would be missing the point as most babies receive their first dose of MMR after their first birthday.  Megan received her's at 15 months, had fever, rash for over 10 days, then AUTISM developed, and now, 18 years later, her measles, mumps and rubella titers are abnormally high and above the normal range of immunity.  Is it possible that these high viral titers are an indication of how or why she now has developed an autoimmune diagnosis?  Will she develop Diabetes in addition to her Autism diagnosis?  When will we get some honest answers and real help for our very ill children?

"Our data suggest that the prevalence of autism spectrum disorder in children with type 1 diabetes attending the Diabetes Clinic at The Hospital for Sick Children, Toronto, may be greater than that in the general population (0.9% [95% CI 0.3–1.5] vs. 0.34–0.67). Certain factors may account for this finding, including a common autoimmune pathogenesis."

Teresa Conrick is Contributing Editor for Age of Autism.

Comments

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

Hi Garbo. Thanks!

Yes, all shows a road to injury. Since Megan never had seizures and these came on in puberty, and then a positive ANA, there is a long process that may start with a match and then burst into a forest fire. I do think too that NMDA receptors are important in this process.

These too can be added in:

Methylmercury increases glutamate extracellular levels in frontal cortex of awake rats" http://www.ncbi.nlm.nih.gov/pubmed/12460659
"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." Then of course there's Hornig et al:

"Neurotoxic effects of postnatal thimerosal are mouse
strain dependent","Hippocampal architectu­re and glutamate receptor and transporte­r immunoreac­tivity are disrupted in SJL mice by postnatal thimerosal­".......NR­1 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."

Thanks again! Always appreciate your great comments!

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.

@JG - We bought our Zapper from http://www.bestzapper.com. This one is nice because there are no handles you have to hold, put the straps on your child and the unit automatically shuts off after a 5 minute zap. (Absolutely NO way you can get burned) We bought the package with the plate Zappicator for zapping our food as well as parts of the body. Dr. Clark's book Cure for All Diseases indicates that Epstein Bar is due to fluke parasites in the pancreas. Thus, I have been using the plate zapper on my son's tummy for a 1/2 hour zap daily along with the daily 5 min wrist zap. Lastly, I have been putting the plate zapper under his pillow after he sleeps for a 30 minutes. Dr. Clark indicated that all the autistic patients she saw had parasites in their brains. Again, this may sound a bit off the wall to some folks, but it is working for us. I zapped for 1 week before trying it on my son. He's been doing great & I will continue to use it on him and our entire family to awaken our own immune systems. (We also do biomed, special diet etc...) PS - If I forget the wrist zap before bed He reminds me that we need to do it and has indicated that he likes it! :)

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.

Have you considered METHYLGLYOXAL toxicity and the effects on enzymes such as glutathionine and the GMO origins?

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.

this photograph looks like a raphael or a manet -- pick your era. beautiful any time.

@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.

After my daughter's Kawaskis she had mood disorder, but not bad enough for me to reliaze that it was more than just a bad day.
Her teen years though - developed into depression.
After another series of HepB and a flu shot in her mid 20s she was not able to sleep - indications of the pituitary signalling too much corisone production which I think led to sleep deprived psychosis.

Also this study says that teenagers with bipolar and mood related problems have an increased volume or enlarged pituitary gland.

http://www.ncbi.nlm.nih.gov/pubmed/18199247

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.

Well, that explains why I developed Hashimoto's thyroiditis as a young adult--within a few weeks of receiving the MMR, Hep B, DPT, and gamma globulin, all supposedly mandatory for a work trip to mainland China back in the 1980's.

Oh, and at the same time, I developed shingles (the worst case my doctor had ever seen) and symptoms of celiac disease/gluten intolerance that then went undiagnosed for decades, but was treated with ever-increasing amoutns of Prilosec, which caused B12 deficiency, earning me yet another round of misdiagnosis, as the doctors tried to diagnose me with Meniere's Disease, and wanted me on prednisone and a truckload of other meds, all of which I rejected in favor of B12 treatment.

Yep. It all fits.

It's amazing that I didn't end up with pancreatitis and/or autism and/or lupus/MS/diabetes.

I can only guess what my health would have been like if it weren't for the fact that I wasn't much of a wheat-eater in the first place.

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

@son in recovery--thank you for this information. My child has the same issues and we would like to explore this. Where did you purchase the zapper?

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.

I have got so much running through my head, I am having trouble focusing!!!!

This is just one piece of amazing information, brought to us "NOT" by the CDC and the NIH -- oh no, but by a mother with an injuried child.

Meanwhile;
The American people have hung their heads in shame for being glutinous/lazy????? Really???

It is not the American people that should be hanging their heads in shame.

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.

I posted last week - my son has Autism, PANDAS and now Epstein Barr. I have been using frequency healing on him for the past 2 weeks and I haven't seen him this happy in months. It is painless, we do it in the comfort of our own home and relatively inexpensive compared to other treatments we have used such as HBOT. His own immune system is awakening! See the following You Tube http://www.youtube.com/watch?v=mfe4M6sbxeA&list=UU7zbipH9fnOXRia_N_m6qeg&index=2&feature=plcp We do not use a Rife machine, instead have bought a zapper since it is less expensive and super easy to use. I encourage everyone that has a child with viral / bacterial issues such as my little guy consider this painless, easy to use method for waking up your child's own immune system. (My son's DAN has patients that use frequency healing and the other DAN office in town treats patients with their own on site Rife Machine.)

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

Thank you for sharing your knowledge, Teresa. I hope this opens doors for treatment for Meg, and all our children. You inspire us all.

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

I echo the comments of Alison regarding your extraordinary diligence and acquired research skills .. my entire family has the greatest respect for all you do.

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

I have more hope in the detective work and research parents like you are doing Teresa than all of mainstream medicine, Autism Speaks, and any government health agency. Deep respect for you.

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