by Sharry Edwards, MEd
Director of the Institute of BioAcoustic Biology
The August 14th, 2010 issue of Science News, "Separating wheat from chaff in celiac disease", reported that a research team led by gastroenterologist Robert Anderson of the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia, had identified specific triggers (gluten sensitivities) associated with celiac disease.
Since our research efforts often evaluate clients who exhibit gluten sensitivity and a myriad of associated diseases, it was imperative that this important information be added to our software databases. I translated the three proteins into BioAcoustic bio-frequency (biomarkers)* and was immediately inundated with an avalanche of novel data showing that the metabolic pathways distorted by these proteins were linked to nearly all systems of the human body; causing immune distortion, acute cellular inflammation and disruptions in cell communication.
The article listed three proteins, w-5 gliadin (wheat), g-3 hordein (barley) and g secalins (rye) that were implicated in the production of the specific anti-gliadin antibody reactions. These proteins, which have been proven to be responsible for the allergic reactions, are associated with grain glutens from which they are derived.
Patent records indicated the grains involved are clones developed in a laboratory by Monsanto, a multinational agricultural biotech conglomerate. This would confirm that the present day epidemic of gluten sensitivities/allergies stem from laboratory created grains. These gluten-distorted, allergic causing, grain clones are being used to create foods that we eat everyday; bread, cereals, crackers, pastry, seasonings, even some packaged chip products contain wheat. As I developed the BioAcoustic correlations I was aghast with the realization of how thoroughly our health is being negatively influenced by these genetically modified foods (GMO's).
Further investigation revealed that the cloned genes contained two substitutions that distorted the way the body processes two sulfur rich amino acids: proline and glutamine. Disturbances in these amino acid substitutions impede the methylation of these two essential nutrients.
BioAcoustically speaking, Glutamine distortions seem to be the most destructive. The enzyme required to utilize glutamine is glutamate decarboxylase (GAD). Glutamate is a key molecule in cellular metabolism and the most abundant excitatory neurotransmitter in a vertebrate nervous system.
In mammals, GAD exists in two isoforms encoded by two different genes - Gad1 and Gad2. GAD1 and GAD2 are expressed in the brain where GABA is used as a neurotransmitter; GAD2 is also expressed in the pancreas.
This led to an evaluation of the GAD genomes and what happens when these genes are activated:
Glutamate decarboxylase aka glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation (part of the process of breaking down for use by the body) of glutamate to GABA (gamma aminobutyric acid) and CO2.
GABA is a natural tranquilizer and an important inhibitory neurotransmitter that helps regulate neuron activity and the body's nanosensors. Starting with the GAD enzyme response and moving toward GABA in conjunction with the active form of B6 (PLP), the nanotransmitters of the body are created and regulated. The movement of electrical energy and hence magnetic potential within the body are controlled by these nanotransmitters.
GAD uses PLP (pyridoxal 5 0-phosphate) as a cofactor. PLP was granted a patent by the US government patent office to the Canadian company, Medicure. PLP is now under the control of the pharmaceutical industry. Its lack is often associated with blood clotting distortions, migraines, neural disorders and seizures.
Nanotransmitters produced in conjunction with GAD metabolism show direct associations with a multitude of diseases: diabetes, autism, arthritis, Parkinson's, ALS, Multiple Sclerosis, joint pain and deterioration, auditory disorders, Celiac Disease, Crohns, Irritable Bowel syndrome, diverticulitis, schizophrenia, bipolar and anxiety disorders, aspartame sensitivity, MSG reactions, Lupus, Fibromyalgia, depression, seizures, brain signaling, the use of calcitonin (cancer related), histidine function (seasonal allergies), cellular inflammation and vaccination reactions.
Of particular importance is GAD's involvement with cancer via Calcitonin, a 32-amino-acid peptide/hormone that participates in calcium and phosphorus metabolism. BioAcoustically Speaking, calcitonin is a major player in the role of how the body handles any cancer threat.
Parkinson's is an incurable, debilitating disease that also shows GAD involvement. The activity of glutamic acid decarboxylase (GAD), the enzyme involved in formation of the inhibitory neurotransmitter γ-aminobutyric acid (GABA), was studied in autopsy brain samples from six Parkinson's patients and 13 controls. The activity of GAD was significantly reduced in brain samples of patients with Parkinson's disease, being about 50 percent; of that in controls. Moreover, levodopa treatment showed a tendency to increase the activity of GAD. The results suggest the involvement of GABA neurons in Parkinson's disease.
A search of the GAD literature stated that acetylcholine, γ-aminobutyric acid, dopamine, calcitonin gene-related peptides, choline acetyltransferase and enkephalins are involved with the metabolism of GAD. It would be important to include these biochemicals when testing subjects for GAD presence and methylation.
Glutamate is the same Frequency Equivalent* as aspartame and is part of MSG (mono-sodium glutamate). James Oschman in his publication, Energy Medicine, states that cells emit frequency-based signals as a request for needed biochemicals to gather at the site where they are needed. Since Glutamate and Aspartame are the same frequency, this may explain why Aspartame has been implicated in so many muscle and joint disorders.
These observations are based on the mathematical matrix of BioAcoustic Biology developed over the last twenty years by the Sound Health Research Center located in Albany, Ohio, USA. The system allows for the evaluation of any item associated with the body in terms of numeric mathways. Sharry Edwards, the recognized pioneer of this emerging technology states, "I expect this information will be the impetus that opens the world to the potential of BioAcoustic Biology and the hope of allowing access to Self Health care; even after the appearance of a disease process".
Quoting from the original Science News article:
"Three protein fragments are looking like the guilty parties in celiac disease, an intestinal ailment that affects as many as one in 133 people in the United States. These partial proteins, or peptides, are the part of gluten in wheat, rye and barley that triggers the immune systems of celiac patients, damaging the small intestine. An Australian research team reports the new findings in the July 21 Science Translational Medicine."
"This is an impressive and very comprehensive study," says immunologist Ludvig Sollid of the University of Oslo. "The authors find that most celiac patients make a response to these three gluten peptides."
Are GMO producers aware of the damage to health that is being caused? Why are GMO producers and the US government boldly attempting to prevent package warnings that would notify people that they were eating GMO products? Is it greed, ignorance or a misguided attempt to improve our food supply that is in fact poisoning our food, our population, and our genetic pool? Is this assault on our food supply intentionally creating a future that will keep us ill and medication dependent?
* all issues expressed in terms of Frequency Equivalent™ (a "term of use" for BioAcoustic Biology) a numeric representation of a person, place, thing or emotion.
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"Separating wheat from chaff in celiac disease." Science News 178.4 (2010): 8. Web. 25 Oct 2010.
Fasano, Alessio. "Celiac Disease Insights: Clues to Solving Autoimmunity." Scientific American Magazine August 2009: n. pag. Web. 25 Oct 2010.
"Glutamic Acid: Facts, Discussion Forum, and Encyclopedia Article." Absolute Astronomy. Web.
"Showing pathways Glutamate Metabolism." N.p., n.d. Web. 26 Sept 2010.
International Archives of Allergy and Immunology - Vol 152, No 2, 2010: The Diabetic Antigen Glutamic Acid Decarboxylase (GAD 65) in the Human Peripheral Blood. G.P. Tilz, J. Dausset, M. Wiltgen
Diabetes mellitus decreases the expression of calcitonin-gene related peptide, gamma-amino butyric acid and glutamic acid decarboxylase in human pancreatic islet cells. Al-Salam S, Hameed R, Parvez HS, Adeghate E.
J Diabetes Sci Technol. 2009 March; 3(2): 320-330. Published online 2009 March.
The Role of Immunomodulation Therapy in Autoimmune Diabetes, Johnny Ludvigsson, M.D., Ph.D. for the Linköping Diabetes Immune Intervention Study Group, Division of Pediatrics and Diabetes Research Centre, Department of Clinical and Experimental Medicine, Linköping University, Sweden
Physiol Res. 2004;53(3):279-86.
Anti-GAD-positive patients with type 1 diabetes mellitus have higher prevalence of autoimmune thyroiditis than anti-GAD-negative patients with type 1 and type 2 diabetes mellitus. Bárová H, Perusicová J, Hill M, Sterzl I, Vondra K, Masek Z. Third Department of Medicine, General University Hospital, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Decreased GAD67 mRNA levels in cerebellar Purkinje cells in autism: pathophysiological implications. Jane Yip, Jean-Jacques Soghomonian and Gene J. Blatt
Blaylock, MD, Russel L. "The Connection Between MS and Aspartame." Truth In Labeling. N.p., 06 07 2004. Web. 26 Sept 2010.
Journal of the Neurological Sciences, Volume 47, Issue 3, September 1980, Pages 353-364 Abnormal glutamic acid metabolism in multiple sclerosis. A. Westall, G.Hawkins, W. Ellison, Lawrence W. Myers. The Salk Institute, San Diego, CA U.S.A.. Multiple Sclerosis Research Clinic, Department of Neurology, UCLA School of Medicine, Los Angeles, CA U.S.A.
GAD and Irritable Bowel Syndrome. Scand J Gastroenterol. 2007 Nov;42(11):1289-93.
Autoantibodies in patients with gut motility disorders and enteric neuropathy. Törnblom H, Lang B, Clover L, Knowles CH, Vincent A, Lindberg G. Karolinska Institutet, Department of Medicine, Karolinska University Hospital, Huddinge, Stockholm, Sweden.
European Neurlogy - Vol 12, No. 1, 1974. Brain Glutamic Acid Decarboxylase Activity in Parkinson's Disease. U.K. Rinne, H. Laaksonen, P. Riekkinen, V. Sonninen. Department of Neurology, University of Turku, Turku. Eur Neurol 1974;12:13-19 (DOI: 10.1159/000114599)
Neurology. 1971 Oct;21(10):1000-7.Title: Glutamic acid decarboxylase in Parkinson's disease and epilepsy.McGeer PL, McGeer EG, Wada JA.
Eur J Clin Nutr. 2008 Apr;62(4):451-62. Epub 2007 Aug.
Direct and indirect cellular effects of aspartame on the brain. Humphries P, Pretorius E, Naudé H.Department of Anatomy, University of Pretoria, Pretoria, Gauteng, South Africa.
Mol Psychiatry. 2006 Aug;11(8):752-62. Epub 2006 May 23. Association between glutamic acid decarboxylase genes and anxiety disorders, major depression, and neuroticism. Hettema JM, An SS, Neale MC, Bukszar J, van den Oord EJ, Kendler KS, Chen X. Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA 23298-0126, USA.
Ann Rheum Dis. 2008 Jul;67(7):1051-2. Methotrexate and its effect on the anti-GAD titre in two patients with rheumatoid arthritis and diabetes mellitus. van Deutekom AW, Nurmohamed MT, Peters MJ, van Eijk IC, Dijkmans BA, Hamann D, Heine RJ, Simsek S.
Sinclair, Mike. "Migraine prevention by targeting glutamate receptors?." BioMedicine. N.p., 4/28/2009. Web. 22 Sept 2010.
Clinical and Experimental Medicine Volume 3, Number 1, 32-36, DOI: 10.1007/s102380300013. Anticardiolipin, glutamic acid decarboxylase, and antinuclear antibodies in epileptic patients A. Verrotti, R. Greco, E. Altobelli, G. Latini, G. Morgese and F. Chiarelli.
Biochemical Medicine. Volume 21, Issue 1, February 1979, Pages 22-32
Possible implication of an inosinetriphosphate metabolic error and glutamic acid decarboxylase in paranoid schizophrenia. Bernardo S. Vanderheiden. Eastern Pennsylvania Psychiatric Institute, Henry Avenue and Abbottsford Road, Philadelphia, Pennsylvania, 19129 USA, Department of Psychiatry and Human Behavior, Jefferson Medical College, Philadelphia, Pennsylvania 19107 USA
Clinical & Experimental Allergy. Volume 40, Issue 5, pages 820-830, May 2010. The role of interleukin-4Rα in the induction of glutamic acid decarboxylase in airway epithelium following acute house dust mite exposure. J. A. Hirota, A. Budelsky, D. Smith, B. Lipsky, R. Ellis, Y-Y. Xiang, W-Y. Lu, M. D. Inman
Archives of Neurology - Vol 61, No 6, June 2004. Anti-Glutamic Acid Decarboxylase Antibodies in the Serum and Cerebrospinal Fluid of Patients With Stiff-Person Syndrome. Goran Rakocevic, MD; Raghavanpillai Raju, PhD; Marinos C. Dalakas, MD.
Arch Neurol. 2004;61:902-904.GAD and Lupus/Fibromyalgia.
Lupus. 2005;14(6):486-8. Anti-glutamic acid decarboxylase antibodies in a patient with systemic lupus erythematosus and fibromyalgia symptoms. Taylor-Gjevre RM, Gjevre JA. Division of Rheumatology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.
Adams, Jefferson. "Frequency of Autoantibodies in Celiac Disease." Celiac Disease Diagnosis, Testing & Treatment. N.p., 1 29 2010. Web. 26 Sept 2010.
Journal of Neurological Sciences - Volume 250, Issue 1, Pages 124-132 (1 December 2006). GABA A-receptor mRNA expression in the prefrontal and temporal cortex of ALS patients. S. Petria, K. Kollewea, C. Grotheb, A Horic, R Denglera, J Buflera, K. Krampfla