Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration
Christopher A. Shaw and Michael S. Petrikc
Departments of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada
Experimental Medicine, University of British Columbia, Vancouver, British Columbia, Canada
Graduate Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada
J Inorg Biochem. 2009 November ; 103(11): 1555. doi:10.1016/j.jinorgbio.2009.05.019.
Abstract
Gulf War Syndrome is a multi-system disorder afflicting many veterans of Western armies in the 1990–1991 Gulf War. A number of those afflicted may show neurological deficits including various cognitive dysfunctions and motor neuron disease, the latter expression virtually indistinguishable from classical amyotrophic lateral sclerosis (ALS) except for the age of onset. This ALS “cluster” represents the second such ALS cluster described in the literature to date. Possible causes of GWS include several of the adjuvants in the anthrax vaccine and others. The most likely culprit appears to be aluminum hydroxide. In an initial series of experiments, we examined the potential toxicity of aluminum hydroxide in male, outbred CD-1 mice injected subcutaneously in two equivalent-to human doses. After sacrifice, spinal cord and motor cortex samples were examined by immunohistochemistry. Aluminum-treated mice showed significantly increased apoptosis of motor neurons and increases in reactive astrocytes and microglial proliferation within the spinal cord and cortex. Morin stain detected the presence of aluminum in the cytoplasm of motor neurons with some neurons also testing positive for the presence of hyper-phosphorylated tau protein, a pathological hallmark of various neurological diseases, including Alzheimer's disease and frontotemporal dementia. A second series of experiments was conducted on mice injected with six doses of aluminum hydroxide. Behavioural analyses in these mice revealed significant impairments in a number of motor functions as well as diminished spatial memory capacity. The demonstrated neurotoxicity of aluminum hydroxide and its relative ubiquity as an adjuvant suggest that greater scrutiny by the scientific community is warranted.
Keywords: Aluminum hydroxide; Adjuvant; Neurotoxicity; Gulf War Syndrome; Amyotrophic lateral sclerosis
Full paper here
9 comments:
Good information.
Especially as Gardasil contains a large dose of aluminum and there have been some cases of girls developing similar syndromes.
What I have not found discussed enough is the macrophagic myofasciis that is a condition recognized as a reaction to the Al in vaccines
J Inorg Biochem. 2009 Nov;103(11):1571-8. Epub 2009 Aug 20.
Long-term persistence of vaccine-derived aluminum hydroxide is associated with chronic cognitive dysfunction.
Couette M, Boisse MF, Maison P, Brugieres P, Cesaro P, Chevalier X, Gherardi RK, Bachoud-Levi AC, Authier FJ.
Macrophagic myofasciitis (MMF) is an emerging condition, characterized by specific muscle lesions assessing long-term persistence of aluminum hydroxide within macrophages at the site of previous immunization. Affected patients mainly complain of arthromyalgias, chronic fatigue, and cognitive difficulties. We designed a comprehensive battery of neuropsychological tests to prospectively delineate MMF-associated cognitive dysfunction (MACD). Compared to control patients with arthritis and chronic pain, MMF patients had pronounced and specific cognitive impairment. MACD mainly affected (i) both visual and verbal memory; (ii) executive functions, including attention, working memory, and planning; and (iii) left ear extinction at dichotic listening test. Cognitive deficits did not correlate with pain, fatigue, depression, or disease duration. Pathophysiological mechanisms underlying MACD remain to be determined. In conclusion, long-term persistence of vaccine-derived aluminum hydroxide within the body assessed by MMF is associated with cognitive dysfunction, not solely due to chronic pain, fatigue and depression.
Lupus. 2009 Nov;18(13):1213-6.
Vaccines as a trigger for myopathies.
Orbach H, Tanay A.
Department of Medicine B, Wolfson Medical Center, Holon, Israel. orbach@wolfson.health.gov.il
Abstract
Vaccines are considered to be among the greatest medical discoveries, credited with the virtual eradication of some diseases and the consequent improved survival and quality of life of the at-risk population. With that, vaccines are among the environmental factors implicated as triggers for the development of inflammatory myopathies. The sporadic reports on vaccine-induced inflammatory myopathies include cases of hepatitis B virus, bacillus Calmette-Guérin, tetanus, influenza, smallpox, polio, diphtheria, diphtheria-pertussis-tetanus, combination of diphtheria with scarlet fever and diphtheria-pertussis-tetanus with polio vaccines. However, a significant increase in the incidence of dermatomyositis or polymyositis after any massive vaccination campaign has not been reported in the literature. In study patients with inflammatory myopathies, no recent immunization was recorded in any of the patients. Moreover, after the 1976 mass flu vaccination, no increase in the incidence of inflammatory myopathies was observed. Although rare, macrophagic myofasciitis has been reported following vaccination and is attributed to the aluminium hydroxide used as an adjuvant in some vaccines. Prospective multicenter studies are needed to identify potential environmental factors, including vaccines, as potential triggers for inflammatory myopathies
Neuromuscul Disord. 2006 May;16(5):347-52. Epub 2006 Apr 17.
AlOH3-adjuvanted vaccine-induced macrophagic myofasciitis in rats is influenced by the genetic background.
Authier FJ, Sauvat S, Christov C, Chariot P, Raisbeck G, Poron MF, Yiou F, Gherardi R.
Centre de Référence Pour Maladies Neuromusculaires, CHU Henri Mondor, AP-HP, Créteil, France. francois-jerome.authier@hmn.aphp.fr
Abstract
Macrophagic myofasciitis (MMF) is a specific histopathologic lesion involved in the persistence for years of aluminum hydroxide [Al(OH)(3)] at the site of previous intramuscular (i.m.) injection. In order to study mechanisms involved persistence of MMF lesions, we set up an experimental model of MMF-lesion in Sprague-Dawley and Lewis rat, by i.m. injections of 10 microL of an Al(OH)(3)-adjuvanted vaccine. An evaluation carried out over a 12-month period disclosed significant shrinkage of MMF lesions with time. A radioisotopic study did not show significant aluminium uptake by Al(OH)(3)-loaded macrophages. A morphometric approach showed that Lewis rats with Th1-biased immunity had significantly smaller lesions than Sprague-Dawley rats with balanced Th1/Th2 immunity. Concluding, our results indicate that genetic determinatives of cytotoxic T-cell responses could interfere with the clearance process and condition the persistence of vaccine-induced MMF-lesions.
Ear Nose Throat J. 2007 Apr;86(4):238-9.
Vocal fold deposits in macrophagic myofasciitis.
Glynn F, O'Sullivan P.
South Infirmary, Victoria University Hospital, Cork, Ireland.
Abstract
Macrophagic myofasciitis was first reported in 1998. This disease manifests as diffuse myalgia and chronic fatigue. Its pathophysiology has been traced to the presence of an aluminum adjuvant used in vaccines against hepatitis A and B virus and tetanus toxoid; the adjuvant aggregates at the site of injection. One-third of patients with macrophagic myofasciitis develop autoimmune disease. Vocal fold deposits have been described in autoimmune diseases such as sarcoidosis, systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis, Sjögren's syndrome, and Hashimoto's thyroiditis. We report what to the best of our knowledge is the first published case of vocal fold deposits in macrophagic myofasciitis.
I wonder how long these guy's research careers are going to last.
The aluminum adjuvant, complexes with glycine, glycine is needed for GABA A receptors, which is involved in tics, Tourettes. Same things happen upon exposure to chlorine, that oxidizes glycine so you get twitching and tics. So the thing is to chelate the excess aluminum and restore glycine functionality by possibly giving more glycine to restore GABA A function and remove tics.
You can study the effect by doing Ellman's reagent of blood to determine Al complexation, check glutathione levels and oxidation-reduced state to determine how binding of glycine has affected it. There might be a link there. Glutathione is made up of glycine-glutamic acid-cysteine, so that may have an effect, as would the glycine-GABA receptors, GABA A. Note that taurine can also be given to complex Aluminum. Alternatively if the person has a sulfite allergy, then mental retardation through, sulfite oxidase and molybdenum cofactor deficiency results. This is why some vaccines have side effects, and why all babies should be tested for allergies during their first year of birth.
Also I should mention, that Renishaw cells found in grey matter, if glycine release is inhibited, then alpha motor neurons become hyperactive, leading to constant muscle contraction that is typically seen in ALS and gulf war and things.
So, chelate the Aluminum and they should be fine and restore functionality by giving more glycine.
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