Studies Showing the Toxicity of Aluminum in Vaccines
The Toxicity of Aluminum in Allergy Shots
Aluminum-Induced Entropy in Biological Systems: Implications for Neurological Disease
"Al is invariably toxic to living systems and has no known beneficial role in any biological systems. Humans are increasingly exposed to Al from food, water, medicinals, vaccines, and cosmetics, as well as from industrial occupational exposure. Al disrupts biological self-ordering, energy transduction, and signaling systems, thus increasing biosemiotic entropy. Beginning with the biophysics of water, disruption progresses through the macromolecules that are crucial to living processes (DNAs, RNAs, proteoglycans, and proteins). It injures cells, circuits, and subsystems and can cause catastrophic failures ending in death. Al forms toxic complexes with other elements, such as fluorine, and interacts negatively with mercury, lead, and glyphosate. Al negatively impacts the central nervous system in all species that have been studied, including humans. Because of the global impacts of Al on water dynamics and biosemiotic systems, CNS disorders in humans are sensitive indicators of the Al toxicants to which we are being exposed."
Aluminium toxicity in the rat brain: histochemical and immunocytochemical evidence
Brain Res Bull. 2001 May 15;55(2):257-67
"Al (as indicated by the fluorescent Morin staining) was concentrated in white matter of the medial striatum, corpus callosum, and cingulate bundle. Immunoreactivity of astrocytes and phagocytic microglia based on glial fibrillary acidic protein and ED1 markers, respectively, revealed a greater inflammatory response in Al-injected animals compared to controls. Damage of the cingulate bundle in Al-treated animals led to a severe anterograde degeneration of cholinergic terminals in cortex and hippocampus, as indicated by acetylcholinesterase labelling. Our data suggest that the enhancement of inflammation and the interference with cholinergic projections may be the modes of action through which Al may cause learning and memory deficits, and contribute to pathological processes in Alzheimer's disease."
Chronic exposure to aluminum in drinking water increases inflammatory parameters selectively in the brain
J Neurosci Res. 2004 Feb 15;75(4):565-72.
"A link between aluminum (Al) exposure and age-related neurological disorders has long been proposed. Although the exact mechanism by which the metal may influence disease processes is unknown, there is evidence that exposure to Al causes an increase in both oxidative stress and inflammatory events... Insofar as no parallel changes were observed in the serum or liver of treated animals, the proinflammatory effects of the metal may be selective to the brain. Al exposure may not be sufficient to cause abnormal production of the principal component of senile plaques directly but does exacerbate underlying events associated with brain aging and thus could contribute to progression of neurodegeneration."
Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain
J of Neuro Immun. Volume 176, Issues 1–2, July 2006, Pages 16–23
"Inflammatory and oxidative events are up-regulated in the brain of AD patients. It has been reported that in animal models of AD, exposure to aluminum (Al) or copper (Cu) enhanced oxidative events and accumulation of amyloid beta (Aβ) peptides. The present study was designed to evaluate the effect of a 3-month exposure of mice to copper sulfate (8 μM), aluminum lactate (10 or 100 μM), or a combination of the salts. Results suggest that although Al or Cu may independently initiate inflammatory or oxidative events, they may function cooperatively to increase APP levels."
Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incident
"People who were exposed to the contaminated water at Camelford suffered considerable damage to cerebral function, which was not related to anxiety. Follow up studies would be required to determine the longer term prognosis for affected individuals."
Biofactors. 1990 Jul;2(3):163-9.
"Experimental evidence is summarized to support the hypothesis that chronic exposure to low levels of aluminum may lead to neurological disorders. These disorders result from defective phosphorylation--dephosphorylation reactions, reduced glucose utilization and site-specific damage inflicted by free radicals produced by altered iron metabolism."
Modulation of tumor necrosis factor alpha expression in mouse brain after exposure to aluminum in drinking water
Arch Toxicol. 1999 Nov;73(8-9):419-26.
"Aluminum, a known neurotoxic substance and a ground-water pollutant, is a possible contributing factor in various nervous disorders including Alzheimer's disease. It has been hypothesized that cytokines are involved in aluminum neurotoxicity... he expression of TNFalpha mRNA in cerebrum was significantly increased among aluminum-treated groups compared with the control, in a dose-dependent manner... Because the aluminum-induced alteration in cytokine message occurred at aluminum concentrations similar to those noted in contaminated water, these results may be relevant in considering the risk of aluminum neurotoxicity in drinking water."
Aluminum neurotoxicity in preterm infants receiving intravenous-feeding solutions
N Engl J Med. 1997 May 29;336(22):1557-61
Aluminium absorption in infancy
J Paediatr Child Health. 1991 Jun;27(3):164-6.
"The use of aluminium-containing medications and aluminium contamination of infant formulae is common. We aimed to determine whether aluminium absorption occurs after antacid ingestion. Plasma and urinary levels of aluminium were measured before and after antacid therapy in seven infants whose mean gestational age was 36 +/- 2 weeks and postnatal age 11 +/- 5 days. Antacid therapy (400-800 mumol aluminium) was given with feeds for 2 days. Plasma aluminium levels increased and reached toxic levels (0.64 +/- 0.33 mumol/L vs 3.48 +/- 2.86 mumol/L, P = 0.029). Urinary aluminium: creatinine ratio also increased. These results demonstrate that infants absorb
aluminium from antacids and raise the concern of aluminium toxicity."
J Chem Neuroanat. 2000 Jan;17(4):207-15.
"The monthly intracisternal inoculation of aluminum chloride (AlCl3) to young adult New Zealand white rabbits induces motor neuron degeneration marked by intraneuronal neurofilamentous aggregates similar to that observed in amyotrophic lateral sclerosis (ALS). However, in contrast to ALS, this process occurs in the experimental paradigm in the absence of a glial response. In addition, whereas ALS is a fatal disorder, the cessation of aluminum exposure leads to both clinical and neuropathological recovery. Because microglia can influence neuronal regeneration, we have examined the effect of both acute and chronic aluminum exposure on microglial activation in vivo. We have studied microglial morphology in young adult New Zealand white rabbits receiving either single (1000 microg) or repeated sublethal (100 microg monthly) intracisternal inoculums of AlCl3. In addition, rabbits receiving 1000 microg AlCl3 inoculums were studied following an unilateral sciatic axotomy 48 h prior to the AlCl3 exposure. Our studies demonstrate that microglial activation in vivo is inhibited by AlCl3 exposure, and that a correlation exists between the extent of microglia suppression and the potential for recovery. This suggests that microglial activation is an important determinant of neuronal injury."
Gerontology. 02/1997; 43 Suppl 1:16-23.
"Since the first reports of aluminum-induced neurofibrillary degeneration in experimental animals, extensive studies have been performed to clarify the role played by aluminum in the pathogenesis of Alzheimer's disease (AD). Additional evidence implicating aluminum in AD includes elevated levels of aluminum in the AD brain, epidemiologic data linking aluminum exposure to AD, and interactions between aluminum and protein components in the pathologic lesions of AD, i.e., neurofibrillary tangles (NFTs) and senile plaques. As most of this evidence is circumstantial and some of it is not consistent in all reports, the role of aluminum in the pathogenesis of AD has remained controversial. However, the interaction of aluminum with altered forms of tau in the paired helical filaments (PHFs) of neurofibrillary lesions is highly likely to contribute to the formation of NFTs because (1) aluminum and abnormally phosphorylated tau (known as PHF tau) are colocalized in NFTs, and (2) aluminum is known to preferentially interact with such phosphorylated proteins. Recently, it was demonstrated that aluminum binds selectively to PHF tau, induces PHF tau to aggregate, and retards the in vivo proteolysis of PHF tau. These data suggest that aluminum could serve as a cofactor in the formation of NFTs by interacting with PHF tau. This review summarizes the current understanding of how aluminum might contribute to the formation of neurofibrillary lesions from PHF tau in neurons of the AD brain."
Aluminum levels in brain in Alzheimer's disease.
Biol Psychiatry. 1978 Dec;13(6):709-18.
"In both human Alzheimer's disease and aluminum encephalopathy of animals, changes are observed in neurofibrillary structures. We have found that brains from Alzheimer patients contain approximately 1.4 times the aluminum level found in a control series. Some possible methodological problems are discussed. We have proposed a plausible chemical mechanism for the changes of aluminum encephalopathy."
Aluminum pretreatment impairs the ability of astrocytes to protect neurons from glutamate mediated toxicity
Brain Res. 1993 Sep 10;621(2):207-14.
"We have also demonstrated that prior treatment of astrocytes with 100 microM aluminum citrate impairs this ability of astrocytes to promote neuronal survival. No differences, however, were observed in the ability of control and aluminum-treated astrocytes to take up glutamate. These findings suggest that aluminum may cause astrocytes to: (i) secrete a factor that makes neurons more susceptible to glutamate-induced toxicity; (ii) secrete a neuronotoxic factor in the presence of glutamate; or (iii) reduce secretion of a factor that protects neurons from glutamate excitotoxicity."
Aluminum potentiates glutamate-induced calcium accumulation and iron-induced oxygen free radical formation in primary neuronal cultures
Mol Chem Neuropathol. 1997 Sep-Dec;32(1-3):41-57.
Oxidative stress and mitochondrial dysfunction in aluminium neurotoxicity and its amelioration: a review.
Neurotoxicology. 2014 Mar;41:154-66.
"Aluminium is light weight and toxic metal present ubiquitously on earth which has gained considerable attention due to its neurotoxic effects. The widespread use of products made from or containing aluminium is ensuring its presence in our body. There is prolonged retention of a fraction of aluminium that enters the brain, suggesting its potential for accumulation with repeated exposures. There is no known biological role for aluminium within the body but adverse physiological effects of this metal have been observed in mammals. The generation of oxidative stress may be attributed to its toxic consequences in animals and humans. The oxidative stress has been implicated in pathogenesis of various neurodegenerative conditions including Alzheimer's disease and Parkinson's disease. Though it remains unclear whether oxidative stress is a major cause or merely a consequence of cellular dysfunction associated with neurodegenerative diseases, an accumulating body of evidence implicates that impaired mitochondrial energy production and increased mitochondrial oxidative damage is associated with the pathogenesis of neurodegenerative disorders. Being involved in the production of reactive oxygen species, aluminium may impair mitochondrial bioenergetics and may lead to the generation of oxidative stress. In this review, we have discussed the oxidative stress and mitochondrial dysfunctions occurring in Al neurotoxicity. In addition, the ameliorative measures undertaken in aluminium induced oxidative stress and mitochondrial dysfunctions have also been highlighted."