Exposure to aluminium and the subsequent development of a disorder with features of Alzheimer’s disease

D P Perl

doi:10.1136/jnnp.2006.090613

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Exposure to aluminium and the subsequent development of a disorder with features of Alzheimer’s disease

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Re: Alzheimer's Dementia and Aluminum in Drinking Water
Douglas W Cross
Published on: 13 April 2016
Alzheimer's Dementia and Aluminum in Drinking Water
Russell L. Blaylock, M.D.
Published on: 13 April 2016

Published on: 13 April 2016
Re: Alzheimer's Dementia and Aluminum in Drinking Water
- Douglas W Cross, Forensic ecologist
Dear Editor,
Dr Russell Blaylock opens an interesting perspective with respect to the toxicity of the aluminofluoride complex as a potential factor in the Camelford aluminium sulphate incident. It may be relevant to note, therefore, that the key water sample taken at the height of the contamination contained not only 620mg/l of aluminium, but also 7 mg/l of fluoride, presumably present as a contaminant of the o...
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Dear Editor,
Dr Russell Blaylock opens an interesting perspective with respect to the toxicity of the aluminofluoride complex as a potential factor in the Camelford aluminium sulphate incident. It may be relevant to note, therefore, that the key water sample taken at the height of the contamination contained not only 620mg/l of aluminium, but also 7 mg/l of fluoride, presumably present as a contaminant of the original concentrated industrial product delivered to the works. Since no other samples were analysed for fluoride, it is uncertain if this may have played a part in the development of my wife's fatal condition.
The literature on which the British Government's Committee on Toxicity sub-group examining the medical effects of the incident has relied almost universally implies that during exposure to aluminium in drinking water, only a small proportion is absorbed and translocated to the blood; what little does enter the blood is rapidly excreted through the kidneys. In fact, for a small (and currently unknown) proportion of the population of around 20,000 peple exposed during the incident, highly anomalous absorption did occur in a very small number of individuals who showed no previous indication of any clinical susceptibility to aluminium intoxication. In one case, the serum in three blood samples collected from a severely affected male in his late thirties contained 2.89 and 0.59 micromoles of aluminium per litre, 42 and 54 days after exposure. After 68 days it fell to normal (0.15 micromoles/l). This suggests that, by extrapolating back to the time of the incident, his serum aluminium may have been greater than fifty times the accepted normal range. There appears to be no comparable data in the literature for individuals not subject to clinical conditions in which serum aluminium levels may become elevated - for example in dialysis dementia.
A few others are known to have had extremely elevated blood serum aluminium following the incident. In attempting to place the recently published results in context, it is clear that within a large and medically highly diverse population unusual effects may be demonstrated in a small number of highly susceptible individuals. Nor is it inevitable that all such people will develop an identical condition following exposure. The range of long-term medical effects currently evident suggests a that there is a central core of common features, but until a detailed examination of those people in the area with long-term and late- onset conditions that may be associated with their exposure in 1988 has been made, the significance of the recent fatality will remain uncertain.
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Conflict of Interest:
None declared.
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Published on: 13 April 2016
Alzheimer's Dementia and Aluminum in Drinking Water
- Russell L. Blaylock, M.D., Neurosurgeon
Dear Editor,
This case strengthens the correlation between aluminum in drinking water and Alzheimer's dementia. A number of studies have shown a relation between hyperphosporylation of tau and aluminum but of more interest is the observation that aluminum can activate brain microglia, which induces the release of toxic concentrations of inflammatory cytokines, eicosanoids, ROS, lipid peroxidation products and tw...
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Dear Editor,
This case strengthens the correlation between aluminum in drinking water and Alzheimer's dementia. A number of studies have shown a relation between hyperphosporylation of tau and aluminum but of more interest is the observation that aluminum can activate brain microglia, which induces the release of toxic concentrations of inflammatory cytokines, eicosanoids, ROS, lipid peroxidation products and two excitotoxins-glutamate and quinolinic acid. (1)
It is also known that aluminum absorption is 2-3-fold higher in Alzheimer's patients as compared to aged-matched controls and 6-fold higher in Down's syndrome, a condition having the pathologic hallmarks of AD.(2,3) In addition, it has been shown that a number of organic acids, such as lactic, gluconic, malic, citric and oxalic acids, significantly increase aluminum absorption and deposition in the brain. (4)
There is growing evidence that much of the pathological damage caused by aluminum is in fact a result of chemical interaction between fluoride and aluminum. Because of both chemical's high level of reactivity, fluoroaluminum compounds are commonly found in drinking water as well as many plants.
Recent research by Strunecka and co-workers have shown that fluoroaluminum compounds can mimic phosphates and activate G-protein receptors, something of great importance considering the widespread presence of these receptors and substrates in the brain. (5) This includes excitotoxic glutamate receptors. Recent papers have explored the possible mechanisms by which fluoroaluminum compounds could cause AD. (6, 7)
Even extremely small concentrations of the fluoroaluminum compound have been shown to produce significant neuronal loss in the CA1 and CA-4 areas of the hippocampus, reflecting pathological changes also seen in AD.8 Aluminum has also been shown to enhance brain glutamate levels, with the greatest increases seen in the midbrain-hippocampal area.(9) This would aggravate the microglial-induced excitotoxicity triggered by high brain aluminum levels.
Based on the available evidence it would be foolish to continue to add aluminum and especially fluoride and aluminum to public drinking water. Those at special risk would be babies, the elderly, those with neurological disorders or strong family histories for these disorders and those deficient in selenium, calcium, magnesium and ascorbate.
Russell L. Blaylock, M.D.
Neurosurgeon and
Visiting Professor of Biology
Belhaven College
Jackson, MS
References
1. Shirabe T, Irie K, Uchida M. Autopsy case of aluminum encephalopathy. Neuropathology. 2002;22:206-10.
2. Roberts NB, Clough A, Bellia JP, Kim JY. Increased absorption of aluminum from a normal dietary intake in dementia. J Inorg Biochem 1998; 69: 171-6.
3. Moore PB, Edwardson JA, Ferrier IN, et al. Gastrointestinal absorption of aluminum is increased in Down's syndrome. Biol Psych 1997; 41: 488- 92.
4. Domingo JL, Gomez M, Sanchez DJ, Lolbet JM, Corbella J. Effect of various dietary constituents on gastrointestinal absorption of aluminum from drinking water and diet. Res Commun Chem Pharmacol 1993; 79: 377-80.
5. Strunecka A., Struneck_ O., Patocka J. Fluoride plus aluminum: The useful tools in laboratory investigations, but messengers of the false information. Physiol. Res.2002; 51, 557-564.
6. Blaylock, RL. Excitotoxicity: a possible central mechanism in fluoride neurotoxicity. Fluoride 2004; 37: 301-314.
7. Ripova D., Platilova V., Strunecka A., Jirak R., Höschl C. Alterations in calcium homeostasis as biological marker for mild Alzheimer´s disease? Physiol. Res. 53, (2), 2004.
8. Varner JA, jenson KF, Horvath W, Isaacson RL. Chronic administration of aluminum-fluoride or sodium fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res 1998; 784; 284-98.
9. Nayak P and Chatterjee A. Dietary protein restriction cause modification in aluminum-induced alterations in glutamate and GABA system of rat brain. BMC Neuroscience 2004; 4: 4.
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Conflict of Interest:
None declared.
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