1Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, 828 W. 10th Avenue, Vancouver, British Columbia, Canada V5Z 1L8
2Program Experimental Medicine, University of British Columbia, Vancouver, Canada V5Z 1L8
3Program in Neurosciences, University of British Columbia, Vancouver, Canada V5Z 1L8
4MIT Computer Science and Artificial Intelligence Laboratory, 32 Vassar Street, Cambridge, MA 02139, USA
5Hudson, FL 34667, USA
6Department of Communicative Disorders, University of Louisiana, Lafayette, LA 70504-3170, USA
7Internal Medicine Group Practice, PhyNet Inc., 4002 Technology Center, Longview, TX 75605, USA
Received 9 June 2014; Accepted 28 July 2014; Published 2 October 2014
Academic Editor: William Valentine
Over the last 200 years, mining, smelting, and refining of aluminum (Al) in various forms have increasingly exposed living species to this naturally abundant metal. Because of its prevalence in the earth’s crust, prior to its recent uses it was regarded as inert and therefore harmless. However, 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.
Aluminum (Al) is the most common metal and the third most abundant element in the earth’s crust [1–3]. However, it seems to have no beneficial role in the biochemistry of any biota . Until the 1820s when the industrial extraction of Al, primarily from bauxite ore , made it possible to bring Al into food processing, manufacturing, medicines, cosmetics, vaccines, and other applications, Al was almost completely absent from the biosphere . Concerns about the toxicity of ingesting Al were expressed over 100 years ago . Today, biologically ingested or injected forms include salts of Al in processed foods  and medicinal products  such as antacids, glossy coatings for pills, and vaccine adjuvants. The last use, which portrays Al compounds as “helpers”—the English translation of the Latin root of adjuvants—is supposed to shock the recipient’s immune defenses into action, ostensibly to enhance the immunogenicity of the pathogen(s) in the vaccine(s) . Al salts are also found in dyes , cosmetics , antiperspirants [11–14], sunscreens [15, 16], and thousands of material products including foils, food containers, and utensils.
In this paper, we will show that Al is harmful to the CNS, acting in a number of deleterious ways and across multiple levels, to induce biosemiotic entropy . A countervailing view exists [18–20], but the assertions of safety are invariably based on weak epidemiological designs, ones that overwhelm significant negative signals with irrelevant noise factors. Such studies that fail to detect significant negative outcomes neither stand up to rigorous scrutiny nor outweigh better designed research, in a vast and growing literature, showing significant negative impacts sustaining the central hypothesis of this paper. Irrefutable research evidence shows that Al exposure is harmful. Further, results discussed in this paper show that it is counterfactual for researchers to argue that Al is universally safe or beneficial even in trace amounts.
Al is used extensively in food processing, for example, in Al-mordanted dye lakes for food coloring, in coatings for pharmaceutical tablets and vitamin capsules, for emulsifying, as a rising agent, to thicken gravies, and in meat-binders, stabilizing agents and texturizers . Even drinking water is a source of Al exposure, although the amount contained in drinking water is typically far below concentrations in common antacids . However, there is concern that the Al in drinking water may be more easily absorbed than at mealtime, due to the fact that an empty stomach promotes absorption . Alum (Al sulfate or Al potassium sulfate) is commonly used in water treatment plants as a coagulant to allow negatively charged colloidal particles to clump together for easy removal. Epidemiological studies have shown that people living in districts with higher Al burden in drinking water are more likely to be diagnosed with Alzheimer’s disease .
Because tea plants contain a higher concentration of Al than many other plants, and, because tea beverages are consumed in large quantities worldwide, a high incidence of Al exposure comes through drinking tea . Al content in tea ranges from 2 to 6 mg/L . Tea infusions have been analyzed for the speciation of Al content, and it has been determined that it is typically bound to large organic molecules such as polyphenols or to citrate [24, 25]. Tea typically contains much more Al than water, and so tea becomes a significant source of Al for heavy tea drinkers. An experiment to estimate oral Al bioavailability from tea involving 8 rats was conducted by injecting Al citrate into tea leaves, delivering approximately the same amount of Al as is inherently found in tea leaves (0.5 to 1 mg/gm) . The brewed tea was administered through intragastric infusion. Following infusion, peak serum levels of Al were up to 1500-fold above mean pretreatment values.
In a substantial and recent review of research, Walton  concludes that Alzheimer’s disease is a manifestation of chronic Al neurotoxicity in humans. Because Al is similar to iron, it gains access to iron-dependent cells involved in memory. As it accumulates over time in such cells, it causes microtubule depletion and disables neuronal afferents and efferents resulting in the multiregion atrophy characteristic of Alzheimer’s pathology . Table 1 highlights some of the Al compounds to which humans are commonly exposed which are known to have deleterious effects on the central nervous systems (CNS) of both animals and humans , whereas Tables 2 and 3, respectively, present Al intake data, and its physical properties compared to other metals. Table 1 also shows dosage and known effects of each source on animals and/or humans.
Christopher A. Shaw, Stephanie Seneff, Stephen D. Kette, Lucija Tomljenovic, John W. Oller Jr., and Robert M. Davidson, “Aluminum-Induced Entropy in Biological Systems: Implications for Neurological Disease,” Journal of Toxicology, vol. 2014, Article ID 491316, 27 pages, 2014. doi:10.1155/2014/491316