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Third only to oxygen and silicon in its prevalence, aluminum is estimated to be the most abundant metal in the Earth's crust. The following are all potential sources: tap water (especially if clarified by alum), and corrosion of the sacrificial anode rod (if it contains aluminum) in hot water tanks. Fluoride-treated water increases aluminum bioavailability and uptake. 

Aluminum in consumer drugs is a big problem. Aspirin is commonly buffered with aluminum hydroxide, aluminum glycinate and other aluminum compounds. Aluminum is present in vaccines such as hepatitis A, hepatitis B, diphtheria-tetanus-pertussis, Haemophilus influenzae type b, human papillomavirus and pneumococcus. Aluminum is placed in the vaccines to selectively target the up-regulation of the humoral arm (TH2 cells) of children’s immune systems, to drive the production of antibodies. (This topic deserves its own 100-page paper.)


An examination of labels on consumer products will reveal that many of them contain aluminum. Vaginal douches contain potassium aluminum sulfate, ammonium aluminum sulfate, and alum. Some antacids contain aluminum hydroxide, dihydroxyaluminum, and aluminum oxide. Anti-diarrheal drugs contain aluminum magnesium silicate and kaolin, an aluminum salt. 


With regard to aluminum in foods, the abrupt and dramatic switch from a largely unprocessed to a largely processed diet (the so-called “Western” diet) has only increased aluminum bioavailability, especially human oral exposure. Such additives are found in dairy (milk, processed cheese, yogurt), staples (cereals, flours, grains), and sweets (sugar, jams, jellies, baking sodas, powdered or crystalline dessert products). Use in food ranges from anticaking agents, to buffers, emulsifying agents, firming agents, leavening agents, neutralizing agents and texturizers.


Other sources include: antiperspirants, food additives, lipstick, hemorrhoid medications, and "softened" water. 

Sources of Exposure




Atomic mass: 26.9815

aluminum in tap water

Target Tissues

Aluminum toxicity is usually found in patients with renal impairment. Acute intoxication is extremely rare; however, in persons in whom aluminum clearance is impaired, it can be a source of significant toxicity. Aluminum accumulates progressively in bone, lung, liver, kidney and brain. Of the total body burden of aluminum, about one-half is in the skeleton, and about one-fourth is in the lungs. Research shows that aluminum builds up in the body over time; thus, the health hazard to older people is greater.

It appears that humans do not need aluminum for any biochemical purpose. Approximately 95% of an aluminum load becomes bound to transferrin and albumin intravascularly and is then eliminated renally. In healthy subjects, only 0.3% of orally administered aluminum is absorbed via the gastrointestinal (GI) tract, and the kidneys effectively eliminate aluminum from the human body. When the GI barrier is bypassed, such as by intravenous infusion, intramuscular injection (vaccines) or in the presence of advanced renal dysfunction, aluminum has a potential to significantly accumulate. 


Absorption from the GI tract is normally minimal, being decreased by the presence of dietary phosphates, but increased by the presence of citric or malic acids (carboxylic acids). Individuals with kidney disorders such as azotemia or uremia may absorb increased quantities of this element. Current evidence shows that aluminum exposure becomes most toxic when dietary magnesium is low. Excretion of aluminum from blood is primarily by urine, while RBC-bound aluminum is mostly excreted via the bile. 


Once in the body, aluminum follows increasing concentrations of phosphate. It may also bind to transferrin in the blood and to citric or malic acids (carboxyl acids). Binding and increasing transport also occurs with the amino acid glycine. Aluminum may bind to DNA, ATP, NADP, NADPH or phosphorylated proteins, once inside the cell. Aluminum impairs production of alpha-ketoglutaric acid in cell mitochondria by interfering with the enzyme, isocitrate dehydrogenase. Low alpha-ketoglutaric acid may then lead to disordered nitrogen balance that may impair protein synthesis, especially in neurological tissues. This depletion in alpha-ketoglutarate also causes an interference with bone mineralization, binds to brain calmodulin, and may enhance acetylcholine turnover that results in its depletion and neuronal plaques.


Aluminum is present in the following U.S. childhood vaccines: hepatitis A, hepatitis B, diphtheria-tetanus-pertussis (DTaP, Tdap), Haemophilus influenzae type b (Hib), human papillomavirus (HPV) and pneumococcus infection. Each of these vaccines contains aluminum, and multiple doses (booster shots) are required. Hence, babies are injected with 1,225 mcg of aluminum instantaneously at age 2 months, and 4,925 mcg of accumulated aluminum by age 18 months. As a result, vaccinated children following the CDC recommendations are exposed to up to 6 mg of aluminum in the first 2 years of life. Experimental research clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. Aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences. 

Signs & Symptoms Research

aluminum research

There are numerous studies that have examined aluminum’s potential to induce toxic effects in humans exposed via inhalation, oral, dermal exposure or by injection with vaccines. Most of these findings are supported by many laboratory animal studies. Occupational exposure studies and animal studies suggest that the lungs and nervous system may be the most sensitive targets of toxicity following inhalation exposure. Most of the animal studies have focused on neurotoxicity and neurodevelopmental toxicity. 


Neurodegenerative changes in the brain, manifested as intraneuronal hyperphosphorylated neurofilamentous aggregates, is a characteristic response to aluminum in certain species and nonnatural exposure situations generally involving direct application to brain tissue, particularly intracerebral and intracisternal administration and in vitro incubation in rabbits, cats, ferrets, and nonhuman primates. 


There is an interesting parallel between the incidence of Alzheimer’s disease and similar memory disorders, and the amount of aluminum in drinking water. Aluminum emerged as a potential cause of Alzheimer’s disease when a 1965 study observed neurofibrillary tangle-like degeneration after directly injecting aluminum into rabbit brains, i.e., lesions similar but not identical to those considered a hallmark of Alzheimer’s disease. A 1973 study followed up with the report of higher levels of aluminum in post-mortem Alzheimer’s disease brain samples. A study published in Lancet involved an evaluation of the geographical relationship between the aluminum content of drinking water and the prevalence of Alzheimer’s over a ten-year period. The study reported a 50% increase in the risk of Alzheimer’s disease in areas with high concentrations of aluminum. Even a small presence of aluminum in water has an effect. Researchers learned that the risk of Alzheimer’s was 1.5 times higher when the aluminum concentration exceeded 0.11 mg/l than in areas where the concentration was 0.01 mg/l. There was no evidence of any relationship between any other form of dementia, including epilepsy, and the presence of aluminum in drinking water. 


It is interesting that about 50% of British drinking water is also treated with iron, which is also suspected of being a co-factor in dementia. These studies have been corroborated by studies done in other countries (other than the United States, in which such a study would be a conflict of interest with the industry), especially in Norway and Australia.


It is also interesting that studies of motor-neuron diseases in Guam, where a tremendous increase in amyotrophic lateral sclerosis (ALS) has occurred, found parallels between ALS and high concentrations of aluminum in drinking water. Swedish studies of the Guam ALS problem concluded that mortality from motor-neuron disease, especially among women, varies with the local water concentration of aluminum. Ten percent of native Guamanians die of brain disease. Fifteen percent of Mariana Island natives die of neurodegenerative disease. Why? Part of the answer is that there are high levels of aluminum in the drinking water. There are also high levels of aluminum in the food.


Research conducted in 1988 by the Medical Research Council revealed that long-term exposure to aluminum contributed to plaque deposits in the cerebral cortex and aluminum deposition in neurons. Patients with loss of memory frequently have high blood aluminum levels above 20 ppb. When magnesium, zinc and vitamin C are administered, the high blood aluminum level decreases to normal (less than 10 ppb) and memory improves. 


Many human studies have examined the occurrence of cancer among aluminum industry workers and found a higher-than-expected cancer mortality rate, but this may also be due to other potent carcinogens to which they are exposed, such as polycyclic aromatic hydrocarbons (PAHs) and tobacco smoke. Available cancer studies in animals have not found biologically relevant increases in malignant tumors. The International Agency for Research on Cancer (IARC) concluded that aluminum production was carcinogenic to humans and that pitch volatiles have consistently been suggested in epidemiological studies as being possible causative agents. The Department of Health and Human Services and the EPA have not evaluated the human carcinogenic potential of aluminum.


Certain vaccines contain aluminum salts as adjuvants. Despite almost 90 years of widespread use of aluminum adjuvants, medical science's understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds.


Some people develop macrophagic myofasciitis (MMF) after receiving an aluminum-containing vaccine. MMF is characterized by an aluminum-filled lesion (wound) at the site of an earlier vaccination. MMF lesions occur when the aluminum adjuvant from a vaccine remains embedded in the muscle tissue and causes a continuous immune reaction. The lesions are persistent, long-term granulomas (or inflammatory tumors) found in the quadriceps in children and deltoid muscles of adults, common vaccination sites. Several vaccines contain aluminum hydroxide, which has been identified as the causal factor of MMF lesions.

aluminum in childhood vaccines

Nutrients Known to be Protective Against Aluminum

Silica, phosphorus, magnesium, zinc, iron, calcium, glycine, and vitamin C are antagonistic for aluminum uptake and retention. The chemical affinity of silica for aluminum has been shown to reduce the bioavailability of aluminum in studies of human gastrointestinal absorption. Mg, Na2EDTA has been clinically shown to be an effective IV chelating agent for aluminum.

As with all detoxification protocols, the type, dose and duration of detoxification agents should always be individually assessed and administered by a licensed medical practitioner. 

Protocols for Aluminum Detoxification

The following may serve as a basic guideline for detoxification of excess aluminum from chronic exposure. After 60 days, laboratory and electrodermal screening should be used to reassess the protocol. Before initiating a detoxification program, a CBC with chemistry, including a thyroid panel with lipids should be performed. In addition, whole blood elements to assess the mineral status and a urine creatinine clearance should be performed every 60 days when using synthetic detoxifying agents (EDTA). Administration of synthetic agents may cause a depletion of essential elements such as zinc, iron, calcium, magnesium, copper and other trace minerals. Of greatest concern is potential kidney toxicity that can occur when the body releases its aluminum stores for excretion through the kidneys. Those with underlying kidney disease may not be able to undergo aggressive aluminum detoxification therapy. 


To evaluate aluminum toxicity a 24-hour urine analysis is the most definitive test. An oral dose of glycine, 80-mg/Kg body weight, given in divided doses over a 24-hour urine collection period provides a non-invasive, diagnostic procedure for flushing out aluminum. Glycine is an excellent complexing agent for aluminum. However, glycine by itself is not recommended as a daily or periodic detoxification remedy. Because it has been shown to move aluminum about, it may increase aluminum uptake and transport into other tissues.


  1. First, remove any known sources of aluminum.

  2. Assess whole blood cell element analysis to determine mineral nutrient deficiency and supplement appropriately.

  3. Supplement with a silica source. Silica is found in all tissues and organs of the body including the skin, hair, nails, teeth, bones, tendons and ligaments. It restores the necessary balance between calcium and magnesium - so not only does it help eliminate excess aluminum, but is nutritional as well. Silica comes in powder and colloidal forms and may be taken daily. Silica supplements can product toxicity in people at doses over 100 mg per day, but horsetail supplements (which are a natural source of silica) have less toxicity at higher doses than other sources of silica. A recommended daily intake of silica has only been established for adults aged 19-50 years with a range of 10-15 mg per day. The best way to eat a diet rich in silica is to include a lot of raw organic radish, alfalfa, cucumber, romaine lettuce, watercress, capsicum, wheatgrass and marjoram. 

  4. Vitamin C may be utilized to help detoxify aluminum excess. Administer gram quantities to bowel tolerance. 

  5. Administer magnesium glycinate 100 to 300 mg daily (watch for diarrhea and if present, reduce dose of magnesium).

  6. Algal cells have a remarkable ability to take up and accumulate heavy metals from their external environment. The primary ones used for toxic metal excess is Chlorella vulgaris, a green microalga, and Laminaria japonica, a brown alga. Chlorella and Laminaria japonica are both chelators, moving toxic metals out of the body, and transporters, moving metals from deeper stores to more readily removal areas. Both work in unison with each other and can remove toxic metals from the body through urinary excretion. Administer 1000 to 2000 mg of Laminaria japonica concentrate (Modifilan) daily and 1000 to 2000 mg of chlorella. Adjust dosage to bowel tolerance; may be taken for long periods of time.

  7. Cilantro works well with alga to chelate, or bind, up toxic metals. The issue with cilantro taken alone is that although it chelates metals, it does not remove them in the urine. This means they can recirculate to deposit elsewhere in the body. Therefore, taken with algas, metals are more effectively eliminated in the urine.

  8. Shilajit is an ancient traditional medicine (Tibetan and Ayurvedic) that has been ascribed a number of pharmacological activities - and has been used for ages as a rejuvenator and for treating a number of disease conditions. It is an effective detoxifier of metals and contains over 60 minerals. Modern scientific research has systematically validated a number of properties of shilajit and has proven that shilajit is truly a panacea. It is important to purchase the highest grade.

  9. Instruct patient to drink adequate amount of pure water (Adult’s urine volume should be about 2 liters per day).


More aggressive treatment for aluminum excess involves the use of magnesium disodium ethylene diamine tetraacetate (Mg, Na2EDTA) chelation. EDTA is an excellent chelator of trivalent ions that are in the bloodstream. The glycine may assist the Al excretion and can transfer it to the EDTA. Check for renal clearance first. The protocol for IV EDTA chelation is available from the American College for Advancement in Medicine (ACAM).  


If you are unfamiliar with EDTA therapy, you may wish to refer the patient to a physician who is board certified by the American Board of Chelation Therapy (ABCT).

In conventional medicine, the treatment of acute aluminum toxicity is often with desferrioxamine, a synthetic chelator of aluminum and iron. Desferrioxamine (DFO) is used primarily as an iron-chelating agent but does have affinity for aluminum as well. DFO has a high and almost specific affinity for the ferric ion. It is poorly absorbed from the GI tract, but when administered by mouth it can chelate iron within the GI tract. DFO used to be thought of as an agent with anti-oxidant potential as it chelates ferric iron in various parts of the body. However, there is evidence suggesting that it may paradoxically and adversely affect red blood cells by inducing intracellular oxidant stress. Also, DFO increases the growth of human Kaposi's sarcoma (KS) xenografts in immunodeficient mice. According to investigators in Belgium, this drug should be avoided in patients with KS. With this chelator, there is also the risk of inadvertently mobilizing large amounts of aluminum into the brain, which may enhance encephalopathy rather than improving it. Hence, due to these potential side effects, DFO is not recommended for aluminum excess due to chronic exposure.


aluminum bibliography

1. Acharya SB, Frotan MH, Goel RK, Tripathi SK, Das PK. 1988. Pharmacological actions of Shilajit. Indian J Exp Biol 26: 775–777.


2. Al Juhaiman, Layla A. Estimating Aluminum leaching from Aluminum cook wares in different meat extracts and milk. Journal of Saudi Chemical Society 14.1 (2010): 131-137. 


3. Alexandrov PN, Kruck TP, Lukiw WJ. Nanomolar aluminum induces expression of the inflammatory systemic biomarker C-reactive protein (CRP) in human brain microvessel endothelial cells (hBMECs). J Inorg Biochem 2015; 152:210-213.

4. Bellia JP, Birchall JD, Roberts NB. The role of silicic acid in the renal excretion of aluminium. Ann Clin Lab Sci. 1996 May-Jun; 26(3):227-33.


5. Bellou, Vanesa, et al. Systematic evaluation of the associations between environmental risk factors and dementia: An umbrella review of systematic reviews and meta-analyses. Alzheimer's & Dementia 13.4 (2017): 406-418.

6. Chopra RN, Chopra IC, Handa KL, Kapoor KD. 1958. In Indigenous Drugs of India. U.N. Dhar & Sons: Calcutta, 457–461.


7. Crapper, D. R., S. S. Krishnan, and A. J. Dalton. Brain aluminum distribution in Alzheimer's disease and experimental neurofibrillary degeneration. Science 180.4085 (1973): 511-513.


8. Crépeaux, Guillemette, et al. Non-linear dose-response of aluminium hydroxide adjuvant particles: Selective low dose neurotoxicity. Toxicology 375 (2017): 48-57.


9. De Filippis LF, Pallaghy CK. 1994. Heavy metals: source and biological effects. In: Rai LC, Gaur JP, Soeder CJ, eds. Algae and water pollution. Stuttgart, Germany: E. Schweizerbart’sche Verlagsbuchhandlung, 31–77.


10. Exley C, Tollervey A, Gray G, Roberts, Birchall JD (1993) Silicon, aluminium and the biological availability of phosphorus in algae. Proceedings of the Royal Society of London Series B, 253, pp. 93-99.


11. Fukuda, S. H. I. G. E. H. A. R. U., et al. Preventive Effect of Chinese Parsley (Coriandrum sativum, Cilantro) on Aluminum Deposition in ICR Mice. J Ethnopharmacol 77.2-3 (2001): 203-8.


12. Ghosal S. 1990. Chemistry of Shilajit, an immunomodulatory Ayurvedic rasayan. Pure Appl Chem (IUPAC) 62: 1285–1288. 


13. Ghosal S. 2006. Biological effects of shilajit. In Shilajit in perspective, Ghosal S. (ed.). Narosa Publishing House, New Delhi, 132–156.


14. Ghosal S, Bhaumik S, Chattopadhyay S. 1995a. Shilajit induced morphometric and functional changes in mouse peritoneal macrophages. Phytother Res 9: 194–198.


15. Ghosal S, Kawanishi K, Saiki K. 1995e. Shilajit odour Part 3. The chemistry of shilajit odour. Indian J Chem 34B: 40– 44. Ghosal S, Lal J, Jaiswal AK, Bhattacharya SK. 1993a. Effects of Shilajit and its active constituents on learning and memory in rats. Phytother Res 7: 29–34.


16. Gruis KL, Teener JW, Blaivas M. Pediatric macrophagic myofasciitis associated with motor delay. Clin Neuropathol 2006;25(4):172-179. 

17. Jorhem, Lars, and Georg Haegglund. Aluminium in foodstuffs and diets in Sweden. Zeitschrift für Lebensmitteluntersuchung und Forschung A 194.1 (1992): 38-42.


18. Kapaki, Elisabeth N., et al. Cerebrospinal fluid aluminum levels in Alzheimer's disease. Biological psychiatry 33.8 (1993): 679-681.


19. Kawahara M, Kato-Negishi M. Link between aluminum and the pathogenesis of Alzheimer’s disease: the integration of the aluminum and amyloid cascade hypotheses. Int J Alzheimers Dis 2011;2011:276393.


20. Klatzo, Igor, Henryk Wiśniewski, and Eugene Streicher. Experimental production of neurofibrillary degeneration: I. Light microscopic observations. Journal of Neuropathology & Experimental Neurology 24.2 (1965): 187-199.

21. Krewski, Daniel, et al. Human health risk assessment for aluminium, aluminium oxide, and aluminium hydroxide. Journal of Toxicology and Environmental Health, Part B 10.S1 (2007): 1-269. 


22. Lacson AG, D’Cruz CA, Gilbert-Barness E, et al. Aluminum phagocytosis in quadriceps muscle following vaccination in children: relationship to macrophagic myofasciitis. Pediatr Dev Pathol 2002;5(2):151-158. 


23. Lancet, Jan. 14, 1989, pp.59-62, Geographical relation between Alzheimer’s disease and aluminum in drinking water. 


24. Nevo Y, Kutai M, Jossiphov J, et al. Childhood macrophagic myofasciitis - consanguinity and clinicopathological features. Neuromuscul Disord 2004;14(4):246-252. 


25. Pourgheysari H, Hajizadeh Y, Tarrahi MJ, Ebrahimi A. Association between Aluminum and Silicon Concentrations in Isfahan Drinking Water and Their Health Risk Assessments. Int J Prev Med. 2015; 6:111. Epub 2015 Nov 12.


26. Reinke, Claudia M., Jörg Breitkreutz, and Hans Leuenberger. Aluminium in over-the-counter drugs. Drug Safety 26.14 (2003): 1011-1025.


27. Rivas E, Gómez-Arnáiz M, Ricoy JR, et al. Macrophagic myofasciitis in childhood: a controversial entity. Pediatr Neurol 2005;33(5):350-356. 


28. Sharma MC, Prentice A, Schmidt PF, Sharma N, Goebel HH. Macrophagic myofasciitis in a 3-month-old child. Journal of Pediatr Neurol 2004;2(4):225-229.


29. Shaw CA, Li D, Tomljenovic L. Are there negative CNS impacts of aluminum adjuvants used in vaccines and immunotherapy? Immunotherapy 2014;6(10):1055-1071. 


30. Shaw, C. A., and L. Tomljenovic. Aluminum in the central nervous system (CNS): toxicity in humans and animals, vaccine adjuvants, and autoimmunity. Immunologic research. 56.2-3 (2013): 304-316.


31. Shaw CA, Li Y, Tomljenovic L. Administration of aluminum to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes. J Inorg Biochem 2013;128:237-244.


32. Vignal, C., P. Desreumaux, and M. Body-Malapel. "Gut: An underestimated target organ for Aluminum." Morphologie 100.329 (2016): 75-84. 

33. Vogt, T., Water quality and health - a study of possible relationship between aluminum in drinking water and dementia. Central Bureau of Statistics of Norway, 1986; Jorm A., et al., Differences in mortality from dementia in Australia: an analysis of death certificate data.


34. Wang, L., D. Z. Su, and Y. F. Wang. Studies on the aluminium content in Chinese foods and the maximum permitted levels of aluminum in wheat flour products. Biomedical and environmental sciences: BES 7.1 (1994): 91-99.

35. Wang, Zengjin, et al. Chronic exposure to aluminum and risk of Alzheimer’s disease: A meta-analysis. Neuroscience letters 610 (2016): 200-206. 


36. Willhite, Calvin C., et al. Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts. Critical reviews in toxicology 44.sup4 (2014): 1-80. 


37. Yokel, Robert A. Aluminum in food–the nature and contribution of food additives. (2012): 203. 

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