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A Very Old Friend - Aluminum - Its 'Benefits' Appear to Be On The Who's Who List of LH/CFS/Post Wax

Updated: Apr 29

This article is not medical advice. Please seek the advice of your Primary Care Physician or an M.D before beginning any health related regimen.

A few of the benefits associated with high aluminum intake:

  1. Metabolic impairment: impairs glycolysis and Kreb’s cycle;

    1. Inhibits the formation of Alpha Ketoglutarate:

      1. "Al inhibits the reverse reaction, i.e. GDH-catalyzed conversion of glutamate to a-ketoglutarate"[10]

      2. Inhibition of Aconitase, "the concomitant inhibition of aconitase by Al could further contribute to the decreased production of a-ketoglutarate"[10]

  2. Inhibits cartilage formation

  3. Inhibits FECH, the last gene in the production of heme, by 63% [2]

  4. Promotes lipid and protein oxidation

  5. Disrupts cell membrane permeability and receptor function, increases osmotic fragility, Inhibits bone formation and mineralization by increasing osteoclastic activity and reducing osteoblastic activity inhibits membrane ATPases, leading to high intracellular calcium

    1. Excess intracellular calcium induces NOX5[8]

  6. Promotes free unbound iron linked to Fenton Reaction and oxidative stress by inhibiting formation of heme bound iron.

    1. Unbound iron gets inserted into SOD2 instead of Manganese, disrupting SOD2 and creating excess super oxide.

  7. Disrupts mineral metabolism of Fe, P, Ca, Zn, Cu by altering intestinal absorption and cellular uptake

  8. Induces NADPH Oxidase(s) [7], and thus the production of Free radicals hydrogen peroxide, super oxide, and induction of NOS2 leading to mast cell degranulation, and histamine issues.

  9. Endocrine disruption: parathyroid hormone, testosterone, luteinizing hormone, follicle stimulating hormone, estradiol, norepinephrine, cortisol, thyroid hormone, insulin

  10. Oxidative stress, lipid peroxidation

  11. Pro-inflammatory: organ inflammation in lung, intestine, heart, and testis

  12. Immunosupression: induces lymphocyte apoptosis and dysfunction, inhibits lymphocyte proliferation, causes macrophage dysfunction

  13. Protein denaturation and transformation

  14. Enzymatic stimulation or inhibition

  15. Genotoxicity: reduced cell proliferation and differentiation, dysneurogenesis

  16. Amyloidogenic and anti-amyloidolytic

  17. Acts as metalloestrogen, promotes proliferation and migration of breast cancer cells

  18. Induces teratogenesis causing fetal and neonatal defects

  19. Induces apoptosis, eryptosis, tissue necrosis

  20. Induces hypertension (systolic and arterial)

  21. Causes ischaemic stroke and thrombosis

  22. Induces contact allergy

  23. Inhibits the biological function of vitamin D in the intestine linked to calcium absorption

  24. aluminum inhibits vitamin D-dependent calcium absorption [11]

  25. aluminum may inhibit the expression of vitamin D-dependent genes [11]

  26. "We argue that acquired vitamin D resistance provides a plausible pathomechanism for the development of autoimmune diseases, which could be treated using high-dose vitamin D3 therapy"[12]

Inhibitors of dietary absorption: phytates, polyphenols, phosphate (beans, cheese, oats), silicon, sialic Acid

Promoters of dietary absorption: Chronic Kidney Disease, Magnesium and Calcium Ion Deficiency, Citrate, Maltol, Lactate, Flouride

Chelators: Deferoxamine, Malic Acid, Citric Acid, Malonic Acid, Oxalic Acid, Succinic Acid

"In previous studies, aluminium was found to retard bacterial growth and enhance porphyrin formation in Arthrobacter aurescens RS-2. The aim of this study was to establish the mechanism of action of aluminium which leads to increased porphyrin production. Cultures of Arthrobacter aurescens RS-2 were incubated in the absence and presence of 0.74 mM aluminium. After 6 and 24 h of incubation, various parameters of the haem biosynthetic pathway were determined. After 6 h of incubation with aluminium, the activities of the enzymes aminolevulinate synthase (ALAS), aminolevulinate dehydratase (ALAD), porphobilinogen deaminase (PBGD) and uroporphyrinogen decarboxylase (UROD) were increased by 120, 170, 190 and 203%, respectively, while that of ferrochelatase (FC) was found to be unchanged. However, after 24 h of incubation, no change in the activities of ALAS and ALAD was noted, while an about 2-fold increase in PBGD and UROD activities were observed. FC activity was decreased by 63%. It was concluded that aluminum exerts its effect by inducing the enzymes PBGD and UROD rather than by a direct or indirect effect on ALAS. Its effect on the final step in the haem biosynthetic pathway is discussed."[2]

"Malic and succinic acids were the most effective. Malic acid and DFOA were the most effective in increasing the urinary excretion of aluminum. Citric acid was the most effective in increasing the fecal excretion of aluminum. Malonic, oxalic and succinic acids had no overall beneficial effects. Citric acid would appear to be the most effective agent of those tested in the prevention of acute aluminum intoxication."[3]

Spirulina and Okra

"Aluminum (Al) is a versatile element commonly employed in various industries and water treatment processes. However, its presence in aquatic ecosystems can elicit adverse effects on organisms, particularly the Danio rerio fish species. Aluminum exposure has been associated with a spectrum of issues, ranging from oxidative stress to behavioral anomalies, reproductive disruptions, and morphological alterations in these organisms. This research aimed to assess the impact of aluminum chloride (AlCl3) on D. rerio embryos and explore strategies to mitigate its effects. Three dietary groups (commercial, okra-spirulina, and spirulina) were studied, focusing on embryonic development, oxidative damage, and gene expression changes. The study revealed that diets enriched with spirulina and okra-spirulina effectively reduced aluminum-induced embryotoxicity, oxidative stress, and gene expression alterations, surpassing the commercial diet. However, all AlCl3-exposed groups experienced adverse effects on embryonic development, including hatching anomalies, structural deformities, and cardiac delays. The okra-spirulina group showed milder toxic responses. In conclusion, this study highlights the potential of spirulina and okra-spirulina diets in mitigating aluminum-triggered oxidative stress and apoptosis in D. rerio. It underscores the need for future research on embryonic development and carries significant implications for environmental conservation and the well-being of aquatic organisms in aluminum-contaminated environments."[4]


"The sterile stems belonging to the Equisetum species are often used in traditional medicine of various nations, including Romanians. They are highly efficient in treating urinary tract infections, cardiovascular diseases, respiratory tract infections, and medical skin conditions due to their content of polyphenolic derivatives that have been isolated. In this regard, this study aimed to provide the chemical composition of the extracts obtained from the Equisetum species (E. pratense, E. sylvaticum, E. telmateia) and to investigate the biological action in vitro and in vivo. For the chemical characterization of the analyzed Equisetum species extracts, studies were performed by using ultra-high-performance liquid chromatography (UHPLC-DAD). In vitro evaluation of the antioxidant activity of the plant extracts obtained from these species of Equisetum genus was determined. The neuroprotective activity of these three ethanolic extracts from the Equisetum species using zebrafish tests was determined in vivo. All obtained results were statistically significant. The results indicate that E. sylvaticum extract has a significant antioxidant activity; whereas, E. pratense extract had anxiolytic and antidepressant effects significantly higher than the other two extracts used. All these determinations indicate promising results for the antioxidant in vitro tests and neuroprotective activity of in vivo tests, particularly mediated by their active principles."[5]

"Aluminum serum concentration is almost equal to whole blood aluminum levels in a normal situation. Almost 90% of plasma aluminum is bound to transferrin, between 7 to 8% with citrate, and less than 1% binds to phosphate and hydroxide. Approximately 60% of the body aluminum is stored in the bones, 25% in the lung, 10% in the muscle, 3% in the liver, and 1% in the brain [19, 22]. Inside the cells, aluminum is stored in the lysosomes of brain neurons, liver (except the Kupffer cells), spleen, myocytes of the heart, mesenchymal glomerular cells, epithelial cells of the kidneys, and mitochondria of osteoblasts"[13]

"Although aluminum (Al), a known environmental toxin, has been implicated in a variety of neurological disorders, the molecular mechanism responsible for these conditions is not fully understood. In this report, we demonstrate the ability of Al to trigger mitochondrial dysfunction and ineffective adenosine triphosphate (ATP) production. This situation severely affected cytoskeletal dynamics. Whereas the control cells had well-defined structures, the Al-exposed astrocytoma cells appeared as globular structures. Creatine kinase (CK) and profilin-2, two critical modulators of cellular morphology, were markedly diminished in the astrocytoma cells treated with Al. Antioxidants such as alpha-ketoglutarate and N-acetylcysteine mitigated the occurrence of the globular-shaped cells promoted by Al toxicity. Taken together, these data reveal an intricate link between ATP metabolism and astrocytic dysfunction and provide molecular insights into the pathogenesis of Al-induced neurological diseases."[14]

"Effect of aluminum on the NADPH supply and glutathione regeneration in mitochondria was analyzed. Reduced glutathione acted as a principal scavenger of reactive oxygen species in mitochondria. Aluminum inhibited the regeneration of glutathione from the oxidized form, and the effect was due to the inhibition of NADP-isocitrate dehydrogenase the only enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the glutathione regeneration dependent on NADPH supply by malic enzyme and NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate dehydrogenase dependent glutathione formation. Aluminum can cause oxidative damage on cellular biological processes by inhibiting glutathione regeneration through the inhibition of NADPH supply in mitochondria, but only a little inhibitory effect on the glutathione generation in cytosol."[15]

"Aluminum inhibited both the cytosolic and mitochondrial hexokinase activities in rat brain. The IC50 values were between 4 and 9 microM. Aluminum was effective at mildly acidic (pH 6.8) or slightly alkaline (pH 7.2-7.5) pH, in the presence of a physiological level of magnesium (0.5 mM). However, saturating (8 mM) magnesium antagonized the effect of aluminum on both forms of hexokinase activity. Other enzymes examined were considerably less sensitive to inhibition by aluminum. The IC50 of aluminum for phosphofructokinase was 1.8 mM and for lactate dehydrogenase 0.4 mM. At 10-600 microM, aluminum actually stimulated pyruvate kinase. Aluminum also inhibited lactate production by rat brain extracts: this effect was much more marked with glucose as substrate than with glucose-6-phosphate. However, the IC50 for inhibiting lactate production using glucose as substrate was 280 microM, higher than that required to inhibit hexokinase. This concentration of aluminum is comparable to those reportedly found in the brains of patients who had died with dialysis dementia and in the brains of some of the patients who had died with Alzheimer disease. Inhibition of carbohydrate utilization may be one of the mechanisms by which aluminum can act as a neurotoxin."[16]

"Here, we investigate the impact of Mn on physiology, and its association with gut dysbiosis as well as neuropathologies such as autism, Alzheimer's disease (AD), depression, anxiety syndrome, Parkinson's disease (PD), and prion diseases. Glutamate overexpression in the brain in association with autism, AD, and other neurological diseases can be explained by Mn deficiency. Mn superoxide dismutase protects mitochondria from oxidative damage, and mitochondrial dysfunction is a key feature of autism and Alzheimer’s. Chondroitin sulfate synthesis depends on Mn, and its deficiency leads to osteoporosis and osteomalacia. Lactobacillus, depleted in autism, depend critically on Mn for antioxidant protection. Lactobacillus probiotics can treat anxiety, which is a comorbidity of autism and chronic fatigue syndrome. Reduced gut Lactobacillus leads to overgrowth of the pathogen, Salmonella, which is resistant to glyphosate toxicity, and Mn plays a role here as well. Sperm motility depends on Mn, and this may partially explain increased rates of infertility and birth defects. We further reason that, under conditions of adequate Mn in the diet, glyphosate, through its disruption of bile acid homeostasis, ironically promotes toxic accumulation of Mn in the brainstem, leading to conditions such as PD and prion diseases."[17]

"Celiac disease, and, more generally, gluten intolerance, is a growing problem worldwide, but especially in North America and Europe, where an estimated 5% of the population now suffers from it. Symptoms include nausea, diarrhea, skin rashes, macrocytic anemia and depression. It is a multifactorial disease associated with numerous nutritional deficiencies as well as reproductive issues and increased risk to thyroid disease, kidney failure and cancer. Here, we propose that glyphosate, the active ingredient in the herbicide, Roundup(®), is the most important causal factor in this epidemic. Fish exposed to glyphosate develop digestive problems that are reminiscent of celiac disease. Celiac disease is associated with imbalances in gut bacteria that can be fully explained by the known effects of glyphosate on gut bacteria. Characteristics of celiac disease point to impairment in many cytochrome P450 enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut. Glyphosate is known to inhibit cytochrome P450 enzymes. Deficiencies in iron, cobalt, molybdenum, copper and other rare metals associated with celiac disease can be attributed to glyphosate's strong ability to chelate these elements. Deficiencies in tryptophan, tyrosine, methionine and selenomethionine associated with celiac disease match glyphosate's known depletion of these amino acids. Celiac disease patients have an increased risk to non-Hodgkin's lymphoma, which has also been implicated in glyphosate exposure. Reproductive issues associated with celiac disease, such as infertility, miscarriages, and birth defects, can also be explained by glyphosate. Glyphosate residues in wheat and other crops are likely increasing recently due to the growing practice of crop desiccation just prior to the harvest. We argue that the practice of "ripening" sugar cane with glyphosate may explain the recent surge in kidney failure among agricultural workers in Central America. We conclude with a plea to governments to reconsider policies regarding the safety of glyphosate residues in foods."[18]


  1. Mechanism of aluminum-induced porphyrin synthesis in bacteria. By Mamet, et. al. Published: BioMetals. January 1996. pages 73–77.

  2. Comparative effects of several chelating agents on the toxicity, distribution and excretion of aluminium. By J L DomingoHum Toxicology. . 1988 May;7(3):259-62. doi: 10.1177/096032718800700305. PMID: 3391623. DOI: 10.1177/096032718800700305

  3. Dietary solutions for aluminum embryotoxicity: A study in Danio rerio using spirulina and okra-spirulina diets. Erika Mariana García-Avalos, et. al. Sci Total Environ. . 2024 Feb 1:910:168510. doi: 10.1016/j.scitotenv.2023.168510. Epub 2023 Nov 15. PMID: 37977388. DOI: 10.1016/j.scitotenv.2023.168510

  4. Neuroprotective and Antioxidant Enhancing Properties of Selective Equisetum Extracts Denisa Batir-Marin, et. al. . Molecules. 2021 May; 26(9): 2565. Published online 2021 Apr 28. doi: 10.3390/molecules26092565 PMCID: PMC8124630. PMID: 33924900

  5. Low levels of aluminum can lead to behavioral and morphological changes associated with Alzheimer’s disease and age-related neurodegeneration. By Stephen C. Bondy. NeuroToxicology 52 (2016) 222–229.

  6. Aluminum induces oxidative burst, cell wall NADH peroxidase activity, and DNA damage in root cells of Allium cepa L. By V Mohan M Achary, et. al. Environ Mol Mutagen. . 2012 Aug;53(7):550-60. doi: 10.1002/em.21719. Epub 2012 Aug 2. PMID: 22865669 DOI: 10.1002/em.21719

  7. Mechanisms of Signal TransductionMechanism of Ca2+ Activation of the NADPH Oxidase 5 (NOX5). By Botond Bánfi, et. al. Volume 279, Issue 18, 30 April 2004, Pages 18583-18591

  8. Effects of aluminum on activity of Krebs cycle enzymes and glutamate dehydrogenase in rat brain homogenate. By P. Zatta. Eur. J. Biochem. 267, 3049±3055 (2000) q FEBS 2000. P. Zatta, CNR Center on Metalloproteins, Department of Biology, University of Padova, Viale G. Colombo 3, 35131, Padova, Italy. Fax: 1 39 49 827 6330; Tel.: 1 39 49 827 6331; E-mail:

  9. Aluminum Toxicity Alters the Regulation of Calbindin-D28k Protein and mRNA Expression in Chick Intestine. By Cox, et. al. The Journal of Nutrition. Volume 131, Issue 7, July 2001, Pages 2007-2013.

  10. Vitamin D Resistance as a Possible Cause of Autoimmune Diseases: A Hypothesis Confirmed by a Therapeutic High-Dose Vitamin D Protocol. By Dirk Lemke. Front Immunol. 2021; 12: 655739. Published online 2021 Apr 7. doi: 10.3389/fimmu.2021.655739 PMCID: PMC8058406. PMID: 33897704

  11. Aluminum Poisoning with Emphasis on Its Mechanism and Treatment of Intoxication Mehrdad Rafati Rahimzadeh. Emerg Med Int. 2022; 2022: 1480553. Published online 2022 Jan 11. doi: 10.1155/2022/1480553 PMCID: PMC8767391. PMID: 35070453

  12. Aluminum-induced Defective Mitochondrial Metabolism Perturbs Cytoskeletal Dynamics in Human Astrocytoma Cells. By Lemire, et. al. May 2009. Journal of Neuroscience Research 87(6):1474-83. DOI:10.1002/jnr.21965. Source PubMed

  13. Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria. By Murakami, et. al. December 2004. Journal of Cellular Biochemistry 93(6):1267-71. DOI:10.1002/jcb.20261.

  14. Inhibition of brain glycolysis by aluminum. By J C Lai. J Neurochem. . 1984 Feb;42(2):438-46. doi: 10.1111/j.1471-4159.1984.tb02697.x. PMID: 6229606. DOI: 10.1111/j.1471-4159.1984.tb02697.x

  15. Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies. Anthony Samsel and Stephanie Seneff Surg Neurol Int. 2015; 6: 45. Published online 2015 Mar 24. doi: 10.4103/2152-7806.153876 PMCID: PMC4392553. PMID: 25883837

  16. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. By Anthony Samsel , Stephanie Seneff . Interdiscip Toxicology. 2013 Dec;6(4):159-84. doi: 10.2478/intox-2013-0026. PMID: 24678255. PMCID: PMC3945755. DOI: 10.2478/intox-2013-0026

  17. Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. By Seneff, Samsel. Date issued 2013-04. URI. Department Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory. Journal Entropy

  18. Glyphosate pathways to modern diseases VI: Prions, amyloidoses and autoimmune neurological diseases. By Anthony Samsel, and Stephanie Seneff. Journal of Biological Physics and Chemistry 17 (2017) 8–32 Received 16 November 2016; accepted 15 March 2017.  2017 Collegium Basilea & AMSI doi: 10.4024/25SA16A.jbpc.17.01


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