The Link Between Aluminum and Mental Disorders
Reassessing Aluminum as a Modifiable Risk Factor for Mental Illnesses.
If we are going to reverse the mental illness epidemic in America, we need research on mild, long-term aluminum chelation protocols funding by NIH: deferoxamine (aka desferoxamine), intranasal insulin, silicic acid, cilantro, and glutathione enhancers. And we need to stop inject aluminum into ourselves. Join me in calling on Dr. Jay Bhattacharya to have his Program Officers write calls for proposals for this urgent area of clinical research to reverse iatrogenic disease caused by injected aluminum.
Aluminum (Al) is a highly abundant metal with no known physiological role in the human body. Despite its frequent use in industrial, pharmaceutical, and consumer products, aluminum is a known neurotoxin. Chronic exposure has been implicated in the pathogenesis of multiple neuropsychiatric and neurodegenerative disorders. While aluminum toxicity was once dismissed as irrelevant due to assumed poor absorption and rapid clearance, a growing body of research shows that aluminum bioaccumulates in vulnerable tissues (Tomljenovic et al., 2013) , particularly the brain, and may be a major avoidable risk factor in the development of Alzheimer’s disease (AD; Armstrong et al., 2019), autism spectrum disorder (ASD; Boretti, 2021; Roe, 2022), dialysis encephalopathy (Alfrey et al., 1978; Mach et al. 1988), and other cognitive and behavioral disorders such as acute aluminum intoxication, which requires chelation therapy.
Aluminum exerts its neurotoxicity through several well-documented mechanisms:
Oxidative Stress: Aluminum promotes the generation of reactive oxygen species (ROS), lipid peroxidation, and oxidative DNA damage, leading to mitochondrial dysfunction and neuronal death.
Mitochondrial Disruption: Aluminum impairs mitochondrial energy metabolism and promotes apoptotic pathways, contributing to neurodegeneration.
Metal Mimicry and Ion Disruption: By mimicking essential ions such as Ca²⁺ and Fe³⁺, aluminum disrupts neuronal signaling, membrane potentials, and ferritin iron storage systems.
Epigenetic Modulation: Aluminum alters DNA methylation patterns, histone acetylation, and the expression of microRNAs (e.g., miR-29a/b, miR-124; Aschne et al., 2024), contributing to dysregulated amyloid precursor protein (APP) and tau pathology in Alzheimer’s disease (Kandimalla et al., 2016;Huat et al., 2019).
Autophagy Dysfunction: Aluminum impairs neuronal autophagy, compromising the clearance of misfolded proteins such as β-amyloid and hyperphosphorylated tau (Sanajou et al., 2023; Makhdoomi et al., 2023).
Importantly, aluminum tolerance is not uniform across individuals. It depends on the rate of aluminum absorption, distribution, metabolism, and excretion (ADME)—all of which are genetically modulated. The CNS is affected to some degree by everyone (Bryliński et al. 2023). But polymorphisms in genes governing renal function, blood-brain barrier integrity, and metal transport proteins (e.g., transferrin, DMT1), and detoxification efficiency influence an individual’s chronic aluminum burden. Those with impaired clearance capacity due to their genetic milieu will experience neurotoxic effects from exposures deemed “safe” in the general population.
Aluminum and Alzheimer’s Disease
Tissue Accumulation: Aluminum preferentially accumulates in brain regions vulnerable in AD, including hippocampal and cortical areas (McLachlan et al, 1986). It is found in neurofibrillary tangles, senile plaques, and even within neuronal nuclei.
Causality: Walton (2013 & 2014) applied Bradford Hill's causality criteria, concluding that aluminum fulfills the requirements for a causal role in sporadic AD. Chronic low-level ingestion leads to cumulative deposition in brain regions central to cognition and memory, mimicking the disease’s anatomical progression.
Modifiers of Risk: Iron metabolism, aging, and inflammation enhance aluminum uptake and neurotoxicity. Aluminum may dysregulate iron homeostasis, leading to synergistic oxidative damage (Walton, 2014). Osteoporosis release stored aluminum in the bone (Roos, 2014), thus reassurances that it just compartmentalizes to the bone are of no help.
Chelation Evidence: Trials using desferrioxamine, which breaks of aluminum from amyloid, have demonstrated slowed cognitive decline in AD patients.
Dialysis Encephalopathy
Clinical Entity: Dialysis encephalopathy, or "dialysis dementia," is a well-characterized syndrome resulting from chronic aluminum accumulation in patients receiving dialysis with aluminum-contaminated water or aluminum-based phosphate binders.
Symptoms and Reversibility: Hallmarks include aphasia, myoclonus, seizures, and progressive cognitive decline. Removal of aluminum from dialysate solutions has virtually eradicated the condition, offering one of the clearest examples of aluminum-induced neurotoxicity in humans.
Other Neuropsychiatric and Neurodegenerative Conditions
Major Depressive Disorder (MDD): Elevated serum aluminum has been associated with MDD and other mood disorders, potentially via neuroinflammation and hippocampal dysfunction (Baj et al., 2023).
Parkinson’s Disease, ALS, MS: High aluminum levels have been reported in patients with Parkinson’s disease (Doroszkiewicz et al., 2023), amyotrophic lateral sclerosis, and multiple sclerosis, although causal attribution remains under investigation.
Macrophagic Myofasciitis (MMF): Associated with aluminum hydroxide-containing vaccines, MMF involves persistent myalgias and cognitive deficits tied to immune activation and retention of aluminum at the injection site.
Controversies and Confounding Arguments
Some aluminum apologists have argued that the small proportion of orally ingested aluminum absorbed (<1%) makes systemic toxicity unlikely. Others suggest that observed aluminum in diseased brains reflects a consequence, not a cause, of neurodegeneration.
However:
Aluminum bioaccumulates over decades and can exceed clearance capacity, especially in genetically susceptible individuals.
Many environmental exposures (e.g., fluoride, citrates) enhance aluminum absorption.
Studies demonstrating reduced cognitive decline via chelation therapy and decreased incidence of dialysis dementia after removing aluminum exposures provide strong experimental support.
Aluminum Causes Autoimmunity. Neurodegenerative Disease Have a Huge Unaddressed Autoimmune Component
In preparing my lecture on neurodegenerative diseases for my one-of-a-kind course Autoimmunity and Human Health at IPAK-EDU, I was struck by how important autoimmunity is in neurodegenerative disease. You can access that lecture and the full course:
Conclusion
Aluminum is a potent neurotoxin that acts through well-defined biological mechanisms. Its association with Alzheimer’s disease, autism spectrum disorder, and dialysis-related encephalopathy is supported by human and animal studies, tissue analyses, and mechanistic data. Importantly, individual aluminum tolerance varies by genetic capacity to absorb, retain, and excrete aluminum, making some populations more vulnerable at lower doses. A reassessment of aluminum’s role in mental disorders is urgently needed, with public health policies aimed at minimizing chronic exposure and identifying at-risk subgroups.
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Yes ! Chris Exley’s research with silicic acid? Lost funding because it threatened the orthodoxy of amyloid plaque & therefore big pharma useless drugs & profit
Why no mention of Dr Chris Exley?