top of page

James Lyons-Weiler: How aluminium leads to brain injury



Aluminium is the most abundant metallic element in Earth’s crust. Because of its chemical activity, aluminium never occurs in the metallic form in nature, but its compounds are present to a greater or lesser extent in almost all rocks, vegetation, and animals.


It is commonly used as an adjuvant in vaccines. Aluminium that has been injected is linked to the onset of autoimmune diseases. It has also been linked to proteins found in the brains of people with Alzheimer’s disease. Below James Lyons-Weiler explains how aluminium is neurotoxic; it induces neurons to commit suicide.


“The evidence is clear. Here is a small sample of the damning literature. We must now help the public avoid this threat to public health,” he says.




Aluminium is a ubiquitous element found in the Earth’s crust, where it was bound to silica for nearly all of the 3.8 billion years of organic evolution on this planet.


Since the late 1800s, it has found its way into various aspects of human life, from cookware to vaccines. While it is generally considered safe for most applications, it is not: emerging evidence shows that it has neurotoxic effects, particularly in the context of neurodegenerative diseases like Alzheimer’s. Here we explore the mechanisms through which aluminium exposure leads to brain injury.


Mechanisms of Aluminium Neurotoxicity


Oxidative Stress


Aluminium has been identified as a neurotoxic agent that results in oxidative damage to cellular biomarkers. Oxidative stress is a well-known factor in the pathogenesis of neurodegenerative diseases, and aluminium’s role in exacerbating this cannot be ignored.


“Aluminium is an environmentally abundant potential neurotoxic agent that may result in oxidative damage to a range of cellular biomarkers.” (REVIEW)


Neuronal Apoptosis


[Neuronal apoptosis is an intrinsic suicide program by which a neuron orchestrates its own destruction.]


Aluminium has been shown to induce neuronal apoptosis both in vivo and in vitro. Apoptosis, or programmed cell death, is a critical mechanism in the development of neurodegenerative diseases.


“Aluminium induces neuronal apoptosis in vivo as well as in vitro, either by endoplasmic stress from the unfolded protein response, by mitochondrial dysfunction, or a combination of them.” (REVIEW with 167 citations therein)


Tau Protein and Amyloid-beta Accumulation


Aluminium exposure has been linked to the accumulation of tau protein and Amyloid-beta (Aβ) in the brain, both of which are hallmark features of Alzheimer’s disease.



Evidence


Historical Context


The earliest evidence of aluminium’s potential involvement in Alzheimer’s disease dates back to the 1960s, from independent laboratories in the United States and Canada.


“The first successful attempt to obtain purified aluminium metal was accomplished by the Danish physicist and chemist Hans Christian Orsted in 1824, however, it was not until about ~140 years later that aluminium’s capacity for neurological disruption and neurotoxicity was convincingly established.” (LINK)


Animal Models


An aluminium-based rat model for Alzheimer’s disease exhibited oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration, providing compelling evidence for Aluminium’s neurotoxic effects.


“An aluminium-based rat model for Alzheimer’s disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration.” (STUDY)


Aluminium injections in mice cause motor deficits and motor neuron degeneration (STUDY).


Sheep injected with aluminium adjuvants develop autoimmune diseases (STUDY).


Hormesis


The argument often made in favour of aluminium safety is that the doses used in medical interventions are low. Non-linear dose/response curves reflect hormesis, in which, paradoxically, low doses can have an increased risk of toxicity. With aluminium adjuvants, low-dose exposures over time can still lead to accumulation and associated risks. Moreover, the “low-dose” argument does not consider the potential for repeated exposures through multiple vaccinations or other medical treatments. The concept of hormesis, where low-dose exposures could have non-linear toxic effects, is evidenced by the study by G. Crépeaux et al. on selective low-dose neurotoxicity[LINK].


Synergistic Toxicity


The concept of synergistic toxicity is crucial here. Aluminium may not act alone but can interact with other toxins or medications a person might be exposed to. For example, aluminium’s impact could be more severe in someone who is also exposed to high levels of lead or mercury.


Other Health Effects


Aluminium hydroxide has been linked to the onset of autoimmune diseases. It can trigger an overactive immune response, leading to the body attacking its tissues, as seen in conditions like lupus and rheumatoid arthritis. The concept of pathogenic priming suggests that exposure to aluminium hydroxide could make the immune system more susceptible to future exposures, via repeated vaccinations, natural infection, or both, leading to autoimmune diseases.


Ethical and Public Health Implications


Given these risks, the ethical dimension cannot be ignored. Is it justifiable to expose populations to a substance with such a risk profile without thorough, long-term safety studies? The precautionary principle should apply here, advocating for the least harmful path until more is known.


Conclusion


It is now well understood that pharmaceutical companies employ aluminium hydroxide – the same form of aluminium found in some vaccines – to induce autoimmunity in animals so they can test the efficacy of their products to reduce the symptoms caused by aluminium hydroxide.

The neurotoxic effects of aluminium are well-known. From inducing oxidative stress to promoting neuronal apoptosis and the accumulation of harmful proteins, Aluminium’s role in neurodegenerative diseases is now abundantly clear.


The use of aluminium hydroxide as an adjuvant raises several red flags for public health concerns that can no longer be ignored. From bioaccumulation and neurotoxicity to its role in autoimmune diseases, the evidence suggests a need for a re-evaluation of its widespread use in medical interventions.


Further research is needed to fully understand the extent of the effects of avoiding aluminium in all forms on all aspects of brain and general health.


References


Dey M, Singh RK. Chronic oral exposure of Aluminium chloride in rat modulates molecular and functional neurotoxic markers relevant to Alzheimer’s disease. Toxicol Mech Methods. 2022 Oct;32(8):616-627. doi: 10.1080/15376516.2022.2058898. Epub 2022 Apr 7. PMID: 35341471.

G. Crépeaux, et al. Non-linear dose-response of aluminium hydroxide adjuvant particles: selective low dose neurotoxicity. Toxicology, 2017.

Kandimalla R, Vallamkondu J, Corgiat EB, Gill KD. Understanding Aspects of Aluminium Exposure in Alzheimer’s Disease Development. Brain Pathol. 2016 Mar;26(2):139-54. doi: 10.1111/bpa.12333. Epub 2015 Dec 8. PMID: 26494454; PMCID: PMC8028870. https://pubmed.ncbi.nlm.nih.gov/26494454/

Luján L, Pérez M, Salazar E, Álvarez N, Gimeno M, Pinczowski P, Irusta S, Santamaría J, Insausti N, Cortés Y, Figueras L, Cuartielles I, Vila M, Fantova E, Chapullé JL. Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA syndrome) in commercial sheep. Immunol Res. 2013 Jul;56(2-3):317-24. doi: 10.1007/s12026-013-8404-0. PMID: 23579772. https://pubmed.ncbi.nlm.nih.gov/23579772/

Shaw, C.A., Petrik, M.S. Aluminium hydroxide injections lead to motor deficits and motor neuron degeneration. Journal of Inorganic Biochemistry, 2009.


About the Author


James Lyons-Weiler is a research scientist and author of the books ‘Cures vs. Profits’, ‘Environmental and Genetic Causes of Autism’, and ‘Ebola: An Evolving Story’. He shares his research and interpretation on the IPAK Knowledge website and through courses offered by IPAK Edu. He also publishes articles on his Substack page ‘Popular Rationalism’ HERE.


Commenti


bottom of page