Dr. Weeks’ Comment: This is instructive reading on how one bad paper can cause everyone to look somewhere else for the cause of Alzheimer’s disease. The evidence actually supports a causative role for aluminum in the brain leading to Alzheimer’s. otherwise stated: “No aluminum, no Alzheimer’s”
The Aluminium (Aluminum) Industry is Becoming Desperate
Feb 07, 2022
Forty years, an academic lifetime, is a long time thinking and writing about aluminium and life. You are ‘noticed’ from the publication of your first paper. You are ignored while industry ambassadors nudge and cajole line managers into acting as friendly deterrents. Your perseverance is tolerated while you build a portfolio of ‘interesting’ research. Out of the blue censorship appears through the actions of your institution. When censorship fails, you are cancelled. Collusion of academia with industry and Government in stopping scientific research was my recent fate ( https://www.aluminiumresearchgroup.com/history). A fate that in truth seems to have largely gone unnoticed by mainstream and alternative media alike.
Why has the aluminium industry chosen this time to use its influence in bringing our research to an end? I contend that it is because it is running scared of recent research published by my group. Specifically, our research on Alzheimer’s disease showing unequivocally that susceptibility to developing Alzheimer’s disease equates to a predisposition to accumulate aluminium in brain tissue. This is the alarming (for industry) conclusion of our recent research on familial Alzheimer’s disease.
Aluminium is a cause of Alzheimer’s disease and while the aluminium industry may not have known this already they certainly suspected this for many years. However, perhaps the straw that broke the camel’s back was not our research on Alzheimer’s disease but our work on aluminium adjuvants used in vaccination. We showed how infiltrating cells at vaccination sites accumulate aluminium adjuvant in their cytoplasm. How these cells laden with aluminium migrate not only to lymph nodes but throughout the body and most critically into brain tissue. We identified a mechanism whereby neurotoxic amounts of aluminium could be rapidly transported and deposited in brain tissue. A mechanism whereby aluminium adjuvants could produce and encephalopathy in a vaccinated infant. The aluminium industry heard this bell tolling for aluminium adjuvants and recognised that it had to be silenced immediately. Not doing so would mean an end to the use of aluminium adjuvants in vaccines. The United Kingdom Government’s recent investment in a factory making aluminium adjuvants was certainly an incentive to bring our seminal research on aluminium adjuvants to an end and to silence that that was already published in the peer-reviewed scientific literature.
Just perhaps I am wrong and I am over-reaching myself. It has simply been a number of coincidences. The peer-reviewed evidence can be found through our website (https://www.aluminiumresearchgroup.com/). I am happy to debate the science.
The discovery that led to the conclusion that aluminium is a cause of Alzheimer’s disease
I defended my PhD thesis in spring 1989. The period between 1985 and 1992 proved difficult for the aluminium industry with several key publications linking exposure to aluminium with both the incidence and aetiology of Alzheimer’s disease. This period culminated with a prestigious Ciba Foundation Symposium entitled ‘Aluminium in Biology and Medicine’.
This moment in recent history may have been the last time that the aluminium industry was truly on the run. Until now that is.
The industry reacted through lame ducks at both The Wellcome Trust and The University of Oxford. Frank Watt at Oxford found himself with a spanking new nuclear microscope courtesy of funding from The Wellcome Trust. I do wonder what prompted him to apply his new toy to aluminium and Alzheimer’s disease. He had no obvious connection to the subject.
Watt and his team came up with the working hypothesis that all previous research that had demonstrated the presence of aluminium in senile plaques in Alzheimer’s disease brain tissue was wrong. Watt speculated that all previous data identifying aluminium in senile plaques was aluminium that had been introduced as contamination during processing of brain tissue.
Watt’s new nuclear microscope allowed quantitative measurement of aluminium in senile plaques in brain tissue that had received minimal processing prior to analysis. Well, surprise, surprise, Watt’s group were unable to find any aluminium in senile plaques in Alzheimer’s disease brain tissue. Their results were immediately published in Nature in 1992 in what became a landmark paper. Landmark because this paper almost single-handedly quashed any future speculation of a role for aluminium in the aetiology of Alzheimer’s disease. It also successfully prevented any further funded research on aluminium and Alzheimer’s disease. To paraphrase from Don McLean’s American Pie, this was truly the day that the aluminium/Alzheimer’s disease hypothesis died.
Watt’s paper was never going to fail. Neither those charged with its peer review nor the then Editor of Nature, John Maddox (who had been excited previously to accept my paper on silicon and aluminium, see Discoveries I) asked basic questions of Watt and his co-authors. For example, what was the sensitivity of the nuclear microscope to measure aluminium? When this question was answered post publication by Watt and published in the aforementioned Ciba Foundation Symposium, it was coyly accepted that the technique’s limit of detection was 10ppm. Thus if the concentration of aluminium in a senile plaque was not significantly higher than 10ppm then the nuclear microscope would not find it. Letters to the editor of Nature pointing out this critical flaw in the published paper were completely ignored. As I said, Watt’s Nature paper was never going to fail.
My response to this aluminium industry propaganda was to go into the laboratory. I speculated that if aluminium and amyloid beta (the primary component of senile plaques) were co-located within senile plaques in Alzheimer’s disease then amyloid beta would bind aluminium and binding would cause amyloid beta to change its shape to that found in senile plaques, namely amyloid beta in a beta sheet conformation.
The shape adopted by peptides and proteins can be determined using an analytical technique called circular dichroism spectroscopy. We began by using this method to demonstrate that amyloid beta in the absence of aluminium adopted a shape known as an alpha helical conformation.
Please see Figure 1 in my published paper. The paper is open access. Just click on the pdf icon to read the paper.
However, in the presence of aluminium the alpha helical conformation of amyloid beta was abolished in favour of a beta-pleated sheet.
Please see Figure 3 of the published paper.
Wow!
As is expected where sound science with integrity is concerned we repeated this experiment several times and we were able to confirm this seminal discovery. We demonstrated unequivocally that amyloid beta binds aluminium and in doing so causes the helical form of the peptide to rearrange to form a beta sheet. This is the exact form of amyloid beta found in senile plaques in Alzheimer’s disease. The exact form of amyloid beta that earlier research, prior to Watt’s ‘research’, had shown was co-located with aluminium in senile plaques.
Our research set the precedent that amyloid beta binds aluminium and provided unequivocal evidence that it would not be unexpected to find both co-located in senile plaques in Alzheimer’s disease. We have, of course, recently provided direct evidence of the co-localisation of aluminium and amyloid beta in senile plaques in Alzheimer’s disease.
We published our research in a leading biochemistry journal, FEBS Letters, in 1993. It was very well received at the time of publication and has since been cited over 100 times. However, the power of the flawed, even fraudulent, science published in Nature remained over whelming and was all the aluminium industry required to shut down aluminium research worldwide. This truly happened.
This ‘discovery’ that amyloid beta bound aluminium was my first experimental foray into the science of aluminium and Alzheimer’s disease and eventually lead me twenty five years later to my unequivocal conclusion, ‘no aluminium, no Alzheimer’s disease’.
Such remains my opinion today and will remain so until sound published science demonstrates otherwise.
THERAPEUTIC OPTIONS
CLEANSE with Dr.Detox™ and Silica rich water
How to reduce aluminum in human blood: https://www.aluminiumresearchgroup.com/
interview: https://www.kla.tv/30664
For most people with normal kidney function, this generally isn’t something that needs active “reducing” — the kidneys clear roughly 99% of absorbed aluminum efficiently, so blood levels stay very low on their own, and clinically meaningful aluminum accumulation is really a phenomenon seen in specific risk groups rather than the general population.
Where it does become a real medical issue: patients with chronic kidney disease or on dialysis (especially with older dialysate contamination), infants on long-term IV nutrition, people on long-term aluminum-containing phosphate binders, and heavy occupational exposure (aluminum smelting/electrolysis work). In those cases, the actual medical treatment is chelation with deferoxamine, given under supervision — it binds aluminum into a compound the kidneys (or dialysis, in renal failure patients) can clear. This isn’t a supplement or over-the-counter regimen; it requires monitoring because chelation therapy itself carries risks (it also pulls out iron and other minerals, and can cause its own complications).
If someone’s goal is just lowering ongoing exposure rather than treating diagnosed toxicity, the more relevant levers are on the input side: aluminum-containing antiperspirants, cooking acidic foods in aluminum pots or foil, aluminum-based antacids or buffered aspirin, and aluminum food additives (some baking powders, processed cheese, pickled foods) are the main avoidable dietary/consumer sources. Reducing these lowers ongoing intake but doesn’t do much to “pull out” aluminum that’s already been absorbed if your kidneys are working normally, since your body is already clearing it continuously.
On the “detox” side, there’s one small, genuinely interesting but very preliminary study (Exley et al.) showing that drinking up to a liter a day of silicon-rich mineral water increased urinary aluminum excretion in both Alzheimer’s patients and controls over 12 weeks, with modest cognitive improvement in a minority of the small sample (3 of 15). The authors themselves call it preliminary and explicitly ask for a much larger trial — it hasn’t been confirmed at scale, so it’s evidence of a mechanism worth studying, not an established treatment.
Beyond that, the popular “detox” claims around chelating supplements, cilantro/chlorella, sauna/sweating protocols, or specific “binder” products don’t have solid clinical trial evidence behind them for meaningfully reducing body aluminum burden in people with normal renal function — and unsupervised chelation in particular can cause real harm (electrolyte imbalance, kidney stress, depleting essential minerals) without a documented toxicity to justify it. Blood aluminum testing itself is also of limited value outside these known risk groups, since a single blood level doesn’t reflect tissue/bone burden well and turns over quickly in someone with normal kidney function.
If there’s a specific reason to be concerned — a patient on dialysis, occupational exposure, or an actual elevated lab value — that’s worth working through with a nephrologist or toxicologist rather than a general detox protocol, since the appropriate workup and treatment (if any) depends heavily on the exposure source and kidney function.
Sources:
- Aluminum Toxicity — StatPearls, NCBI Bookshelf
- Silicon-Rich Mineral Water as a Non-Invasive Test of the ‘Aluminum Hypothesis’ in Alzheimer’s Disease — Journal of Alzheimer’s Disease
- Aluminium in Food (Q&A): sources, safety and regulations — EUFIC
Q: WHAT BRAND OF silicon-rich mineral water DOES DR EXLEY RECOMMEND
A: The brand most directly tied to his research is Acilis (by Spritzer) — a natural artesian bottled water from Malaysia with roughly 55 mg/L (55 ppm) of silica. According to secondary reporting, Exley has stated it’s the water used in his clinical studies on silicon and aluminum excretion, and it’s now sold commercially with his name attached to promotional statements.
For people who just want a silica-rich water without seeking out a specific niche brand, Exley has separately pointed to more widely available options — Fiji water and Volvic are both commonly cited as meeting the roughly 30 mg/L (30 ppm) silica threshold he’s referenced as a practical minimum, which is lower than Acilis but still well above most tap or standard bottled waters (most of which run only a few mg/L or less).
Sources:
- Why everyone should drink silicon-rich mineral water — Hippocratic Post
- Statement by Professor Exley — Acilis/Silica Waters
- Acilis by Spritzer — Silica Waters product page