Where’s the science?
“The results demonstrated that Al(III) induced the transformation of the initial random coil structure to the β-sheet configuration in the Aβ40 peptides. These structural changes facilitated the aggregation of Aβ40.”
Meanwhile, denial train. Choo choo!
“Here’s the evidence behind the presence of metals such as copper, zinc, iron and aluminium.”
The first three are needed by the body and not neurotoxins.
“But the evidence doesn’t yet show whether this relationship actually causes Alzheimer’s disease.”
Have you tried checking?
“It is also unclear whether reducing metals in the brain via drugs or reducing our exposure would have any effect.”
It is unclear whether Caesar was stabbed but there is a lot of blood and all these knives might’ve had some effect.
“These metals are essential to the healthy function of our brain,”
Aluminium is not necessary for any bodily function.
But it makes food manufacturing dirt cheap!
“The body is able to tolerate these metals in small amounts by clearing through the kidneys. ”
Well, clearly not.
“These include aluminium and lead, for example it has been shown that if they are not taken out by the kidneys through organ failure or by exposure to extremely high doses these metals are able to deposit in the brain.
These metals are known to cause negative effects in the brain and have been implicated in several neurological conditions.”
Safe as lead, guys!
And no that’s outdated, the body doesn’t really clear it. See end.
“In 1965, researchers found that rabbits injected with an extremely high dose of aluminium developed toxic tau tangles in their brains. This led to speculation that aluminium from cans, cookware, processed foods and even the water supply could be causing dementia.”
But the can manufacturers were slipped a bribe because they recently had to switch from toxic tin.
That generation’s children now seem to be presenting with unprecedented Alzheimer’s…. coincidence?
“Importantly, these results were only seen with extremely high exposures that far exceed the levels that can enter the body through food or potentially through contact with aluminium cookware.”
That limit does not exist and assumes perfect health – no alcoholism, polluted air, toxic water, stress, chronic diseases.
“As yet no study or group of studies has been able to confirm that aluminium is involved in the development of Alzheimer’s disease.”
Ethics and finding the funding.
Also a half-lie, there are many studies. As you’ll see.
“Aluminium is seen in the normal, healthy brain.”
No, it isn’t.
Not ever. Not at all.
It shouldn’t get past the barrier.
Normal for the modern world is not healthy.
Opening line here: “Aluminium is neurotoxic.”
Back to the liars:
“Although aluminium has been seen in amyloid plaques there is no solid evidence that aluminium is increased in the brains of people with Alzheimer’s disease.”
Yes there was, you’re ignoring it.
They dissected Alzheimer’s patients and found it in there.
“No convincing relationship between amount of exposure or aluminium in the body and the development of Alzheimer’s disease has been established.”
Wait before it didn’t exist and in the very next sentence, it isn’t convincing?
“Aluminium in food and drink is in a form that is not easily absorbed in to the body. Hence the amount taken up is less than 1% of the amount present in food and drink.”
Bullshit. It’s the most processed form it goes through the whole digestive tract and then into the bloodstream like food nutrients.
Less than 1% – per meal or drink. PER meal or drink.
“Most of the aluminium taken into the body is cleaned out by the kidneys.”
And wouldn’t it be the liver?
“failed to find a convincing causal association between aluminium exposure in humans and Alzheimer’s disease.”
Give us the data instead of finding excuses to hide it.
1991, before the cash cow was in full milking rotation
“exposure to aluminium has been implicated by epidemiological studies and the finding of aluminium in the cerebral plaques and tangles.”
3 decades later? Still covering it up?
While they blame copper:
“a high brain tissue ratio of copper to aluminium protects against neurotoxicity associated with the deposition of amyloid-b and the amyloid cascade hypothesis.”
“The study on 60 aged human brains identified a number of relationships between the degree of severity of amyloid-b neuropathology and the metal content of tissue from the donor brains. The latter was recently published for aluminium, copper and iron (House et al. (2012) Metallomics 4, 56-65).
Relationships, PLURAL and severity.
“Specifically, the extent and severity of amyloid-b deposition was inversely related to the copper content of brain tissue. Lower copper resulted in more severe and more extensive deposition of amyloid-b in the donor brain.”
But obviously you’re crazy to read about it.
“The research suggested that for those individuals with moderate to severe amyloid pathology, a copper to aluminium ratio of less than 20 predicted dementia.”
“Professor Exley said: “The hypothesis requires further testing but if proven correct it could explain why some individuals with senile plaques do not suffer from dementia. The implication being that a high brain tissue ratio of copper to aluminium protects against neurotoxicity associated with the deposition of amyloid-b and the amyloid cascade hypothesis.””
Aluminium-specific chelators reduce symptoms. Coincidence?
Effect is seen with low levels too:
“By this means, the body burden of aluminum in humans has increased. Epidemiological and experimental findings indicate that aluminum is not as harmless as was previously thought, and that aluminum may contribute to the inception and advancement of Alzheimer’s disease. Epidemiological data is reinforced by indications that aluminum exposure can result in excess inflammatory activity within the brain.”
“Evidence is presented that reinforces the likelihood that aluminum is a factor speeding the rate of brain aging. Such acceleration would inevitably enlarge the incidence of age-related neurological diseases.”
Maybe most Baby Boomers would be okay if their brains weren’t poisoned?
“However, disruption of these mechanisms, or absorption of detrimental metals with no known biological function, alter the ionic balance and can result in a disease state, including several neurodegenerative disorders such as Alzheimer’s disease. Understanding the complex structural and functional interactions of metal ions with the various intracellular and extracellular components of the central nervous system, under normal conditions and during neurodegeneration, is essential for the development of effective therapies.”
I hope you plan on someone in Big Pharma coming to kill you for developing therapies.
Opening line: “Aluminum has been identified as a neurotoxin for over 100 years.”
As safe as lead or mercury.
You know where the society said no studies?
“A 2008 systematic review of studies that included aluminum exposure through drinking water, diet, and occupation found 23 studies demonstrated an increased risk for Alzheimer’s disease with elevated aluminum exposure, 3 found that there was no connection…”
Cover-up? Where’s the science?
I can’t seem to find it, guys!
“We screened 4784 studies and included 60 in the review. Risk factors were considered in six categories: air quality, toxic heavy metals, other metals, other trace elements, occupational-related exposures, and miscellaneous environmental factors. Few studies took a life course approach. There is at least moderate evidence implicating the following risk factors: air pollution; aluminium; silicon; selenium; pesticides; vitamin D deficiency; and electric and magnetic fields.”
Life course is ideal.
There is a threshold.
“Our article examines the question of whether environmental and therapeutic aluminum exposure increases the risk of disease. To this end, Alzheimer’s disease and breast cancer are taken as critical endpoints. Aluminum’s neurotoxic effects in humans and its embryotoxic effects in animal models have been proven (4).”
“An inevitable consequence of humans living in
the Aluminium Age is the presence of aluminium in the
brain. This non-essential, neurotoxic metal gains entry to
the brain throughout all stages of human development,
from the foetus through to old age. Human exposure to
myriad forms of this ubiquitous and omnipresent metal
makes its presence in the brain inevitable, while the
structure and physiology of the brain makes it particularly
susceptible to the accumulation of aluminium with age. In
spite of aluminium’s complete lack of biological essentiality,
it actually participates avidly in brain biochemistry
and substitutes for essential metals in critical biochemical
processes. The degree to which such substitutions are disruptive
and are manifested as biological effects will depend
upon the biological availability of aluminium in any particular
physical or chemical compartment, and will under
all circumstances be exerting an energy load on the brain.
In short, the brain must expend energy in its ‘unconscious’
response to an exposure to biologically available aluminium.
There are many examples where ‘biological effect’
has resulted in aluminium-induced neurotoxicity and most
potently in conditions that have resulted in an aluminiumassociated
encephalopathy. However, since aluminium is
non-essential and not required by the brain, its biological
availability will only rarely achieve such levels of acuity,
and it is more pertinent to consider and investigate the
brain’s response to much lower though sustained levels of
biologically reactive aluminium. This is the level of
exposure that defines the putative role of aluminium in
chronic neurodegenerative disease and, though thoroughly
investigated in numerous animal models, the chronic toxicity
of aluminium has yet to be addressed experimentally
in humans. A feasible test of the ‘aluminium hypothesis’,
whereby aluminium in the human brain is implicated in
chronic neurodegenerative disease, would be to reduce the
brain’s aluminium load to the lowest possible level by noninvasive
means. The simplest way that this aim can be
fulfilled in a significant and relevant population is by
facilitating the urinary excretion of aluminium through the
regular drinking of a silicic acid-rich mineral water over an
extended time period. This will lower the body and
brain burden of aluminium, and by doing so will test
whether brain aluminium contributes significantly to
chronic neurodegenerative diseases such as Alzheimer’s
Of course, A Drink is cheaper than all the care of the sick patients and you can’t steal their house legally by telling the council they lack competence.
“Certainly aluminium either directly as a
particulate or indirectly following the dissolution of
nanoparticulates could induce an inflammatory action in
the human brain, and this has been demonstrated in animal
models . The immunopotency of aluminiumbased
adjuvants outside their role as adjuvants in vaccine
and allergy therapies seems to have been largely ignored
as a potential mechanism of aluminium toxicity
throughout the body  and especially in the nervous
system . The consistent observation of significant
accumulations of aluminium in the brain should at least
be a warning of the potential for such to participate in
“The brain is an obvious target for aluminium toxicity.
Neurotoxicity is evident under acute conditions such as
encephalopathies, and it is predicted but not necessarily
recognised as such under chronic or everyday exposures to
environmental aluminium. The mechanisms of neurotoxicity
are potentially myriad, while their manifestations as
biochemical changes are probably quite subtle for all but
the most vulnerable groups.”
Headaches, stomach aches, etc. “Brain fog” might be entirely toxin based.
“While the latter must include
the foetus and neonate, there are few indications as to the
identities of others who are susceptible to the neurotoxicity
of aluminium. Since the advent of the Hall-He´roult process
(and thereafter Bayer process) towards the end of the
nineteenth century and our ability to extract aluminium
from its inert ores on an industrial scale, we have all been
living in the Aluminium Age . Now, in the twenty-first
century, we can no longer completely avoid environmental
exposure to aluminium. Since there is as yet no proven
requirement for aluminium in any living organism, never
mind in humans, it would be prudent to reduce our
everyday exposure to avoid aluminium entering the body
and persisting in the human brain .”
It’s used to process junk food, watch How It’s Made.
When people feel better after giving up junk, it might be aluminium exposure reduction.
It would be easy to study: people who eat a lot of junk and people who don’t, Al urine amounts.
“We have begun to
show that this can be achieved by using nature’s own way
of avoiding biologically available aluminium. We have
shown that regular consumption of silicon-rich mineral
waters both reduce our gastrointestinal uptake of aluminium
and, importantly, facilitate our urinary excretion of
systemic aluminium . Life on Earth evolved in spite of
a crust of aluminosilicate . However, the Hall-He´roult
process and the subsequent arrival of an Aluminium Age
have let the aluminium genie out of the bottle. Our final
wish should be that the unique inorganic chemistry of
aluminium and silicic acid will help to put the genie back
where it can be used effectively but, most importantly,
Trans. We evolved to take silicon into our brain but aluminium is taking its place.
It lied on its CV, it needs to be fired.
“This article summarizes the various ways in which Al induces oxidative stress, eventually leading to cell death. It also gives a brief account of manifold epidemiological studies that relate the abundant occurrence of Al in soil and water and the prevalence of AD. Al carriers, their role in AD, Al in neurofibrillary tangles, biochemical reactions altered by Al influx in mitochondria have been briefly discussed.”
One of the key words is apoptosis…
“If aluminium contributes to the development of sporadic AD, it must do so indirectly, perhaps via effects on the synthesis or metabolism of APP, or by contributing generally to the age-related attrition of neurons and thus reducing the threshold for deficits produced by more specific disease-related processes.”
Final study describes a mechanism.
Back-up PDFs are always useful.
Active effect of aluminium on the brain’s self-cleaning.
“Aluminum, as an extremely high charge density cation (Z2/r = 18), has the remarkable capability to both (1) aggregate and compact Aβ42 peptide monomers into higher order, more neurotoxic oligomeric, and fibrillar structures, and (2) impair, at the molecular-genetic* level, the cellular machinery responsible for Aβ42 peptide monomer phagocytosis and clearance from the cell (4–13).”
*Hints at genetic damage.
Apparently the levels we ingest are “physiologically realistic.” As in, it can affect you.