Aluminum exposure may cause Alzheimer’s

Aluminum exposure may cause Alzheimer’s

Scientists now say lifelong exposure to aluminum, a neurotoxin present in deodorant, tinfoil, and other common household items, may contribute to Alzheimer’s. While research is still being conducted, the scientific community has begun to look more at environmental factors than genetics in our fight against Alzheimer’s and dementia. RT correspondent Brigida Santos joins RT’s Simone Del Rosario to explain these findings.

There is a study titled “Aluminum and Alzheimer’s disease: after a century of controversy, is there a plausible link?” from Tomljenovic, Lucija published in Journal of Alzheimer’s Disease, vol. 23, no. 4, pp. 567-598, 2011. DOI: 10.3233/JAD-2010-101494.aluminum-and-alzheimers-disease

aluminum-and-alzheimers-disease

You can find its abstract here:

The brain is a highly compartmentalized organ exceptionally susceptible to accumulation of metabolic errors. Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease of the elderly and is characterized by regional specificity of neural aberrations associated with higher cognitive functions. Aluminum (Al) is the most abundant neurotoxic metal on earth, widely bioavailable to humans and repeatedly shown to accumulate in AD-susceptible neuronal foci. In spite of this, the role of Al in AD has been heavily disputed based on the following claims: 1) bioavailable Al cannot enter the brain in sufficient amounts to cause damage, 2) excess Al is efficiently excreted from the body, and 3) Al accumulation in neurons is a consequence rather than a cause of neuronal loss. Research, however, reveals that: 1) very small amounts of Al are needed to produce neurotoxicity and this criterion is satisfied through dietary Al intake, 2) Al sequesters different transport mechanisms to actively traverse brain barriers, 3) incremental acquisition of small amounts of Al over a lifetime favors its selective accumulation in brain tissues, and 4) since 1911, experimental evidence has repeatedly demonstrated that chronic Al intoxication reproduces neuropathological hallmarks of AD. Misconceptions about Al bioavailability may have mislead scientists regarding the significance of Al in the pathogenesis of AD. The hypothesis that Al significantly contributes to AD is built upon very solid experimental evidence and should not be dismissed. Immediate steps should be taken to lessen human exposure to Al, which may be the single most aggravating and avoidable factor related to AD.

You can also find its conclusions here:

Al is the third most abundant element on earth, widely bioavailable to humans and a definite neurotoxin and AD is the most prevalent neurodegenerative disease at the present age. The hypothesis that Al significantly contributes to AD, more so than any other single factor investigated, is built upon very solid experimental evidence. Al has a direct and active access to the brain where it accumulates in a region-specific manner that highly implicates its involvement in AD. Experimental data clearly shows that all neurophysiological parameters required for AD are efficiently targeted for impairment by Al. The sum of latent neurophysiological alterations which are known to precede overt clinical manifestations of AD and are consistent with Al’s neurotoxic properties are:
1) enhanced amyloidosis,
2) neurofibrillary abnormalities, disruption of axonal transport mechanisms, neurite degeneration, and loss of synapses,
3) deficits in neurotransmission (particularly cholinergic) and impairment of G-protein signal transduction cascades,
4) disruption of neuronal energy metabolism and brain metal homeostasis (particularly calcium iron and magnesium),
5) potentiation of oxidative stress and peroxidation of brain membrane lipids,
6) disruption of brain barriers,
7) alterations in chromatin structure and impairment of transcription, and
8) upregulation of stress-related pro-inflammatory and pro-apoptotic pathways.

The latter may be of special significance since elevated levels of intrinsic inflammation are associated with neural aging and further exacerbated in several neurodegenerative diseases. In stark contradiction with the abundance of research evidence, there appear to be “several hostile intellectual attitudes” that reject the possibility that Al toxicity contributes to the growing incidence of AD. Such widely circulated opinions hamper implementation of preventative plans to lessen exposure to Al, which, according to some leading scientists’ advice, would be the most sound and cost-effective approach to reduce the growing incidence of Alzheimer’s type dementia. Given the great socio-economical impact of AD, immediate steps should be taken to minimize human exposure to Al, the single most avoidable factor that poses a serious risk for developing AD. The failure of government health policy makers to take into account the most recent animal studies, as well as epidemiological data which clearly relate long-term Al ingestion at levels relevant to human exposure to an increased risk of cognitive impairment and dementia of the Alzheimer-type, leads to human AD cases as a major means for demonstrating the neurotoxic potential of Al. This practice is unacceptable but unfortunately prevalent at the present time: “Current dietary patterns in the USA are akin to a grand-scale experiment whereby some individuals are consuming large quantities of aluminum while others are not, the long term effects of which have not been investigated”. It would appear that the practical considerations of warnings given by William Gies are now 100 years overdue “These studies have convinced me that the use in food of aluminum or any other aluminum compound is a dangerous practice. That the aluminum ion is very toxic is well known. That aluminized food yields soluble aluminum compounds to gastric juice (and stomach contents) has been demonstrated. That such soluble aluminum is in part absorbed and carried to all parts of the body by the blood can no longer be doubted. That the organism can “tolerate” such treatment without suffering harmful consequences has not been shown. It is believed that the facts in this paper will give emphasis to my conviction that aluminum should be excluded from food”.

The same rationale would apply for Al in skin-care products, antiperspirants, pharmaceuticals, and perhaps significantly in vaccines, at least until independent research is available to demonstrate that these products can be used safely. In particular, Al in adjuvant form carries a risk for long-term brain inflammation, cytotoxicity, and associated neurological complications, and may thus have profound and widespread adverse health consequences. We are long overdue for a comprehensive evaluation of the overall impact of Al on human health. With regards to AD, such an evaluation should include studies designed to elucidate the molecular mechanisms involved in the neurotoxicity caused by chronic Al intake and its association with the metabolism of other compounds such as iron. Special emphasis should be given to Al species which are most relevant to human exposure (e.g., fluoroaluminates, Al hydroxide, Al sulfate). As for the reasons for the current complacency about Al toxicity to humans from bioavailable sources, some on the other side of the issue have noted that: “Some have argued that I should have been more vocal about the fact that paid consultants for the aluminum industry served as consistent and vocal critics of our findings. I always felt, perhaps naively, that our data were properly collected, honestly and completely reported and were essentially correct. Accordingly, I have felt that the truth would eventually be known and ultimately accepted” . Food for thought?

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