I am often told that the link to Alzheimer’s disease and aluminum is inconclusive. If you don’t look for it you won’t find it. However there is plenty of evidence if you look for it.
Lets start with the link below which is a Comparative Toxicogenomics Database. It provides information on various chemicals and the diseases that they cause. We will look at these three listed below as they are all neurotoxins.
CTD is a robust, publicly available database that aims to advance understanding about how environmental exposures affect human health. It provides manually curated information about chemical–gene/protein interactions, chemical–disease and gene–disease relationships. These data are integrated with functional and pathway data to aid in development of hypotheses about the mechanisms underlying environmentally influenced diseases.
Even though very little mercury is found in our drinking water, I just want to make people aware of the effects that it can have on the brain.
Mike Adams, the Health Ranger
Believe it or not, there are still millions of people, doctors, pharmacists and even journalists who do not yet realize there is a very high concentration of mercury in influenza vaccines given to pregnant women, children and senior citizens. Most people, you see, have been lied to by the media which has stated over and over again that mercury was removed from all vaccines.
That’s simply not true.
It’s still there. And toxic mercury is present in influenza vaccines at a level that’s literally 25,000 times higher than the EPA limit of mercury in drinking water. It’s 100 times higher than the highest level of mercury contamination I’ve ever tested in ocean fish.
Third from top of the list Autism
Top of the list Alzheimer
What most people fail to understand is that when chemicals enter the body, they don’t remain isolated. You may get chemicals entering the body from different sources at different times. But as they work their way around the body some may combine with other chemicals which can have devastating effects, as the experiments below shows. What kind of impact can this have on an unborn or newborn child?
“And combination of substances in toxicology can be greater than the sum of its parts. “With lead and mercury, for instance, a toxicity rating of 1 for each mercury and lead equals not 2, but 60 when combined.”—Hal Huggins
Toxics can make each other more toxic.
“A small dose of mercury that kills 1 in 100 rats and a dose of aluminum that will kill 1 in 100 rats, when combined have a striking effect: all the rats die.
Doses of mercury that have a 1 percent mortality will have a 100 percent mortality rate if some aluminum is there.”
Toxins where ever they come from have a cumulative, synergistic toxic affect on all of us. They slowly degrade and diminish us bit by bit. For some it can come a lot quicker. The scientific facts speak for themselves.
Did you know that aluminum is being added to our water and the science has shown that aluminum is linked to Alzheimer’s disease.
The synergistic toxic affect of Aluminum and fluoride combined.
“In l999, EPA convened a group of experts to carefully consider the results of the Varner et al. (1998) study,” USEPA spokesman, Charles Fox wrote in a September 5, 2000 letter to US Congressman Ken Calvert, Chairman, House Subcommittee on Energy and the Environment. Fox continued, “As a result of that conference, EPA has requested that the National Toxicology Program consider the possibility of conducting additional studies of the neurotoxicity of aluminum that include verification of the results observed in the Varner et al. Study.” ntp.niehs.nih.gov/ntp/htdocs/lt_rpts/tr393.pdf
All three studies found that aluminum-fluoride interactions are associated with brain and kidney damage in laboratory animals. Aside from brain and kidney damage, there was an 80% mortality rate in the animals fed doses of sodium fluoride and aluminum similar to those found in artificially fluoridated drinking water.
Alum (aluminum sulfate) is most frequently used by water companies to improve the appearance of drinking water, to make it clear. For many years, aluminum has been known to be neurotoxic to humans and animals.
The Varner team said that, “Striking parallels were seen between aluminum-induced alterations” in cerebral blood vessels that are associated with Alzheimer’s disease and other forms of presenile dementia. They concluded that the alterations of the blood vessels may be a primary event triggering neuro-degenerative diseases.
Varner and associates appear to have found TOXIC SYNERGISTIC ACTION between FLUORIDE and ALUMINIUM in drinking water. This has now been made a part of PUBLIC RECORD in the US FEDERAL REGISTER as of December 4, 2000.
Promoters of fluoridation can no longer get away with the “unequivocal statement” that fluoride is a “free ion” in water”, OR that “it completely dissociates and doesn’t react with other minerals in drinking water.”
Following the Varner, et al aluminium fluoride studies in which 80% of the experimental rats died before the end of the experiment the United States Environmental Protection Agency was sufficiently alarmed to push the National Toxicology Program (NTP) to do further research.
Varner and associates appear to have found TOXIC SYNERGISTIC ACTION between FLUORIDE and ALUMINIUM in drinking water. This has now been made a part of PUBLIC RECORD in the US FEDERAL REGISTER as of December 4, 2000.
WHAT DOES THIS MEAN?
For the first time, synergistic action is officially acknowledged, along with the fact that FLUORIDE in the water COMBINES WITH OTHER MINERALS.
Higher levels of aluminium and fluoride in drinking water are related to the onset of dementia, according to a ground-breaking study of thousands of Scots…….
The proof is in the science. Not the pseudo corporate science that is always being presented to us by corporate controlled government.
It’s time to wake up, before you loose your mind literally and take action.
Americans are losing their minds to Alzheimer’s disease. It’s an epidemic. And it’s not typical of what’s going on in the rest of the world.
The World Health Organization (WHO) estimates that there are 18 million people with Alzheimer’s. Over 4 1/2 million Americans have the disease. We account for 25% of all Alzheimer’s cases, even though we represent only 4.6% of the world’s population. Europe is experiencing half our rate of disease. For Americans over 85 years of age, 50% are thought to have Alzheimer’s.
The question is, “Why?”………
The Age of Aluminum profiles people whose health has been seriously impacted by unwitting exposure to aluminum, along with leading scientists as they explore the links between this known neurotoxin and a growing epidemic of chronic illnesses and disabilities.
For those seeking answers to why breast cancer, dementia, autism, autoimmunity, allergies, and chronic fatigue are on the rise,
The Age of Aluminum is a must-see film.
Go read the ingredients on your tube of toothpaste. It’ll list one or two ‘active ingredients’…notice the combined total amounts of ‘active ingredients’ is usually less than 1%. What about the other 99%?
Senile dementia is a progressive degenerative brain disease associated with old age. Its symptoms include short-term memory loss, slowness in thought and movement, confusion, disorientation, depression, difficulty communicating, and loss of physical function. Alzheimers disease accounts for about half of all senile dementia cases. Although there are many theories about what causes Alzheimers, the fact is, its origins remain poorly understood. One theory proposed that the common occurrence of being exposed to aluminum could cause Alzheimers dementia. Aluminum, the theory postulated, becomes concentrated in the characteristic lesions (senile plaques and neurofibrillary tangles) that develop in the brain during the course of the disease. At first, medical scientists thought this theory was absurd. Aluminum, they believed, accumulated merely as a result of a destructive process caused by some other factor. In recent years, however, the aluminum hypothesis has been gaining respect. For example, studies have discovered a direct association between the level of aluminum in municipal drinking water and the risk of Alzheimers dementia. One study found aluminum in drinking water was related to only this specific type of dementia;1 another found that the probability of the association being due to chance was only 1 in 24, with a 46 percent increased risk for people drinking water with the highest aluminum levels. 2 The use of aluminum-containing antiperspirants–but not the use of antiperspirants and deodorants in general–has also been associated with a risk of Alzheimers dementia, with a trend toward a higher risk corresponding with increasing frequency of use. 3 This relationship does not extend to aluminum-containing antacids, 4 which may simply be evidence that the aluminum in antacids is not absorbed–the process of absorption through the gut mucosa is quite different from absorption through the skin. We also know that serum aluminum concentrations increase with age. Aluminum may accumulate slowly over our lifetimes or we may absorb it more easily as we age. Moreover, there is evidence that people with probable Alzheimers disease have serum aluminum levels that are often significantly higher than those of people with other types of dementia, as well healthy people of similar ages.5 Further evidence that aluminum fosters the development of Alzheimers dementia comes from a scientific (placebo-controlled) trial of desferrioxamine, a drug that removes aluminum from the body by binding with it. While regular administration of the drug failed to stop the disease from progressing, desferrioxamine did significantly reduce the rate of decline in the ability of a group of people with Alzheimers dementia to care for themselves.6 Although the aluminum/Alzheimers link remains unproven, I believe that waiting for definitive proof before taking a few easy and protective measures is foolhardy–and more scientists are starting to agree.7,8 Perhaps one person in 10 age 65 or older suffers from dementia; by age 80 that figure rises to one in five. This is too common an illness to ignore preventive measures until we can know for certain why it develops.
Aluminum has been linked to diseases such as cancer, autism, and Alzheimer’s. This toxic material is entering the human body via everyday consumption of food, water, cosmetics and an increasing number of vaccinations.
“Professor Christopher Exley, often referred to as Mr. Aluminum, has been studying the effects of aluminum on the human body for thirty years and has become increasingly worried. In a recent video presentation, he explained that, despite the fact that aluminum has been regularly used as an adjuvant in vaccination for many years, little is known about its effect on the human body. He made it clear that we should accept that aluminum is toxic and that toxicity may take many different forms. He stated that wherever it ends up in the body, it has the potential to do harm.
This is certainly something to consider, especially when none of us can be certain where an aluminum adjuvant will accumulate once it has been vaccinated into our body.
Professor Exley continued by stating that:
If aluminum is in the brain, it can produce neurodegeneration and problems associated with the brain; if it is in the bone, it can produce bone disease. Wherever it ends up in the body, it has the potential to cause toxicity, whether it is in humans, fish or any other living organism.”…..
This study describes alterations in the nervous system resulting from chronic administration of the fluoroaluminum complex (AlF3) or equivalent levels of fluoride (F) in the form of sodium-fluoride (NaF). Twenty seven adult male Long-Evans rats were administered one of three treatments for 52 weeks: the control group was administered double distilled deionized drinking water (ddw). The aluminum-treated group received ddw with 0.5 ppm AlF3 and the NaF group received ddw with 2.1 ppm NaF containing the equivalent amount of F as in the AlF3 ddw. Tissue aluminum (Al) levels of brain, liver and kidney were assessed with the Direct Current Plasma (DCP) technique and its distribution assessed with Morin histochemistry. Histological sections of brain were stained with hematoxylin & eosin (H&E), Cresyl violet, Bielschowsky silver stain, or immunohistochemically for beta-amyloid, amyloid A, and IgM. No differences were found between the body weights of rats in the different treatment groups although more rats died in the AlF3 group than in the control group. The Al levels in samples of brain and kidney were higher in both the AlF3 and NaF groups relative to controls. The effects of the two treatments on cerebrovascular and neuronal integrity were qualitatively and quantitatively different. These alterations were greater in animals in the AlF3 group than in the NaF group and greater in the NaF group than in controls.
Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Varner JA, Jensen KF, Horvath W, Isaacson RL, Psychology Department, Binghamton University, Binghamton, NY, USA. Brain Res 1998 Feb 16;784(1-2):284-98
The pathophysiology of Alzheimer’s disease (AD) is related to the alterations in neurotransmission, beta-amyloid production, plaque formation and cytoskeletal abnormalities. The question of aluminium relevance to the etiology of AD cannot yet be adequately answered. Aluminium is currently regarded as the putative risk factor for the disease. Our paper shows that some of pathologic changes are not raised by aluminium alone, but by the aluminofluoride complexes. These complexes may act as the initial signal stimulating impairment of homeostasis, degeneration and death of the cells. By influencing energy metabolism these complexes can accelerate the aging and impair the functions of the nervous system. In respect to the etiology of AD, the long term action of aluminofluoride complexes may represent a serious and powerful risk factor for the development of AD.”
Reassessment of the role of aluminum in the development of Alzheimer’s disease. Strunecka A, Patocka J, Katedra fyziologie a vyvojove biologie Prirodovedecke fakulty Univerzity Karlovy, Praha. Cesk Fysiol 1999 Feb;48(1):9-15
This study examined the behavioral effects of chronic ingestion of various monofluoroaluminum complexes (AlF3) in drinking water. Forty young adult male Long-Evans rats were divided into four groups of 10 rats each. The groups received different concentrations of AlF3 in the drinking water from three sample solutions having a total Al concentration of 0.5, 5.0, and 50 ppm, respectively, or double-distilled deionized water on an ad lib. basis for 45 weeks. General decline of bodily appearance was observed in the lowest concentration AlF3 group, and animals in this group succumbed in greater numbers during the course of the study than those in any other group. Examinations of performance in an open field, an analysis of walking patterns, and a balance beam test did not find any difficulties indicative of motor disorder. Indeed, on the initial trial on the balance beam, the AlF3-treated animals exhibited superior performance. No group differences were found in behavior assessed by spontaneous alternation or by a modified Morris water maze test. When retested in the Morris maze after a low dose of scopolamine (0.4 mg/kg), the control animals took longer to reach the platform while the AlF3-treated rats were not affected. In an olfactory preference test, the AlF3-treated animals failed to show preferences exhibited by the controls, indicating a possible olfactory impairment. The level of Al in the brains of the AlF3-exposed rats, as determined by direct current plasma analysis, was almost double that of the control animals. There was a similar trend for the Al content found in the kidneys.
Chronic aluminum fluoride administration. I. Behavioral observations. Varner JA, Horvath WJ, Huie CW, Naslund HR, Isaacson RL, Department of Psychology, Binghamton University, New York 13902-6000. Behav Neural Biol 1994 May;61(3):233-41
Aluminofluoride complexes: new phosphate analogues for laboratory investigations and potential danger for living organisms.
©Anna Struneckáa & Jirí Patockab
aCharles University, Faculty of Sciences, Department of Physiology and Developmental Physiology, Prague bDepartment of Toxicology, Purkynì Military Medical Academy, Hradec Králové, Czech Republic
Running title: Pharmacological implications of aluminofluoride complexes
Corresponding author: Anna Strunecká
Department of Physiology and Developmental Physiology,
Faculty of Sciences, Charles University, Vinièná
7, 128 00, Prague 2, Czech Republic
Telephone: (42) – 02/21953239
Fax no.: (42) – 02/299713
A list of non-standard abbreviations used in the paper: AD, Alzheimer´s disease; [AlF4]–, aluminofluoride complexes; cAMP, cyclic adenosine monophosphate; G proteins, guanine nucleotide binding proteins; GDP, guanosine diphosphate; GTP, guanosine triphosphate; 1,4,5-IP3, inositol-1,4,5-trisphosphate; PIP2, phosphatidylinositol 4,5-bis-phosphate.
Aluminofluoride complexes have been widely used in laboratory investigations for stimulation of various guanine nucleotide binding proteins. These fluorometallic complexes cannot be obtained through any catalogue or drug store. They are formed in water solutions containing fluoride and traces of aluminium in the form of the soluble ionic complexes, Aluminofluoride complexes have been recognised to act as phosphate analogues. Reflecting many studies which utilise aluminofluoride complexes in laboratory investigations, the effects of these fluorometallic complexes on various cells and tissues as observed, can be reviewed. With the appearance of acid rain and the use of aluminium in industry, there has been a dramatic increase in the amount of uncomplexed aluminium in ecosystems. In view of the ubiquity of phosphate in cell metabolism, aluminofluoride complexes represent a strong potential danger for living organisms including humans. The possibility of pathophysiological consequences of their long-term action is not fully recognised at this point.
During the last decade aluminofluoride complexes have been widely used in laboratory investigations as the tool for stimulation of various guanine nucleotide binding proteins (G proteins). Knowledge about the role of G proteins in signal transduction has expanded enormously , as over one hundred G protein-coupled receptors have been described (Gilman, 1987). Physiological agonists of these receptors include neurotransmitters and hormones, such as dopamine, epinephrine, norepinephrine, serotonin, acetylcholine, glucagon, vasopressin, neuropeptides, opioids, excitatory aminoacids, prostanoids, purines, photons and odorants. Fluoride anions had been recognised as the activators of the purified guanine nucleotide-binding regulatory component of adenylate cyclase (Rall & Sutherland 1958). Later Sternweis & Gilman (1982) reported that fluoride activation of adenylate cyclase depends on the presence of aluminium traces. The requirement for aluminium is highly specific; of 28 other metal tested, only Be2+ promoted activation of the guanine nucleotide-binding regulatory component of adenylate cyclase by fluoride. [AlF4]– mimics the role of the phosphate only if the phosphate is present and remained unsubstituted. These metallofluoride complexes are only active in conjuction with a bound nucleoside diphosphate. Their effect is more readily seen with G proteins because guanosine diphosphate (GDP) is always tightly bound in the site after the hydrolysis of guanosine triphosphate (GTP). In aqueous solutions, the fluoride anions bind to metal cation and are exchangeable with free fluoride or hydroxyl ions. The complexes are not permanent; equilibria exist between the various possible complexes, and the proportions of multifluorinated species such as AlF3, AlF3(OH) and [AlF4]–, depend on the excess concentration of free F– ions and on the pH of the solution (Bigay et al. 1987; Martin 1988; Chabre 1990).
Chabre (1990) explained an important “functional” difference between a phosphate group and the structurally analogous aluminofluoride complexes. In phosphate, oxygen is covalently bound to the phosphorus and does not exchange with oxygen from solvent. In aluminofluoride complexes, ionic bonds are formed between the electropositive aluminium and the highly electronegative fluorine. While the reaction of a bound phosphate compound with orthophosphate is endergonic and slow, the corresponding reaction with [AlF4]– is rapid and spontaneous. Aluminofluoride complexes bind ionically to the terminal oxygen of GDP -phosphate. Enzyme-bound GDP or ADP could therefore form a complex with [AlF4]– that imitates ATP or GTP in its effect on protein conformation. This effect often causes a structural change that locks the site and prevents the dissociation of the trisphosphate. Free phosphates and nucleotides, when present at milimolar concentrations, do bind ionically to all the fluoride complexes. The action of [AlF4 ]– is not therefore restricted only to guanine nucleotides. These fluorometallic complexes influence the activity of a variety of phosphatases, phosphorylases and kinases (Bigay et al. 1987). In view of the ubiquity of phosphate in cell metabolism, aluminofluoride complexes can represent a strong potential danger for living organisms including humans. The possibility of pathophysiological consequences of their long-term action is not fully recognised at this point. But, reflecting many studies which utilise aluminofluoride complexes in laboratory investigations, the effects of these fluorometallic complexes on various cells and tissues as observed, can be reviewed. It might seem difficult to decide if these experiments present a potential toxicological risk for the human population in the future. In this article we review some of the evidence for pathophysiological effects of aluminium and fluoride on living organism.
II. PHYSIOLOGICAL AND BIOCHEMICAL ACTION OF [AlF4]– IN VARIOUS CELLS AND TISSUES
Liver. Isolated parenchymal cells, hepatocytes, maintain responsiveness to hormones and serve as model cells equipped with very complex biochemical pathways. The stimulation of glycolysis by vasopressin, angiotensin II, and 1-adrenergic agonists is mediated in the liver through the increase of the Ca2+ size=4>cytosolic level. It has been demonstrated that the phosphoinositide signaling second messenger system is activated and involved in these events (Werve et al. 1985). Blackmore et al. (1985; 1988) demonstrated in their studies that the treatment of isolated hepatocytes with NaF produced the efflux of Ca2+, the rise in free cytosolic Ca2+, the decrease in phosphatidylinositol 4,5-bis-phosphate (PIP2)content and the increase in inositol-1,4,5-trisphosphate (1,4,5-IP3 ) and diacylglycerol. The level of intracellular cyclic adenosine monophosphate (cAMP) was decreased. All these changes were concentration dependent. The effects of low doses of NaF (2-15 mM) were potentiated by AlCl3 and this potentiation was abolished by Al3+ chelator desferoxamine. Fluoride anions in the presence of aluminium thus mimicked the action of Ca2+-mobilizing hormones glucagon and vasopressin in hepatocytes. The effects of submaximal doses of [AlF4]– were potentiated by submaximal doses of vasopressin, angiotensin II, and 1-adrenergic agonists. Using phorbol myristate acetate, the activator of protein kinase C, the conclusion was made that [AlF4]– mimics the effects of Ca2+ mobilizing hormones by activating the G protein which couples the hormone receptor to phospholipase C specific to PIP2 (Blackmore & Exton 1986). The phosphate-analogue model of [AlF4]– action is not restricted to guanine nucleotides in the liver. Blackmore et al. (1985) observed the activation of phosphorylase and inactivation of glycogen synthase after the activation of fluoride in the presence of AlCl3 in hepatocytes. [AlF4]– transforms the liver to the organ involved in glycogenolysis, fatty acid oxidation and lipolysis.
Brain. G protein-coupled receptors and G protein-mediated cell responses are of key importance in the processes of neurotransmission and intercellular signaling in the brain. Phosphoinositide metabolism is coupled to several neurotransmitter receptors in the central nervous system including cholinergic, adrenergic, dopaminergic and histaminergic receptors. [AlF4]– has been widely used to stimulate phosphoinositide hydrolysis. The ability of [AlF4]– to mimic the effects of Ca2+-mobilizing hormones suggests the coupling of hormone receptors to phosphoinositide breakdown through G proteins (Rana & Hokin 1990).
Candura et al. (1991) observed that aluminium salts and NaF mimicked the action of GTP(S) in stimulating phosphoinositide turnover and generation of inositol phosphates in rat cerebral cortical membranes. A much greater hydrolysis of phosphoinositides was observed when AlCl3 and NaF were present together, supporting the concept that [AlF4]– is the active stimulatory species. Nadakavukaren et al. (1990) demonstrated accumulation of inositol phosphates in the suprachiasmatic nuclei region of rat hypothalamus over a 40 min incubation with [AlF4]–. Hypothalamic suprachiasmatic nuclei were suggested as the site of a biological clock responsible for generation of circadian rhythms. Melatonin receptors are involved in this function. Melatonin can facilitate secretion via a cholera and pertussis toxins-insensitive mechanism which can be inhibited by aluminum fluoride. [AlF4]– blocked the increase in cAMP stimulation by forskolin, being as effective as melatonin and increased intracellular calcium ( Morgan et al. 1991).
When rat hippocampal slices were exposed to 10 mM NaF and 10 µM AlCl3 for a brief period of time (12-15 min), spike amplitude fell to very low levels. Upon washout, spike amplitude recovered beyond control values and in half of the preparations a prolonged enhancement of spike amplitude (greater than 2 hours) occurred. If AlCl3 was omitted from fluoride-containing saline, enhancement of spike amplitude, when observed, was brief. These experiments show that brief exposure to [AlF4]– induces prolonged enhancement of synaptic transmission in rat hippocampal slices (Publicover 1991).
Tremendous possibilities of multiple molecular interactions of aluminium, fluoride and aluminofluoride complexes probably exist in the brain. Understanding the action of [AlF4]– in the brain warrants further investigation.
Kidney. The effects of aluminofluoride complexes on the kidney were studied using glomerular mesangial cells, proximal tubular cells, and inner medullary collecting tubule cells of rat kidney.
The ion transporting processes are affected by [AlF4]– in kidney tubular cells. [AlF4]– stimulates adenylate cyclase, inhibits amiloride-sensitive Na/H exchange regulated by cAMP-dependent protein kinase, enhances epidermal growth factor-stimulated prostaglandin production, and mimics vasopressin and bradykinin induced Ca2+ mobilisation. It is suggested that [AlF4]–can affect the activity of many other ion channels and enzymes in the kidney (Zhou et al.1990).
Cells of blood. [AlF4]– induces shape changes and aggregation in platelets ( Rendu et al. 1990). Incubation of platelets with NaF (5-10 mM) induced only slight morphological changes. Addition of 10 µM AlCl3 resulted in aggregation. One min after addition of AlCl3, most of the granules were concentrated in the center of the cell, but some were extruding their contents by direct exocytosis. No myosin light-chain phosphorylation typical for the platelet response was observed after fluoride activation in the presence of aluminium. It has been reported that [AlF4]– impairs the polymerisation-depolymerisation cycle of tubulin (Chabre 1990).
Rapid and dynamic changes of the actin network are of vital importance for the motility of human neutrophils. Bengtsson et al. (1990) observed [AlF4]– induction of a pronounced and sustained increase in a filamentous form of actin in intact human neutrophils. This effect parallels an increase in cytosolic Ca2+ level, indicating that phospholipase C (PLC) is activated.
Shape changes and disorganisation of the spectrin network were observed after addition of 1 mM NaF and 10 µM AlCl3 in human red blood cells (Strunecká et al. 1991). Cells lost their membrane material and became smaller.
Osteoblasts and osteoclasts. Caverzasio et al. (1996) found that traces of aluminium markedly enhanced the stimulation of inorganic phosphate transport induced by fluoride in osteoblasts, suggesting that a fluoroaluminium complex might be responsible for fluoride -induced regulatory pathway. Analysis of the role of tyrosine phosphorylation in mediating this cellular response indicates that this signal transduction pathway is also involved in the stimulation of inorganic phosphate transport activity by fluoride. Aluminium potentiates the effect of fluoride on tyrosine phosphorylation and osteoblast replication in vitro and bone mass in vivo. The combination of fluoride and aluminium modulates a growth factor-dependent tyrosine kinase pathway enhancing mitogen-activated protein kinase and osteoblastic proliferation. Studies in ewes show that at a low dose fluoride stimulates the recruitment and lifespan of osteoblasts; at higher doses, fluoride decreases osteoblast activity (Chavassieux et al. 1991). The hormone calcitonin inhibits osteoclastic bone resorption. The activation of calcitonin involves two separate effects on the osteoclast: abolition of cell motility and marked cellular retraction. [AlF4]– produces both effects. Calcitonin elicited a biphasic elevation of cytosolic calcium level in isolated osteoclasts. Exposure of osteoclasts to [AlF4]–resulted in a marked concentration-dependent inhibition of bone resorption (Moonga et al. 1993).
Energy metabolism. ATP generation in mitochondria requires the association of F1 subunit with F0 transmembrane subunit transporting protons. The binding of ADP and Pi in a catalytic site of F1 triggers conformational changes which lock both of them into the site and induce the formation of pyrophosphate bonds by eliminating a water molecule (Chabre 1990). Lunardi et al. (1988) reported the inhibition of mitochondrial ATPase activity in the presence of [AlF4]–. This inhibition is not reversed by elution of fluoride from solution or by addition of strong chelators of aluminium. No significant release of the complex occured over a period of days. [AlF4]– inhibits many ATPases, phosphatases and phosphorylases. The intervention of aluminofluoride complexes in the energy transformation processes may thus affect the energy metabolism of the entire organism.
III. EVIDENCE FOR IMPLICATION OF ALUMINIUM, FLUORIDE AND ALUMINOFLUORIDE COMPLEXES IN PATHOLOGY
Elevated aluminium levels have been implicated as the cause of dialysis encephalopathy or dementia in renal failure patients after three to seven years of hemodialysis treatment (Alfrey et al. 1976; Meiri et al. 1991). Speech disorders precede dementia and convulsions. The mode of death has been reported as sudden cardiac arrest usually associated with acute pulmonary oedema (Elliot et al. 1978).
Increased serum fluoride concentration and fluoride intoxication have been also observed in chronic hemodialysis patients (Chaleil et al. 1986 ). Arnow et al. (1994) reported that 12 of 15 patients receiving dialysis treatment in one room became acutely ill, with severe pruritus, multiple nonspecific symptoms, and/or fatal ventricular fibrillation (3 patients). Death was associated with longer hemodialysis time and increased age compared with other patients who became ill. Serum concentrations of fluoride in the sick patients were markedly increased to as high as 716 µM. The source of fluoride was the temporary deionization system used to purify water for hemodialysis.
NaF is so far clinically used as the potent stimulator of bone formation. However, there are conflicting reports on the effect of fluoride on trabecular bone formation and bone strength. Osteosclerosis in workers exposed to fluoride and aluminium (industrial fluorosis) led to the use of fluoride as a treatment to increase bone mass in osteoporosis patients. Caverzasio et al. (1996) administered fluoride and aluminium subcutaneously to rats for 8 months. Their results suggest that the combination of fluoride and aluminium modulates a growth factor-dependent tyrosine kinase pathway enhancing mitogen-activated protein kinase and osteoblastic proliferation and bone mass. The authors concluded that these effects are consistent with the crucial role of aluminium in osteosclerosis observed in industrial fluorosis.
Soyseth et al. (1994) investigated the relation between plasma fluoride levels and bronchial responsiveness in a longitudinal study in aluminium potroom workers who reported work-related asthmatic symptoms. A positive association was found between bronchial responsiveness and plasma fluoride levels. Plasma fluoride levels were associated with the total atmospheric fluoride concentration.
The effects of aluminofluoride complexes have been also studied in connection with impairment of blood circulation. As a model for G protein-induced cardiopulmonary dysfunction, fluoride infusion (0.9 mol/l in 0.9% NaCl at 15 µl.kg-1.min-1 for 3 h i.v.) in the presence and absence of AlCl3 (0.6 µg.kg-1.min-1) into pigs anaesthetised with pentobarbital sodium was used (Dodam & Olson, 1995). NaF, with or without AlCl3, induced progressive deterioration of cardiopulmonary function after 1 h of infusion. Recent studies provide evidence that apoptosis of pancreatic cells is important in the early etiology of both type I and type II diabetes mellitus. Loweth et al. (1996) employed fluoride and show that this agent induces apoptosis in clonal pancreatic cells and also in the cells of normal rat islets of Langerhans. The process may reflect the formation of [AlF4]– since it was inhibited by the aluminum chelator deferoxamine.
Conroy et al. (1995) reported that treatment of thymic lobes cells with fluoroaluminate provoked apoptosis of a wider range of thymocyte subtypes. Oguro et al. (1990) studied the cytotoxicity of NaF on fibroblast-like cells from 5 Japanese whole foetuses and found that the growth of the cells was markedly impaired by fluoride. In a living organism, fibroblasts must be able to move into areas of newly forming tissue and to secrete molecules that helps glue together the tissue. Laboratory investigations clearly indicate that both production of extracellular matrix and cell movement can be affected by the action of [AlF4]–.
Because a higher amount of aluminium was found in the human brain with Alzheimer’s disease (AD) than in brains of age-matched healthy controls, the hypothesis that the accumulation of toxic amounts of aluminium in the brain is the cause of neurofibrillary changes and dementia has been discussed very often (McDermott et al. 1979; Zatta et al. 1988; Patocka et al. 1996). A positive correlation between the incidence of Alzheimer’s disease and concentrations of aluminium in drinking water was reported by some authors (Martyn et al. 1989; Flaten 1990). Neither the increased content of aluminium in the brain nor the results of ecological studies can explain why aluminium constitutes a risk. Aluminium is currently regarded as the putative risk factor for the etiology of this disease. The recent fundamental research of pathogenesis of AD has brought evidence that this disease is connected with the alterations in neurotransmission, -amyloid production, plaque formation, and cytoskeletal abnormalities in brain tissue. We suggest that some of pathologic changes are not raised by aluminium alone, but by the aluminofluoride complexes (Strunecká 1999). AD could be an example demonstrating the diversified and multidimensional nature of the integration of the nervous system. However, aluminofluoride complexes may act as the initial signal stimulating impairment of homeostasis, degeneration and death of the cells. By influencing energy metabolism these complexes can accelerate the aging and impair the functions of the nervous system. In respect to the etiology of AD, the long term action of [AlF4]– may represent a serious and powerful risk factor for the development of this devastating disease.
Aluminofluoride complexes appear as a new class of phosphate analogues for laboratory investigations. Experimental data clearly indicate that aluminofluoride complexes may mimic or potentiate the action of numerous extracellular signals and significantly affect many cellular responses. The principle of amplification of the initial signal during its conversion into the functional response has been a widely accepted tenet in cell physiology. Aluminofluoride complexes may therefore act with powerful pharmacological efficacy. The interpretation of laboratory investigations using isolated animal and human cells or tissues on the intact human organism could be discussed. It seems that, in an evolutionary sense, the natural barrier systems such as low aluminium absorption in the gastrointestinal tract, and various physiological ligands, such as transferrin, citrate, phosphate and silicic acid, were efficient buffers preventing the increased intake of this metal in natural conditions (Wilhelm et al. 1990). With the appearance of acid rains and due to the use of aluminium in industry, there has been a dramatic increase in the amount of aluminium appearing in ecosystems, nourishment and water sources (Cooke & Gould 1991). The increasing content of aluminium and fluorides in environment and food chains has raised the possibility that the near future will supply us with more data about the danger of aluminofluoride complexes for the human race.
Supported by Grant Agency of Charles University, Prague (Grant No. 113/1998/BBio/PF).
- Alfrey AC, Le Gendre GR, Kachny WD, The dialysis encephalopathy syndrome. Possible aluminium intoxication. NEJM 1976;294:187-188.
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A health report on drinking water treatment linking Alzheimer‘s mental health disease in the elderly to drinking water treated with aluminium sulphate, alumina, by municiple treatment filtration filter systems.
Aluminum – Why a Concern in Drinking Water?
For years, researchers have puzzled over the surprisingly high levels of aluminum that turn up in the shrivelled brains of Alzheimer’s disease victims. While some scientists believe that the aluminum deposits are only a side effect of Alzheimer’s, a growing number of investigators say that aluminum may play a central role in causing the disease that afflicts mostly elderly people. Aluminum occurs naturally in some waters but is also introduced as aluminum sulphate by some municipal water departments to remove fine particles, colour and bacteria. Municipal water departments usually control the water to a slightly alkaline condition, i.e., pH between 7 and 8. In alkaline conditions aluminum precipitates as fine solid particles, which are then filtered out by means of sand filters. However, sand filters become less efficient for particles as small as 4 to 5 microns and therefore fine particles slip through.
The latest evidence of a link emerged when Australian scientists reported that aluminum used to purify water accumulated in the brains of laboratory rats. The Australian study focused new interest on the issue at a time when Ottawa’s environmental health directorate is preparing to propose Canada’s first national guidelines for aluminum levels in drinking water. The Australian study was important, said the directorate’s chief, Dr. Barry Thomas, because it showed that aluminum in drinking water can be absorbed by the body. “As to whether it actually causes memory loss and brain damage,” added Thomas, “there is not conclusive evidence. But we fear that it may.” Although tiny amounts of aluminum are used in a variety of products, including antacids, antiperspirants, and some processed foods, the metal is pervasively present in drinking water. The reason: municipalities in Canada and other countries often use aluminum sulphate, or alum, to remove mineral particles from water in filtration plants, a process that leaves an aluminum residue in the water.
In the past, studies in Canada and other countries have pointed to links between aluminum and Alzheimer’s. University of Toronto researchers found in a 1991 study that they could slow the rate of deterioration in Alzheimer’s patients by treating them with a drug that removed some aluminum from their brains………
HUDSON WD (1966) Studies of distribution system capacity in seven cities. J. AWWA 58 (2) 157-164. JASIM SY, FRASER JC, HUCK PM, URFER D and ANDERSON WB (1997)
Pilot scale investigation of the reduction of aluminum in drinking water.
Aluminium, which is a neurotoxin, has previously been associated with an increased risk of developing Alzheimer’s.
Fed-up dentists expose the evil practices of modern dentistry: toxic filling, fluoride poisoning and more
WAR ON HEALTH-ALUMINUM IN OUR PILLS-TOXIC CHEMICALS IN EVERYTHING – MEDICINE & FOOD MAKING US ILL – PROFITABLE SLOW KILL!!!
WAR ON HEALTH – The Pharmaceutical Industry has become the #1 cause of disease and death in America by poisoning people with its toxic chemicals, so that they become future revenue generating patients. The FDA receives 40% of their budgets from drug companies! THE FDA IS KILLING AMERICANS EVERY DAY…
Clearly there is enough evidence to question the safety of adding these neurotoxins to our water
The precautionary principle denotes a duty to prevent harm, when it is within our power to do so, even when all the evidence is not in. This principle has been codified in several international treaties to which Canada is a signatory.
by UNESCO, 2005,
(United Nations Educational, Scientific, and Cultural Organization), 2005,
page 14, Box 2
When human activities may lead to morally unacceptable harm that is scientifically plausible but uncertain, actions shall be taken to avoid or diminish that harm. Morally unacceptable harm refers to harm to humans or the environment that is
- threatening to human life or health, or
• serious and effectively irreversible, or
• inequitable to present or future generations, or
• imposed without adequate consideration of the human rights of those affected.
The judgement of plausibility should be grounded in scientific analysis. Analysis should be ongoing so that chosen actions are subject to review. Uncertainty may apply to, but need not be limited to, causality or the bounds of the possible harm.
Actions are interventions that are undertaken before harm occurs that seek to avoid or diminish the harm. Actions should be chosen that are proportional to the seriousness of the potential harm, with consideration of their positive and negative consequences, and with an assessment of the moral implications of both action and inaction. The choice of action should be the result of a participatory process.