Guest guest Posted September 3, 2005 Report Share Posted September 3, 2005 Hi Amy, There are specific water filters made just to remove the fluoride from our water. Fluoride is NOT good--it's toxic and used to be used as RAT poison!!! Fluoride is linked to a severe form of childhood and teenage cancer in boys (I'll see if I can find the reference for this). Fluoride actually causes MORE tooth decay!!! Fluoride was grandfathered in (it was NOT checked for toxicity) because it was already in use as rat poison before the FDA rules regarding testing drugs were put into effect. In short, your dentist is misinformed. There is widespread acceptance for purposely avoiding fluoride among both the autism community, and individuals interested in healthy living. You will notice that a lot of the toothpaste at health food stores if fluoride-free. I'll see if I can find you some more articles about this. Remember, dentists are the same people that put amalgams containing mercury in our teeth!!!!!!!!!!!!!!!!!!!!!!!!!! Dentists take an oath preventing them from advising us to get our amalgams out. UNBELIEVABLE!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! At 04:38 AM 9/3/2005 -0700, you wrote: >Hi everyone: > >My ASD son uses non fluoride toothpaste. I just >visited a pediatric dentist for his first check up and >he was really concerned that my son doesn't get any >fluoride. I explained to him about trying to reduce >his toxic load based on his metals test and that he >gets no chemicals or artificial anything. > >He did understand this and knows some of patients who >are chelating. (he's a special needs dentist) >However, he said of all the patients he >knows...fluoride was never a problem. > >He said that for my sons permanent teeth he needs the >fluoride to keep the enamel strong and to of course, >keep the teeth from decaying. > >Any thoughts on the importance of fluoride for our >kids? Isn't there any " natural " way to prevent >cavities and make teeth strong at the same time? > >thanks. Amy > > > >____________________________________________________ >Start your day with - make it your home page ><http://www./r/hs>http://www./r/hs > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 3, 2005 Report Share Posted September 3, 2005 My little brother died of osteosarcoma when he was 14 due to high fluoride in our municipal water (in So. Cal). THE OBSERVER , LONDON Monday, Jun 13, 2005,Page 6 Fluoride in tap water can cause bone cancer in boys, a disturbing new study indicates, although there is no evidence of a link for girls. New US research suggests that boys exposed to fluoride between the ages of five and 10 will suffer an increased rate of osteosarcoma -- bone cancer -- between the ages of 10 and 19. In the UK, fluoride is added to tap water on the advice of bodies such as the British Dental Association. The Department of Health maintains that it is a cost-effective public health measure that helps prevent tooth decay in children. The increased cancer risks, identified in a newly available study conducted at the Harvard School of Dental Health, were found at fluoride exposure levels common in the US and other countries. It was the first examination of the link between exposure to the chemical at the critical period of a child's development and the age of onset of bone cancer. Although osteosarcoma is rare, accounting for only about 3 percent of childhood cancers, it is especially dangerous. The mortality rate in the first five years is about 50 percent, and nearly all survivors have limbs amputated, usually legs. The research has been made available by the Environmental Working Group (EWG), a respected Washington-based research organization. The group reports that it has assembled a " strong body of peer-reviewed evidence " and has asked that fluoride in tap water be added to the US government's classified list of substances known or anticipated to cause cancer in humans. " This is a very specific cancer in a defined population of children, " said Wiles, the group's co-founder. " When you focus in and look for the incidence of tumors, you see the increase. We recognize the potential benefits of fluoride to dental health, " Wiles said, " but I've spent 20 years in public health, trying to protect kids from toxic exposure. Even with DDT, you don't have the consistently strong data that the compound can cause cancer as you now have with fluoride. " Half of all fluoride ingested is stored in the body, accumulating in calcifying tissue such as teeth and bones and in the pineal gland in the brain, although more than 90 percent is taken into the bones. Anti-fluoride campaigners argue that the whole issue has become highly politically sensitive. If health scares about fluoride were to be recognized in the courts, the litigation, especially in the US, could be expected to run for decades. Consequently, scientists have been inhibited from publicizing any adverse findings. The new evidence only emerged by a circuitous process. It was contained in a Harvard dissertation by Dr Elise Bassin at the Harvard School of Dental Medicine. The dissertation, completed in April 2001, obviously had merit because Bassin was awarded her doctorate. However it has not been published. Environmental organizations were repeatedly denied access to it, and even bodies such as the US National Academy of Sciences could not get hold of a copy. Eventually two researchers from the Fluoride Action Network were allowed to read it in the rare books and special collections room at Harvard medical library. On Sep 3, 2005, at 6:52 AM, R. Owen wrote: > Fluoride is linked to a severe form of childhood and teenage > cancer in boys (I'll see if I can find the reference for this). Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 3, 2005 Report Share Posted September 3, 2005 When my middle son was a baby, his doctor switched him at three months to Poly-Vi- Fluor vitamins instead of Poly-Vi-Sol...only difference, new vitamin contained fluoride. Immediately he developed a chloracne type-rash and even got a sebaceous cyst on his cheek which had to be surgically removed. This alerted me to the fact that fluoride sensitivities were present in my family, and I discovered that large cysts on my own chin which came up and often became infected were only present when I used fluoride toothpaste. My daughter gets the same kind of reaction. It is HARD to find fluoride-free toothpaste sometimes, outside of a health food store. I use Desert Essence tea tree oil kind. When I had a support group for interstitial cystitis patients in upstate NY, one woman had blood tests to determine what delayed (IgG) reactions she had, and the main allergy that was causing her severe bladder pain was fluoride in the water. Another friend was disabled as a child from juvenile arthritis that only came up when they moved into a county with fluoridated water (in NYC I believe), and recovered after she got away from it. I would be tempted to go tell the dentist to go peddle his poisons somewhere else. Peace, Kathy E. > Hi Amy, > > There are specific water filters made just to remove the fluoride from our > water. Fluoride is NOT good--it's toxic and used to be used as RAT > poison!!! Fluoride is linked to a severe form of childhood and teenage > cancer in boys (I'll see if I can find the reference for this). Fluoride > actually causes MORE tooth decay!!! Fluoride was grandfathered in (it was > NOT checked for toxicity) because it was already in use as rat poison > before the FDA rules regarding testing drugs were put into effect. In > short, your dentist is misinformed. > > There is widespread acceptance for purposely avoiding fluoride among both > the autism community, and individuals interested in healthy living. You > will notice that a lot of the toothpaste at health food stores if > fluoride-free. I'll see if I can find you some more articles about > this. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 3, 2005 Report Share Posted September 3, 2005 Hi: Flouride is a neurotoxin. It's great your dentist is sensitive to toxicity in general but perhaps he doesn't know that fluoride has been shown to INCREASE the toxicity of other toxins like aluminum. Am scrambling today - as every day these days - and don't have time to post everything I have but was able to pull this last one up quickly. BTW - Thanks to everyone who responded to my diarrhea question. I like the macaroon suggestion the bestbut didn't get a chance to try it. Josie ___________________________________________________________________ Fluoride 2004;37(4):301-314 Research Review 301 Fluoride 2004;37(4) Dr Blaylock, a Board-certified neurosurgeon, Visiting Professor of Biology at Belhaven College, , Mississippi, and member of the Editorial Board of the Journal of the American Nutraceutical Association (JANA), is the author of three books on excitotoxicity: Excitoxicity: the taste that kills, Health and nutrition secrets, and Natural strategies for cancer patients. EXCITOTOXICITY: A POSSIBLE CENTRAL MECHANISM IN FLUORIDE NEUROTOXICITY L Blaylocka Ridgeland, MS, USA SUMMARY: Recent evidence indicates that fluoride produces neuronal destruction and synaptic injury by a mechanism that involves free radical production and lipid peroxidation. For a number of pathological disorders of the central nervous system (CNS), excitotoxicity plays a critical role. Various studies have shown that many of the neurotoxic metals, such as mercury, lead, aluminum, and iron also injure neural elements in the CNS by an excitotoxic mechanism. Free radical generation and lipid peroxidation, especially in the face of hypomagnesemia and low neuronal energy production, also magnify excitotoxic sensitivity of neurons and their elements. This paper reviews briefly some of the studies that point to a common mechanism for the CNS neurotoxic effects of fluoride and calls for research directed toward further elucidation of this mechanism. Keywords: Aspartate; Excitotoxicity; Fluoride neurotoxicity; Fluoroaluminum complexes; Glutamate; 4-Hydroxynonenal; Melatonin; Neurodegeneration; Peroxynitrite; Reactive nitrogen species; Reactive oxygen species. INTRODUCTION Compelling evidence indicates that fluoride produces injury to the central nervous system (CNS) by several mechanisms. Of particular interest is the ability of fluoride to induce free radical generation and lipid peroxidation in the brain, especially in the hippocampus. In addition, fluoride enhances aluminum absorption from the gastrointestinal mucosa and across the blood-brain barrier. Of particular concern is the recent demonstration that fluoride readily forms a chemical complex with aluminum, similar to the phosphate ion, which is toxic to neurons at low concentrations and can act as an activator of G-proteins, a membrane link to second messenger activation. While it appears that the toxicity of fluoride is secondary to many widely divergent and unrelated processes, there is compelling evidence that a central mechanism may be involved called excitotoxicity (Figure and Table). aFor correspondence: L Blaylock, MD, 315 Rolling Meadows Road, Ridgeland, MS 39157, USA. E-mail: blay6307@... 302 Blaylock Fluoride 2004;37(4) Figure. Possible mechanisms for neurodegenerative effects of fluoride and aluminum as related to excitotoxicity. The broken arrow represents the effects of both elements. In a recent series of papers, I argue that excitotoxicity is also the central mechanism of autism and the Gulf War Syndrome.2-4 The process involves accumulation of acidic amino acids in the synaptic cleft Figure. Possible mechanisms for neurodegenerative effects of fluoride and aluminum as related to excitotoxicity. The broken arrow represents the effects of both elements. WHAT IS EXCITOTOXICITY? Excitotoxicity is a common mechanism seen in many neurological disorders, including strokes, brain trauma, CNS infections, autoimmune disorders, multiple sclerosis, heavy metal toxicity, brain tumors, and the majority of neurodegenerative diseases, such as Alzheimer's dementia, Parkinson's disease, and Lou Gehrig's disease (amyotrophic lateral sclerosis, ALS).1 In a recent series of papers, I argue that excitotoxicity is also the central mechanism of autism and the Gulf War Syndrome.2-4 Fluoride Aluminum Microglial Activation Impair transp Reactive oxygen species and reactive nitrogen species/ Lipid peroxidation products (4-HNE) Reduced GSHPx,G Excitoxicity: a possible central mechanism in fluoride neurotoxicity 303 Fluoride 2004;37(4) The process involves accumulation of acidic amino acids in the synaptic cleft for a prolonged period. These special amino acids include cysteine, cysteine sulfinic acid, cysteic acid, and homocysteine, as well as the neurotransmitters glutamate and aspartate. The neurotransmitters glutamate and aspartate normally activate a series of glutamate receptors on the postsynaptic membrane that leads to neuronal excitation. In fact, glutamate is the most abundant neurotransmitter in the CNS and is responsible for attention, alertness, and learning. It is also the most neurotoxic. If the excitatory amino acids are not removed quickly from the synaptic cleft, the postsynaptic neurons become overstimulated, leading to either synaptic destruction and dendritic retraction or, should the stimulation be prolonged and intense, neuronal destruction by both apoptosis and necrosis.5 It is for these reasons that extracellular glutamate levels are carefully regulated by a series of glutamate transporters, which remove the glutamate for storage, either in the presynaptic neuron terminal or surrounding astrocytes (glia).6 Table. Comparison of the effects of fluoride/aluminium and excitotoxicity Fluoride/Aluminium Excitotoxicity Increased brain reactive oxygen species (ROS) and reactive nitrogen species (RNS) yes yes Increased lipid peroxidation (LPO) yes yes Decreased glutathione yes yes Decreased superoxide dismutase (SOD) yes yes Elevated brain ascorbate yes yes Hippocampal apoptosis necrosis yes yes G-protein activation yes yes Synaptic injury yes yes Impaired glutamate uptake yes yes Microglial activation ? for fluoride yes for aluminium yes ROS in other tissues ? for fluoride yes for aluminium yes DNA injury yes yes 304 Blaylock Fluoride 2004;37(4) This excitotoxic process was originally discovered by two ophthalmologists, Lucas and Newhouse in 19577 and given the name excitotoxicity by Dr Olney in 1969.8 Since its discovery, a great deal has been learned about the mechanism of excitotoxicity, the receptors involved, and the glutamate uptake system. In addition, much has been discovered about other toxins that can activate this destructive process. Recently, glutamate receptors have been found in numerous peripheral tissues, including the testes, lungs, pancreatic islet cells, cardiac nerves, ovaries, endothelial cells, immune cells, and bone osteoblasts.9 COMMON MECHANISMS 1.Free radical generation Glutamate receptors are found in numerous types of neurons, including those that utilize other neurotransmitters, such as GABA (gamma-aminobutyric acid), dopamine, norepinephrine, and serotonin.10 There are two basic types of glutamate receptors, ion-gated channels (ionotrophic) and metabotropic receptors. 11 Three ionotrophic receptor types have been identified, based on their affinity for selective agonists. These include N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and kainate receptors. Neurons frequently contain more than one of these receptors types on the synaptic membranes. The ionotrophic receptors control the passage of sodium, potassium, and calcium through membrane channels, which in turn initiates neuronal depolarization (excitation). Most important to the excitotoxic process is calcium accumulation within the cytosol following glutamate receptor activation. Intracellular calcium triggers numerous cellular reactions including the activation of nitric oxide synthase and protein kinase C.12 These in turn can activate free radical generation and lipid peroxidation as well as eicosanoid activation, should glutamate persist too long in its receptor.13 These processes play a major role in excitotoxic injury and neuronal death. Three types of metabotropic receptors and eight subtypes of these receptors have been identified through cloning techniques. They operate mainly by GTP (guanine triphosphate) binding proteins or G-proteins. 14 When these receptors are stimulated by glutamate, the G-protein within the cell membrane is activated, which in turn activates several second messengers within the neuron, including IP3 (inositol 1,4,5-trisphosphate), cAMP (cyclic adenine monophosphate), or cGMP (cyclic guanine monophosphate). There is also evidence that they regulate intracellular calcium.16 Two of the metabotropic receptors are thought to be neuroprotective and one is capable of triggering excitotoxicity. Free radicals and lipid peroxidation products generated by excitotoxicity have been shown to damage dendrites and synaptic connections, and, if unrelieved, lead to neuronal destruction.16 Likewise, free radicals caused by other processes have been shown to trigger excitotoxicity by impairing glutamate removal and by activating microglia, which contain abundant stores of glutamate.17 Excitoxicity: a possible central mechanism in fluoride neurotoxicity 305 Fluoride 2004;37(4) It has also been shown that one of the lipid peroxidation products, 4-hydroxynonenal (4-HNE), specifically impairs synaptic function and inhibits glutamate removal by the glutamate transport proteins.18 This lipid peroxidation product, though less abundant than malondialdehyde, is significantly more neurotoxic. Any process that precipitates lipid peroxidation also precipitates the production of 4-HNE. Therefore, even if fluoride does not directly trigger excitotoxicity, it will do so indirectly by impairing glutamate removal and by generating reactive oxygen intermediates and lipid peroxidation products. A study from China found that sodium fluoride significantly increased nitric oxide synthase (NOS) activity.19 Interestingly, excitotoxins also stimulated NOS activity, which increases intracellular nitric oxide (NO) content. This is of particular importance because NO combines readily with superoxide forming the very powerfully toxic peroxynitrite radical, which plays a major role in all neurodegenerative diseases, primarily by damaging mitochondrial energy production, inhibiting glutamate re-uptake, and stimulating lipid peroxidation.20- 21 Fluoride has also been shown to inhibit superoxide dismutase, which would increase intracellular levels of the superoxide radical, the substrate for peroxynitrite formation. 22 Another related neurotoxin, aluminum, is known to produce a dramatic increase in brain free radical generation and lipid peroxidation both directly and by increasing neuronal and glial iron levels.23 In addition, melanin has a high affinity for aluminum, making neuromelanin-containing neurons in the substantia nigra pars compacta significantly more vulnerable to free radical and lipid peroxidation injury.24 Aluminum accumulation and focal increases in reactive oxygen species and lipid peroxidation in this nucleus have been demonstrated in Parkinson's disease.25 Another mechanism by which fluoride might increase brain free radical generation and lipid peroxidation would be through activation of protein kinase C by a fluoroaluminum complex. It is known that a major mechanism by which glutamate induces excitotoxicity is activation of protein kinase C. Blocking this enzyme affords significant protection against excitotoxicity. Lead dramatically increases protein kinase C activity in a manner similar to glutamate, thereby triggering excitotoxicity.26 Fluoride, in the form of silicofluorides in drinking water has been found to increase blood lead levels significantly, indicating an indirect connection between fluoride, free radical generation, and excitotoxicity.27 Because of the intimate connection between excitotoxicity, free radical generation, and lipid peroxidation, one can safely assume that fluoride can at least initiate the process indirectly and because of chronic exposure seen with water fluoridation, one would expect an eventual increase in neurodegeneration-associate disorders such as Alzheimer's dementia, ALS, and Parkinson's disease. 2. Inhibition of antioxidant enzymes Closely connected with excitotoxicity-precipitated free radical generation and lipid peroxidation is the eventual depletion of antioxidant defenses. Several stud306 Blaylock Fluoride 2004;37(4) ies have demonstrated that fluoride toxicity, as well as excitotoxic injury, is associated with selective antioxidant depletion.28-30 Fluoride has been shown to inhibit certain antioxidant enzymes and molecules, such as superoxide dismutase (SOD), glutathione reductase, glutathione peroxidase, catalase, and glutathione.31 This would not only increase free radical injury but would also enhance excitotoxicity, since reactive oxygen species as well as nitrogen species and lipid peroxidation products can trigger the excitotoxic process. 32 Antioxidant enzyme inhibition would necessarily enhance the toxicity of other neurotoxic elements, pesticides, herbicides, and environmental pollutants. Another mechanism for magnifying the harmful effects of both fluoride and excitotoxins on the brain would be inhibition of melatonin. Melatonin, a hormone produced by the pineal gland, has been shown to have powerful neutralizing effects on free radicals and lipid peroxidation and to increase the levels of several of the antioxidant enzymes in the brain including SOD, glutathione reductase, glutathione peroxidase, catalase, and glutathione itself.33 A recent study has shown that fluoride significantly inhibits the release of melatonin from the pineal gland and that fluoride accumulates in the gland in very large concentrations in individuals drinking fluoridated water.34 Ironically, glutamate and aspartate also powerfully inhibit melatonin release from the pineal gland and do so by a metabotropic receptor.35 Conceivably, fluoride inhibits release of pineal melatonin by elevating glutamate levels. Since no research has been reported looking for this connection we do not know. A recent study revealed that babies with the lowest melatonin production had the most neurobehavioral problems.36 Melatonin levels are also lower in the cerebrospinal fluid (CSF) of Alzheimer's patients as compared with normal individuals. 37 The fact that fluoride lowers melatonin production would indicate that risk of neurodegeneration in both instances would be elevated.38 3. Inhibition of mitochondrial energy enzymes Another connection between glutamate excitotoxicity and fluoride toxicity is related to inhibition of brain energy production. Several studies have shown that anything which suppresses neuronal energy production, especially mitochondrial energy production, greatly enhances excitotoxic sensitivity.39-41 In fact, when neuronal energy production is low, even physiological levels of excitotoxins such as glutamate can trigger excitotoxicity. Fluoride is also known to inhibit cellular energy producing enzymes, including mitochondrial electron transport enzymes. It does this both directly, as in the case of glycolytic and Kreb's cycle enzymes,42 and indirectly, as in the case of the mitochondrial enzymes by the effect of peroxynitrite.43 Vani and Reddy demonstrated suppression of both antioxidant enzymes and energy generating enzymes in female mice treated with 20 mg of fluoride/kg bw for 14 days.22 The importance of neuronal energy suppression by fluoride lies in the fact that that mitochondrial energy suppression is intimately connected as an early event to neurodegenerative diseases such as Alzheimer's dementia and Parkinson's disExcitoxicity: a possible central mechanism in fluoride neurotoxicity 307 Fluoride 2004;37(4) ease.44-46 Since fluoride can inhibit these enzymes, even in low concentrations, there is an increased likelihood that excitotoxicity plays a significant role in this process. Likewise, it should be appreciated that Mullenix et al have shown that fluoride accumulates in various brain areas of the rat, particularly the hippocampus, resulting in higher fluoride levels in the brain than are seen in the blood.47 The hippocampus is one of the most sensitive areas of the brain to a multitude of neurotoxic events. 4. Inhibition of glutamate transporters One of the most important ways glutamate concentrations are controlled in the nervous system is by a series of glutamate transport proteins. Thus far, five such transporters have been demonstrated by cloning techniques.48 Of particular importance are GLAST (cloned glutamate/aspartate transporter) and GLT-1 (glutamate transporter-1). These transporters are associated with either the glial cells or the neurons themselves. The glial transporters (GLAST and GLT-1) bind to synaptically released glutamate and transport it to the interior of the glial cells. The neuronal transporters bind the glutamate and transfer it to the interior of the presynaptic terminal. Considerable evidence points to impairment of these transporters as major players in neurodevelopmental disorders and neurodegenerative diseases.49 The function of these transporters is altered by a number of commonly encountered toxins including mercury,50 aluminum,51 iron,52 cytokines,53 eicosanoids (PGE2),54 and 4-HNE.55 In fact, mercury has been shown to inhibit the glutamate transporters at concentrations below those that are cytotoxic.56 Anything that increases free radical generation and lipid peroxidation impairs glutamate transport. Aluminum inhibition of glutamate transporters is of special interest because of the frequent and ready interaction of aluminum and fluoride to form a biologically reactive complex. Although no one has apparently examined the occurrence of fluoride-aluminum complexes as the common inhibitor involved, the possibility is quite high. This is because of the chemical avidity of fluoride for aluminum and the fact they frequently occur together in nature. Even without the direct involvement of a fluoroaluminum complex, the fact that fluoride is known to cause a seven-fold increase in the absorption of aluminum past gut barriers is of significant concern.57 In addition, fluoride enhances the passage across the blood-brain barrier. In several studies, fluoride added to drinking water doubled brain aluminum levels, thus increasing the likelihood of glutamate transporter inhibition.58,59 Aluminum glutamate, which is formed in the GI tract, has been shown to alter the blood-brain barrier making it more permeable to normally excluded toxins.60 In addition, it enhanced both aluminum and glutamate concentrations in the brain, significantly increasing the risk of excitotoxicity. 308 Blaylock Fluoride 2004;37(4) THE ALUMINUM-FLUORIDE CONNECTION As mentioned in the introduction, aluminum interacts with fluoride to form a fluoroaluminum complex that mimics phosphate groups in biological systems.61 By this mechanism, it could also activate the G-proteins in cell membranes. As we have seen, the metabotropic receptors are activated by a G-protein mechanism. In addition, numerous cells in the body utilize the G-protein second messenger receptor system, including endothelial cells, lymphocytes, osteoblasts, other neurotransmitters (dopamine, norepinephrine, acetylcholine, serotonin, neuropeptides, and opioids), and glucagon. Activation of metabotropic excitatory receptors by an aluminum-fluoride complex could initiate excitotoxicity as shown by Lan and coworkers.62 Because the aluminum-fluoride complex accumulates in the brain, it would also be expected to cause prolonged neurotoxicity, leading eventually to neurodegeneration and synaptic loss. The aluminum-fluoride complex has been shown to produce neuronal loss in the CA1 and CA-4 areas of the hippocampus when given to animals as 0.5 ppm in drinking water.59 The toxic effect may be related to a combination of effects, including impairment of energy-producing enzymes, impaired dephosphorylation of hyperphosphorylated tau-protein, increased neuronal iron concentration, elevated free radical and lipid peroxidation levels, and impaired DNA repair, all of which are related to excitotoxicity. Another toxic effect of aluminum, and possibly a fluoroaluminum complex, is the activation of microglia. These are resident immune cells within the nervous system, which are normally quiescent, but are easily activated by a number of environmental and biological agents, such as viruses, mycoplasma, bacteria, aluminum, mercury, and several pesticides.63 Once activated, microglia generate and secrete a number of neurotoxic compounds, including two powerful excitotoxins: glutamate and quinolinic acid.64 The combination of excitotoxin secretion and cytokine production greatly increases the concentration of free radicals and lipid peroxidation products in the brain. No one has looked at the possibility of fluoride-induced microglial activation. Yet, one would expect the fluoroaluminum complex to activate microglia, since aluminum alone is a powerful activator.65 Chronic microglial activation has been associated with a number of neurodegenerative processes, including strokes, multiple sclerosis, brain trauma, experimental allergic encephalomyelitis (EAE), Alzheimer's dementia, Parkinson's disease, and ALS.3 Because both aluminum and fluoride accumulate in the brain and have their highest concentrations in the hippocampus and neocortex, one would expect chronic microglial activation as well. At least one study noted reactive gliosis (microglial activation) in association with fluoride brain toxicity.66 Excitoxicity: a possible central mechanism in fluoride neurotoxicity 309 Fluoride 2004;37(4) FLUORIDE: A SPECIAL DANGER TO THE DEVELOPING BRAIN The brain undergoes one of the fastest growth and development rates of any portion of the human body during embryogenesis. This occurs especially during the last trimester and first two years of life, a period called the brain growth spurt. This involves not only the rapid development of synaptic connections (synaptogenesis) and pathway development, but also refinement of all of the synaptic connection made during this period. One way glutamate does this is by stimulating the growth cones that guide neural pathways to their intended destination. The brain develops far greater synaptic connections than are needed during this " brain growth spurt " and as a result, synaptic connections are removed in a process referred to as pruning. Connected to this pruning process, as well as to synaptogenesis and pathway development, is the level of glutamate within the brain. The rise and fall of brain glutamate levels during development controls these processes, and is finely tuned throughout brain development.67 Too much glutamate overprunes the synapses and dendrites, whereas too little results in an excess of un-needed connections.68 Both can result in severe neurodevelopmental problems. Recent studies have revealed that the glutamate transport proteins also play a significant role in the development of the brain.69,70 As shown by these studies, anything that alters transporter function can affect brain development. By interfering with neuronal energy production, neurotransmitter levels (especially glutamate), free radical generation and growth cone function, fluoride can have significant harmful effects on neurodevelopment. In addition, fluoride has also been found to inhibit thyroid function and thereby alter early neuron migration in the developing fetus.71 This can result in irreversible changes in the fetal brain. A CALL FOR FURTHER RESEARCH It is obvious from this short review that more research needs to be done in this area. We need data on both the effects of fluoride and fluoroaluminum on the glutamate transporter proteins and on the exact mechanism of free radical generation being caused by fluoride. In addition, we need studies to see if fluoride can cause chronic microglial activation and neurodegeneration. Because of the growing number of studies showing a strong connection between aluminum accumulation in the brain and neurodegenerative diseases, studies need to be done to see if the aluminum in neurofibrillary tangles and senile plaques is in fact fluoroaluminum. Further studies are also needed to see if fluoroaluminum passes along olfactory axons into the entorhinal area as has been demonstrated for aluminum itself.72 This would not only provide direct access to the area of the brain showing the earliest changes of Alzheimer's dementia, but would allow lower concentrations in the drinking water to produce higher concentrations in the hippocampal area than would be attainable from blood. 310 Blaylock Fluoride 2004;37(4) In addition, special studies are needed using silicofluorides to see if their toxicity to the nervous system differs from that of sodium fluoride. Along this same line, we need data on the possibility of additive and even synergic toxicities when fluoride is combined with mercury, lead, cadmium, and other known neurotoxins. Although progress has been made on nutrient-based neuroprotection against fluoride toxicity, more research needs to be pursued.73-77 Chinoy and Sharma found that both vitamin E and D3 reversed the toxic effect of fluoride on male reproductive organs and that a combination of the two antioxidants completely reversed the toxicity.78 In a recent study, Chinoy and Shah found that a combination of vitamin C and E and calcium could reverse the toxic effects of both fluoride and arsenic on multiple biochemical parameters, including suppression of dehydroascorbic acid, glutathione, glutathione peroxidase, and SOD in the brains of mice.79 If excitotoxicity indeed plays a significant role in fluoride toxicity, we need to apply some of the methods used to protect against excitotoxicity, such as increasing the intake of methylcobalamin, melatonin, selenium, the B vitamins, vitamins C, E, D, and K, along with metabolic stimulants such as pyruvate, malate, CoQ10, acetyl-L-carnitine, R-lipoic acid, and ginkgo biloba. Of special importance is supplementation with magnesium, which has been shown to block the NMDA glutamate receptor and decrease free radical production. One area of particular interest is the use of flavonoids as neuroprotectants. Plant flavonoids are known to be the most versatile and powerful antioxidants known, and one of the few antioxidants that will neutralize peroxynitrite.80 In addition, they can chelate metals, reduce inflammation, block eicosanoid production, and inhibit enzymes such as protein kinase C, which is critical to excitotoxicity and lead neurotoxicity.81 A recent study by Juzyszyn and co-workers found that quercetin sulfonate, a water-soluble form of the flavonoid quercetin, protected liver and kidney cells from ammonium fluoride suppression of mitochondrial energy production.82 Finally, we need more data on the concentration and accumulation of fluoride in other calcified areas of the brain beside the pineal gland. For example, calcification of the basal ganglion is seen in a small number of individuals. In the past, this was considered an asymptomatic condition occurring in 0.3% of the population examined.83 While basal ganglion calcification has been noted in a number of disorders, of particular interest is its appearance in Down's syndrome. One study on autopsied Down's brains found calcification in 45% in the area of the basal ganglion and increased calcification there with increasing age.84 Newer studies have shown that a significant number of these individuals have symptoms related to basal ganglion dysfunction as well as neuropsychiatric disturbances.85 In addition, recent studies has shown that excitotoxicity induces calcification deposits in the brain, which also contain aluminosilicates.86 Should these calcifications accumulate fluoride in high concentrations as found in pineal calcifications, one would expect damage to adjacent neurons and glia. With widespread fluoridation of drinking water, one would also expect higher fluoride concentrations in these calcified structures than in the past. Excitoxicity: a possible central mechanism in fluoride neurotoxicity 311 Fluoride 2004;37(4) It is obvious from this review that there is an intimate connection between the neurotoxicity of fluoride, aluminum, and glutamate that needs further attention. It is also obvious that excitotoxicity plays some role in this process, perhaps a central one. REFERENCES 1 Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurological disorders. N Eng J Med 1994;330:613-22. 2 Blaylock RL. The central role of excitotoxicity in autism spectrum disorders. Journal of the American Nutraceutical Association (JANA) 2003;6:7-19. 3 Blaylock RL. Interaction of cytokines, excitotoxins and reactive nitrogen and oxygen species in autism spectrum disorders. Journal of the American Nutraceutical Association (JANA) 2003;6:21- 35. 4 Blaylock RL Chronic microglial activation and excitotoxicity secondary to excessive immune stimulation: Possible factors in Gulf War Syndrome and autism. Journal of American Physicians and Surgeons 2004;9:46-51. 5 Szatkowski M, Attwell D. Triggering and execution of neuronal death in brain ischemia: two phases of glutamate release by different mechanisms. Trends Neurosci 1994;17:359-65. 6 Jensen AA, Brauner-Osborne H. Pharmacological characterization of human excitatory amino acid transporters EAAT1, EAAT2 and EAAT3 in a fluorescence-based membrane potential assay. Biochem Pharmacol 2004;67:2115-27. 7 Lucas DR, Newhouse JP. The toxic effect of sodium L-glutamate on the inner layers of the retina. AMA Arch Ophthalmol 1957;58:193-201. 8 Olney JW. Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate. Sci 1969; 164:719-21. 9 Hinoi E, Takarada T, Ueshima T, Tsuchihashi Y, Yoneda Y. Glutamate signaling in peripheral tissues. Eur J Biochem. 2004;271:1-13. 10 Trudeau LE. Glutamate co-transmission as an emerging concept in monoamine neuron function. J Psychiatry Neurosci. 2004;29:296-310. 11 Simeone TA, RM, Rho JM. Molecular biology and ontogeny of glutamate receptors in the mammalian central nervous system. J. Child Neurol 2004;19:343-60. 12 Lan JY, Skeberdis VA, Jover T, Grooms SY, Lin Y, Araneda RC, et al. Protein kinase C modulates NMDA receptor trafficking and gating. Nat Neurosci 2001;4:382-90. 13 Babu GN, Bawari M, Ali MM. Lipid peroxidation potential and antioxidant status of circumventricular organs of rat brain following neonatal monosodium glutamate. Neurotoxicology 1994;15:773-7. 14 Minoshima T, Nakanishi S. Structural organization of the mouse metabotropic glutamate receptor subtype 3 gene and its regulation by growth factors in cultured cortical astrocytes. J Biochem (Tokyo) 1999;126:889-96. 15 Baskys A. Metabotropic receptors and 'slow' excitatory actions of glutamate agonists in the hippocampus. Trends Neurosci 1992;15:92-6. 16 Isokawa M, Levesque MF. Increased NMDA responses and dendritic degeneration in human epileptic hippocampal neurons in slices. Neurosci Lett 1991;132:212-6. 17 Pellegrini-Giampietro DE, Cherici G, Alesiani M, Carla V, Moroni F. Excitatory amino acid release from rat hippocampal slices as a consequence of free-radical formation. J Neurochem 1988;51:1960-3. 18 Blanc EM, Keller JN, Fernandez S, Mattson MP. 4-Hydroxynonenal, a lipid peroxidation product, impairs glutamate transport in cortical astrocytes. Glia 1998;22:149-60. 19 Xu S, Shu B, Chen Z. Effect of fluoride on activities of nitric oxide synthase in rat brain [abstract]. Fluoride 2001;34:84. 20 Cassina R, Radi R. Differential inhibitory action of nitric oxide and peroxynitrite on mitochondrial electron transport. Arch Biochem Biophys 1996;328:309-16. 312 Blaylock Fluoride 2004;37(4) 21 Bolanos JP, Almeida A, V, Peuchen S, Land JM, JB. Nitric oxide-mediated mitochondrial damage in the brain: mechanisms and implications for neurodegenerative diseases. J Neurochem 1997:68:2227-40. 22 Vani LM, Reddy KP. Effects of fluoride accumulation on some enzymes of brain and gastrocnemius muscle of mice. Fluoride 2000; 33:17-26. 23 Mundy WR, Freudenrich TM, Kodavanti PR. Aluminum potentiates glutamate-induced calcium accumulation and iron-induced oxygen free radical formation in primary neuronal cultures. Mol Chem Neuropathol 1997;32:41-57. 24 Meglio L, Oteiza PI. Aluminum enhances melanin-induced lipid peroxidation. Neurochem Res 1999;24:1001-8. 25 Good PF, Olanow CW, Perl DP. Neuromelanin-containing neurons of the substantia nigra accumulate iron and aluminum in Parkinson's disease: A LAMMA study. Brain Res 1992;593: 343-6. 26 Naarala JT, Loikkanen JJ, Ruotsalainen MH, Savilainen KM. Lead amplifies glutamate-induced oxidative stress. Free Radic Biol Med 1995;19:689-93. 27 Coplan MJ, Masters RD. Silicofluorides and fluoridation. Fluoride 2001;34: 161-4. 28 Shivarajashankara YM, Shivashankara AR, Bhat GP, Rao SH, Brain lipid peroxidation and antioxidant systems of young rats in chronic fluoride intoxication. Fluoride 2002;35:197-203. 29 Inkielewicz I, Krechniak J Fluoride effects on glutathione peroxidase and lipid peroxidation in rats. Fluoride 2004;37:7-12. 30 Singh K, Ahluwalia P. Studies on the effect of monosodium glutamate [MSG] administration on some antioxidant enzymes in the arterial tissue of adult male mice. J Nutr Sci Vitaminol (Tokyo) 2003; 49:145-8. 31 Li J, Cao S. Recent studies on endemic fluorosis in China [editorial]. Fluoride 1994; 27:125-8. 32 Siesjo BK, Bengtsson F. Calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a unifying hypothesis. J Cereb Blood Flow Metab 1989;9:127-40. 33 Reiter RJ, Tan DX, Osuna C, Gitto E. Actions of melatonin in the reduction of oxidative stress: a review. J Biomed Sci 2000;7:444-58. 34 Luke J. Fluoride deposition in the aged human pineal gland. Caries Res 2001;35: 125-8. 35 Yamada H, Yatsushiro S, Ishio S, Hayashi M, Nishi T, Yamamoto A. Metabotropic glutamate receptors negatively regulate melatonin synthesis in rat pinealocytes. J Neurosci 1998; 18:2056-62. 36 Tauman R, Zisapel N, Laudon M, Nehama H, Sivan Y. Melatonin production in infants. Pediatr Neurol 2002;26:379-82. 37 Lima AC, Louzada PR, De Mello FG, Ferreira ST. Neuroprotection against Abeta and glutamate toxicity by melatonin: are GABA receptors involved? Neurotox Res 2003;5:323-7. 38 Gao HX, Zhang LX. Anatagonistic effects of melatonin on glutamate-induced neurotoxicity in rat hippocampal neurons. Sheng Li Xue Bao 1999;51:430-4. 39 Nicholls DG, Budd SL. Mitochondria and neuronal glutamate excitotoxicity. Biochim Biophys Acta 1998;1366:97-112. 40 Beal MF, Hyman BT, Koroshetz W. Do defects in mitochondrial energy metabolism underlie the pathology of neurodegenerative diseases? Trends Neurosci 1993;16:125-31. 41 Henneberry RC. The role of neuronal energy in neurotoxicity of excitatory amino acids. Neurobiol Aging 1989;10:611-3. 42 Dousset JC, Rioufol C, Philibert C, Bourbon P. Effects of inhaled HF on cholesterol, carbohydrate and trioxycarboxylic acid metabolism in guinea pigs. Fluoride 1987;20:137-41. 43 Ebadi M, Sharma SK. Peroxynitrite and mitochondrial dysfunction in the pathogenesis of Parkinson's disease. Antioxid Redox Signal 2003; 5:319-35. 44 Meltzer CC, Zubieta JK, Brandt J, Tune LE, Mayberg HS, Frost JJ. Regional hypometabolism in Alzheimer's disease as measured by positron emission tomography after correction for effects of partial volume averaging. Neurology 1996;47:454-61. 45 Schapira AH, Gu M, Taanman JW, Tabrizi SJ, Seaton T, Cleeter M, et al. Mitochondria in the etiology and pathogenesis of Parkinson's disease. Ann Neurol 1998;44 Suppl 1:S89-S98. Excitoxicity: a possible central mechanism in fluoride neurotoxicity 313 Fluoride 2004;37(4) 46 Gibson GE, Park LC, Zhang H, Sorbi S, Calingasan NY. Oxidative stress and a key metabolic enzyme in Alzheimer brains, cultured cells, and an animal model of chronic oxidative deficits. Ann NY Acad Sci 1999;893:79-94. 47 Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. Neurotoxicology of sodium fluoride in rats. Neurotoxicol Teratol 1995;17: 169-77. 48 Seal RP, Amara SG. Excitatory amino acid transporters: a family in flux. Annu Rev Pharmacol Toxicol 1999; 39:431-56. 49 Maragakis NJ, Rothstein JD. Glutamate transporters: animal models to neurologic disease. Neurobiol Dis 2004; 15:461-73. 50 s N. Specificity and reversibility of the inhibition by HgCl2 of glutamate transport in astrocyte cultures. J Neurochem 1988; 50:1117-22. 51 Sass JB, Ang LC, Juurlink BH. Aluminum pretreatment impairs the ability of astrocytes to protect neurons from glutamate mediated toxicity. Brain Res 1993;621:207-14. 52 Ueda Y, Willmore LJ. Sequential changes in glutamate transporter protein levels during Fe3+- induced epileptogenesis. Epilepsy Res 2000; 39:201-9. 53 Hu S, Sheng WS, Ehrlich LC, PK, Chao CC. Cytokine effects on glutamate uptake by human astrocytes. Neuroimmunomodulation 2000;7:153-9. 54 Lundy DF, McBean GJ. Pre-incubation of synaptosomes with arachidonic acid potentiates inhibition of [3H] D-aspartate transport. Eur J Pharmacol 1995;291:273-9. 55 Keller JN, Mark RJ, Bruce AJ, Blanc E, Rothstein JD, Uchida K et al. 4-Hydroxynonenal, an aldehydic product of membrane lipid peroxidation, impairs glutamate transport and mitochondrial function in synaptosomes. Neuroscience 1997;80:685-96. 56 Aschner M, Du YL,Gannon M, Kimelberg HK. Methylmercury-induced alterations in excitatory amino acid transport in rat primary astrocyte cultures. Brain Res 1993;602:181-6. 57 Allain P, Gauchard F, Krari N. Enhancement of aluminum digestive absorption by fluoride in rats. Res Commun Mol Pathol Pharmacol 1996;91:225-31. 58 Varner JA, Horvath WJ, Huie CW, Naslund HR, Isaacson RL. Chronic aluminum fluoride administration. I. Behavioral observations. Behav Neural Biol 1994;61:233-41. 59 Varner JA, Jenson KF, Horvath W, Isaacson RL. Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res 1998;784:284-98. 60 Deloncle R, Guillard O, Huguet F, Clanet F. Modification of the blood-brain barrier through chronic intoxication by aluminum glutamate. Possible role in the etiology of Alzheimer's disease. Biol Trace Elem Res 1995;47:227-33. 61 Strunecka A, Strunecky O, Patocka J. Fluoride plus aluminum: useful tools in laboratory investigations, but messengers of false information. Physiol Res 2002;51:557-64. 62 Lan JY, Skeberdis VA, Jover T, Zheng X, MV, Zukin RS. Activation of metabotropic glutamate receptor 1 accelerates NMDA receptor trafficking. J Neurosci 2001;21:6058-68. 63 Thoulmond S, Parnet P, Linthorst AC. When cytokines get on your nerves: cytokine networks and CNS pathologies. Trends Neurosci 1996;19:409-10. 64 Tavares RG, Tasca CL, Santos CE, Alves LB, Porciuncula LO, Emanuelli T, et al. Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes. Neurochem Int 2002;40:621-7. 65 Tsunoda M, Sharma RP. Modulation of tumor necrosis factor alpha expression in mouse brain after exposure to aluminum in drinking water. Arch Toxicol 1999;73:419-26. 66 Shivarajashankara YM, Shivashankara AR, Bhat PG, Roa SM, Roa SH. Histological changes in the brain of young fluoride-intoxicated rats. Fluoride 2002;35:12-21. 67 Komuro H, Rakic P. Modulation of neuronal migration by NMDA receptors. Science 1993;260:95- 7. 68 Marret S, Gressens P, Evarard P. Arrest of neuronal migration by excitatory amino acids in hamster developing brain. Proc Natl Acad Sci USA 1996;93:15463-8. 69 Bar-Peled O, Ben-Hur H, Biegon A, Groner Y, Dewhurst S, Furuta A. Distribution of glutamate transporter subtypes during brain development. J Neurochem 1997;69:2571-80. 314 Blaylock Fluoride 2004;37(4) 70 Shibata T, Watanabe M, Tanaka K, Wada K, Inoue Y. Dynamic changes in expression of glutamate transporter mRNAs in developing brain. Neuroreport 1996;7:705-9. 71 Trabelsi M, Guermazi F, Zeghal N. Effect of fluoride on thyroid function and cerebellar development in mice. Fluoride 2001;34:165-73. 72 Perl DP, Good PF. Uptake of aluminum into central nervous system along nasal-olfactory pathways. Lancet 1987;1:1028. 73 Susheela AK, Bhatnagar M. Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants. Mol Cell Biochem 2002;234- 235:335-40. 74 Guna Sherlin DM, Verma RJ. Vitamin D ameliorates fluoride-induced embryotoxicity in pregnant rats. Neurotoxicol Teratol 2001;23:197-201. 75 Verma RJ, Sherlin DM. Vitamin C ameliorates fluoride-induced embryotoxicity in pregnant rats. Hum Exp Toxicol 2001:619-23. [abstract in Fluoride 2002;35:131]. 76 Chinoy NJ, Sequeira E, Narayana MV. Effects of vitamin C and calcium on the reversibility of fluoride- induced alterations in spermatozoa of rabbits. Fluoride 1991;24:29-39. 77 Gupta SK, Gupta RC, Seth AK, Gupta A. Reversal of fluorosis in children. Acta Paediatr Jpn 1996;38:513-9. 78 Chinoy NJ, Sharma A. Amelioration of fluoride toxicity by vitamins E and D in reproductive functions of male mice. Fluoride 1998;31:203-16. 79 Chinoy NJ, Shah SD. Biochemical effects of sodium fluoride and arsenic trioxide toxicity and their reversal in the brain of mice. Fluoride 2004;37(2):80-7. 80 Blaylock RL. Neurodegeneration and aging of the central nervous system: prevention and treatment by phytochemicals and metabolic nutrients. Integrative Med 1998;1:117-33. 81 Blaylock RL. New developments in the prevention and treatment of neurodegenerative diseases using nutraceuticals and metabolic stimulants. Journal of the American Nutraceutical Association (JANA) 2002;5:15-32. 82 Juzyszyn Z, Czerny B, Myoeliwiec Z, Put A, Enhancement of kidney and liver respiratory activity by quercetin sulfonates in rats chronically exposed to ammonium fluoride. Fluoride 2002;35: 161- 7. 83 Marasco JA Jr, Feczko WA. Basal ganglia calcification in Down's syndrome. Comput Tomogr 1979;3:111-3. 84 Takashima S, Becker LE. Basal ganglia calcification in Down's syndrome. J Neurol Neurosurg Psychiatry 1985;48:61-4. 85 Chiu HF, Lam LC, Shum PP, Li KW. Idiopathic calcification of the basal ganglia. Postgrad Med J 1993;69:68-70. 86 May N, Prats A, Riveros A, Andres N, Bernal F. Basal ganglia calcification induced by excitotoxicity: an experimental model characterized by electron microscopy and X-ray microanalysis. Acta Neuropathol (Berl) 1999;98:217-25. Published by the International Society for Fluoride Research http://homepages.ihug.co.nz/~spittle/fluoride-journal.htm Editorial Office: 727 Brighton Road, Ocean View, Dunedin 9051, New Zealand Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 4, 2005 Report Share Posted September 4, 2005 i refuse to use flouride in our toothpaste. i have read it is extremely bad for you on mercola.com i believe and also in natural cures they don't want you to know. i use spry toothpaste with xylitol. xylitol is a natural antibacterial and helps to promote healthy teeth. you can google xylitol to get info on it, there are many good things about it. you can also add some to thier juices and bake with it. jenny > Hi everyone: > > My ASD son uses non fluoride toothpaste. I just > visited a pediatric dentist for his first check up and > he was really concerned that my son doesn't get any > fluoride. I explained to him about trying to reduce > his toxic load based on his metals test and that he > gets no chemicals or artificial anything. > > He did understand this and knows some of patients who > are chelating. (he's a special needs dentist) > However, he said of all the patients he > knows...fluoride was never a problem. > > He said that for my sons permanent teeth he needs the > fluoride to keep the enamel strong and to of course, > keep the teeth from decaying. > > Any thoughts on the importance of fluoride for our > kids? Isn't there any " natural " way to prevent > cavities and make teeth strong at the same time? > > thanks. Amy > > > > ____________________________________________________ > Start your day with - make it your home page > http://www./r/hs Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 4, 2005 Report Share Posted September 4, 2005 My daughter,too goes to a pediatric/special needs dentist and he agreed that fluoride wasn't needed. In fact, he went so far as to say he wouldn't even push toothpaste-just brushing (we use the toddler fluoride free paste.) He offered to give my daughter flavor-free toothpaste and to not use flavoring in the glue stuff she needed to attach something in her mouth...we tasted the NASTY stuff though and told him to go ahead and add some flavor. ICK! --- In , Amy Allnutt <aallnutt2004@y...> wrote: > Hi everyone: > > My ASD son uses non fluoride toothpaste. I just > visited a pediatric dentist for his first check up and > he was really concerned that my son doesn't get any > fluoride. I explained to him about trying to reduce > his toxic load based on his metals test and that he > gets no chemicals or artificial anything. > > He did understand this and knows some of patients who > are chelating. (he's a special needs dentist) > However, he said of all the patients he > knows...fluoride was never a problem. > > He said that for my sons permanent teeth he needs the > fluoride to keep the enamel strong and to of course, > keep the teeth from decaying. > > Any thoughts on the importance of fluoride for our > kids? Isn't there any " natural " way to prevent > cavities and make teeth strong at the same time? > > thanks. Amy > > > > ____________________________________________________ > Start your day with - make it your home page > http://www./r/hs Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 6, 2005 Report Share Posted September 6, 2005 > He did understand this and knows some of patients who > are chelating. (he's a special needs dentist) > However, he said of all the patients he > knows...fluoride was never a problem. I have read some really nasty regression stories about fluoride. These sites will have more info and research etc http://www.slweb.org/ http://www.flouridealert.org/ http://www.nofluoride.com/ Dana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 6, 2005 Report Share Posted September 6, 2005 Hi Amy, , either of you in the UK and can tell me the contact details for your dentist? My Son's teeth are full of plaque and I think its as a result of combating a huge bacteria problem he's had (we had a 2week course of oral vancomycin, and that's when the discolouration set in. PS Flouride - no way would I let it near my son. Can't remember where I read this but it affects our kids like Chloride. Perhaps Dana has a view on this . All I know is its bad bad bad and we won't have it in our house! Eileen and ASD aged 3 david_j_mead <david_j_mead@...> wrote: My daughter,too goes to a pediatric/special needs dentist and he agreed that fluoride wasn't needed. In fact, he went so far as to say he wouldn't even push toothpaste-just brushing (we use the toddler fluoride free paste.) He offered to give my daughter flavor-free toothpaste and to not use flavoring in the glue stuff she needed to attach something in her mouth...we tasted the NASTY stuff though and told him to go ahead and add some flavor. ICK! --- In , Amy Allnutt <aallnutt2004@y...> wrote: > Hi everyone: > > My ASD son uses non fluoride toothpaste. I just > visited a pediatric dentist for his first check up and > he was really concerned that my son doesn't get any > fluoride. I explained to him about trying to reduce > his toxic load based on his metals test and that he > gets no chemicals or artificial anything. > > He did understand this and knows some of patients who > are chelating. (he's a special needs dentist) > However, he said of all the patients he > knows...fluoride was never a problem. > > He said that for my sons permanent teeth he needs the > fluoride to keep the enamel strong and to of course, > keep the teeth from decaying. > > Any thoughts on the importance of fluoride for our > kids? Isn't there any " natural " way to prevent > cavities and make teeth strong at the same time? > > thanks. Amy > > > > ____________________________________________________ > Start your day with - make it your home page > http://www./r/hs Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 6, 2005 Report Share Posted September 6, 2005 If you really want to clean his teeth and avoid a dentist altogether try a Sonic Care toothbrush. They aren't too expensive and they really do work, even with just water. I love them because they make my teeth feel like I had been to the dentist. And yes, flouride is really bad...we don't use it either. JMO! Eileen McLennan <eileen_mclennan@...> wrote: Hi Amy, , either of you in the UK and can tell me the contact details for your dentist? My Son's teeth are full of plaque and I think its as a result of combating a huge bacteria problem he's had (we had a 2week course of oral vancomycin, and that's when the discolouration set in. PS Flouride - no way would I let it near my son. Can't remember where I read this but it affects our kids like Chloride. Perhaps Dana has a view on this . All I know is its bad bad bad and we won't have it in our house! Eileen and ASD aged 3 david_j_mead <david_j_mead@...> wrote: My daughter,too goes to a pediatric/special needs dentist and he agreed that fluoride wasn't needed. In fact, he went so far as to say he wouldn't even push toothpaste-just brushing (we use the toddler fluoride free paste.) He offered to give my daughter flavor-free toothpaste and to not use flavoring in the glue stuff she needed to attach something in her mouth...we tasted the NASTY stuff though and told him to go ahead and add some flavor. ICK! --- In , Amy Allnutt <aallnutt2004@y...> wrote: > Hi everyone: > > My ASD son uses non fluoride toothpaste. I just > visited a pediatric dentist for his first check up and > he was really concerned that my son doesn't get any > fluoride. I explained to him about trying to reduce > his toxic load based on his metals test and that he > gets no chemicals or artificial anything. > > He did understand this and knows some of patients who > are chelating. (he's a special needs dentist) > However, he said of all the patients he > knows...fluoride was never a problem. > > He said that for my sons permanent teeth he needs the > fluoride to keep the enamel strong and to of course, > keep the teeth from decaying. > > Any thoughts on the importance of fluoride for our > kids? Isn't there any " natural " way to prevent > cavities and make teeth strong at the same time? > > thanks. Amy > > > > ____________________________________________________ > Start your day with - make it your home page > http://www./r/hs Quote Link to comment Share on other sites More sharing options...
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