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Dentists Oppose Fluoridation; You Should Too
Two hundred and eleven dentists signed a statement asking Congress to
ban water fluoridation. And, according to the Wealthy Dentist, 15% of dentists oppose water fluoridation. Professionals Urge End to Water Fluoridation New York - February 24, 2008 -- In a statement first released August 9, 2007, almost 2,000 professionals urge Congress to stop water fluoridation until Congressional hearings are conducted. They cite new scientific evidence that fluoridation, long promoted to fight tooth decay, is ineffective and has serious health risks. (http:// http://www.fluorideaction.org/statem...gust.2007.html) Signers include a Nobel Prize winner, three members of the prestigious 2006 National Research Council (NRC) panel that reported on fluoride's toxicology, two officers in the Union representing professionals at EPA headquarters, the President of the International Society of Doctors for the Environment, and hundreds of medical, dental, academic, scientific and environmental professionals, worldwide. Signer Dr. Arvid Carlsson, winner of the 2000 Nobel Prize for Medicine, says, "Fluoridation is against all principles of modern pharmacology. It's really obsolete." An Online Action Petition to Congress in support of the Professionals' Statement is available on FAN's web site, www.fluorideaction.org/congress .. "The NRC report dramatically changed scientific understanding of fluoride's health risks," says Paul Connett, PhD, Executive Director, Fluoride Action Network. "Government officials who continue to promote fluoridation must testify under oath as to why they are ignoring the powerful evidence of harm in the NRC report," he added. An Assistant NY State Attorney General calls the report "the most up- to-date expert authority on the health effects of fluoride exposure." The Professionals' Statement also references: -- The new American Dental Association policy recommending infant formula NOT be prepared with fluoridated water. -- The CDC's concession that the predominant benefit of fluoride is topical not systemic. -- CDC data showing that dental fluorosis, caused by fluoride over- exposure, now impacts one third of American children. -- Major research indicating little difference in decay rates between fluoridated and non-fluoridated communities. -- A Harvard study indicating a possible link between fluoridation and bone cancer. -- The silicofluoride chemicals used for fluoridation are contaminated industrial waste and have never been FDA- approved for human ingestion. The Environmental Working Group (EWG), a DC watchdog, revealed that a Harvard professor concealed the fluoridation/bone cancer connection for three years. EWG President Ken Cook states, "It is time for the US to recognize that fluoridation has serious risks that far outweigh any minor benefits, and unlike many other environmental issues, it's as easy to end as turning off a valve at the water plant." Further, researchers reporting in the Oct 6 2007 British Medical Journal indicate that fluoridation, touted as a safe cavity preventive, never was proven safe or effective and may be unethical. (1) Partially, as a result of the professionals' statement, at least one city, Cobleskill NY, stopped 54 years of water fluoridation. See: http://www.fluoridealert.org/news/2998.html In New York State, the Central Bridge Water District stopped fluoridation in 2006, Homer in 2005, Canton in 2003. Oneida rejected fluoridation in 2002. Ithaca rejected fluoridation in 2002. Johnstown rejected it in 1999. Before that several towns in Nassau County stopped fluoridation. Suffolk County rejected fluoridation in the 1990's. Many communities rejected or stopped fluoridation over the years. See: http://www.fluoridealert.org/communities.htm On October 2, Juneau Alaska voters rejected fluoridation despite the American Dental Association's $150,000 political campaign to return fluoride into the water supply after the legislative body voted it out. References: (1) "Adding fluoride to water supplies," British Medical Journal, KK Cheng, Iain Chalmers, Trevor A. Sheldon, October 6, 2007 |
#2
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Fluoride damages the mitochondira, the compartment within cells that converts food into useable energy. Below article indicates fluoride damages the oral gum cells' mito. Involvement of both mitochondrial- and death receptor-dependent apoptotic pathways regulated by Bcl-2 family in sodium fluoride- induced apoptosis of the human gingival fibroblasts. Sodium fluoride (NaF) has been shown to be cytotoxic and produces inflammatory responses in humans. However, the cellular mechanisms underlying the NaF-induced cytotoxicity in periodontal tissues are unclear. This study examined whether or not NaF induces apoptosis in human gingival fibroblasts (HGF), and its underlying mechanisms by monitoring various apoptosis-associated processes. NaF reduced the cell viability of HGF in a dose- and time-dependent manner. NaF increased TUNEL-positive cell and induced apoptosis with concomitant chromatin condensation and DNA fragmentation in HGF. In addition, NaF increased the level of cytochrome c released from the mitochondria into the cytosol, enhanced the caspase-9, -8 and -3 activities, the cleavage of poly (ADP-ribose) polymerase (PARP), and up-regulated the voltage-dependent anion channel (VDAC) 1. However, NaF did not affect the production of reactive oxygen species (ROS) which is a strong apoptotic inducer. Furthermore, NaF up-regulated the Fas-ligand (Fas- L), a ligand of death receptor. Bcl-2, a member of the anti-apoptotic Bcl-2 family, was down-regulated, whereas the expression of Bax, a member of the pro-apoptotic Bcl-2 family, was unaffected in the NaF- treated HGF. These results suggest that NaF induces apoptosis in HGF through both the mitochondria-mediated pathways regulated by the Bcl-2 family and death receptor-mediated pathway. PMID: 18069112 |
#3
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates the mito of cells that create tooth enamel are damaged by fluoride. Ultrastructural morphometric analysis of ameloblasts exposed to fluoride during tooth development. Since a considerable amount of the world population is exposed to high doses of fluoride, it is of special concern to investigate its action mechanisms during dental enamel development. In this study, the toxicity of fluoride in ameloblasts during enamel development was evaluated by means of ultrastructural morphometric analysis. A total of 18 male Wistar rats were distributed into three groups. In Group I, the animals received deionized drinking water ad libitum (negative control) and in Groups II and III, they received sodium fluorided (NaF) drinking water at doses of 7 and 100 ppm ad libitum, respectively, for 6 weeks. Morphometric data were expressed as volume density of the most significant organelles present in the secretory and maturation phases of amelogenesis such as RER, granules, lysosomes, phagic vacuoles, microfilaments and mitochondria. The results showed that the volume density of mitochondria in the 100 ppm experimental group was 29% (P 0.05) higher than the control group in secretory ameloblasts. No remarkable differences were found in maturation ameloblasts for all organelles evaluated. Taken together, these data indicate that NaF at high doses is able to induce cellular damage in secretory ameloblasts, whereas no noxious effect was observed during maturation stage of amelogenesis as depicted by ultrastructural analysis. PMID: 17077986 |
#4
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride damages mito of rat liver cells. Effect of fluoride on activities of enzyme and ultrastructure in primary cultured rat hepatocytes OBJECTIVE: To study the cell viability, activities of enzyme and ultrastructure changes induced by sodium fluoride in primary cultured rat hepatocytes. METHODS: Hepatocytes were isolated using half-in situ collagenase digestion method. Cellular viability was determined by MTT method. The activities of ALT and AST were determined by spectrophotography method. The ultrastructure changes of hepatocyte were observed under transmission electron microscope. RESULTS: After cultured with various concentrations of fluoride for 24 hours, a dose- dependent decrease of cell viability was detected in the hepatocytes. The activities of AST and ALT in the 2 mmol/L and 4 mmol/L groups were significantly higher than the control group (P 0.05). Transmission electron microscope study showed that in fluoride treated hepatocytes the changes included swollen mitochondria and disordered, disrupted endoplasm reticulum. CONCLUSION: Excessive fluoride induced significant toxicity in primary cultured hepatocytes which manifested the injuries of membrane and organell plasma membrane. PMID: 15862017 |
#5
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride damages mito of rat liver and pancreas cells. Ultrastructural study of the mitochondria in the submandibular gland, the pancreas and the liver of young rats, exposed to NaF in drinking water. The aim of the experiment was to determine the effect of fluoride on ultrastructural changes in the submandibular gland, the pancreas and the liver. The experimental rats received fluoride in aqueous solutions of sodium fluoride at concentrations of 10.6 NaF/dm3 and 32.0 NaF/dm3. In the ultrastructural examination, mitochondria were most damaged. PMID: 15638415 |
#6
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates that fluoride derivates can be used to damage mito thus cause cell death. Fluoride curcumin derivatives: new mitochondrial uncoupling agents. The mitochondrial effects of two fluoride curcumin derivatives were studied. They induced the collapse of mitochondrial membrane potential (DeltaPsi), increased mitochondrial respiration, and decreased O(2)*- production and promoted Ca(2+) release. These effects were reversed by the recoupling agent 6-Ketocholestanol, but not by cyclosporin A, an inhibitor of the permeability transition pore (PTP), suggesting that these compounds act as uncoupling agents. This idea was reinforced by the analysis of the physico-chemical properties of the compounds indicating, that they are mainly in the anionic form in the mitochondrial membrane. Moreover, they are able to induce PTP opening by promoting the oxidation of thiol groups and the release of cytochrome c, making these two molecules potential candidates for induction of apoptosis. PMID: 15225605 |
#7
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride fed animals performed poorly in performance tests due to mito damage in brain cells. Neurotoxicity of fluoride: neurodegeneration in hippocampus of female mice. Light microscopic study of hippocampal sub-regions demonstrated significant number of degenerated nerve cell bodies in the CA3, CA4 and dentate gyrus(Dg) areas of sodium fluoride administered adult female mice. Ultrastructural studies revealed neurodegenrative characteristics like involution of cell membranes, swelling of mitochondria, clumping of chromatin material etc, can be observed in cell bodies of CA3, CA4 and dentate gyrus (Dg). Fluoride intoxicated animals also performed poorly in motor co-ordination tests and maze tests. Inability to perform well increased with higher fluoride concentration in drinking water. PMID: 12622200 |
#8
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride derivates damage mito in rabbit kidney cells. Fluoride ion toxicity in rabbit kidney thick ascending limb cells. BACKGROUND AND OBJECTIVE: Some halogenated agents, especially methoxyflurane, because of a higher level of fluoride production, induce a renal concentrating defect that could be related to an ascending limb impairment. We investigated the mechanisms of fluoride toxicity on an immortalized cell line. METHODS: Cells were cultured for 2, 6 or 24 h in the presence of fluoride. Toxicity evaluation was based on: cell numbers, protein content, leucine-incorporation, lactate dehydrogenase (LDH) and N-acetyl-beta-glucosaminidase (NAG) releases, Na-K-ATPase and Na-K-2Cl activities, electron microscope studies. Infrared analysis and fluoride microdetermination allowed crystal components. RESULTS: At 5 mmol after 24 h, fluoride decreased cell numbers (-14%, *P 0.05), protein content (-16%*), leucine incorporation (-54%*), Na-K-2Cl activity (-84%*), increased LDH (+145%*) and NAG release (+190%*). Na-K-ATPase was more sensitive and impaired from 1 mmol for 24h and after 2 h at 5 mmol. Crystal formation in mitochondria occurred after 6 h at 5 mmol. Infra-red analysis and fluoride microdetermination established that crystals contained sodium, phosphate and fluoride. CONCLUSIONS: The results suggest that the Na-K-ATPase pump is a major target for fluoride toxicity in Henle's loop. PMID: 12095014 |
#9
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride damages of mito of human tooth pulp cells. Cytotoxicity of fluoride on human pulp cell cultures in vitro. OBJECTIVES: Numerous studies have revealed that conventional glass- ionomer cements might release fluoride into an aqueous environment. The objective of this study was to examine the effects of fluoride on human pulp cells in vitro. STUDY DESIGN: H33258 fluorescence, cell proliferation, protein synthesis, and mitochondrial activity assay were used to investigate the pathobiological effects of fluoride on cultured human pulp cells. RESULTS: Fluoride was found to be a cytotoxic agent to cultured human pulp cells by inhibiting cell growth, proliferation, mitochondrial activity, and protein synthesis. CONCLUSIONS: Fluoride release has significant potential for pulpal toxicity. PMID: 11174602 |
#10
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Dentists Oppose Fluoridation; You Should Too
Professionals Urge End to Water Fluoridation
Below abstract indicates fluoride derivative inhibits mito function in cows. Structure of bovine mitochondrial F(1)-ATPase inhibited by Mg(2+) ADP and aluminium fluoride. BACKGROUND: The globular domain of the membrane-associated F(1)F(o)- ATP synthase complex can be detached intact as a water-soluble fragment known as F(1)-ATPase. It consists of five different subunits, alpha, beta, gamma, delta and epsilon, assembled with the stoichiometry 3:3:1:1:1. In the crystal structure of bovine F(1)- ATPase determined previously at 2.8 A resolution, the three catalytic beta subunits and the three noncatalytic alpha subunits are arranged alternately around a central alpha-helical coiled coil in the gamma subunit. In the crystals, the catalytic sites have different nucleotide occupancies. One contains the triphosphate form of the nucleotide, the second contains the diphosphate, and the third is unoccupied. Fluoroaluminate complexes have been shown to mimic the transition state in several ATP and GTP hydrolases. In order to understand more about its catalytic mechanism, F(1)-ATPase was inhibited with Mg(2+)ADP and aluminium fluoride and the structure of the inhibited complex was determined by X-ray crystallography. RESULTS: The structure of bovine F(1)-ATPase inhibited with Mg(2+)ADP and aluminium fluoride determined at 2.5 A resolution differs little from the original structure with bound AMP-PNP and ADP. The nucleotide occupancies of the alpha and beta subunits are unchanged except that both aluminium trifluoride and Mg(2+)ADP are bound in the nucleotide- binding site of the beta(DP) subunit. The presence of aluminium fluoride is accompanied by only minor adjustments in the surrounding protein. CONCLUSIONS: The structure appears to mimic a possible transition state. The coordination of the aluminofluoride group has many features in common with other aluminofluoride-NTP hydrolase complexes. Apparently, once nucleotide is bound to the catalytic beta subunit, no additional major structural changes are required for catalysis to occur. PMID: 10873854 |
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