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Re: Fluoride - Demand AARP Take Action

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Dr. Sauerheber for your barely legible response.  

 

For the m-teenth time now, could you please provide a link and a citation to an FDA website in which the FDA calls optimally fluoridated water a "drug?"  Since this was the entire premise of your rant, that would be necessary to back up what you were trying to say.

 

You haven't been able to provide such evidence before, so I don't expect miracles now.

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Re: Fluoride - Demand AARP Take Action

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Hi David,

 

Such good questions.  Unfortunately, you seem to either fail to read my posts or read so fast you miss the answers.  I have responded repeatedly on your two questions.  Please slow down and read carefully.

 

To your first question on how to do a prospective RCT, consider several options.  

a.   Easiest to do an RCT with fluoride pills  The intent of fluoridation is to increase fluoride exposure (increase background dosage).  Fluoride pills have the same alleged benefit as putting the fluoride pill in water and swallowing the water.   In other words, have two sets of pills, one a fluoride pill and another a placebo pill.  Give the pills to people and keep track of who gets which pill  If an RCT were done with pills and demonstrated effective at a specific dosage and safe at that dosage, FDA approval could be applied for and approved.   Make swallowing fluoride legal with FDA approval.   If fluoride pills were legal, promoters of fluoridation would have a rather strong case.   The biggest problem would be to gain ethical approval.  With so many studies demonstrating harm, I doubt a university human studies ethics board would approve the study.   If an RCT is unethical, certainly forcing people to ingest the fluoride without consent should be questioned.

 

b.  There are communities in the North of Canada/Alaska and other remote communities in countries where water is trucked to the community.  A prospective RCT could be done with these communities. Again, the biggest hurdel would be ethics approval.  Too many studies showing harm.

 

David, we put a man on the moon, certainly we can make the swallowing of fluoride with the intent to prevent disease. . . legal and supported by the best of science.  The biggest problem to an RCT would be ethics.

 

To your second question of why fluoride used with the intent to prevent disease requires FDA approval.

 

   FDA approval is required by both Federal and all state laws.    21 USC 321 (g)(1)(B) states, "Articles intended for use in the . . . prevention of disease."   

 

The intent of fluoride is to prevent dental caries, a disease.   

If one argues that fluoride is not a drug, then fluoride is regulated under poison laws.  However, fluoride is exempt from poison laws when regulated under drug laws.  No exemption is made when diluted with water.

 

Fluoride is listed as a drug in all Pharmacopias and laws define drugs as those listed in the US Pharmacopia.

Fluoride is called a drug by the FDA.  See FDA.gov.   You can contact the FDA and ask the FDA if ingestion of fluoride is FDA approved whether in pills or liquids or disolved in water.

 

Note:  Drug Digest in 1975 notified 35 fluoride manufacturers:  

“. . .there is no substantial evidence of drug effectiveness as prescribed, recommended or suggested in its labeling. . . marketing is in violation of the new drug provisions of the Federal Food, Drug, and Cosmetic Act; they have, therefore, requested that marketing of these products be discontinued.”        

 

Read the FDA web site on Drug approval.  See FDA.gov Look under "drugs."  Then look at resources on the left side.   Look at how the FDA defines "drugs."  No exception to a drug just because it is diluted with water.  The intent of use defines the substance as a drug.

 

Now look at your toothpaste.  If fluoride is added, the toothpaste has a label, "Drug Facts."

Fluoride is approved in toothpaste with the label "Do Not Swallow."   Because, swallowing fluoride is not approved.

 

Now look at the Safe Drinking Water Act:

 

SDWA: “No national primary drinking water regulation may require the addition of any substance for preventive health care purposes unrelated to contamination of drinking water. ”42 USC 300g-1(b)(11):

 

For clarity, I asked the EPA and EPA in a FOIA request responded,

“The Safe Drinking Water Act prohibits the deliberate addition of any substance to drinking water for health-related purposes other than disinfection of the water.”

                                                                 FOIA Request HQ-FOI-01418-10 

 

Some have suggested they are simply adjusting the natural concentration of fluoride in water, and that is true.  But the intent, saying again, "INTENT" of use makes fluoride a drug and drugs are under FDA jurisdiction.   If fluoride were added to kill bacteria, then it would be legal, but fluoride is added to prevent disease.

 

At one time the natural concentration of lithium concentration was considered.  Lithium was considered so safe, safe for everyone, and would help those in need.  But lithium addition to water was stopped because it is a drug and found not safe for everyone.

 

Many other substances are found naturally in water but are not safe in larger quantities, concentrations.

 

Thanks for your questions, go to FDA.gov and they have much more.

 

Bill Osmunson DDS MPH

 

 

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Re: Fluoride - Demand AARP Take Action

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This has been addtessed repeatedly in earlier posts. The FEW  ruled that fluoride added into water is an uncontrolled use of an unapproved dtug. 

And regardless of whether one prefers  to call fluoride , which is added to treat human tissue , either a drug or a supplement, is irrelevant since the FDA has sole authority to regulate both drugs and supplements -- regardless of the method of dissemination.

Some argue fluoride is,a food but the FDA ruled that fluoride is not considered safe to add to foods.

Current FDA staff considers fluoride to be a toxic agent under  the toxic substances control act and that the EPA needs to deal with the problem, while  the EPA states that fluoride is added to mitigate caries and thus needs to be regulated by the FDA. Neither agency currently regulates fluoridation. 

This ,is  all old news.

 

 

Richard Sauerheber, Ph.D.
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Re: Fluoride - Demand AARP Take Action

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Message 814 of 1,417

Dr. Bill, 

 

Could you remind us all again how you would undertake an RTC with community water fluoridation?  

 

And why exactly would the practice of community water fluoridation need FDA approval?  Correct me if I am wrong, but aren't we talking about optimally fluoridated water?  Could you show me anywhere on this FDA regulated product (bottled water - the FDA has regulatory authority over bottled water because it is considered a "food") where the word "Drug," or the phrase "Drug Facts" are used?  This is the label from a bottle of optimally fluoridated water.

 

https://nutritiondata.self.com/facts/beverages/9231/2

 

Could you please cite any Federal Regulatory Authority which considers optimally fluoridated water a "Drug"?

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Re: Fluoride - Demand AARP Take Action

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CarryAnne,

 

Thank you for those studies.

 

No one actually reading the research regarding the dosage of fluoride we are getting and the serious harm to our brains from too much fluoride would promote ingesting even more fluoride.  Makes no sense to intentionally harm brains.

 

Combine the current fluoride neurotoxic studies along with past studies and fluoridation will and must stop.  

 

To make matters worse, some attempt to reassure us that fluoride is effective in mitigating dental caries.  Unfortunately the research makes claims more by default, estimates, and assumptions rather than good research evidence.  The claim is often, "caries declined, so the effect must have been fluoride."   

 

It is time for promoters to provide RCT studies and gain FDA approval, show the evidence or stop forcing people to ingest excess fluoride.  

 

Bill Osmunson DDS MPH

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Re: Fluoride - Demand AARP Take Action

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It's not even half way through the month, and look at the newest studies damning fluoridation as a public harm policy in just the past few days. 

 

THYROID: 18% of people drinking 'optimally' fluoridated water in Canadian communities at risk of low thyroid function because fluoride interferes with iodine. Many of them will be sub-clinical and do not know they have low thyroid, which nevertheless increases their risk for diabetes, high cholesterol, and other problems. Overall 9% of the population is diagnosed with low thyroid. 

https://www.sciencedirect.com/science/article/pii/S016041201830833X

 

PREGNANT WOMEN: Pregnant Canadian women drinking  'optimally' fluoridated water had twice the fluoride exposure per individual testing as compared to pregnant women in non-fluoridated communities - and consistent with the range in the Mexican women whose children had up to 6 points lowered IQ based on prenatal exposure to fluoride (from salt).  https://www.sciencedirect.com/science/article/pii/S0013935116302808

 

LEARNING DISABILITIES: Over 200 children who were individually tested had attention deficit disorder apparently caused by their prenatal exposure to fluoride. This is the 3rd report out of the NIH sponsored 12 year study that seems to have been designed with the intention of showing no ill effect, but instead has three times to date confirmed low dose prenatal exposure to fluoride consistent with exposure in 'optimally' fluoridated communities causes subtle but permanent brain damage. https://www.sciencedirect.com/science/article/pii/S0160412018311814

 

OVERDOSED BABIES: Over one third of babies (37%) in fluoridated American communities consume in unsafe amounts of fluoride in excess of the upper limits of fluoride considered safe per government regulations. Even 4 % of babies in non-fluoridated communities also are overdosed on fluoride. At the very least, this puts these children at high risk for developing dental fluorosis, mottled teeth, a condition associated with more learning disabilities, broken bones and kidney disease. http://jocpd.org/doi/10.17796/1053-4625-43.1.7 

 

GOVERNMENT BIAS: A National Toxicology Program’s animal experiment used the wrong rats, the wrong dose, and the wrong study design in order to manufacture a finding of no prenatal or postnatal effect, apparently in an effort to protect policy instead of people. https://www.sciencedirect.com/science/article/pii/S0306987718308600

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Re: Fluoride - Demand AARP Take Action

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Message 817 of 1,417

Johnny,

 

Further to the list of studies below evaluating the mechanism of fluoride's neurotoxicity, here are a few studies specifically affecting the fetus.  These become even more significant when we add the Bashash et al study https://www.ncbi.nlm.nih.gov/pubmed/28937959 and their conclusion:

 

"CONCLUSIONS:

In this study, higher prenatal fluoride exposure, in the general range of exposures reported for other general population samples of pregnant women and nonpregnant adults, was associated with lower scores on tests of cognitive function in the offspring at age 4 and 6-12 y. https://doi.org/10.1289/EHP655."

 

They did not report a "no effect" urine fluoride concentration.   

 

Johnny, science has demonstrated for years that brain damage is happening to the developing brain from the increased fluoride exposure caused by fluoridation.  

 

 

 

FETUS

Mechanism of Low Learning and Memory Abilities: Niu (2014)“Both fluoride and lead can cross the blood-brain barrier and produce toxic effects on the central neural system, resulting in low learning and memory abilities, especially in children. In order to identify the proteomic pattern in the cortex of young animals, from the beginning of fertilization to the age of postnatal day 56, pregnant female mice and pups were administrated with 150 mg sodium fluoride/L and/or 300 mg lead acetate/L in their drinking water. Two-dimensional electrophoresis (2-DE) combined with mass spectrometry (MS) was applied to identify differently expressed protein spots. Results showed that there were eight proteins in the cortex that significantly changed, whose biological functions were involved in (1) energy metabolism (Ndufs1, Atp5h, Atp6v1b2), (2) cytoskeleton (Spna2, Tuba1a, Tubb2a), (3) glycation repair (Hdhd2), and (4) cell stress response (Hspa8). Based on the previous and current studies, ATPase, Spna2, and Hspa8 were shared by fluoride and lead both as common target molecules.”

 

Potential Toxicity: NRC (2006) p 164, In general, average cord blood concentrations are approximately 60% of maternal serum concentrations, with proportionally lesser amounts present as higher maternal serum concentrations. . . . Therefore potential toxicity to the developing embryo and fetus in the setting of high maternal ingestion of fluoride has been a concern evaluated in both animal and humans.” 

 

Harm to Fetus: Yu (1996 and English 2008) “The mothers of the ten fetuses that formed the subject group for this study all had dental fluorosis, with a corresponding increase in urinary fluoride, indicating that these pregnant women were suffering from chronic fluoride poisoning. The excess fluoride of the mother was passed through the placental barrier into the fetus, and from there through the blood-brain barrier to accumulate in the fetal brain, leading to a significant rise in bone and brain fluoride levels. Our results are consistent with earlier reports. Previous experiments have shown that the brains of fetuses from endemic fluorosis areas as well as fluoride-poisoned rats manifest morphological changes. Following experimental testing of the monoamine neurotransmitters in fetuses from fluorosis endemic areas, the present study found lowered levels of norepinephrine and elevated levels of epinephrine. The presence of norepinephrine in the brain allows the organism to become alert, and guards against the intensification of reflex reactions and other behavior. Norepinephrine also plays a role in the regulation of complex response mechanisms, emotions, cerebrocardiovascular function, etc. When norepinephrine levels drop the ability to maintain an appropriate state of activation in the central nervous system is weakened. The elevated levels of epinephrine could be due to a blockage of the pathway that transforms epinephrine into norepinephrine or possibly due to suppression of the relevant metabolic enzymes, causing the brain levels of epinephrine to increase, and the levels of norepinephrine to decrease.”

 

Mechanism of Harm to Fetus:  Dong (1993) “The contents of five types of amino-acid neurotransmitters and three types of monoamine neurotransmitters in the brains of fetuses aborted through induced labor in a chronic fluorosis-endemic area were determined. Findings revealed that the content of the excitatory amino acid, aspartic acid, was significantly lower than in the fetuses from the non-endemic area whereas the content of the inhibitory amino acid, taurine, was significantly higher; the content of the major spinal cord-inhibitory glycine was significantly reduced. Among the monoamine neurotransmitters, the content of norepinephrine was significantly reduced; the contents of 5-hydroxytryptamine in the frontal and the occipital lobes were elevated and the content of 5-hydroxytryptamine in the parietal lobe (precentral and postcentral gyri) was reduced.”

 

Harm to Fetus with Stunted Neuronal Development: Du (1992) “It is known that fluoride can cross the placenta from the mother’s blood to the developing fetus. However, the theory there is a direct link between fluoride effects and brain cell damage is still controversial due to lack of adequate evidence. In order to determine if there are any adverse effects on the developing human brain, especially starting from formation of the embryo, fetuses from an endemic fluorosis area at the 5th–8th month of gestation were compared with those from a non-endemic area. RESULTS: Normal Purkinje cells from the non-endemic fluorosis area were observed in single or parallel lines and were well organized in the fetal cerebellum. Purkinje cells of fetuses from the endemic fluorosis area were abnormally disorganized and had a thicker granulated layer in the cerebellum. Other dysmorphology, including higher nucleus-cytoplasm ratio of brain cones, hippocampus cones, and Purkinje cone cells, supports the theory that fluoride has an adverse effect on brain development. SEM analysis also found reduced neurons of brain cortex, decreased numerical density, volume density, and surface density in those fetuses from the endemic fluorosis area. In summary, the passage of fluorine through the placenta of mothers with chronic fluorosis and its accumulation within the brain of the fetus impacts the developing central nervous system and stunts neuron development.

 

Toxic to Nerve Development:  Li (2004) “The effects of excessive fluoride intake during pregnancy on neonatal neurobehavioral development and the neurodevelopment toxicity of fluoride were evaluated. Ninety-one normal neonates delivered at the department of obstetrics and gynecology in five hospitals of Zhaozhou County, Heilongjiang Province, China were randomly selected from December 2002 to January 2003. The subjects were divided into two groups (high fluoride and control) based on the fluoride content in the drinking water of the pregnant women. . . . There were significant differences in the neonatal behavioral neurological assessment score and neonatal behavioral score between the subjects in the endemic fluoride areas and the control group. . . . [N]eurobehavioural capability and agonistic muscle tension from the high fluoride group were impaired, resulting in a statistically significant lower overall (total) assessment score than in the control group (p<0.05). . . . [V]arious neurobehavioral capabilities, such as non-biological visual, biological visual, and auditory directional reactions of the neonates from the high fluoride group lagged behind those of the control group with differences that are statistically significant (p<0.05). . . . NBNA examination can help to detect mild damage to brain functions. The results of the examination indicate that high fluoride levels can cause adverse effects in the neurobehavioral development of neonates. . . . The present observations indicate that fluoride, as a toxic material to nerve development, can have an adverse impact on the neurobehavioral development of neonates and can cause abnormal changes of neurobehavioral capability during the neonate period with a negative impact on the future development of both the body and intelligence of the neonate. Therefore, in endemic fluoride areas, great effort should be made to reduce fluoride level in the water.

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Re: Fluoride - Demand AARP Take Action

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Message 818 of 1,417

Johnny,

 

I've pulled together a few research studies on the mechanism of fluoride neurotoxicity.  As toxiclologists and scientists know, a key aspect to understanding toxicity of a substance is to understand the mechanism of how the substance affects the body, organs and cells.    Due to limits on space, here are a few incomplete clips from studies for your consideration.  Although brief, you will get the idea. . . .

 

 

Mechanism, Low Glucose Utilization and Neurodegnerative changes:  Jiang (2014) “Fluorine, a toxic and reactive element, is widely prevalent throughout the environment and can induce toxicity when absorbed into the body. This study was to explore the possible mechanisms of developmental neurotoxicity in rats treated with different levels of sodium fluoride (NaF). The rats’ intelligence, as well as changes in neuronal morphology, glucose absorption, and functional gene expression within the brain were determined using the Morris water maze test, transmission electron microscopy, small-animal magnetic resonance imaging and Positron emission tomography and computed tomography, and Western blotting techniques. We found that NaF treatment-impaired learning and memory in these rats. Furthermore, NaF caused neuronal degeneration, decreased brain glucose utilization, decreased the protein expression of glucose transporter 1 and glial fibrillary acidic protein, and increased levels of brain-derived neurotrophic factor in the rat brains. The developmental neurotoxicity of fluoride may be closely associated with low glucose utilization and neurodegenerative changes.”

 

If fluoride reduces glucose utilization, would fluoride increase obesity?  Just asking.   Good research project.

 

Mechanism: Object Recognition Memory: Han (2014) “This study aimed to investigate the effects of long-term fluoride exposure on object recognition memory and mRNA expression of soluble N-ethylmaleimidesensitive fusion protein attachment protein receptors (SNARE) complex (synaptosome-associated protein of 25 kDa (SNAP-25), vesicle-associated membrane protein 2 (VAMP-2), and syntaxin 1A) in the hippocampus of male mice. . . . Taken together, these results indicated that long-term fluoride administration can enhance the excitement of male mice, impair recognition memory, and upregulate VAMP-2 mRNA expression, which are involved in the adverse effects of fluoride on the object recognition memory of nervous system.”

 

Mechanism of Neurodegenerative diseases:  Pal (2014) “Fluoride, a well-established environmental carcinogen, has been found to cause various neurodegenerative diseases in human. Sub-acute exposure to fluoride at a dose of 20mg/kgb.w./day for 30 days caused significant alteration in pro-oxidant/anti-oxidant status of brain tissue as reflected by perturbation of reduced glutathione content, increased lipid peroxidation, protein carbonylation, nitric oxide and free hydroxyl radical production and decreased activities of antioxidant enzymes. . . .  Resveratrol was found to inhibit changes in metabolic activities restoring antioxidant status, biogenic amine level and structural organization of the brain. Our findings indicated that resveratrol imparted antioxidative role in ameliorating fluoride-induced metabolic and oxidative stress in different regions of the brain.”

 

 

Mechanism of Harm and Amelioration of Harm:  Sardar (2014)  “Beneficial effects of oleanolic acid on fluoride-induced oxidative stress and certain metabolic dysfunctions were studied in four regions of rat brain. Male Wistar rats were treated with sodium fluoride at a dose of 20 mg/kg b.w./day (orally) for 30 days . Results indicate marked reduction in acidic, basic and neutral protein contents due to fluoride toxicity in cerebrum, cerebellum, pons and medulla. DNA, RNA contents significantly decreased in those regions after fluoride exposure. A. . .  Appreciable counteractive effects of oleanolic acid against fluoride-induced changes in protein and nucleic acid contents, proteolytic enzyme activities and other oxidative stress parameters indicate that oleanolic acid has potential antioxidative effects against fluoride-induced oxidative brain damage.”

 

Mechanism of Known Harm: Hamza (2015) “Sodium fluoride (NaF) intoxication (brain, kidney, liver, oxidative stress, reproductive toxicity, testes, anti-oxidants) is associated with oxidative stress and altered antioxidant defense mechanism.”  

 

Mechanism of Known Damage: Zhang (2015) “To explore the mechanisms by which chronic fluorosis damages the brain, we determined the levels of the advanced glycation end-products (AGEs), the receptor for AGE (RAGE), NADPH oxidase-2 (NOX2), reactive oxygen species (ROS) and malondialdehyde (MDA) in the brains of rats /and or SH-SY5Y cells exposed to different levels of sodium fluoride (5 or 50ppm in the drinking water for 3 or 6 months and in the incubation medium for as long as 48hr, respectively).. . . In conclusion, our present results indicate that excessive fluoride can activate the AGE/RAGE pathway, which might in turn enhance oxidative stress.”

 

Mechanism of Locomotor Activity, Exploratory Behavior Suppression, Spacial Learning and Memory Loss:  Zhang (2015)  “Results showed that in rats with chronic fluorosis compared with the controls, locomotor activity and exploratory behavior were significantly or very significantly suppressed, spatial learning and memory ability were significantly declined;. synaptic membrane fluidity and the protein level of PSD-95 of hippocampus were greatly decreased. The data indicated that the changes of synaptosome membrane fluidity and PSD-95 expression level in hippocampus might be the one synaptic mechanism of learning-memory injury induced by chronic fluorosis in brain.”

 

Mechanism of Deficit in Learning and Memory: Dong (2014): “To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. . . . Our results suggest that the mechanism for the deficits in learning and memory of rats with chronic fluorosis may be associated with the decreased expressions of M1 and M3 in mAChRs, in which the changes in the receptors might be the result of the high level of oxidative stress occurring in the disease.”

 

Mechanism of Central Neural System Injury: Niu (2014) “Fluoride and lead are two common pollutants in the environment. Previous investigations have found that high fluoride exposure can increase the lead burden. In this experiment, in order to study on the molecular mechanisms of central neural system injury induced by the above two elements, differently expressed protein spots in hippocampus of male mice treated with 150 mg sodium fluoride/L and/or 300 mg lead acetate/L in their drinking water were detected by two-dimensional electrophoresis (2-DE) and mass spectrometry (MS). The behavior tests showed that 56 days of fluoride and lead administration significantly reduced the vertical activity and lowered the memory ability of mice. In addition, results of 2-DE and MS revealed that nine spots demonstrated above a twofold change in the same trend in all treatment groups, which were mainly related with (1) energy metabolism, (2) cell stress response/chaperones, (3) cytoskeleton development, (4) protein metabolism, and (5) cell surface signal transduction. The findings could provide potential biomarkers for lesion in nervous system induced by fluoride and lead exposure.”

 

Mechanism of Apoptosis: Lou (2014) “The aim of the study was to investigate the influence of chronic fluorosis on apoptosis and the expression of Bax and Bcl-2 in the cerebral cortices of rats in an attempt to elucidate molecular mechanisms. . . . The results showed that the animal model of chronic fluorosis was successfully established in the study. In the cortices of the rat brains with chronic fluorosis, as compared to controls, the percentage of apoptotic neurons was significantly increased, with a dose-dependent tendency between the rate of apoptosis and the F contents in drinking water. The expression of Bax and Bcl-2, at both the protein and mRNA levels, was clearly elevated in the rat brains with chronic fluorosis. . . . .”

 

Mechanism of Neurotoxicity: Zhou (2014) “A significant decrease of TGF-B1 was found, in both the gene and protein levels, while no significant change occurred in the levels of IL-4, IL-1B, IL-6, and TNF-a gene. Fluoride may damage the hippocampus by significantly decreasing the expression of TGF-B1 gene and protein, possibly by an unknown post-transcriptional mechanism. . . . .”

 

Mechanism and Known Harm:  Reddy (2014) “Aims: This study was designed to evaluate the effect of sodium fluoride (NaF) in inducing neuroimmunological, oxidative and antioxidative damage. . . .  Results: Increase in the NaF concentration resulted in increased fluoride deposition in brain tissue. This increased fluoride content led to increased levels of certain neurotransmitters such as epinephrine, histamine, serotonin and glutamate and decreased levels of norepinephrine, acetylcholine and dopamine in a dose-dependent manner. NaF exposure led to the decrease in the levels of CD4, NK cells and IgG1 coupled with marked increase in lipid peroxidation and impairment of the antioxidative defense system.  Conclusion: The result of the study emphasizes the toxic role of high NaF doses on the neurological and immunological functions.”

 

Chromosomal anomalies and Primary DNA Damage: Tiwari (2010) “Our study has supported the role of As [arsenic] and F [fluoride] as potent genotoxic agents, since in vitro exposure of both caused increased chromosomal anomalies along with primary DNA damage, in human peripheral blood cultures.”

 

Known Harm Measured by Deficits in Attention, Auditory Retention, Physicial Dexterity and Acuity and Emotional States:  Guo (2001, English translation 2008) “In recent years, the damage fluoride inflicts on nonskeletal organs, and in particular the nervous system, has received a great deal of attention. . . .  RESULTS: The results of the NCTB testing in this investigation revealed significant differences among the fluoride-exposed groups for various indices as compared to reference standards and the controls, with particular deficits in attention, auditory retention, and physical dexterity and acuity as well as abnormal emotional states.  . . . There is a definite relationship between the damage caused by fluoride and the level of exposure.”

 

Mechanism of DNA Damage: Zhang (2008) “Some recent studies have suggested that DNA damage may be a potential neurotoxic mechanism of fluoride. The tail length, as measured by an ocular micrometer, is increased in fluoride-treated human embryonic hepatocytes in a previous study carried out to investigate the geneotic effect of fluoride (Wang et al., 2004). In the present study, we performed OTM and percentage of DNA in the tail as indices of DNA damage. OTM, multiplication of the tail length and percentage of DNA in the tail, objectively and sensitively reflects the effect of fluoride on DNA damage. Our findings showed that fluoride-induced DNA damage and OTM was more a sensitive measure than percentage of DNA in the tail. The correlation analysis showed a positive correlation between ROS formation and OTM level (r2=0.583, P < 0.05), which indicated that ROS might play an important role in the course of DNA damage.”

 

Known Genotoxic: Zhang (2009) “Twenty four agents were used to evaluate this screening assay. We selected the agents, ranging from DNA alkylating agents, oxidative agent, radiation, DNAcross- linking agent, nongenotoxic carcinogens, precarcinogenic agents, which included . . . sodium fluoride, acrylamide . . . . The results showed that all 20 tested known carcinogenic and genotoxic agents were able to induce gadd153-Luc expression at a sublethal dose.. . . .”

 

Known Genotoxic, Mutagenic, Teratogenic: Ercivas (2009) “In this study we concluded that NaF, in 5 and 10 lg/ml NaF concentrations cause genotoxic alterations. So genotoxic, mutagenic and teratogenic effects of NaF need to be carefully screened and evaluated together with other long-term effects using in vitro and in vivo animal test models.”

 

Mechanism of Known DNA Damage: Wang(2004)“As cells were exposed to higher doses of fluoride, the percentage of L-02 cells with DNA damage increased. This result is consistent with other studies... Therefore, considering previous studies, we think that fluoride can cause lipid peroxidation, DNA damage and apoptosis, and that there is a positive relationship among these changes.”

 

Mechanism of Known Harm: Aardema (1989) “Based on these results and those previously reported for NaF and APC, it is proposed that NaF-induced aberrations may occur by an indirect mechanism involving the inhibition of DNA synthesis/repair.”

 

Mechanism of Known Harm: Lasne (1988) “Sodium fluoride was found to induce morphological transformation of SHE cells seeded on a feeder layer of X-irradiated cells at high concentrations (75-125 micrograms/ml). When the cells were seeded in the absence of a feeder-layer, the transformation frequencies increased in a dose-dependent manner with the concentrations of sodium fluoride ranging from 0 to the highly toxic concentration of 200 micrograms/ml. In the BALB/3T3 cell system, sodium fluoride was negative in the standard Kakunaga procedure, while through the experiment designed by table L8 (2(7] of the orthogonal method, an initiating-like effect and a weak promoting activity were detected within the concentrations ranging from a 25 micrograms/ml to a 50 micrograms/ml concentration which is highly toxic for BALB/3T3 cells. From these results, it is suggested that, besides a genetic mode of action, sodium fluoride could possibly act through a non-genotoxic mechanism.”

 

Known Mutagenic: 1990 NTP “In summary, sodium fluoride is mutagenic in cultured mammalian cells and produces transformation of Syrian hamster cells in vitro. The reports of in vivo cytogenetic studies are mixed, but the preponderance of the evidence indicates that sodium fluoride can induce chromosome aberrations and sister chromatid exchanges in cultured mammalian cells. These mutagenic and clastogenic effects in cultured cells are supported by positive effects in Drosophila germ cell tests that measure point mutations and chromosome breakage. In vivo tests in rodents for chromosome aberrations provide mixed results that cannot readily be resolved because of differences in protocols and insufficient detail in some study reports to allow a thorough analysis. The mechanism(s) by which these effects result from exposure to sodium fluoride is not known.”

 

Preponderance of Evidence: 2001 Bassin “The effects of fluoride as a mutagen, carcinogen, and antimutagen are inconsistent, but the preponderance of evidence in cultured mammalian cells indicate that sodium fluoride can induce chromosome aberrations and sister chromatid exchanges.”

 

Known DNA Damage: Chen (2000) “To investigate the effects of fluoride on DNA damage as well as the effects of selenium and zinc against fluoride respectively or jointly in pallium neural cells of rats, single cell gel electrophoresis was used to detect the DNA damage of neural cells prepared in vitro. The results showed that the degree of DNA damage in the fluoride group and the selenium group were significantly greater than that in control group (P < 0.01). The damage in the fluoride group was even more serious. The damage in the fluoride + selenium group and fluoride + zinc group was slighter than that in the fluoride group but with no significant difference. The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group(P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively.

 

Known Genotoxic Rivedal (2000) ”In the present work, 13 compounds [chlordane, Arochlor 1260, di(2-ethylhexyl)phthalate, 1,1,1-trichloro-2, 2-bis(4-chlorophenyl)ethane, limonene, sodium fluoride, ethionine, o-anisidine, benzoyl peroxide, o-vanadate, phenobarbital, 12-O-tetradecanoylphorbol 13-acetate and clofibrate] have been tested for their ability to induce morphological transformation and affect intercellular communication in Syrian hamster embryo (SHE) cells... In vitro morphological transformation of SHE cells is now one of the most frequently used cell transformation systems. Around 500 chemicals have been tested in this system, and a good correlation has been obtained with the ability of compounds from different chemical groups to cause tumours in animals and humans. The SHE cell transformation assay also responds to tumour promoters and carcinogens not detected by tests for genotoxicity... [N]ine of the 13 tested substances (TPA, o-vanadate, DEPH, phenobarbital, Arochlor 1260, clofibrate, o-anisidine, limonene and NaF) are considered positive for induction of morphological transformation.” 

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Re: Fluoride is Neurotoxic - Demand AARP Take Action

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Message 819 of 1,417

Johnny,

 

Background:  

 

Too many are ingesting too much fluoride.  60% of adolescents show signs, biomarker, of excess fluoride exposure.

 

 

A. A recent review of fluoride for the Irish Department of Health, Sutton (2015).   “The evidence base examining the association between health effects and community water fluoridation is scarce”  and “Having examined the evidence, and given the paucity of studies of appropriate design, further research, would be required in order to provide definitive proof. . . .“    

 

For 70 years Governments have continued to dispense fluoride based on a “paucity of studies of appropriate design.”  Intentional fluoride exposure under police powers, solely for therapeutic intent, should be suspended until such proof of efficacy and safety is provided.  

 

B. The Public Health Service recommendation in 2015 (PHS 2015) estimates about 60% of fluoride exposure for adults and 40%-70% for children is from water fluoridation.  The PHS (2015) does not mention infants on formula with fluoridated water who would get close to 100% of their fluoride from water at 0.7 ppm or greater. 

 

C. There are some streams of evidence the FDA should consider which are fundamental to common sense even though they may not fit within a prescribed research format such as PECO and protocol approach, such as intent of use, lack of physiologic requirement, ethics, mother’s milk, and the FDA’s withdrawal of NDA and fluoride dental products’ warnings, etc.

1. For example, mother’s milk: Only the NRC 2006 report seriously addressed mother’s milk which has undetectable fluoride in most samples and mean concentration of 0.004 ppm.  Infants on formula made with 0.7 ppm fluoridated water are ingesting 175 times more fluoride than mother’s milk.   Perhaps the survival of our species has been dependent on mother’s milk.  The paucity of high quality studies on fluoride’s safety and efficacy do not outweigh the historical record of mother’s milk.  Mother’s milk is considered the nutritional standard for infants against which all other substitutes are judged.  Reviewers of science usually omit or avoid the most fundamental, historical, obvious scientific evidence of nature’s dosage of fluoride for infants, in part because dosage of 175 times more than mother’s milk of a highly toxic substance without consent sounds hellish.  

The undisputed evidence of the virtual lack of fluoride in mother’s milk must be the dosage considered optimal for infants unless overwhelming proof that mother’s milk is deficient or defective is provided. 

 

CDC reports about 13% of infants are exclusively breast fed through six months.

Hujoel (2009) provides the graph below confirming an increase of dental fluorosis in formula fed infants.

 

Primarily, English speaking Government agencies dispense fluoride with assumed dental caries reduction and without any high quality studies.  Yet promoters  demand high quality “proof” of harm.  

 

2. Another stream of evidence  is the FDA . The FDA requires a label (variable wording) on fluoride toothpaste because fluoridated toothpaste makes a therapeutic claim that it “helps protect against cavities.  Fluoride is a drug,   The label says, “Drug Facts.”  “do not swallow,” use a “pea size.”  The pea size pictured is about twice the size the FDA is referring to.  A pea size of toothpaste has 0.25 mg of fluoride, the same as each  glass of fluoridated water.  Diluting a quarter milligram of fluoride in a glass of public water does not make the fluoride safe. 

 

Governments do not make sense when they warn not to swallow the same amount of fluoride as they require each person to swallow in each glass of water.

 

 

3. We should consider Congress as a stream of evidence.  

“21 U.S.C. 321 CHAPTER II—DEFINITIONS (g)(1) The term "drug" means (A) articles recognized in the official United States Pharmacopoeia, official Homoeopathic Pharmacopoeia of the United States, or official National Formulary, or any supplement to any of them;”  Sodium Fluoride is listed in the 2007 US Pharmacopoeia pages 3194-3196.   Congress and the President have clearly defined drugs, and fluoride is listed as one of the drugs.  Fluoride is exempt from Federal and state “poison” and “highly toxic” laws as a drug and not exempt as a food. State Board’s of Pharmacy have determined fluoride is a drug.

 

The ingestion of fluoride with the intent to mitigate dental caries is not approved by the FDA CDER and is therefore an unapproved drug.

 

D. Reviews of potential harm from fluoride ingestion have a selection criteria usually limited to human studies and usually conclude, “Ecological studies are not adequate to infer causality.”  

 

Reviews have in part been a house of cards, narrow in focus, assumed efficacy, and/or failed to consider evidence from all streams of evidence. 

 

E. Prospective Randomized Controlled Human Trials (RCT) testing children to see how much, for example, their IQ decreases, at various ages, dosages, synergistic chemicals, health status and nutritional variables would certainly increase confidence but would be unethical.  Determining the toxicological endpoint of chemicals such as fluoride for a public health (population wide) non contagious disease by dispensing of toxicants requires a significant factor of uncertainty to protect everyone, especially when benefit is controversial.  Therefore, the FDA should review the science with the premise, “if in doubt, do no harm.”

 

F. Ethically, clinical evidence for efficacy for toxic substances administered with therapeutic intent must be a different scientific standard and methodology than evidence of safety and harm for random or unavoidable toxins.   Fluoride is different than an industrial toxic product because it is administered by Governments without individual consent, label or legend and without efficacy and toxicity oversight. 

 

 

G. “Weight of evidence” for an ecological study maybe stronger than an individual study when the bigger picture is evaluated such as: sample size, precision of measurements, choosing an appropriate sample, avoiding biases such as confounders, age, gender, race of cohorts, objective or subjective evidence, etc.   

 

 

 

H. Current human studies have centered on IQ as a measurement tool of neurotoxicity for humans.  Rocha-Amador (2009) reminds us that IQ is only one form of testing for chemical neurotoxicity:

“Intuitively, though it might seem that an IQ test would be an ideal measure [for determining the neurotoxic effects of a chemical], this assumption would be ill founded, because some toxicants could affect only specific functions, such as attention, memory, language, or visuospatial abilities without clear decrements on IQ scores. Furthermore, the exposure dose as well as mixtures of toxicants are important factors that also need to be considered.”  

 

Yazdi et. al. concluded that “neurobehavioural testing is useful for detecting impairment of psychomotor performance and memory that is associated with occupational F exposure.” 

 

I. A neurotoxic substance has been defined as a substance which alters the normal activity of the nervous system in such a way as to cause damage to nervous tissue.  Symptoms of this alteration may appear immediately after exposure or be delayed. The range of symptoms include loss of IQ but also include limb weakness or numbness, loss of memory, vision, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems, sexual dysfunction and pain. 

 

J. Although research on the neurotoxicity of fluoride is robust enough to suspend artificial fluoridation, the research finding harm is in its infancy.  Research will become more refined, focused and demonstrate even higher risk for subpopulations.  An uncertainty factor must be included for safety.   Each day of delay, leaves many at risk.  

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Re: Fluoride - Demand AARP Take Action

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Message 820 of 1,417

Johnny,

 

You desire to end the back and forth because you do not have the decency to apologize for slandering and defaming me to city councils.   If you look at my slides, I gave credit for the photos.  Cosmetic dentistry of a Pedodontist might be malpractice, I am not making that judgment.  But General Dentists do cosmetic dentistry every day.  We could go into details, but your apology is requested.

 

However, whether ingesting fluoride makes teeth harder and less caries prone is a secondary issue to the EXCESS EXPOSURE.   Too many are ingesting too much fluoride.

 

You have not disputed nor have you disagreed with the fundamental issue that 60% of adolescents with various degrees of dental fluorosis is too much.  

 

You have to agree that water fluoridation supplements the fluoride exposure from other sources.  With 60% getting too much fluoride, a cessation of water fluoridation is essential.  

Johnny,

 

The fact is you said you would address your defamation and slander if I responded to the NTP study. I did and will more.  But the "True Fact" is you have not appologized privately or publicly.  If you have, please send me a video or copy of the letter to the Potsdam Village Council.  

 

Bill

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