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Fluoride Causes Diabetes



This brief literature review and bibliography presents evidence that Fluoride, through fluoridation of public drinking water, causes Diabetes as well as injury to existing diabetics.
Fluoride Causes Diabetes A literature review
Geoff Pain March 2015
Fluoride is a low-dose endocrine disruptor. The focus of this brief review and bibliography is the
effect of Fluoride on insulin production, sensitivity and resultant Diabetes. No distinction was made
in searching the literature between Diabetes Insipidus, Type 1 Diabetes Mellitus caused by the
pancreas not producing adequate amounts of insulin, and Type 2 Diabetes Mellitus caused by the
body’s cells becoming less responsive to insulin that is produced.
Previous studies have emphasized the adverse impact of Fluoride on diabetic patients because they
typically consume much larger quantities of water than average humans and have impaired kidney
function leading to higher risk from the diverse toxic effects of Fluoride [see for example Prystupa
2011, NRC 2006, Marier 1977]. It has also been shown that Fluoride toxicity is greater in diabetics
[Banu Priya et al. 1997].
Diabetics suffer impaired glucose tolerance (IGT), hypertension, hyperlipoproteinemia and coronary
disease. They have a higher risk of death from breast cancer [Youlden et al. 2009], pancreatic cancer
[Michaud 2004], uterine cancer [Purdie 2001] and colorectal cancer [Youlden 2008 ]. Diabetics also
suffer reduced bone mass and strength through Fluoride exposure [Dunipace et al. 1996].
Diabetics have a higher incidence of chronic kidney disease which leads to impaired renal clearance
of fluoride [Hanhijarvi 1974], the “vicious cycle”. The Australian Institute of Health and Welfare has
forecast the proportion of diabetics undergoing transplants or dialysis would rise to 64 per cent in
2020 from 45 per cent in 2009 [Henderson 2012].
The total number of Australians being treated for end-stage kidney disease is forecast to rise by up
to 80 per cent to about 4300 in the coming decade.
Diabetic women have a higher risk of premature birth and low birth weight children [Patel 1975].
The immense scale of the Diabetes problem is summarized by the World Health Organization
[Bergman et al. 2013] as follows: “The number of diabetics in the world is expected to increase from
194 million in 2003 to 330 million in 2030 with three of four affected individuals living in developing
countries. The global health expenditure on diabetes alone is expected to rise to US$ 490 billion in
2030 12% of all per capita health-care expenditures [Zhang et al. 2010]. The burden of premature
death from diabetes in developing countries is similar to that of HIV/AIDS, yet the problem is largely
unrecognised in these areas. “
There has been an explosion in the incidence of diabetes in the developed countries over the last 40
years [Bergman et al 2013] which matches the timescale of deliberate fluoridation of public water
supplies in those countries.
There is strong evidence that Fluoride causes Diabetes.
Fluoride directly reduces insulin synthesis in rats [Lin et al. 1976]. Microcirculatory defects, increased
capillary permeability and altered protein biosynthesis in the pancreas is associated with Fluoride
exposure. Because human hormones interact with each other, the known adverse effect of Fluoride
on melatonin production and the knock-on effect on insulin should also be considered [Rasmussen
et al. 1999]. The fact that Fluoride causes hypothyroidism also exacerbates the damage to diabetics
through reduction of peripheral glucose metabolism [Cettour-Rose 2005].
A genetically inherited condition demonstrates an association between pineal gland hyperplasia and
insulin resistance [West et al. 1980].
Blood fluoride level of just 234 ppb after a single acute exposure caused significant impairment in
glucose metabolism, as evident by sharp rises in blood glucose and decreases in insulin [Whitford
1987]. Similar results have been measured in rats and human volunteers [Rigalli et al. 1990, Suketa
1985 ].
Short-term acute exposures to high levels of fluoride generated by metabolism of the fluorinated
anesthetic methoxylflurane impairs the kidney’s ability to concentrate urine and produces a diabetes
insipidus-like condition marked by excessive urination [Mazze 1977].
Pancreas pathological morphometry analysis via β cells [Hu et al. 2012] of rats exposed to Fluoride
showed increased islet size. The same rats exhibited increased alkaline phosphatise and osteocalcin,
increase of serum insulin level and a general decrease of glucagon level.
Rats with Fluoride induced diabetes that were encouraged to exercise demonstrated accelerated
skeletal fluorosis [Lombarte 2013]. Diabetic rats also show enhanced contractile responses of
arteries to sodium fluoride which directly stimulates GTP-binding proteins (G-proteins) [Weber
Insulin resistance in humans caused by chronic Fluoride exposure from drinking water is well known
[Bergman et al. 2013, Vandenberg et al. 2012, Chiba et al. 2012, Menoya et al. 2008, Stephen 1994,
Trivedi et al. 1993].
In chronic exposures, effects on glucose metabolism occurred when plasma fluoride concentrations
exceeded 0.1 mg/L (5 µmol/L) [Rigalli et al. 1992, 1995], or just one 15th the concentration allowed in
Australian drinking water. The US National Research Council [2006] stated “In general, impaired
glucose metabolism appears to be associated with serum or plasma fluoride concentrations of about
0.1 mg/L or greater in both animals and humans.
Townsville in the state of Queensland, Australia, fluoridated since 1964, suffers 10% higher rate of
diabetes than the rest of non-fluoridated Queensland [PHIDU 2005]. Townsville also suffers higher
rates of hospital admissions for unspecified dental conditions as well as asthma, congestive heart
failure, convulsions and epilepsy, congestive obstructive pulmonary disease, ear nose and throat
conditions and pyelonephritis. Townsville also suffers increased death rates due to circulatory
system, ischaemic heart disease, cerebrovascular disease Stroke, chronic lower respiratory disease
and cancer of the trachea [Queensland Hospital Data 2005-2006]. Townsville can therefore be
considered a randomised control trial centre for Fluoride toxicology.
Workers in the phosphate fertilizer industry are exposed to Fluoride and experience higher incidence
of diabetes as well as skeletal fluorosis [Renke 1987].
Workers in the cryolite industry also suffer Chronic Fluoride Intoxication (CFI) and have lower insulin
and increased C-peptide serum levels [Tokar 1992]. It was shown that the incidence of diabetes
increased with years of exposure. The observed lower serum insulin levels in Fluoride intoxication
might be due to associated liver damage [Tokar 1992]. Liver damage has also been observed by
Vasant and Narasimhacharya [2013a] who state “Exposure to fluoride through drinking water not
only significantly increased plasma glucose and lipid profiles, but also elevated both hepatic and
renal lipid peroxidation, hepatic lipid profiles and G-6-Pase activity with a reduction in plasma HDL-C,
hepatic glycogen content, hexokinase activity and antioxidant status”.
Fluoride induced hyperglycemia has been stated to be mainly due to increased hepatic
glycogenolysis [Varadacharyulu et al. 1997]. Rabbits fed 16 mg of Fluoride per day exhibited
hyperglycemia as well as reduction of bone strength through fluorosis [Turner 1997].
People exposed to high Fluoride levels in their drinking water suffer a high incidence of skeletal
fluorosis. As demonstrated by Xie et al. [2000] they exhibit a higher and longer lasting blood glucose
level after an oral glucose tolerance test (OGTT). Those with diagnosed skeletal fluorosis
demonstrate high levels of serum insulin.
Diabetics are exposed to an acceleration of their disease due to water fluoridation. They typically
drink much larger volumes of water [Prystupa 2011] and accumulate more Fluoride.
The mechanisms by which Fluoride induces diabetes most likely include antagonism to calcium and
magnesium centred biochemistry [De Valk 1999]. Insulin secretion (both basal and glucose-
stimulated) by isolated islets of Langerhans in vitro is inhibited as a function of fluoride
concentrations [Rigalli et al. 1990, 1995].
Diabetics are more susceptible to Fluoride induced arterial contraction [Hattori et al. 2000]
increasing risk of cardiovascular disease.
Fluoride induced diabetes will also cause damage to the periodontum and tooth loss [AHMAC 2001].
Diabetics are a “Sensitive Subpopulation” or “Vulnerable Group” and no attempt has been made by
Australian health authorities to warn diabetics about Fluoride toxicity or protect them from harmful
I am grateful to Professor Paul Connett and the Fluoride Action Network whose online database
facilitated identification of relevant studies. See
Note: Those marked * were deliberately excluded from the NMRC 2007 Review.
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... This is an issue of interest in the context of the effects of fluorine compounds on glucose metabolism. Studies in both humans and animals have shown that excessive fluoride intake alters blood glucose levels by affecting the regulation of metabolic pathways and release of hormones involved in carbohydrate metabolism [226]. A population-based study on the consumption of fluoridated tap water showed that additional fluoridation of tap water (0.7-1.2 ppm) was associated with an increase in the incidence and prevalence of diabetes from 2005 to 2010 in the United States [227]. ...
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The purpose of this review is to attempt to outline the potential role of fluoride in the pathogenesis of brain tumours, including glioblastoma (GBM). In this paper, we show for the first time that fluoride can potentially affect the generally accepted signalling pathways implicated in the formation and clinical course of GBM. Fluorine compounds easily cross the blood–brain barrier. Enhanced oxidative stress, disruption of multiple cellular pathways, and microglial activation are just a few examples of recent reports on the role of fluoride in the central nervous system (CNS). We sought to present the key mechanisms underlying the development and invasiveness of GBM, as well as evidence on the current state of knowledge about the pleiotropic, direct, or indirect involvement of fluoride in the regulation of these mechanisms in various tissues, including neural and tumour tissue. The effects of fluoride on the human body are still a matter of controversy. However, given the growing incidence of brain tumours, especially in children, and numerous reports on the effects of fluoride on the CNS, it is worth taking a closer look at these mechanisms in the context of brain tumours, including gliomas.
... Fluoride causes diabetes by reducing insulin production and insulin receptor function as reviewed previously [Pain 2015b]. Diabetes is the leading cause of kidney failure, accounting for 44% of all new cases of kidney failure in the USA in [NIDDK 2008. ...
Technical Report
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Fluoride causes excess suffering and death by initiating and exacerbating kidney disease, which in turn causes a cascade of secondary, often fatal, diseases. This review demonstrates that proponents of water Fluoridation have attempted to suppress evidence of harm to the population at large and especially vulnerable groups with impaired renal function.
... There is clear evidence that Fluoride causes Diabetes [Pain 2015d]. Diabetics are at increased risk of Fluoride toxicity and cardiovascular disease [Hattori 2000]. ...
Technical Report
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Fluoride uptake in coronary arteries is associated with an increased cardiovascular risk of sudden death. Fluoride causes enhanced deposition of doped Hydroxyapatite which leads to inflammation and sites for fatty deposits of atherosclerosis. Fluoride interferes with numerous enzyme systems resulting in elevation of key risk factors for cardiovascular disease. Fluoride causes oxidative stress and degeneration of heart muscle. Fluoride inhibits Thyroid function with consequential damage to heart function. Fluoride increases risk of sudden death from ruptured aorta. Diabetes, caused or exacerbated by Fluoride, further increases risk of cardiovascular death and disability.
... One of the most significant findings against Fluoride is the discovery that hydroxyapatite enhances the mitogenesis of mammary cells, amplifying the malignant process and resulting in accelerated tumor growth [Wilson 2014]. Recently Fluoride, delivered by mandated fluoridation, has been linked to Hypothyroidism [Peckham 2015], Diabetes and Obesity [Vandenberg 2012, Pain 2015b], Pre-term Birth and Impaired Neurodevelopment [McArthur 2015] and Attention Deficit Hyperactivity Disorder (ADHD) [Malin 2015]. ...
Technical Report
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Fluoride, Asbestos, Uranium, Lead and Tobacco (FAULT) are multibillion dollar industries that have caused immeasurable harm to humans who have recently discovered that decades of propaganda claims that the products are “safe and effective” are demonstrably false. Each of these industries has a history of denial of harm, suppression of evidence, attempts to avoid litigation and compensation of victims. In a last ditch attempt to retain public drinking water as a conduit for disposal of Fluoride, an industrial waste product, myth-mongers are attempting to promulgate the “Big Lie” that Fluoride is a nutrient.
Technical Report
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Cataract blindness affects tens of millions of people, many of whom will never have access to lens replacement surgery. Fluoride from various sources including drinking water, tea, salt and drugs, enhances and stabilizes crystal growth of Hydroxyapatite within the eye. Fluoride is identified as the major risk for cataract and contributes to risk of other eye diseases including macular degeneration.
Technical Report
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Australia's National Health and Medical Research Council states that the only harm arising from water Fluoridation and total dietary Fluoride intake is Dental Fluorosis. This guide provides a quick reference to harms known by toxicologists to be caused by Fluoride, including those still under intensive research and recognized by other administrations.
Technical Report
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Fluoride is a developmental neurotoxin that has been linked to human brain damage since the 1920s when Fluoride induced cretinism was investigated and confirmed with animal studies. With advances in imaging, chemical analytical techniques including proteomics, detailed molecular mechanisms of Fluoride damage to the brain, spinal cord and nerve networks have been investigated with ever increasing levels of detail. The current peer-reviewed scientific publication rate regarding Fluoride neurotoxicity is about one paper per week. This literature guide provides a snapshot of the science as easily obtained in early 2017, to help inform those interested in the depth of knowledge and where the ongoing studies are directed.
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The aim of this study was to determine if streptozotocin-induced diabetes in rats as a model for Type-1 human diabetes causes changes in the levels of fluoride (F) and biogenic elements in the bones and serum in the initial stage of the disease. Twenty-two female Wistar rats were given streptozotocin to induce diabetes; after 10 days the femoral bones and blood were collected for determination of F by potentiometric analysis, Ca and Mg by atomic absorption spectrometry, and estradiol by electroluminescence. At various levels of significance, F, Ca, and Mg increased in the bones. In the serum, F decreased, but Ca, Mg, and estradiol increased. The results indicate that diabetes in the early stages affects uptake of F, Ca, and Mg intake into the bones, which may result in defective crystal formation and an increase of amorphous mineral structure in the bone.
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Forty seven-week-old male castrated Wistar rats were randomly divided evenly into a control group and a fluoride (F) group. The latter was given a single dose of NaF from a solution containing 1.0 mg F ion/kg bw, administered by gavage. After 30 min, the following experiments were performed: intravenous insulin tolerance test (0.75 U/kg bw) and determination of the insulin receptor substrate (pp 185-IRS-1/IRS/2) tyrosine phosphorylation status. The acute treatment with NaF promoted increased blood glycemia, but there were no significant changes in the insulin sensitivity and in the pp185 tyrosine phosphorylation status in the muscular or in the white adipose tissues.
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With half the animals as controls without fluoride (F) in their drinking water, 16 of 32 seven-week-old castrated male Wistar rats were administered NaF in their drinking water and F contained in food pellets (estimated total F intake: 4.0 mg F/kg bw/day). After 42 days, determinations were made of the insulin receptor substrate (pp185-IRS-1/IRS/2), tyrosine phosphorylation status, and the extent of glycemia and insulinemia. This chronic treatment with F promoted: 1) decrease in the pp185 tyrosine phosphorylation status in the muscle tissue but not in the liver; 2) increase in the plasma F level; 3) no alteration in glycemia and insulinemia; 4) an increase in insulin resistance.
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The incidence of type 1 diabetes has increased substantially in Finland, but the exact trigger for the onset of T1D is still unknown. We know that use of amoxicillin and anti-cariogenic fluoride tablets is a common practice for children in Finland. It seems that beta-cell destruction is initiated by modification of the proinsulin by combined effects of fluoride (F2) and amoxicillin. Amoxicillin especially when used together with clavulanic acid results in an acid environment around the beta cells that promotes the conversion of F2 to hydrogen fluoride (HF). Unlike F2, HF can diffuse easily into the beta cell cytosol. Because the cytosol has a neutral pH, virtually all HF reverts to F2 in the cytosol and F2 cannot easily diffuse out of the cell. Exposure to excess F2 promotes proinsulin covalent dimerization and simultaneously hyperexpression of MHC Class I molecules. Proinsulin dimers then migrate to the cell membrane with MHC class I molecules, accumulate at the beta-cell membrane and produces a powerful immunogenic stimulus for the cytotoxic T-cells. Production of cytotoxic cytokines from the infiltrating T cells initiates the destruction of beta cells. In Finnish children, this might be helped along by a higher beta-cell activity and by a reactive thymus-dependent immune system induced by higher levels of thyroid hormones and calcitonin respectively. After repeated similar attacks, more and more effector T cells are raised and more and more beta cells are destroyed, and clinical diabetes occurs.
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: Wistar rats were given 20 ppm fluoride in drinking water, or single administration of 115 mg/kg alloxan i.m. to induce diabetes, or single administra-tion of 115 mg/kg alloxan i.m. followed by 20 ppm fluoride for 31 days. Blood sugar level increased in rats given alloxan and alloxan + fluoride. Body weight gain in rats given alloxan + fluoride decreased significantly compared to other groups. Decrease in hemoglobin and glutamic oxaloacetate transaminase (GOT) was seen only in rats given alloxan + fluoride. In this group alkaline phospha-tase, the target enzyme in fluoride toxicosis, increased considerably. The toxicity of fluoride in diabetic rats was further reflected in organ weight data. This investigation shows that fluoride toxicity is greater in diabetic rats.
Fluoride is known to cause both local and systemic alterations in animals and humans, such as dental fluorosis and disturbances in glucose homeostasis. The effects of fluoride are dose dependent and can produce decreased insulin secretion, inhibition of glycolysis, glycogen depletion, hyperglycemia, and insulin resistance. Because excessive ingestion of fluoride during tooth brushing can lead to deterioration in health, the use of low-fluoride dentifrices is recommended for young children with diabetes.
The aim of this study was to determine how metabolic and functional changes in diabetes affect the fluoride intake, distribution, and concentration in bone tissue; and whether alterations in fluoride metabolism in diabetes may influence the severity of the disorder. Two groups of rats received 0 (C) or 10 ppm (F10) fluoride via drinking water for three weeks, ad libitum. Two other groups were treated with a single dose of streptozotocin to induce diabetes, and also received 0 (D) or 10 ppm fluoride (DF10). The quantity of fluoride consumed via water by the DF10 animals was calculated daily and an equal amount was added to the drinking water of another group of non-diabetic animals (FF). In the diabetic group (DF10) the intake of fluoride gradually increased, hyperglycemia was more severe, and renal hypertrophy was expressed less than in the diabetic group (D) which consumed deionized water. The femoral fluoride concentration increased in proportion to fluoride intake. The high fluoride intake of FF animals resulted, when compared to DF10 ones, in a further increase in the bone tissue and in relatively less elevation in plasma fluoride concentrations. It is concluded that (i) fluoride supply via drinking water may enhance the severity of diabetes in rats, and (ii) due to diabetic metabolic and functional imbalance, the fluoride metabolism may also change.
Fluorosis is a major health problem in many parts of the world. The present work focuses on investigating the utility of nutrient and antioxidant rich grains- ragi, jowar, bajra, maize in formulation of basal, high carbohydrate low protein and low carbohydrate high protein diets in mitigating fluoride toxicity. Exposure to fluoride through drinking water not only significantly increased plasma glucose and lipid profiles, but also elevated both hepatic and renal lipid peroxidation, hepatic lipid profiles and G-6-Pase activity with a reduction in plasma HDL-C, hepatic glycogen content, hexokinase activity and antioxidant status. Even though basal and high carbohydrate diets did not significantly alter plasma glucose, lipid profiles in fluoride administered animals, protein enriched multigrain diet significantly decreased plasma glucose and lipid levels. However, the multigrain basal and high carbohydrate diets influenced the hepatic glycogen, lipid profiles, hexokinase and G-6-Pase activities, hepatic and renal lipid peroxidation and antioxidant status though not as significantly as that of multigrain diet enriched with protein. Thus the results of the present study indicate that both a multigrain diet rich in nutrients and antioxidants, and fortified with protein is useful in mitigating the fluoride toxicity.
A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure.