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Abstract

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
1996].
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
exposure.
Acknowledgment
I am grateful to Professor Paul Connett and the Fluoride Action Network whose online database
facilitated identification of relevant studies. See FluorideAlert.org
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... 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. ...
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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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